Detecting melanoma early, when it is easier to treat, remains a “paramount goal,” but guidelines surrounding optimal melanoma screening practices and diagnostic evaluations need greater clarity, according to the authors of a new consensus statement.

That is why a group of expert panelists evaluated the existing evidence and a range of clinical scenarios to help clarify the optimal strategies for early detection and assessment of cutaneous melanoma.

Overall, the panelists agreed that a risk-stratified approach is likely the most appropriate strategy for melanoma screening and follow-up and supported the use of visual and dermoscopic examination. However, the panelists did not reach consensus on the role for gene expression profile (GEP) testing in clinical decision-making, citing the need for these assays to be validated in large randomized clinical trials.

In an accompanying editorial, two experts highlighted the importance of carefully evaluating the role of diagnostic tests.

“Diagnostic tests such as GEP must face critical scrutiny; if not, there are immediate concerns for patient care, such as the patient being erroneously informed that they do not have cancer or told that they do have cancer when they do not,” write Alan C. Geller, MPH, RN, from the Harvard T.H. Chan School of Public Health, Boston, and Marvin A. Weinstock, MD, PhD, from Brown University, Providence, R.I.

The consensus statement was published online in JAMA Dermatology.
 

The need for guidance

Although focusing melanoma screening on higher-risk populations may be cost effective, compared with population-based screening, the major guidelines lack consistent guidance to support a risk-stratified approach to skin cancer screening and best practices on diagnosing cutaneous melanoma.

In the prebiopsy setting, the appropriate use of diagnostic tools for evaluating the need for biopsy remain poorly defined, and, in the post-biopsy setting, questions remain concerning the diagnostic accuracy of molecular techniques, diagnostic GEP testing, next-generation sequencing, and immunohistochemical assessment for various markers of melanoma.

To provide consensus recommendations on optimal screening practices, prebiopsy and postbiopsy diagnostics, and prognostic assessment of cutaneous melanoma, a group of 42 panelists voted on hypothetical scenarios via an emailed survey. The panel then came together for a consensus conference, which included 51 experts who discussed their approach to the various clinical case scenarios. Most attendees (45 of the 51) answered a follow-up survey for their final recommendations.

The panelists reached a consensus, with 70% agreement, to support a risk-stratified approach to melanoma screening in clinical settings and public screening events. The experts agreed that higher-risk individuals (those with a relative risk of 5 or greater) could be appropriately screened by a general dermatologist or pigmented lesion evaluation. Higher-risk individuals included those with severe skin damage from the sun, systemic immunosuppression, or a personal history of nonmelanoma or melanoma skin cancer.

Panelists agreed that those at general or lower risk (RR < 2) could be screened by a primary care provider or through regular self- or partner examinations, whereas those at moderate risk could be screened by their primary care clinician or general dermatologist. The experts observed “a shift in acceptance” of primary care physicians screening the general population, and an acknowledgement of the importance of self- and partner examinations as screening adjuncts for all populations.

In the prebiopsy setting, panelists reached consensus that visual and dermoscopic examination was appropriate for evaluating patients with “no new, changing, or unusual skin lesions or with a new lesion that is not visually concerning.”

The panelists also reached consensus that lesions deemed clinically suspicious for cancer or showing features of cancer on reflectance confocal microscopy should be biopsied. Although most respondents (86%) did not currently use epidermal tape stripping routinely, they agreed that, in a hypothetical situation where epidermal tape stripping was used, that lesions positive for PRAME or LINC should be biopsied.

In the postbiopsy setting, views on the use of GEP scores varied. Although panelists agreed that a low-risk prognostic GEP score should not outweigh concerning histologic features when patients are selected to undergo sentinel lymph node biopsy (SLNB), they did not reach consensus for imaging recommendations in the setting of a high-risk prognostic GEP score and low-risk histology and/or negative nodal status.

“The panelists await future, well-designed prospective studies to determine if use of these and newer technologies improves the care of patients with melanoma,” the panelists write.

In the editorial, Mr. Geller and Dr. Weinstock highlighted concerns about the cost and potential access issues associated with these newer technologies, given that the current cost of GEP testing exceeds $7,000.

The editorialists also emphasize that “going forward, the field should be advanced by tackling one of the more pressing, common, potentially morbid, and costly procedures – the prognostic use of sentinel lymph node biopsy.”

Of critical importance is “whether GEP can reduce morbidity and cost by safely reducing the number of SLNBs performed,” Mr. Geller and Dr. Weinstock write.

The funding for the administration and facilitation of the consensus development conference and the development of the manuscript was provided by Dermtech, in an unrestricted award overseen by the Melanoma Research Foundation and managed and executed at UPMC by the principal investigator. Several of the coauthors disclosed relationships with industry. Mr. Geller is a contributor to UptoDate for which he receives royalties. Dr. Weinstock receives consulting fees from AbbVie.

A version of this article first appeared on Medscape.com.

Detecting melanoma early, when it is easier to treat, remains a “paramount goal,” but guidelines surrounding optimal melanoma screening practices and diagnostic evaluations need greater clarity, according to the authors of a new consensus statement.

That is why a group of expert panelists evaluated the existing evidence and a range of clinical scenarios to help clarify the optimal strategies for early detection and assessment of cutaneous melanoma.

Overall, the panelists agreed that a risk-stratified approach is likely the most appropriate strategy for melanoma screening and follow-up and supported the use of visual and dermoscopic examination. However, the panelists did not reach consensus on the role for gene expression profile (GEP) testing in clinical decision-making, citing the need for these assays to be validated in large randomized clinical trials.

In an accompanying editorial, two experts highlighted the importance of carefully evaluating the role of diagnostic tests.

“Diagnostic tests such as GEP must face critical scrutiny; if not, there are immediate concerns for patient care, such as the patient being erroneously informed that they do not have cancer or told that they do have cancer when they do not,” write Alan C. Geller, MPH, RN, from the Harvard T.H. Chan School of Public Health, Boston, and Marvin A. Weinstock, MD, PhD, from Brown University, Providence, R.I.

The consensus statement was published online in JAMA Dermatology.
 

The need for guidance

Although focusing melanoma screening on higher-risk populations may be cost effective, compared with population-based screening, the major guidelines lack consistent guidance to support a risk-stratified approach to skin cancer screening and best practices on diagnosing cutaneous melanoma.

In the prebiopsy setting, the appropriate use of diagnostic tools for evaluating the need for biopsy remain poorly defined, and, in the post-biopsy setting, questions remain concerning the diagnostic accuracy of molecular techniques, diagnostic GEP testing, next-generation sequencing, and immunohistochemical assessment for various markers of melanoma.

To provide consensus recommendations on optimal screening practices, prebiopsy and postbiopsy diagnostics, and prognostic assessment of cutaneous melanoma, a group of 42 panelists voted on hypothetical scenarios via an emailed survey. The panel then came together for a consensus conference, which included 51 experts who discussed their approach to the various clinical case scenarios. Most attendees (45 of the 51) answered a follow-up survey for their final recommendations.

The panelists reached a consensus, with 70% agreement, to support a risk-stratified approach to melanoma screening in clinical settings and public screening events. The experts agreed that higher-risk individuals (those with a relative risk of 5 or greater) could be appropriately screened by a general dermatologist or pigmented lesion evaluation. Higher-risk individuals included those with severe skin damage from the sun, systemic immunosuppression, or a personal history of nonmelanoma or melanoma skin cancer.

Panelists agreed that those at general or lower risk (RR < 2) could be screened by a primary care provider or through regular self- or partner examinations, whereas those at moderate risk could be screened by their primary care clinician or general dermatologist. The experts observed “a shift in acceptance” of primary care physicians screening the general population, and an acknowledgement of the importance of self- and partner examinations as screening adjuncts for all populations.

In the prebiopsy setting, panelists reached consensus that visual and dermoscopic examination was appropriate for evaluating patients with “no new, changing, or unusual skin lesions or with a new lesion that is not visually concerning.”

The panelists also reached consensus that lesions deemed clinically suspicious for cancer or showing features of cancer on reflectance confocal microscopy should be biopsied. Although most respondents (86%) did not currently use epidermal tape stripping routinely, they agreed that, in a hypothetical situation where epidermal tape stripping was used, that lesions positive for PRAME or LINC should be biopsied.

In the postbiopsy setting, views on the use of GEP scores varied. Although panelists agreed that a low-risk prognostic GEP score should not outweigh concerning histologic features when patients are selected to undergo sentinel lymph node biopsy (SLNB), they did not reach consensus for imaging recommendations in the setting of a high-risk prognostic GEP score and low-risk histology and/or negative nodal status.

“The panelists await future, well-designed prospective studies to determine if use of these and newer technologies improves the care of patients with melanoma,” the panelists write.

In the editorial, Mr. Geller and Dr. Weinstock highlighted concerns about the cost and potential access issues associated with these newer technologies, given that the current cost of GEP testing exceeds $7,000.

The editorialists also emphasize that “going forward, the field should be advanced by tackling one of the more pressing, common, potentially morbid, and costly procedures – the prognostic use of sentinel lymph node biopsy.”

Of critical importance is “whether GEP can reduce morbidity and cost by safely reducing the number of SLNBs performed,” Mr. Geller and Dr. Weinstock write.

The funding for the administration and facilitation of the consensus development conference and the development of the manuscript was provided by Dermtech, in an unrestricted award overseen by the Melanoma Research Foundation and managed and executed at UPMC by the principal investigator. Several of the coauthors disclosed relationships with industry. Mr. Geller is a contributor to UptoDate for which he receives royalties. Dr. Weinstock receives consulting fees from AbbVie.

A version of this article first appeared on Medscape.com.

Detecting melanoma early, when it is easier to treat, remains a “paramount goal,” but guidelines surrounding optimal melanoma screening practices and diagnostic evaluations need greater clarity, according to the authors of a new consensus statement.

That is why a group of expert panelists evaluated the existing evidence and a range of clinical scenarios to help clarify the optimal strategies for early detection and assessment of cutaneous melanoma.

Overall, the panelists agreed that a risk-stratified approach is likely the most appropriate strategy for melanoma screening and follow-up and supported the use of visual and dermoscopic examination. However, the panelists did not reach consensus on the role for gene expression profile (GEP) testing in clinical decision-making, citing the need for these assays to be validated in large randomized clinical trials.

In an accompanying editorial, two experts highlighted the importance of carefully evaluating the role of diagnostic tests.

“Diagnostic tests such as GEP must face critical scrutiny; if not, there are immediate concerns for patient care, such as the patient being erroneously informed that they do not have cancer or told that they do have cancer when they do not,” write Alan C. Geller, MPH, RN, from the Harvard T.H. Chan School of Public Health, Boston, and Marvin A. Weinstock, MD, PhD, from Brown University, Providence, R.I.

The consensus statement was published online in JAMA Dermatology.
 

The need for guidance

Although focusing melanoma screening on higher-risk populations may be cost effective, compared with population-based screening, the major guidelines lack consistent guidance to support a risk-stratified approach to skin cancer screening and best practices on diagnosing cutaneous melanoma.

In the prebiopsy setting, the appropriate use of diagnostic tools for evaluating the need for biopsy remain poorly defined, and, in the post-biopsy setting, questions remain concerning the diagnostic accuracy of molecular techniques, diagnostic GEP testing, next-generation sequencing, and immunohistochemical assessment for various markers of melanoma.

To provide consensus recommendations on optimal screening practices, prebiopsy and postbiopsy diagnostics, and prognostic assessment of cutaneous melanoma, a group of 42 panelists voted on hypothetical scenarios via an emailed survey. The panel then came together for a consensus conference, which included 51 experts who discussed their approach to the various clinical case scenarios. Most attendees (45 of the 51) answered a follow-up survey for their final recommendations.

The panelists reached a consensus, with 70% agreement, to support a risk-stratified approach to melanoma screening in clinical settings and public screening events. The experts agreed that higher-risk individuals (those with a relative risk of 5 or greater) could be appropriately screened by a general dermatologist or pigmented lesion evaluation. Higher-risk individuals included those with severe skin damage from the sun, systemic immunosuppression, or a personal history of nonmelanoma or melanoma skin cancer.

Panelists agreed that those at general or lower risk (RR < 2) could be screened by a primary care provider or through regular self- or partner examinations, whereas those at moderate risk could be screened by their primary care clinician or general dermatologist. The experts observed “a shift in acceptance” of primary care physicians screening the general population, and an acknowledgement of the importance of self- and partner examinations as screening adjuncts for all populations.

In the prebiopsy setting, panelists reached consensus that visual and dermoscopic examination was appropriate for evaluating patients with “no new, changing, or unusual skin lesions or with a new lesion that is not visually concerning.”

The panelists also reached consensus that lesions deemed clinically suspicious for cancer or showing features of cancer on reflectance confocal microscopy should be biopsied. Although most respondents (86%) did not currently use epidermal tape stripping routinely, they agreed that, in a hypothetical situation where epidermal tape stripping was used, that lesions positive for PRAME or LINC should be biopsied.

In the postbiopsy setting, views on the use of GEP scores varied. Although panelists agreed that a low-risk prognostic GEP score should not outweigh concerning histologic features when patients are selected to undergo sentinel lymph node biopsy (SLNB), they did not reach consensus for imaging recommendations in the setting of a high-risk prognostic GEP score and low-risk histology and/or negative nodal status.

“The panelists await future, well-designed prospective studies to determine if use of these and newer technologies improves the care of patients with melanoma,” the panelists write.

In the editorial, Mr. Geller and Dr. Weinstock highlighted concerns about the cost and potential access issues associated with these newer technologies, given that the current cost of GEP testing exceeds $7,000.

The editorialists also emphasize that “going forward, the field should be advanced by tackling one of the more pressing, common, potentially morbid, and costly procedures – the prognostic use of sentinel lymph node biopsy.”

Of critical importance is “whether GEP can reduce morbidity and cost by safely reducing the number of SLNBs performed,” Mr. Geller and Dr. Weinstock write.

The funding for the administration and facilitation of the consensus development conference and the development of the manuscript was provided by Dermtech, in an unrestricted award overseen by the Melanoma Research Foundation and managed and executed at UPMC by the principal investigator. Several of the coauthors disclosed relationships with industry. Mr. Geller is a contributor to UptoDate for which he receives royalties. Dr. Weinstock receives consulting fees from AbbVie.

A version of this article first appeared on Medscape.com.

A few years ago, my partner emailed me about a consult.
 

“Dr. Carter, I had the pleasure of seeing Mrs. Smith today for a preconception consult for chronic hypertension. As a high-risk Black woman, she wants to know what we’re going to do to make sure that she doesn’t die in pregnancy or childbirth. I told her that you’re better equipped to answer this question.”

I was early in my career, and the only thing I could assume that equipped me to answer this question over my partners was my identity as a Black woman living in America.

Mrs. Smith was copied on the message and replied with a long list of follow-up questions and a request for an in-person meeting with me. I was conflicted. As a friend, daughter, and mother, I understood her fear and wanted to be there for her. As a newly appointed assistant professor on the tenure track with 20% clinical time, my clinical responsibilities easily exceeded 50% (in part, because I failed to set boundaries). I spent countless hours of uncompensated time serving on diversity, equity, and inclusion initiatives and mentoring and volunteering for multiple community organizations; I was acutely aware that I would be measured against colleagues who rise through the ranks, unencumbered by these social, moral, and ethical responsibilities, collectively known as the “Black tax.”¹

I knew from prior experiences and the tone of Mrs. Smith’s email that it would be a tough, long meeting that would set a precedent of concierge level care that only promised to intensify once she became pregnant. I agonized over my reply. How could I balance providing compassionate care for this patient with my young research program, which I hoped to nurture so that it would one day grow to have population-level impact?

It took me 2 days to finally reply to the message with a kind, but firm, email stating that I would be happy to see her for a follow-up preconception visit. It was my attempt to balance accessibility with boundaries. She did not reply.

Did I fail her?

The fact that I still think of Mrs. Smith may indicate that I did the wrong thing. In fact, writing the first draft of this letter was a therapeutic experience, and I addressed it to Mrs. Smith. As I shared the experience and letter with friends in the field, however, everyone had similar stories. The letter continued to pass between colleagues, who each made it infinitely better. This collective process created the beautiful love letter to Black birthing people that we share here.

We call upon all of our obstetric clinician colleagues to educate themselves to be equally, ethically, and equitably equipped to care for and serve historically marginalized women and birthing people. We hope that this letter will aid in the journey, and we encourage you to share it with patients to open conversations that are too often left closed.

Continue to: Our love letter to Black women and birthing people...

Our love letter to Black women and birthing people

We see you, we hear you, we know you are scared, and we are you. In recent years, the press has amplified gross inequities in maternal care and outcomes that we, as Black birth workers, midwives, and physicians, already knew to be true. We grieve, along with you regarding the recently reported pregnancy-related deaths of Mrs. Kira Johnson,² Dr. Shalon Irving,³ Dr. Chaniece Wallace,⁴ and so many other names we do not know because their stories did not receive national attention, but we know that they represented the best of us, and they are gone too soon. As Black birth workers, midwives, physicians, and more, we have a front-row seat to the United States’ serious obstetric racism, manifested in biased clinical interactions, unjust hospital policies, and an inequitable health care system that leads to disparities in maternal morbidity and mortality for Black women.

Unfortunately, this is not anything new, and the legacy dates back to slavery and the disregard for Black people in this country. What has changed is our increased awareness of these health injustices. This collective consciousness of the risk that is carried with our pregnancies casts a shadow of fear over a period that should be full of the joy and promise of new life. We fear that our personhood will be disregarded, our pain will be ignored, and our voices silenced by a medical system that has sought to dominate our bodies and experiment on them without our permission.⁵ While this history is reprehensible, and our collective risk as Black people is disproportionately high, our purpose in writing this letter is to help Black birthing people recapture the joy and celebration that should be theirs in pregnancy and in the journey to parenthood.

As Black birth workers, we see Black pregnant patients desperately seeking safety, security, and breaking down barriers to find us for their pregnancy care. Often, they are terrified and looking for kinship and community in our offices. In rural areas patients may drive up to 4 hours in distance for an appointment, and during appointments entrust us with their stories of feeling unheard in the medical system. When we anecdotally asked about what they feared about pregnancy, childbirth, and the postpartum period and thought was their risk of dying during pregnancy or childbirth, answers ranged from 1% to 60%. Our actual risk of dying from a pregnancy-related cause, as a Black woman, is 0.0414% (41.4 Black maternal deaths per 100,000 live births).⁶ To put that in perspective, our risk of dying is higher walking down the street or driving a car.⁷

What is the source of the fear? Based on past and present injustices inflicted on people with historically marginalized identities, we have every right to be scared; but, make no mistake that fear comes at a cost, and Black birthing people are the ones paying the bill! Stress and chronic worry are associated with poor pregnancy outcomes, and so this completely justifiable fear, at the population level, is not serving us well personally.⁸ Unfortunately, lost in the messaging about racial inequities in maternal mortality is the reality that the vast majority of Black people and babies will survive, thrive, and have healthy pregnancy outcomes, despite the terrifying population-level statistics and horrific stories of discrimination and neglect that make us feel like our pregnancies and personal peril are synonymous.

While it is true that our absolute individual, personal risk is lower than population-level statistics convey, let us be clear: We are furious about what is happening to Black people! It is immoral that Black patients in the richest country in the world are 3-4 times more likely to die of a pregnancy-related cause than White women,⁹ and we are more likely to experience pregnancy complications and “near misses” when death is narrowly avoided. Research has done an excellent job defining reproductive health disparities in this country, but prioritizing and funding meaningful strategies, policies, and programs to close this gap have not taken precedence—especially initiatives and research that are headed by Black women.^10–12 This is largely because researchers and health care systems continue evaluating strategies that focus on behavior change and narratives that identify individual responsibility as a sole cause of inequity.

Let us be clear, Black people and our behaviors are not the problem.¹³ The problems are White supremacy, classism, sexism, heteropatriarchy, and obstetric racism.^1-21 These must be recognized and addressed across all levels of power. We endorse systems-level changes that are at the root of promoting health equity in our reproductive outcomes. These changes include paid parental leave, Medicaid expansion/extension, reimbursement for doula and lactation services, increased access to perinatal mental health and wellness services, and so much more. (See the Black Mamas Matter Alliance Toolkit: https://blackmamas matter.org/our-work/toolkits/.)

Continue to: Pearls for reassurance...

Pearls for reassurance

While the inequities and their solutions are grounded in the need for systemic change,²² we realize that these population-level solutions feel abstract when our sisters and siblings ask us, “So what can I do to advocate for myself and my baby, right now in this pregnancy?” To be clear, no amount of personal hypervigilance on our part as Black pregnancy-capable people is going to fix these problems, which are systemic; however, we want to provide a few pearls that may be helpful for patient self-advocacy and reassurance:

1. Seek culturally and ethnically congruent care. We intuitively want to find a clinician who looks like us, but sadly, in the United States only 5% of physicians and 2% of midwives are Black. Demand exceeds supply for Black patients who are seeking racially congruent care. Nonetheless, it is critical that you find a physician or midwife who centers you and  provides support and care that affirms the strengths and assets of you, your family, and your community when cultural and ethnic congruency are not possible for you and your pregnancy. 
2. Ask how your clinicians are actively working to ensure optimal and equitable experiences for Black birthing individuals. We recommend asking your clinician and/or hospital what, if anything, they are doing to address health care inequities, obstetric racism, or implicit bias in their pregnancy and postpartum care. Many groups (including some authors of this letter) are working on measures to address obstetric racism. An acknowledgement of initiatives to mitigate inequities is a meaningful first step. You can suggest that they look into it while you explore your options, as this work is rapidly emerging in many areas of the country. 
3. Plan for well-person care. The best time to optimize pregnancy and birth outcomes is before you get pregnant. Set up an appointment with a midwife, ObGyn, or your primary care physician before you get pregnant. Discuss your concerns about pregnancy and use this time to optimize your health. This also provides an opportunity to build a relationship with your physician/ midwife and their group to evaluate whether they curate an environment where you feel seen, heard, and valued when you go for annual exams or problem visits. If you do not get that sense after a couple of visits, find a place where you do. 
4. Advocate for a second opinion. If something does not sound right to you or you have questions that were not adequately answered, it is your prerogative to seek a second opinion; a clinician should never be offended by this. 
5. Consider these factors, for those who deliver in a hospital (by choice or necessity): 

   a. 24/7 access to obstetricians and dedicated anesthesiologists in the hospital

   b. trauma-informed medical/mental health/social services

   c. lactation consultation

   d. supportive trial of labor after cesarean delivery policy

   e. massive blood transfusion  protocol. 

6. Seek doula support! It always helps to have another set of eyes and ears to help advocate for you, especially when you are in pain during pregnancy, childbirth, or in the postpartum period, or are having difficulty advocating for yourself. There is also evidence that women supported by doulas have better pregnancy-related outcomes and experiences.²³ Many major cities in the United States have started to provide race-concordant doula care for Black birthing people  for free.²⁴
7.  Don’t forget about your mental health. As stated, chronic stress from racism impacts birth outcomes. Having a mental health clinician is a great way to mitigate adverse effects of prolonged tension.^25–27
8. Ask your clinician, hospital, or insurance company about participating in group prenatal care and/or nurse home visiting models²⁸ because both are associated with improved birth outcomes.²⁹ Many institutions are implementing group care that provides race-concordant care.^30,31 
9. Ask your clinician, hospital, or local health department for recommendations to a lactation consultant or educator who can support your efforts in breast/ chest/body-feeding. 

We invite you to consider this truth

You, alone, do not carry the entire population-level risk of Black birthing people on your shoulders. We all carry a piece of it. We, along with many allies, advocates, and activists, are outraged and angered by generations of racism and mistreatment of Black birthing people in our health systems and hospitals. We are channeling our frustration and disgust to demand substantive and sustainable change.

Our purpose here is to provide love and reassurance to our sisters and siblings who are going through their pregnancies with thoughts about our nation’s past and present failures to promote health equity for us and our babies. Our purpose is neither to minimize the public health crisis of Black infant and maternal morbidity and mortality nor is it to absolve clinicians, health systems, or governments from taking responsibility for these shameful outcomes or making meaningful changes to address them. In fact, we love taking care of our community by providing the best clinical care we can to our patients. We call upon all of our clinical colleagues to educate themselves to be ethically and equitably equipped to provide health care for Black pregnant patients. Finally, to birthing Black families, please remember this: If you choose to have a baby, the outcome and experience must align with what is right for you and your baby to survive and thrive. So much of the joys of pregnancy have been stolen, but we will recapture the celebration that should be ours in pregnancy and the journey to parenthood.

Sincerely,

Ebony B. Carter, MD, MPH
Maternal Fetal Medicine
Washington University School of Medicine
St. Louis, Missouri

Karen A. Scott, MD, MPH
Birthing Cultural Rigor, LLC
Nashville, Tennessee

Andrea Jackson, MD, MAS
ObGyn
University of California,
San Francisco

Sara Whetstone, MD, MHS
ObGyn
University of California, 
San Francisco

Traci Johnson, MD
ObGyn
University of Missouri 
School of Medicine
Kansas City, Missouri

Sarahn Wheeler, MD
Maternal Fetal Medicine
Duke University School of Medicine
Durham, North Carolina

Asmara Gebre, CNM
Midwife
Zuckerberg San Francisco General Hospital
San Francisco, California

Joia Crear-Perry, MD
ObGyn
National Birth Equity Collaborative
New Orleans, Louisiana

Dineo Khabele, MD
Gynecologic Oncology
Washington University School of Medicine
St. Louis, Missouri

Judette Louis, MD, MPH
Maternal Fetal Medicine
University of South Florida College of Medicine
Tampa, Florida

Yvonne Smith, MSN, RN
Director
Barnes-Jewish Hospital
St. Louis, Missouri

Laura Riley, MD
Maternal Fetal Medicine
Weill Cornell Medicine
New York, New York

Antoinette Liddell, MSN, RN
Care Coordinator
Barnes-Jewish Hospital
St. Louis, Missouri

Cynthia Gyamfi-Bannerman, MD
Maternal Fetal Medicine
Columbia University Irving Medical Center
New York, New York

Rasheda Pippens, MSN, RN
Nurse Educator
Barnes-Jewish Hospital
St. Louis, Missouri

Ayaba Worjoloh-Clemens, MD
ObGyn
Atlanta, Georgia

Allison Bryant, MD, MPH
Maternal Fetal Medicine
Massachusetts General Hospital
Boston, Massachusetts

Sheri L. Foote, CNM
Midwife
Zuckerberg San Francisco General Hospital
San Francisco, California

J. Lindsay Sillas, MD
ObGyn
Bella OB/GYN
Houston, Texas

Cynthia Rogers, MD
Psychiatrist
Washington University School of Medicine
St. Louis, Missouri

Audra R. Meadows, MD, MPH
ObGyn
University of California, San Diego

AeuMuro G. Lake, MD
Urogynecologist
Urogynecology and Healing Arts
Seattle, Washington

Nancy Moore, MSN, RN, WHNP-BC
Nurse Practitioner
Barnes-Jewish Hospital
St. Louis, Missouri

Zoë Julian, MD, MPH
ObGyn
University of Alabama at Birmingham

Janice M. Tinsley, MN, RNC-OB
Zuckerberg San Francisco General Hospital
San Francisco, California

Jamila B. Perritt, MD, MPH
ObGyn
Washington, DC

Joy A. Cooper, MD, MSc
ObGyn
Culture Care
Oakland, California

Arthurine K. Zakama, MD
ObGyn
University of California,San Francisco

Alissa Erogbogbo, MD
OB Hospitalist
Los Altos, California

Sanithia L. Williams, MD
ObGyn
Huntsville, Alabama

Audra Williams, MD, MPH
ObGyn
University of Alabama, Birmingham

Hedwige “Didi” Saint Louis, MD, MPH
OB Hospitalist
Morehouse School of Medicine
Atlanta, Georgia

Cherise Cokley, MD
OB Hospitalist
Community Hospital
Munster, Indiana

J’Leise Sosa, MD, MPH
ObGyn
Buffalo, New York

A few years ago, my partner emailed me about a consult.
 

“Dr. Carter, I had the pleasure of seeing Mrs. Smith today for a preconception consult for chronic hypertension. As a high-risk Black woman, she wants to know what we’re going to do to make sure that she doesn’t die in pregnancy or childbirth. I told her that you’re better equipped to answer this question.”

I was early in my career, and the only thing I could assume that equipped me to answer this question over my partners was my identity as a Black woman living in America.

Mrs. Smith was copied on the message and replied with a long list of follow-up questions and a request for an in-person meeting with me. I was conflicted. As a friend, daughter, and mother, I understood her fear and wanted to be there for her. As a newly appointed assistant professor on the tenure track with 20% clinical time, my clinical responsibilities easily exceeded 50% (in part, because I failed to set boundaries). I spent countless hours of uncompensated time serving on diversity, equity, and inclusion initiatives and mentoring and volunteering for multiple community organizations; I was acutely aware that I would be measured against colleagues who rise through the ranks, unencumbered by these social, moral, and ethical responsibilities, collectively known as the “Black tax.”¹

I knew from prior experiences and the tone of Mrs. Smith’s email that it would be a tough, long meeting that would set a precedent of concierge level care that only promised to intensify once she became pregnant. I agonized over my reply. How could I balance providing compassionate care for this patient with my young research program, which I hoped to nurture so that it would one day grow to have population-level impact?

It took me 2 days to finally reply to the message with a kind, but firm, email stating that I would be happy to see her for a follow-up preconception visit. It was my attempt to balance accessibility with boundaries. She did not reply.

Did I fail her?

The fact that I still think of Mrs. Smith may indicate that I did the wrong thing. In fact, writing the first draft of this letter was a therapeutic experience, and I addressed it to Mrs. Smith. As I shared the experience and letter with friends in the field, however, everyone had similar stories. The letter continued to pass between colleagues, who each made it infinitely better. This collective process created the beautiful love letter to Black birthing people that we share here.

We call upon all of our obstetric clinician colleagues to educate themselves to be equally, ethically, and equitably equipped to care for and serve historically marginalized women and birthing people. We hope that this letter will aid in the journey, and we encourage you to share it with patients to open conversations that are too often left closed.

Continue to: Our love letter to Black women and birthing people...

Our love letter to Black women and birthing people

We see you, we hear you, we know you are scared, and we are you. In recent years, the press has amplified gross inequities in maternal care and outcomes that we, as Black birth workers, midwives, and physicians, already knew to be true. We grieve, along with you regarding the recently reported pregnancy-related deaths of Mrs. Kira Johnson,² Dr. Shalon Irving,³ Dr. Chaniece Wallace,⁴ and so many other names we do not know because their stories did not receive national attention, but we know that they represented the best of us, and they are gone too soon. As Black birth workers, midwives, physicians, and more, we have a front-row seat to the United States’ serious obstetric racism, manifested in biased clinical interactions, unjust hospital policies, and an inequitable health care system that leads to disparities in maternal morbidity and mortality for Black women.

Unfortunately, this is not anything new, and the legacy dates back to slavery and the disregard for Black people in this country. What has changed is our increased awareness of these health injustices. This collective consciousness of the risk that is carried with our pregnancies casts a shadow of fear over a period that should be full of the joy and promise of new life. We fear that our personhood will be disregarded, our pain will be ignored, and our voices silenced by a medical system that has sought to dominate our bodies and experiment on them without our permission.⁵ While this history is reprehensible, and our collective risk as Black people is disproportionately high, our purpose in writing this letter is to help Black birthing people recapture the joy and celebration that should be theirs in pregnancy and in the journey to parenthood.

As Black birth workers, we see Black pregnant patients desperately seeking safety, security, and breaking down barriers to find us for their pregnancy care. Often, they are terrified and looking for kinship and community in our offices. In rural areas patients may drive up to 4 hours in distance for an appointment, and during appointments entrust us with their stories of feeling unheard in the medical system. When we anecdotally asked about what they feared about pregnancy, childbirth, and the postpartum period and thought was their risk of dying during pregnancy or childbirth, answers ranged from 1% to 60%. Our actual risk of dying from a pregnancy-related cause, as a Black woman, is 0.0414% (41.4 Black maternal deaths per 100,000 live births).⁶ To put that in perspective, our risk of dying is higher walking down the street or driving a car.⁷

What is the source of the fear? Based on past and present injustices inflicted on people with historically marginalized identities, we have every right to be scared; but, make no mistake that fear comes at a cost, and Black birthing people are the ones paying the bill! Stress and chronic worry are associated with poor pregnancy outcomes, and so this completely justifiable fear, at the population level, is not serving us well personally.⁸ Unfortunately, lost in the messaging about racial inequities in maternal mortality is the reality that the vast majority of Black people and babies will survive, thrive, and have healthy pregnancy outcomes, despite the terrifying population-level statistics and horrific stories of discrimination and neglect that make us feel like our pregnancies and personal peril are synonymous.

While it is true that our absolute individual, personal risk is lower than population-level statistics convey, let us be clear: We are furious about what is happening to Black people! It is immoral that Black patients in the richest country in the world are 3-4 times more likely to die of a pregnancy-related cause than White women,⁹ and we are more likely to experience pregnancy complications and “near misses” when death is narrowly avoided. Research has done an excellent job defining reproductive health disparities in this country, but prioritizing and funding meaningful strategies, policies, and programs to close this gap have not taken precedence—especially initiatives and research that are headed by Black women.^10–12 This is largely because researchers and health care systems continue evaluating strategies that focus on behavior change and narratives that identify individual responsibility as a sole cause of inequity.

Let us be clear, Black people and our behaviors are not the problem.¹³ The problems are White supremacy, classism, sexism, heteropatriarchy, and obstetric racism.^1-21 These must be recognized and addressed across all levels of power. We endorse systems-level changes that are at the root of promoting health equity in our reproductive outcomes. These changes include paid parental leave, Medicaid expansion/extension, reimbursement for doula and lactation services, increased access to perinatal mental health and wellness services, and so much more. (See the Black Mamas Matter Alliance Toolkit: https://blackmamas matter.org/our-work/toolkits/.)

Continue to: Pearls for reassurance...

Pearls for reassurance

While the inequities and their solutions are grounded in the need for systemic change,²² we realize that these population-level solutions feel abstract when our sisters and siblings ask us, “So what can I do to advocate for myself and my baby, right now in this pregnancy?” To be clear, no amount of personal hypervigilance on our part as Black pregnancy-capable people is going to fix these problems, which are systemic; however, we want to provide a few pearls that may be helpful for patient self-advocacy and reassurance:

1. Seek culturally and ethnically congruent care. We intuitively want to find a clinician who looks like us, but sadly, in the United States only 5% of physicians and 2% of midwives are Black. Demand exceeds supply for Black patients who are seeking racially congruent care. Nonetheless, it is critical that you find a physician or midwife who centers you and  provides support and care that affirms the strengths and assets of you, your family, and your community when cultural and ethnic congruency are not possible for you and your pregnancy. 
2. Ask how your clinicians are actively working to ensure optimal and equitable experiences for Black birthing individuals. We recommend asking your clinician and/or hospital what, if anything, they are doing to address health care inequities, obstetric racism, or implicit bias in their pregnancy and postpartum care. Many groups (including some authors of this letter) are working on measures to address obstetric racism. An acknowledgement of initiatives to mitigate inequities is a meaningful first step. You can suggest that they look into it while you explore your options, as this work is rapidly emerging in many areas of the country. 
3. Plan for well-person care. The best time to optimize pregnancy and birth outcomes is before you get pregnant. Set up an appointment with a midwife, ObGyn, or your primary care physician before you get pregnant. Discuss your concerns about pregnancy and use this time to optimize your health. This also provides an opportunity to build a relationship with your physician/ midwife and their group to evaluate whether they curate an environment where you feel seen, heard, and valued when you go for annual exams or problem visits. If you do not get that sense after a couple of visits, find a place where you do. 
4. Advocate for a second opinion. If something does not sound right to you or you have questions that were not adequately answered, it is your prerogative to seek a second opinion; a clinician should never be offended by this. 
5. Consider these factors, for those who deliver in a hospital (by choice or necessity): 

   a. 24/7 access to obstetricians and dedicated anesthesiologists in the hospital

   b. trauma-informed medical/mental health/social services

   c. lactation consultation

   d. supportive trial of labor after cesarean delivery policy

   e. massive blood transfusion  protocol. 

6. Seek doula support! It always helps to have another set of eyes and ears to help advocate for you, especially when you are in pain during pregnancy, childbirth, or in the postpartum period, or are having difficulty advocating for yourself. There is also evidence that women supported by doulas have better pregnancy-related outcomes and experiences.²³ Many major cities in the United States have started to provide race-concordant doula care for Black birthing people  for free.²⁴
7.  Don’t forget about your mental health. As stated, chronic stress from racism impacts birth outcomes. Having a mental health clinician is a great way to mitigate adverse effects of prolonged tension.^25–27
8. Ask your clinician, hospital, or insurance company about participating in group prenatal care and/or nurse home visiting models²⁸ because both are associated with improved birth outcomes.²⁹ Many institutions are implementing group care that provides race-concordant care.^30,31 
9. Ask your clinician, hospital, or local health department for recommendations to a lactation consultant or educator who can support your efforts in breast/ chest/body-feeding. 

We invite you to consider this truth

You, alone, do not carry the entire population-level risk of Black birthing people on your shoulders. We all carry a piece of it. We, along with many allies, advocates, and activists, are outraged and angered by generations of racism and mistreatment of Black birthing people in our health systems and hospitals. We are channeling our frustration and disgust to demand substantive and sustainable change.

Our purpose here is to provide love and reassurance to our sisters and siblings who are going through their pregnancies with thoughts about our nation’s past and present failures to promote health equity for us and our babies. Our purpose is neither to minimize the public health crisis of Black infant and maternal morbidity and mortality nor is it to absolve clinicians, health systems, or governments from taking responsibility for these shameful outcomes or making meaningful changes to address them. In fact, we love taking care of our community by providing the best clinical care we can to our patients. We call upon all of our clinical colleagues to educate themselves to be ethically and equitably equipped to provide health care for Black pregnant patients. Finally, to birthing Black families, please remember this: If you choose to have a baby, the outcome and experience must align with what is right for you and your baby to survive and thrive. So much of the joys of pregnancy have been stolen, but we will recapture the celebration that should be ours in pregnancy and the journey to parenthood.

Sincerely,

Ebony B. Carter, MD, MPH
Maternal Fetal Medicine
Washington University School of Medicine
St. Louis, Missouri

Karen A. Scott, MD, MPH
Birthing Cultural Rigor, LLC
Nashville, Tennessee

Andrea Jackson, MD, MAS
ObGyn
University of California,
San Francisco

Sara Whetstone, MD, MHS
ObGyn
University of California, 
San Francisco

Traci Johnson, MD
ObGyn
University of Missouri 
School of Medicine
Kansas City, Missouri

Sarahn Wheeler, MD
Maternal Fetal Medicine
Duke University School of Medicine
Durham, North Carolina

Asmara Gebre, CNM
Midwife
Zuckerberg San Francisco General Hospital
San Francisco, California

Joia Crear-Perry, MD
ObGyn
National Birth Equity Collaborative
New Orleans, Louisiana

Dineo Khabele, MD
Gynecologic Oncology
Washington University School of Medicine
St. Louis, Missouri

Judette Louis, MD, MPH
Maternal Fetal Medicine
University of South Florida College of Medicine
Tampa, Florida

Yvonne Smith, MSN, RN
Director
Barnes-Jewish Hospital
St. Louis, Missouri

Laura Riley, MD
Maternal Fetal Medicine
Weill Cornell Medicine
New York, New York

Antoinette Liddell, MSN, RN
Care Coordinator
Barnes-Jewish Hospital
St. Louis, Missouri

Cynthia Gyamfi-Bannerman, MD
Maternal Fetal Medicine
Columbia University Irving Medical Center
New York, New York

Rasheda Pippens, MSN, RN
Nurse Educator
Barnes-Jewish Hospital
St. Louis, Missouri

Ayaba Worjoloh-Clemens, MD
ObGyn
Atlanta, Georgia

Allison Bryant, MD, MPH
Maternal Fetal Medicine
Massachusetts General Hospital
Boston, Massachusetts

Sheri L. Foote, CNM
Midwife
Zuckerberg San Francisco General Hospital
San Francisco, California

J. Lindsay Sillas, MD
ObGyn
Bella OB/GYN
Houston, Texas

Cynthia Rogers, MD
Psychiatrist
Washington University School of Medicine
St. Louis, Missouri

Audra R. Meadows, MD, MPH
ObGyn
University of California, San Diego

AeuMuro G. Lake, MD
Urogynecologist
Urogynecology and Healing Arts
Seattle, Washington

Nancy Moore, MSN, RN, WHNP-BC
Nurse Practitioner
Barnes-Jewish Hospital
St. Louis, Missouri

Zoë Julian, MD, MPH
ObGyn
University of Alabama at Birmingham

Janice M. Tinsley, MN, RNC-OB
Zuckerberg San Francisco General Hospital
San Francisco, California

Jamila B. Perritt, MD, MPH
ObGyn
Washington, DC

Joy A. Cooper, MD, MSc
ObGyn
Culture Care
Oakland, California

Arthurine K. Zakama, MD
ObGyn
University of California,San Francisco

Alissa Erogbogbo, MD
OB Hospitalist
Los Altos, California

Sanithia L. Williams, MD
ObGyn
Huntsville, Alabama

Audra Williams, MD, MPH
ObGyn
University of Alabama, Birmingham

Hedwige “Didi” Saint Louis, MD, MPH
OB Hospitalist
Morehouse School of Medicine
Atlanta, Georgia

Cherise Cokley, MD
OB Hospitalist
Community Hospital
Munster, Indiana

J’Leise Sosa, MD, MPH
ObGyn
Buffalo, New York

A few years ago, my partner emailed me about a consult.
 

“Dr. Carter, I had the pleasure of seeing Mrs. Smith today for a preconception consult for chronic hypertension. As a high-risk Black woman, she wants to know what we’re going to do to make sure that she doesn’t die in pregnancy or childbirth. I told her that you’re better equipped to answer this question.”

I was early in my career, and the only thing I could assume that equipped me to answer this question over my partners was my identity as a Black woman living in America.

Mrs. Smith was copied on the message and replied with a long list of follow-up questions and a request for an in-person meeting with me. I was conflicted. As a friend, daughter, and mother, I understood her fear and wanted to be there for her. As a newly appointed assistant professor on the tenure track with 20% clinical time, my clinical responsibilities easily exceeded 50% (in part, because I failed to set boundaries). I spent countless hours of uncompensated time serving on diversity, equity, and inclusion initiatives and mentoring and volunteering for multiple community organizations; I was acutely aware that I would be measured against colleagues who rise through the ranks, unencumbered by these social, moral, and ethical responsibilities, collectively known as the “Black tax.”¹

I knew from prior experiences and the tone of Mrs. Smith’s email that it would be a tough, long meeting that would set a precedent of concierge level care that only promised to intensify once she became pregnant. I agonized over my reply. How could I balance providing compassionate care for this patient with my young research program, which I hoped to nurture so that it would one day grow to have population-level impact?

It took me 2 days to finally reply to the message with a kind, but firm, email stating that I would be happy to see her for a follow-up preconception visit. It was my attempt to balance accessibility with boundaries. She did not reply.

Did I fail her?

The fact that I still think of Mrs. Smith may indicate that I did the wrong thing. In fact, writing the first draft of this letter was a therapeutic experience, and I addressed it to Mrs. Smith. As I shared the experience and letter with friends in the field, however, everyone had similar stories. The letter continued to pass between colleagues, who each made it infinitely better. This collective process created the beautiful love letter to Black birthing people that we share here.

We call upon all of our obstetric clinician colleagues to educate themselves to be equally, ethically, and equitably equipped to care for and serve historically marginalized women and birthing people. We hope that this letter will aid in the journey, and we encourage you to share it with patients to open conversations that are too often left closed.

Continue to: Our love letter to Black women and birthing people...

Our love letter to Black women and birthing people

We see you, we hear you, we know you are scared, and we are you. In recent years, the press has amplified gross inequities in maternal care and outcomes that we, as Black birth workers, midwives, and physicians, already knew to be true. We grieve, along with you regarding the recently reported pregnancy-related deaths of Mrs. Kira Johnson,² Dr. Shalon Irving,³ Dr. Chaniece Wallace,⁴ and so many other names we do not know because their stories did not receive national attention, but we know that they represented the best of us, and they are gone too soon. As Black birth workers, midwives, physicians, and more, we have a front-row seat to the United States’ serious obstetric racism, manifested in biased clinical interactions, unjust hospital policies, and an inequitable health care system that leads to disparities in maternal morbidity and mortality for Black women.

Unfortunately, this is not anything new, and the legacy dates back to slavery and the disregard for Black people in this country. What has changed is our increased awareness of these health injustices. This collective consciousness of the risk that is carried with our pregnancies casts a shadow of fear over a period that should be full of the joy and promise of new life. We fear that our personhood will be disregarded, our pain will be ignored, and our voices silenced by a medical system that has sought to dominate our bodies and experiment on them without our permission.⁵ While this history is reprehensible, and our collective risk as Black people is disproportionately high, our purpose in writing this letter is to help Black birthing people recapture the joy and celebration that should be theirs in pregnancy and in the journey to parenthood.

As Black birth workers, we see Black pregnant patients desperately seeking safety, security, and breaking down barriers to find us for their pregnancy care. Often, they are terrified and looking for kinship and community in our offices. In rural areas patients may drive up to 4 hours in distance for an appointment, and during appointments entrust us with their stories of feeling unheard in the medical system. When we anecdotally asked about what they feared about pregnancy, childbirth, and the postpartum period and thought was their risk of dying during pregnancy or childbirth, answers ranged from 1% to 60%. Our actual risk of dying from a pregnancy-related cause, as a Black woman, is 0.0414% (41.4 Black maternal deaths per 100,000 live births).⁶ To put that in perspective, our risk of dying is higher walking down the street or driving a car.⁷

What is the source of the fear? Based on past and present injustices inflicted on people with historically marginalized identities, we have every right to be scared; but, make no mistake that fear comes at a cost, and Black birthing people are the ones paying the bill! Stress and chronic worry are associated with poor pregnancy outcomes, and so this completely justifiable fear, at the population level, is not serving us well personally.⁸ Unfortunately, lost in the messaging about racial inequities in maternal mortality is the reality that the vast majority of Black people and babies will survive, thrive, and have healthy pregnancy outcomes, despite the terrifying population-level statistics and horrific stories of discrimination and neglect that make us feel like our pregnancies and personal peril are synonymous.

While it is true that our absolute individual, personal risk is lower than population-level statistics convey, let us be clear: We are furious about what is happening to Black people! It is immoral that Black patients in the richest country in the world are 3-4 times more likely to die of a pregnancy-related cause than White women,⁹ and we are more likely to experience pregnancy complications and “near misses” when death is narrowly avoided. Research has done an excellent job defining reproductive health disparities in this country, but prioritizing and funding meaningful strategies, policies, and programs to close this gap have not taken precedence—especially initiatives and research that are headed by Black women.^10–12 This is largely because researchers and health care systems continue evaluating strategies that focus on behavior change and narratives that identify individual responsibility as a sole cause of inequity.

Let us be clear, Black people and our behaviors are not the problem.¹³ The problems are White supremacy, classism, sexism, heteropatriarchy, and obstetric racism.^1-21 These must be recognized and addressed across all levels of power. We endorse systems-level changes that are at the root of promoting health equity in our reproductive outcomes. These changes include paid parental leave, Medicaid expansion/extension, reimbursement for doula and lactation services, increased access to perinatal mental health and wellness services, and so much more. (See the Black Mamas Matter Alliance Toolkit: https://blackmamas matter.org/our-work/toolkits/.)

Continue to: Pearls for reassurance...

Pearls for reassurance

While the inequities and their solutions are grounded in the need for systemic change,²² we realize that these population-level solutions feel abstract when our sisters and siblings ask us, “So what can I do to advocate for myself and my baby, right now in this pregnancy?” To be clear, no amount of personal hypervigilance on our part as Black pregnancy-capable people is going to fix these problems, which are systemic; however, we want to provide a few pearls that may be helpful for patient self-advocacy and reassurance:

1. Seek culturally and ethnically congruent care. We intuitively want to find a clinician who looks like us, but sadly, in the United States only 5% of physicians and 2% of midwives are Black. Demand exceeds supply for Black patients who are seeking racially congruent care. Nonetheless, it is critical that you find a physician or midwife who centers you and  provides support and care that affirms the strengths and assets of you, your family, and your community when cultural and ethnic congruency are not possible for you and your pregnancy. 
2. Ask how your clinicians are actively working to ensure optimal and equitable experiences for Black birthing individuals. We recommend asking your clinician and/or hospital what, if anything, they are doing to address health care inequities, obstetric racism, or implicit bias in their pregnancy and postpartum care. Many groups (including some authors of this letter) are working on measures to address obstetric racism. An acknowledgement of initiatives to mitigate inequities is a meaningful first step. You can suggest that they look into it while you explore your options, as this work is rapidly emerging in many areas of the country. 
3. Plan for well-person care. The best time to optimize pregnancy and birth outcomes is before you get pregnant. Set up an appointment with a midwife, ObGyn, or your primary care physician before you get pregnant. Discuss your concerns about pregnancy and use this time to optimize your health. This also provides an opportunity to build a relationship with your physician/ midwife and their group to evaluate whether they curate an environment where you feel seen, heard, and valued when you go for annual exams or problem visits. If you do not get that sense after a couple of visits, find a place where you do. 
4. Advocate for a second opinion. If something does not sound right to you or you have questions that were not adequately answered, it is your prerogative to seek a second opinion; a clinician should never be offended by this. 
5. Consider these factors, for those who deliver in a hospital (by choice or necessity): 

   a. 24/7 access to obstetricians and dedicated anesthesiologists in the hospital

   b. trauma-informed medical/mental health/social services

   c. lactation consultation

   d. supportive trial of labor after cesarean delivery policy

   e. massive blood transfusion  protocol. 

6. Seek doula support! It always helps to have another set of eyes and ears to help advocate for you, especially when you are in pain during pregnancy, childbirth, or in the postpartum period, or are having difficulty advocating for yourself. There is also evidence that women supported by doulas have better pregnancy-related outcomes and experiences.²³ Many major cities in the United States have started to provide race-concordant doula care for Black birthing people  for free.²⁴
7.  Don’t forget about your mental health. As stated, chronic stress from racism impacts birth outcomes. Having a mental health clinician is a great way to mitigate adverse effects of prolonged tension.^25–27
8. Ask your clinician, hospital, or insurance company about participating in group prenatal care and/or nurse home visiting models²⁸ because both are associated with improved birth outcomes.²⁹ Many institutions are implementing group care that provides race-concordant care.^30,31 
9. Ask your clinician, hospital, or local health department for recommendations to a lactation consultant or educator who can support your efforts in breast/ chest/body-feeding. 

We invite you to consider this truth

You, alone, do not carry the entire population-level risk of Black birthing people on your shoulders. We all carry a piece of it. We, along with many allies, advocates, and activists, are outraged and angered by generations of racism and mistreatment of Black birthing people in our health systems and hospitals. We are channeling our frustration and disgust to demand substantive and sustainable change.

Our purpose here is to provide love and reassurance to our sisters and siblings who are going through their pregnancies with thoughts about our nation’s past and present failures to promote health equity for us and our babies. Our purpose is neither to minimize the public health crisis of Black infant and maternal morbidity and mortality nor is it to absolve clinicians, health systems, or governments from taking responsibility for these shameful outcomes or making meaningful changes to address them. In fact, we love taking care of our community by providing the best clinical care we can to our patients. We call upon all of our clinical colleagues to educate themselves to be ethically and equitably equipped to provide health care for Black pregnant patients. Finally, to birthing Black families, please remember this: If you choose to have a baby, the outcome and experience must align with what is right for you and your baby to survive and thrive. So much of the joys of pregnancy have been stolen, but we will recapture the celebration that should be ours in pregnancy and the journey to parenthood.

Sincerely,

Ebony B. Carter, MD, MPH
Maternal Fetal Medicine
Washington University School of Medicine
St. Louis, Missouri

Karen A. Scott, MD, MPH
Birthing Cultural Rigor, LLC
Nashville, Tennessee

Andrea Jackson, MD, MAS
ObGyn
University of California,
San Francisco

Sara Whetstone, MD, MHS
ObGyn
University of California, 
San Francisco

Traci Johnson, MD
ObGyn
University of Missouri 
School of Medicine
Kansas City, Missouri

Sarahn Wheeler, MD
Maternal Fetal Medicine
Duke University School of Medicine
Durham, North Carolina

Asmara Gebre, CNM
Midwife
Zuckerberg San Francisco General Hospital
San Francisco, California

Joia Crear-Perry, MD
ObGyn
National Birth Equity Collaborative
New Orleans, Louisiana

Dineo Khabele, MD
Gynecologic Oncology
Washington University School of Medicine
St. Louis, Missouri

Judette Louis, MD, MPH
Maternal Fetal Medicine
University of South Florida College of Medicine
Tampa, Florida

Yvonne Smith, MSN, RN
Director
Barnes-Jewish Hospital
St. Louis, Missouri

Laura Riley, MD
Maternal Fetal Medicine
Weill Cornell Medicine
New York, New York

Antoinette Liddell, MSN, RN
Care Coordinator
Barnes-Jewish Hospital
St. Louis, Missouri

Cynthia Gyamfi-Bannerman, MD
Maternal Fetal Medicine
Columbia University Irving Medical Center
New York, New York

Rasheda Pippens, MSN, RN
Nurse Educator
Barnes-Jewish Hospital
St. Louis, Missouri

Ayaba Worjoloh-Clemens, MD
ObGyn
Atlanta, Georgia

Allison Bryant, MD, MPH
Maternal Fetal Medicine
Massachusetts General Hospital
Boston, Massachusetts

Sheri L. Foote, CNM
Midwife
Zuckerberg San Francisco General Hospital
San Francisco, California

J. Lindsay Sillas, MD
ObGyn
Bella OB/GYN
Houston, Texas

Cynthia Rogers, MD
Psychiatrist
Washington University School of Medicine
St. Louis, Missouri

Audra R. Meadows, MD, MPH
ObGyn
University of California, San Diego

AeuMuro G. Lake, MD
Urogynecologist
Urogynecology and Healing Arts
Seattle, Washington

Nancy Moore, MSN, RN, WHNP-BC
Nurse Practitioner
Barnes-Jewish Hospital
St. Louis, Missouri

Zoë Julian, MD, MPH
ObGyn
University of Alabama at Birmingham

Janice M. Tinsley, MN, RNC-OB
Zuckerberg San Francisco General Hospital
San Francisco, California

Jamila B. Perritt, MD, MPH
ObGyn
Washington, DC

Joy A. Cooper, MD, MSc
ObGyn
Culture Care
Oakland, California

Arthurine K. Zakama, MD
ObGyn
University of California,San Francisco

Alissa Erogbogbo, MD
OB Hospitalist
Los Altos, California

Sanithia L. Williams, MD
ObGyn
Huntsville, Alabama

Audra Williams, MD, MPH
ObGyn
University of Alabama, Birmingham

Hedwige “Didi” Saint Louis, MD, MPH
OB Hospitalist
Morehouse School of Medicine
Atlanta, Georgia

Cherise Cokley, MD
OB Hospitalist
Community Hospital
Munster, Indiana

J’Leise Sosa, MD, MPH
ObGyn
Buffalo, New York

NEW ORLEANS – Application of a single-use disposable patch to the axillary area for up to 3 minutes led to statistically significant and clinically meaningful benefit for patients with primary axillary hyperhidrosis, results from a pivotal randomized trial showed.

“This is a new kind of device that is going to be a nice tool to have for treating patients who have hyperhidrosis of the axilla,” the study’s lead investigator, David M. Pariser, MD, who practices dermatology in Norfolk, Va., said during a late-breaking abstract session at the annual meeting of the American Academy of Dermatology.

Koldunov/Thinkstock

Adverse events

A total of 13 patients in the active patch group experienced AEs at the treatment site, including six with erythema; four with erosion; two with burning, itching or stinging; and one with underarm odor. “The two procedure-related AEs in the TAT-treated group were compensatory sweating and irritant contact dermatitis due to the adhesive,” said Dr. Pariser said.

Most adverse events resolved in fewer than 2 weeks, and all were mild to moderate. No serious adverse events occurred. Only five adverse events occurred in the sham group.

The TAT patch is currently undergoing review by the Food and Drug Administration, and according to Dr. Pariser, no other body sites have been treated with the device.

Adam Friedman, MD, professor and chair of dermatology at George Washington University, Washington, who was asked to comment on the study, characterized hyperhidrosis as “an exceedingly common medical condition that is commonly overlooked even though it has a tremendous burden on quality of life. I should know, as both someone who manages a large cohort of these patients but also as someone who suffers from it.”

Treatment options “have historically been limited, many of which are off-label and some which are difficult to access due to cost and/or duration/frequency of treatment,” added Dr. Friedman, who was not involved with the study. “The TAT patch offers a new, targeted, in-office, practical procedure-based approach to treat primary axillary hyperhidrosis. Innovation is certainly welcomed and needed, and I am curious to see how this technology is employed in practice once approved.”

The device is being developed by Candesant Biomedical. Dr. Pariser disclosed that he is a consultant or investigator for Bickel Biotechnology, Biofrontera AG, Bristol Myers Squibb, Celgene Corporation, Novartis Pharmaceuticals, Pfizer, Regeneron, and Sanofi.

Dr. Friedman reported having no relevant disclosures.

NEW ORLEANS – Application of a single-use disposable patch to the axillary area for up to 3 minutes led to statistically significant and clinically meaningful benefit for patients with primary axillary hyperhidrosis, results from a pivotal randomized trial showed.

“This is a new kind of device that is going to be a nice tool to have for treating patients who have hyperhidrosis of the axilla,” the study’s lead investigator, David M. Pariser, MD, who practices dermatology in Norfolk, Va., said during a late-breaking abstract session at the annual meeting of the American Academy of Dermatology.

Koldunov/Thinkstock

Adverse events

A total of 13 patients in the active patch group experienced AEs at the treatment site, including six with erythema; four with erosion; two with burning, itching or stinging; and one with underarm odor. “The two procedure-related AEs in the TAT-treated group were compensatory sweating and irritant contact dermatitis due to the adhesive,” said Dr. Pariser said.

Most adverse events resolved in fewer than 2 weeks, and all were mild to moderate. No serious adverse events occurred. Only five adverse events occurred in the sham group.

The TAT patch is currently undergoing review by the Food and Drug Administration, and according to Dr. Pariser, no other body sites have been treated with the device.

Adam Friedman, MD, professor and chair of dermatology at George Washington University, Washington, who was asked to comment on the study, characterized hyperhidrosis as “an exceedingly common medical condition that is commonly overlooked even though it has a tremendous burden on quality of life. I should know, as both someone who manages a large cohort of these patients but also as someone who suffers from it.”

Treatment options “have historically been limited, many of which are off-label and some which are difficult to access due to cost and/or duration/frequency of treatment,” added Dr. Friedman, who was not involved with the study. “The TAT patch offers a new, targeted, in-office, practical procedure-based approach to treat primary axillary hyperhidrosis. Innovation is certainly welcomed and needed, and I am curious to see how this technology is employed in practice once approved.”

The device is being developed by Candesant Biomedical. Dr. Pariser disclosed that he is a consultant or investigator for Bickel Biotechnology, Biofrontera AG, Bristol Myers Squibb, Celgene Corporation, Novartis Pharmaceuticals, Pfizer, Regeneron, and Sanofi.

Dr. Friedman reported having no relevant disclosures.

NEW ORLEANS – Application of a single-use disposable patch to the axillary area for up to 3 minutes led to statistically significant and clinically meaningful benefit for patients with primary axillary hyperhidrosis, results from a pivotal randomized trial showed.

“This is a new kind of device that is going to be a nice tool to have for treating patients who have hyperhidrosis of the axilla,” the study’s lead investigator, David M. Pariser, MD, who practices dermatology in Norfolk, Va., said during a late-breaking abstract session at the annual meeting of the American Academy of Dermatology.

Koldunov/Thinkstock

Adverse events

A total of 13 patients in the active patch group experienced AEs at the treatment site, including six with erythema; four with erosion; two with burning, itching or stinging; and one with underarm odor. “The two procedure-related AEs in the TAT-treated group were compensatory sweating and irritant contact dermatitis due to the adhesive,” said Dr. Pariser said.

Most adverse events resolved in fewer than 2 weeks, and all were mild to moderate. No serious adverse events occurred. Only five adverse events occurred in the sham group.

The TAT patch is currently undergoing review by the Food and Drug Administration, and according to Dr. Pariser, no other body sites have been treated with the device.

Adam Friedman, MD, professor and chair of dermatology at George Washington University, Washington, who was asked to comment on the study, characterized hyperhidrosis as “an exceedingly common medical condition that is commonly overlooked even though it has a tremendous burden on quality of life. I should know, as both someone who manages a large cohort of these patients but also as someone who suffers from it.”

Treatment options “have historically been limited, many of which are off-label and some which are difficult to access due to cost and/or duration/frequency of treatment,” added Dr. Friedman, who was not involved with the study. “The TAT patch offers a new, targeted, in-office, practical procedure-based approach to treat primary axillary hyperhidrosis. Innovation is certainly welcomed and needed, and I am curious to see how this technology is employed in practice once approved.”

The device is being developed by Candesant Biomedical. Dr. Pariser disclosed that he is a consultant or investigator for Bickel Biotechnology, Biofrontera AG, Bristol Myers Squibb, Celgene Corporation, Novartis Pharmaceuticals, Pfizer, Regeneron, and Sanofi.

Dr. Friedman reported having no relevant disclosures.

Recurrent episodic blood loss from normal menstruation is not expected to result in anemia. But without treatment, chronic heavy periods will progress through the stages of low iron stores to iron deficiency and then to anemia. When iron storage levels are low, the bone marrow’s blood cell factory cannot keep up with continued losses. Every patient with heavy menstrual bleeding (HMB) or prolonged menstrual episodes should be tested and treated for iron deficiency and anemia.^1,2

Particular attention should be paid to assessment of iron storage levels with serum ferritin, recognizing that low iron levels progress to anemia once the storage is depleted. Recovery from anemia is much slower in individuals with iron deficiency, so assessment for iron storage also should be included in preoperative assessments and following a diagnosis of acute blood loss anemia.

The mechanics of erythropoiesis, hemoglobin, and oxygen transport

Red blood cells (erythrocytes) have a short life cycle and require constant replacement. Erythrocytes are generated on demand in erythropoiesis by a hormonal signaling process, regardless of whether sufficient components are available.³ Hemoglobin, the main intracellular component of erythrocytes, is comprised of 4 globin chains, which each contain 1 iron atom bound to a heme molecule. After erythrocytes are assembled, they are sent out into circulation for approximately 120 days. A hemoglobin level measures the oxygen-carrying capacity of erythrocytes, and anemia is defined as hemoglobin less than 12 g/dL.

Unless erythrocytes are lost from bleeding, they are decommissioned—that is, the heme molecule is metabolized into bilirubin and excreted, and the iron atoms are recycled back to the bone marrow or to storage.⁴ Ferritin is the storage molecule that binds to iron, a glycoprotein with numerous subunits around a core that can contain about 4,000 iron atoms. Most ferritin is intracellular, but a small proportion is present in serum, where it can be measured.

Serum ferritin is a good marker for the iron supply in healthy individuals because it has high correlation to iron in the bone marrow and correlates to total intracellular storage unless there is inflammation, when mobilization to serum increases. The ferritin level at which the iron supply is deficient to meet demand, defined as iron deficiency, is hotly debated and ranges from less than 15 to 50 ng/mL in menstruating individuals, with higher thresholds based on onset of erythropoiesis signaling and the lower threshold being the World Health Organization recommendation.^5-7 When iron atoms are in short supply, erythrocytes still are generated but they have lower amounts of intracellular hemoglobin, which makes them thinner, smaller, and paler—and less effective at oxygen transport.

CASE Patient seeks treatment for HMB-associated symptoms

A 17-year-old patient presents with HMB, fatigue, and difficulty with concentration. She reports that her periods have been regular and lasting 7 days since menarche at age 13. While they are manageable, they seem to be getting heavier, soaking pads in 2 to 3 hours. The patient reports that she would like to start treatment for her progressively heavy bleeding and prefers lighter scheduled bleeding; she currently does not desire contraception. The patient has no family history of bleeding problems and self-reports no personal history of epistaxis or bleeding with tooth extraction or tonsillectomy. Laboratory tests confirm iron deficiency with a hemoglobin level of 12.5 g/dL (reference range, 12.0–17.5 g/dL) and a serum ferritin level of 8 ng/mL (reference range, 50–420 ng/mL). Results from a coagulopathy panel are normal, as are von Willebrand factor levels.

Untreated iron deficiency will progress to anemia

This patient has iron deficiency without anemia, which warrants significant attention in HMB because without treatment it eventually will progress to anemia. The prevalence of iron deficiency, which makes up half of all causes of anemia, is at least double that of iron deficiency anemia.³

Adult bodies usually contain about 3 to 4 g of iron, with two-thirds in erythrocytes as hemoglobin.⁸ Approximately 40 to 60 mg of iron is recycled daily, 1 to 2 mg/day is lost from sloughed cells and sweat, and at least 1 mg/day is lost during normal menstruation. These losses are balanced with gastrointestinal uptake of 1 to 2 mg/day until bleeding exceeds about 10 mL/day. In this 17-year-old patient, iron stores have likely been on a progressive decline since menarche.

For normally menstruating individuals to maintain iron homeostasis, the daily dietary iron requirement is 18 mg/day. Iron requirements also increase during periods of illness or inflammation due to hormonal signaling in the iron absorption and transport pathway, in athletes due to sweating, foot strike hemolysis and bruising, and during growth spurts.⁹

Continue to: Managing iron deficiency and anemia...

Management of iron deficiency and iron deficiency anemia in the setting of HMB includes:

• workup for the etiology of the abnormal uterine bleeding (TABLE)
• reducing the source of blood loss, and
• iron supplementation to correct the iron deficiency state.

In most cases, workup, reduction, and repletion can occur simultaneously. The goal is not always complete cessation of menstrual bleeding; even short-term therapy can allow time to replenish iron storage. Use a shared decision-making process to assess what is important to the patient, and provide information about relative amounts of bleeding cessation that can be expected with various therapies.¹⁰

Treatment options

Medical treatments to decrease menstrual iron losses are recommended prior to proceeding with surgical interventions.¹¹ Hormonal treatments are the most consistently recommended, with many guidelines citing the 52-mg levonorgestrel-releasing intrauterine device (LNG IUD) as first-line treatment due to its substantial reduction in the amount of bleeding, HMB treatment indication approved by the US Food and Drug Administration (FDA), and evidence of success in those with HMB.¹²

Any progestin or combined hormonal medication with estrogen and a progestin will result in an approximately 60% to 90% bleeding reduction, thus providing many effective options for blood loss while considering patient preferences for bleeding pattern, route of administration, and concomitant benefits. While only 1 oral product (estradiol valerate/dienogest) is FDA approved for managementof HMB, use of any of the commercially available contraceptive products will provide substantial benefit.^11,13

Nonhormonal options, such as antifibrinolytics and nonsteroidal anti-inflammatory drugs (NSAIDs), tend to be listed as second-line therapies or for those who want to avoid hormonal medications. Antifibrinolytics, such as tranexamic acid, require frequent dosing of large pills and result in approximately 40% blood loss reduction, but they are a very successful and well-tolerated method for those seeking on-demand therapy.¹⁴ NSAIDs may result in a slight bleeding reduction, but they are far less effective than other therapies.¹⁵ Antifibrinolytics have a theoretical risk of thrombosis and a contraindication to use with hormonal contraceptives; therefore, concomitant use with estrogen-containing medications is reserved for patients with refractory heavy bleeding or for heavy bleeding days during the hormone-free interval, when benefits likely outweigh potential risk.^16,17

Guidelines for medical management of acute HMB typically cite 3 small comparative studies with high-dose regimens of parenteral conjugated estrogen, combined ethinyl estradiol and progestin, or oral medroxyprogesterone acetate.^18,19 Dosing recommendations for the oral medications include a loading dose followed by a taper regimen that is poorly tolerated and for which there is no evidence of superior effectiveness over the standard dose.^20,21In most cases, initiation of the preferred long-term hormonal medication plan will reduce bleeding significantly within 2 to 3 days. Many clinicians who commonly treat acute HMB prescribe norethindrone acetate 5 mg daily (up to 3 times daily, if needed) for effective and safe menstrual suppression.²²

Iron replenishment: Dosing frequency, dietary iron, and multivitamins

Iron repletion is usually via the oral route unless surgery is imminent, anemia is severe, or the oral route is not tolerated or effective.²³ Oral iron has substantial adverse effects that limit tolerance, including nausea, epigastric pain, diarrhea, and constipation. Fortunately, evidence supports lower oral iron doses than previously used.⁴

Iron homeostasis is controlled by the peptide hormone hepcidin, produced by the liver, which controls mobilization of iron from the gut and spleen and aids iron absorption from the diet and supplements.²⁴ Hepcidin levels decrease in response to high circulating levels of iron, so the ideal iron repletion dose in iron-deficient nonanemic women was determined by assessing the dose response of hepcidin. Researchers compared iron 60 mg daily for 14 days versus every other day for 28 days and found that iron absorption was greater in the every-other-day group (21.8% vs 16.3%).²⁵They concluded that changing iron administration to 60 mg or more in a single dose every other day is most efficient in those with iron deficiency without anemia. Since study participants did not have anemia, research is pending on whether different strategies (such as daily dosing) are more effective for more severe cases. The bottom line is that conventional high-dose divided daily oral iron administration results in reduced iron bioavailability compared with alternate-day dosing.

Increasing dietary iron is insufficient to treat low iron storage, iron deficiency, and iron deficiency anemia. Likewise, multivitamins, which contain very little elemental iron, are not recommended for repletion. Any iron salt with 60 to 120 mg of elemental iron can be used (for examples, ferrous sulfate, ferrous gluconate).²⁵ Once ingested, stomach and pancreatic acids release elemental iron from its bound form. For that reason, absorption may be improved by administering iron at least 1 hour before a meal and avoiding antacids, including milk. Meat proteins and ascorbic acid help maintain the soluble ferrous form and also aid absorption. Tea, coffee, and tannins prevent absorption when polyphenol compounds form an insoluble complex with iron (see box at end of article). Gastrointestinal adverse effects can be minimized by decreasing the dose and taking after meals, although with reduced efficacy.

Intravenous iron treatment raises hemoglobin levels significantly faster than oral administration but is limited by cost and availability, so it is reserved for individuals with a hemoglobin level less than 9 g/dL, prior gastrointestinal or bariatric surgery, imminent surgery, and intolerance, poor adherence, or nonresponse to oral iron therapy. Several approved formulations are available, all with equivalent effectiveness and similar safety profiles. Lower-dose formulations (such as iron sucrose) may require several infusions, but higher-dose intravenous iron products (ferric carboxymaltose, low-molecular weight iron dextran, etc) have a stable carbohydrate shell that inhibits free iron release and improves safety, allowing a single administration.²⁶

Common adverse effects of intravenous iron treatment include a metallic taste and headache during administration. More serious adverse effects, such as hypotension, arthralgia, malaise, and nausea, are usually self-limited. With mild infusion reactions (1 in 200), the infusion can be stopped until symptoms improve and can be resumed at a slower rate.²⁷

Continue to: The role of blood transfusion...

The role of blood transfusion

Blood transfusion is expensive and potentially hazardous, so its use is limited to treatment of acute blood loss or severe anemia.

A one-time red blood cell transfusion does not impact diagnostic criteria to assess for iron deficiency with ferritin, and it does not improve underlying iron deficiency.²⁸Patients with acute blood loss anemia superimposed on chronic blood loss should be screened and treated for iron deficiency even after receiving a transfusion.

Since ferritin levels can rise significantly as an acute phase reactant, even following a hemorrhage, iron deficiency during inflammation is defined as ferritin less than 70 ng/mL.

The potential for iron overload

Since iron is never metabolized or excreted, it is possible to have iron overload following accidental overdose, transfusion dependency, and disorders of iron transport, such as hemochromatosis and thalassemia.

While a low ferritin level always indicates iron deficiency, high ferritin levels can be an acute phase reactant. Ferritin levels greater than 150 ng/mL in healthy menstruating individuals and greater than 500 ng/mL in unhealthy individuals should raise concern for excess iron and should prompt discontinuation of iron intake or workup for conditions at risk for overload.⁵

Oral iron supplements should be stored away from small children, who are at particular risk of toxicity.

How long to treat?

Treatment duration depends on the individual’s degree of iron deficiency, whether anemia is present, and the amount of ongoing blood loss. The main treatment goal is normalization and maintenance of serum ferritin.

Successful treatment should be confirmed with a complete blood count and ferritin level. Hemoglobin levels improve 2 g/dL after 3 weeks of oral iron therapy, but repletion may take 4 to 6 months.^23,29 The American College of Obstetricians and Gynecologists recommends 3 to 6 months of continued iron therapy after resolution of HMB.¹⁹

In a comparative study of treatment for HMB with the 52-mg LNG IUD versus hysterectomy, hemoglobin levels increased in both treatment groups but stayed lower in those with initial anemia.⁸ Ferritin levels normalized only after 5 years and were still lower in individuals with initial anemia.

Increase in hemoglobin is faster after intravenous iron administration but is equivalent to oral therapy by 12 weeks. If management to reduce menstrual losses is discontinued, periodic or maintenance iron repletion will be necessary.

CASE Management plan initiated

This 17-year-old patient with iron deficiency resulting from HMB requests management to reduce menstrual iron losses with a preference for predictable menses. We have already completed a basic workup, which could also include assessment for hypermobility with a Beighton score, as connective tissue disorders also are associated with HMB.³⁰ We discuss the options of cyclic hormonal therapy, antifibrinolytic treatment, and an LNG IUD. The patient is concerned about adherence and wants to avoid unscheduled bleeding, so she opts for a trial of tranexamic acid 1,300 mg 3 times daily for 5 days during menses. This regimen results in a 50% reduction in bleeding amount, which the patient finds satisfactory. Iron repletion with oral ferrous sulfate 325 mg (containing 65 mg of elemental iron) is administered on alternating days with vitamin C taken 1 hour prior to dinner. Repeat laboratory test results at 3 weeks show improvement to a hemoglobin level of 14.2 g/dL and a ferritin level of 12 ng/mL. By 3 months, her ferritin levels are greater than 30 ng/mL and oral iron is administered only during menses.

Summing up

Chronic HMB results in a progressive net loss of iron and eventual anemia. Screening with complete blood count and ferritin and early treatment of low iron storage when ferritin is less than 30 ng/mL will help avoid symptoms. Any amount of reduction of menstrual blood loss can be beneficial, allowing a variety of effective hormonal and nonhormonal treatment options. ●

Recurrent episodic blood loss from normal menstruation is not expected to result in anemia. But without treatment, chronic heavy periods will progress through the stages of low iron stores to iron deficiency and then to anemia. When iron storage levels are low, the bone marrow’s blood cell factory cannot keep up with continued losses. Every patient with heavy menstrual bleeding (HMB) or prolonged menstrual episodes should be tested and treated for iron deficiency and anemia.^1,2

Particular attention should be paid to assessment of iron storage levels with serum ferritin, recognizing that low iron levels progress to anemia once the storage is depleted. Recovery from anemia is much slower in individuals with iron deficiency, so assessment for iron storage also should be included in preoperative assessments and following a diagnosis of acute blood loss anemia.

The mechanics of erythropoiesis, hemoglobin, and oxygen transport

Red blood cells (erythrocytes) have a short life cycle and require constant replacement. Erythrocytes are generated on demand in erythropoiesis by a hormonal signaling process, regardless of whether sufficient components are available.³ Hemoglobin, the main intracellular component of erythrocytes, is comprised of 4 globin chains, which each contain 1 iron atom bound to a heme molecule. After erythrocytes are assembled, they are sent out into circulation for approximately 120 days. A hemoglobin level measures the oxygen-carrying capacity of erythrocytes, and anemia is defined as hemoglobin less than 12 g/dL.

Unless erythrocytes are lost from bleeding, they are decommissioned—that is, the heme molecule is metabolized into bilirubin and excreted, and the iron atoms are recycled back to the bone marrow or to storage.⁴ Ferritin is the storage molecule that binds to iron, a glycoprotein with numerous subunits around a core that can contain about 4,000 iron atoms. Most ferritin is intracellular, but a small proportion is present in serum, where it can be measured.

Serum ferritin is a good marker for the iron supply in healthy individuals because it has high correlation to iron in the bone marrow and correlates to total intracellular storage unless there is inflammation, when mobilization to serum increases. The ferritin level at which the iron supply is deficient to meet demand, defined as iron deficiency, is hotly debated and ranges from less than 15 to 50 ng/mL in menstruating individuals, with higher thresholds based on onset of erythropoiesis signaling and the lower threshold being the World Health Organization recommendation.^5-7 When iron atoms are in short supply, erythrocytes still are generated but they have lower amounts of intracellular hemoglobin, which makes them thinner, smaller, and paler—and less effective at oxygen transport.

CASE Patient seeks treatment for HMB-associated symptoms

A 17-year-old patient presents with HMB, fatigue, and difficulty with concentration. She reports that her periods have been regular and lasting 7 days since menarche at age 13. While they are manageable, they seem to be getting heavier, soaking pads in 2 to 3 hours. The patient reports that she would like to start treatment for her progressively heavy bleeding and prefers lighter scheduled bleeding; she currently does not desire contraception. The patient has no family history of bleeding problems and self-reports no personal history of epistaxis or bleeding with tooth extraction or tonsillectomy. Laboratory tests confirm iron deficiency with a hemoglobin level of 12.5 g/dL (reference range, 12.0–17.5 g/dL) and a serum ferritin level of 8 ng/mL (reference range, 50–420 ng/mL). Results from a coagulopathy panel are normal, as are von Willebrand factor levels.

Untreated iron deficiency will progress to anemia

This patient has iron deficiency without anemia, which warrants significant attention in HMB because without treatment it eventually will progress to anemia. The prevalence of iron deficiency, which makes up half of all causes of anemia, is at least double that of iron deficiency anemia.³

Adult bodies usually contain about 3 to 4 g of iron, with two-thirds in erythrocytes as hemoglobin.⁸ Approximately 40 to 60 mg of iron is recycled daily, 1 to 2 mg/day is lost from sloughed cells and sweat, and at least 1 mg/day is lost during normal menstruation. These losses are balanced with gastrointestinal uptake of 1 to 2 mg/day until bleeding exceeds about 10 mL/day. In this 17-year-old patient, iron stores have likely been on a progressive decline since menarche.

For normally menstruating individuals to maintain iron homeostasis, the daily dietary iron requirement is 18 mg/day. Iron requirements also increase during periods of illness or inflammation due to hormonal signaling in the iron absorption and transport pathway, in athletes due to sweating, foot strike hemolysis and bruising, and during growth spurts.⁹

Continue to: Managing iron deficiency and anemia...

Management of iron deficiency and iron deficiency anemia in the setting of HMB includes:

• workup for the etiology of the abnormal uterine bleeding (TABLE)
• reducing the source of blood loss, and
• iron supplementation to correct the iron deficiency state.

In most cases, workup, reduction, and repletion can occur simultaneously. The goal is not always complete cessation of menstrual bleeding; even short-term therapy can allow time to replenish iron storage. Use a shared decision-making process to assess what is important to the patient, and provide information about relative amounts of bleeding cessation that can be expected with various therapies.¹⁰

Treatment options

Medical treatments to decrease menstrual iron losses are recommended prior to proceeding with surgical interventions.¹¹ Hormonal treatments are the most consistently recommended, with many guidelines citing the 52-mg levonorgestrel-releasing intrauterine device (LNG IUD) as first-line treatment due to its substantial reduction in the amount of bleeding, HMB treatment indication approved by the US Food and Drug Administration (FDA), and evidence of success in those with HMB.¹²

Any progestin or combined hormonal medication with estrogen and a progestin will result in an approximately 60% to 90% bleeding reduction, thus providing many effective options for blood loss while considering patient preferences for bleeding pattern, route of administration, and concomitant benefits. While only 1 oral product (estradiol valerate/dienogest) is FDA approved for managementof HMB, use of any of the commercially available contraceptive products will provide substantial benefit.^11,13

Nonhormonal options, such as antifibrinolytics and nonsteroidal anti-inflammatory drugs (NSAIDs), tend to be listed as second-line therapies or for those who want to avoid hormonal medications. Antifibrinolytics, such as tranexamic acid, require frequent dosing of large pills and result in approximately 40% blood loss reduction, but they are a very successful and well-tolerated method for those seeking on-demand therapy.¹⁴ NSAIDs may result in a slight bleeding reduction, but they are far less effective than other therapies.¹⁵ Antifibrinolytics have a theoretical risk of thrombosis and a contraindication to use with hormonal contraceptives; therefore, concomitant use with estrogen-containing medications is reserved for patients with refractory heavy bleeding or for heavy bleeding days during the hormone-free interval, when benefits likely outweigh potential risk.^16,17

Guidelines for medical management of acute HMB typically cite 3 small comparative studies with high-dose regimens of parenteral conjugated estrogen, combined ethinyl estradiol and progestin, or oral medroxyprogesterone acetate.^18,19 Dosing recommendations for the oral medications include a loading dose followed by a taper regimen that is poorly tolerated and for which there is no evidence of superior effectiveness over the standard dose.^20,21In most cases, initiation of the preferred long-term hormonal medication plan will reduce bleeding significantly within 2 to 3 days. Many clinicians who commonly treat acute HMB prescribe norethindrone acetate 5 mg daily (up to 3 times daily, if needed) for effective and safe menstrual suppression.²²

Iron replenishment: Dosing frequency, dietary iron, and multivitamins

Iron repletion is usually via the oral route unless surgery is imminent, anemia is severe, or the oral route is not tolerated or effective.²³ Oral iron has substantial adverse effects that limit tolerance, including nausea, epigastric pain, diarrhea, and constipation. Fortunately, evidence supports lower oral iron doses than previously used.⁴

Iron homeostasis is controlled by the peptide hormone hepcidin, produced by the liver, which controls mobilization of iron from the gut and spleen and aids iron absorption from the diet and supplements.²⁴ Hepcidin levels decrease in response to high circulating levels of iron, so the ideal iron repletion dose in iron-deficient nonanemic women was determined by assessing the dose response of hepcidin. Researchers compared iron 60 mg daily for 14 days versus every other day for 28 days and found that iron absorption was greater in the every-other-day group (21.8% vs 16.3%).²⁵They concluded that changing iron administration to 60 mg or more in a single dose every other day is most efficient in those with iron deficiency without anemia. Since study participants did not have anemia, research is pending on whether different strategies (such as daily dosing) are more effective for more severe cases. The bottom line is that conventional high-dose divided daily oral iron administration results in reduced iron bioavailability compared with alternate-day dosing.

Increasing dietary iron is insufficient to treat low iron storage, iron deficiency, and iron deficiency anemia. Likewise, multivitamins, which contain very little elemental iron, are not recommended for repletion. Any iron salt with 60 to 120 mg of elemental iron can be used (for examples, ferrous sulfate, ferrous gluconate).²⁵ Once ingested, stomach and pancreatic acids release elemental iron from its bound form. For that reason, absorption may be improved by administering iron at least 1 hour before a meal and avoiding antacids, including milk. Meat proteins and ascorbic acid help maintain the soluble ferrous form and also aid absorption. Tea, coffee, and tannins prevent absorption when polyphenol compounds form an insoluble complex with iron (see box at end of article). Gastrointestinal adverse effects can be minimized by decreasing the dose and taking after meals, although with reduced efficacy.

Intravenous iron treatment raises hemoglobin levels significantly faster than oral administration but is limited by cost and availability, so it is reserved for individuals with a hemoglobin level less than 9 g/dL, prior gastrointestinal or bariatric surgery, imminent surgery, and intolerance, poor adherence, or nonresponse to oral iron therapy. Several approved formulations are available, all with equivalent effectiveness and similar safety profiles. Lower-dose formulations (such as iron sucrose) may require several infusions, but higher-dose intravenous iron products (ferric carboxymaltose, low-molecular weight iron dextran, etc) have a stable carbohydrate shell that inhibits free iron release and improves safety, allowing a single administration.²⁶

Common adverse effects of intravenous iron treatment include a metallic taste and headache during administration. More serious adverse effects, such as hypotension, arthralgia, malaise, and nausea, are usually self-limited. With mild infusion reactions (1 in 200), the infusion can be stopped until symptoms improve and can be resumed at a slower rate.²⁷

Continue to: The role of blood transfusion...

The role of blood transfusion

Blood transfusion is expensive and potentially hazardous, so its use is limited to treatment of acute blood loss or severe anemia.

A one-time red blood cell transfusion does not impact diagnostic criteria to assess for iron deficiency with ferritin, and it does not improve underlying iron deficiency.²⁸Patients with acute blood loss anemia superimposed on chronic blood loss should be screened and treated for iron deficiency even after receiving a transfusion.

Since ferritin levels can rise significantly as an acute phase reactant, even following a hemorrhage, iron deficiency during inflammation is defined as ferritin less than 70 ng/mL.

The potential for iron overload

Since iron is never metabolized or excreted, it is possible to have iron overload following accidental overdose, transfusion dependency, and disorders of iron transport, such as hemochromatosis and thalassemia.

While a low ferritin level always indicates iron deficiency, high ferritin levels can be an acute phase reactant. Ferritin levels greater than 150 ng/mL in healthy menstruating individuals and greater than 500 ng/mL in unhealthy individuals should raise concern for excess iron and should prompt discontinuation of iron intake or workup for conditions at risk for overload.⁵

Oral iron supplements should be stored away from small children, who are at particular risk of toxicity.

How long to treat?

Treatment duration depends on the individual’s degree of iron deficiency, whether anemia is present, and the amount of ongoing blood loss. The main treatment goal is normalization and maintenance of serum ferritin.

Successful treatment should be confirmed with a complete blood count and ferritin level. Hemoglobin levels improve 2 g/dL after 3 weeks of oral iron therapy, but repletion may take 4 to 6 months.^23,29 The American College of Obstetricians and Gynecologists recommends 3 to 6 months of continued iron therapy after resolution of HMB.¹⁹

In a comparative study of treatment for HMB with the 52-mg LNG IUD versus hysterectomy, hemoglobin levels increased in both treatment groups but stayed lower in those with initial anemia.⁸ Ferritin levels normalized only after 5 years and were still lower in individuals with initial anemia.

Increase in hemoglobin is faster after intravenous iron administration but is equivalent to oral therapy by 12 weeks. If management to reduce menstrual losses is discontinued, periodic or maintenance iron repletion will be necessary.

CASE Management plan initiated

This 17-year-old patient with iron deficiency resulting from HMB requests management to reduce menstrual iron losses with a preference for predictable menses. We have already completed a basic workup, which could also include assessment for hypermobility with a Beighton score, as connective tissue disorders also are associated with HMB.³⁰ We discuss the options of cyclic hormonal therapy, antifibrinolytic treatment, and an LNG IUD. The patient is concerned about adherence and wants to avoid unscheduled bleeding, so she opts for a trial of tranexamic acid 1,300 mg 3 times daily for 5 days during menses. This regimen results in a 50% reduction in bleeding amount, which the patient finds satisfactory. Iron repletion with oral ferrous sulfate 325 mg (containing 65 mg of elemental iron) is administered on alternating days with vitamin C taken 1 hour prior to dinner. Repeat laboratory test results at 3 weeks show improvement to a hemoglobin level of 14.2 g/dL and a ferritin level of 12 ng/mL. By 3 months, her ferritin levels are greater than 30 ng/mL and oral iron is administered only during menses.

Summing up

Chronic HMB results in a progressive net loss of iron and eventual anemia. Screening with complete blood count and ferritin and early treatment of low iron storage when ferritin is less than 30 ng/mL will help avoid symptoms. Any amount of reduction of menstrual blood loss can be beneficial, allowing a variety of effective hormonal and nonhormonal treatment options. ●

Recurrent episodic blood loss from normal menstruation is not expected to result in anemia. But without treatment, chronic heavy periods will progress through the stages of low iron stores to iron deficiency and then to anemia. When iron storage levels are low, the bone marrow’s blood cell factory cannot keep up with continued losses. Every patient with heavy menstrual bleeding (HMB) or prolonged menstrual episodes should be tested and treated for iron deficiency and anemia.^1,2

Particular attention should be paid to assessment of iron storage levels with serum ferritin, recognizing that low iron levels progress to anemia once the storage is depleted. Recovery from anemia is much slower in individuals with iron deficiency, so assessment for iron storage also should be included in preoperative assessments and following a diagnosis of acute blood loss anemia.

The mechanics of erythropoiesis, hemoglobin, and oxygen transport

Red blood cells (erythrocytes) have a short life cycle and require constant replacement. Erythrocytes are generated on demand in erythropoiesis by a hormonal signaling process, regardless of whether sufficient components are available.³ Hemoglobin, the main intracellular component of erythrocytes, is comprised of 4 globin chains, which each contain 1 iron atom bound to a heme molecule. After erythrocytes are assembled, they are sent out into circulation for approximately 120 days. A hemoglobin level measures the oxygen-carrying capacity of erythrocytes, and anemia is defined as hemoglobin less than 12 g/dL.

Unless erythrocytes are lost from bleeding, they are decommissioned—that is, the heme molecule is metabolized into bilirubin and excreted, and the iron atoms are recycled back to the bone marrow or to storage.⁴ Ferritin is the storage molecule that binds to iron, a glycoprotein with numerous subunits around a core that can contain about 4,000 iron atoms. Most ferritin is intracellular, but a small proportion is present in serum, where it can be measured.

Serum ferritin is a good marker for the iron supply in healthy individuals because it has high correlation to iron in the bone marrow and correlates to total intracellular storage unless there is inflammation, when mobilization to serum increases. The ferritin level at which the iron supply is deficient to meet demand, defined as iron deficiency, is hotly debated and ranges from less than 15 to 50 ng/mL in menstruating individuals, with higher thresholds based on onset of erythropoiesis signaling and the lower threshold being the World Health Organization recommendation.^5-7 When iron atoms are in short supply, erythrocytes still are generated but they have lower amounts of intracellular hemoglobin, which makes them thinner, smaller, and paler—and less effective at oxygen transport.

CASE Patient seeks treatment for HMB-associated symptoms

A 17-year-old patient presents with HMB, fatigue, and difficulty with concentration. She reports that her periods have been regular and lasting 7 days since menarche at age 13. While they are manageable, they seem to be getting heavier, soaking pads in 2 to 3 hours. The patient reports that she would like to start treatment for her progressively heavy bleeding and prefers lighter scheduled bleeding; she currently does not desire contraception. The patient has no family history of bleeding problems and self-reports no personal history of epistaxis or bleeding with tooth extraction or tonsillectomy. Laboratory tests confirm iron deficiency with a hemoglobin level of 12.5 g/dL (reference range, 12.0–17.5 g/dL) and a serum ferritin level of 8 ng/mL (reference range, 50–420 ng/mL). Results from a coagulopathy panel are normal, as are von Willebrand factor levels.

Untreated iron deficiency will progress to anemia

This patient has iron deficiency without anemia, which warrants significant attention in HMB because without treatment it eventually will progress to anemia. The prevalence of iron deficiency, which makes up half of all causes of anemia, is at least double that of iron deficiency anemia.³

Adult bodies usually contain about 3 to 4 g of iron, with two-thirds in erythrocytes as hemoglobin.⁸ Approximately 40 to 60 mg of iron is recycled daily, 1 to 2 mg/day is lost from sloughed cells and sweat, and at least 1 mg/day is lost during normal menstruation. These losses are balanced with gastrointestinal uptake of 1 to 2 mg/day until bleeding exceeds about 10 mL/day. In this 17-year-old patient, iron stores have likely been on a progressive decline since menarche.

For normally menstruating individuals to maintain iron homeostasis, the daily dietary iron requirement is 18 mg/day. Iron requirements also increase during periods of illness or inflammation due to hormonal signaling in the iron absorption and transport pathway, in athletes due to sweating, foot strike hemolysis and bruising, and during growth spurts.⁹

Continue to: Managing iron deficiency and anemia...

Management of iron deficiency and iron deficiency anemia in the setting of HMB includes:

• workup for the etiology of the abnormal uterine bleeding (TABLE)
• reducing the source of blood loss, and
• iron supplementation to correct the iron deficiency state.

In most cases, workup, reduction, and repletion can occur simultaneously. The goal is not always complete cessation of menstrual bleeding; even short-term therapy can allow time to replenish iron storage. Use a shared decision-making process to assess what is important to the patient, and provide information about relative amounts of bleeding cessation that can be expected with various therapies.¹⁰

Treatment options

Medical treatments to decrease menstrual iron losses are recommended prior to proceeding with surgical interventions.¹¹ Hormonal treatments are the most consistently recommended, with many guidelines citing the 52-mg levonorgestrel-releasing intrauterine device (LNG IUD) as first-line treatment due to its substantial reduction in the amount of bleeding, HMB treatment indication approved by the US Food and Drug Administration (FDA), and evidence of success in those with HMB.¹²

Any progestin or combined hormonal medication with estrogen and a progestin will result in an approximately 60% to 90% bleeding reduction, thus providing many effective options for blood loss while considering patient preferences for bleeding pattern, route of administration, and concomitant benefits. While only 1 oral product (estradiol valerate/dienogest) is FDA approved for managementof HMB, use of any of the commercially available contraceptive products will provide substantial benefit.^11,13

Nonhormonal options, such as antifibrinolytics and nonsteroidal anti-inflammatory drugs (NSAIDs), tend to be listed as second-line therapies or for those who want to avoid hormonal medications. Antifibrinolytics, such as tranexamic acid, require frequent dosing of large pills and result in approximately 40% blood loss reduction, but they are a very successful and well-tolerated method for those seeking on-demand therapy.¹⁴ NSAIDs may result in a slight bleeding reduction, but they are far less effective than other therapies.¹⁵ Antifibrinolytics have a theoretical risk of thrombosis and a contraindication to use with hormonal contraceptives; therefore, concomitant use with estrogen-containing medications is reserved for patients with refractory heavy bleeding or for heavy bleeding days during the hormone-free interval, when benefits likely outweigh potential risk.^16,17

Guidelines for medical management of acute HMB typically cite 3 small comparative studies with high-dose regimens of parenteral conjugated estrogen, combined ethinyl estradiol and progestin, or oral medroxyprogesterone acetate.^18,19 Dosing recommendations for the oral medications include a loading dose followed by a taper regimen that is poorly tolerated and for which there is no evidence of superior effectiveness over the standard dose.^20,21In most cases, initiation of the preferred long-term hormonal medication plan will reduce bleeding significantly within 2 to 3 days. Many clinicians who commonly treat acute HMB prescribe norethindrone acetate 5 mg daily (up to 3 times daily, if needed) for effective and safe menstrual suppression.²²

Iron replenishment: Dosing frequency, dietary iron, and multivitamins

Iron repletion is usually via the oral route unless surgery is imminent, anemia is severe, or the oral route is not tolerated or effective.²³ Oral iron has substantial adverse effects that limit tolerance, including nausea, epigastric pain, diarrhea, and constipation. Fortunately, evidence supports lower oral iron doses than previously used.⁴

Iron homeostasis is controlled by the peptide hormone hepcidin, produced by the liver, which controls mobilization of iron from the gut and spleen and aids iron absorption from the diet and supplements.²⁴ Hepcidin levels decrease in response to high circulating levels of iron, so the ideal iron repletion dose in iron-deficient nonanemic women was determined by assessing the dose response of hepcidin. Researchers compared iron 60 mg daily for 14 days versus every other day for 28 days and found that iron absorption was greater in the every-other-day group (21.8% vs 16.3%).²⁵They concluded that changing iron administration to 60 mg or more in a single dose every other day is most efficient in those with iron deficiency without anemia. Since study participants did not have anemia, research is pending on whether different strategies (such as daily dosing) are more effective for more severe cases. The bottom line is that conventional high-dose divided daily oral iron administration results in reduced iron bioavailability compared with alternate-day dosing.

Increasing dietary iron is insufficient to treat low iron storage, iron deficiency, and iron deficiency anemia. Likewise, multivitamins, which contain very little elemental iron, are not recommended for repletion. Any iron salt with 60 to 120 mg of elemental iron can be used (for examples, ferrous sulfate, ferrous gluconate).²⁵ Once ingested, stomach and pancreatic acids release elemental iron from its bound form. For that reason, absorption may be improved by administering iron at least 1 hour before a meal and avoiding antacids, including milk. Meat proteins and ascorbic acid help maintain the soluble ferrous form and also aid absorption. Tea, coffee, and tannins prevent absorption when polyphenol compounds form an insoluble complex with iron (see box at end of article). Gastrointestinal adverse effects can be minimized by decreasing the dose and taking after meals, although with reduced efficacy.

Intravenous iron treatment raises hemoglobin levels significantly faster than oral administration but is limited by cost and availability, so it is reserved for individuals with a hemoglobin level less than 9 g/dL, prior gastrointestinal or bariatric surgery, imminent surgery, and intolerance, poor adherence, or nonresponse to oral iron therapy. Several approved formulations are available, all with equivalent effectiveness and similar safety profiles. Lower-dose formulations (such as iron sucrose) may require several infusions, but higher-dose intravenous iron products (ferric carboxymaltose, low-molecular weight iron dextran, etc) have a stable carbohydrate shell that inhibits free iron release and improves safety, allowing a single administration.²⁶

Common adverse effects of intravenous iron treatment include a metallic taste and headache during administration. More serious adverse effects, such as hypotension, arthralgia, malaise, and nausea, are usually self-limited. With mild infusion reactions (1 in 200), the infusion can be stopped until symptoms improve and can be resumed at a slower rate.²⁷

Continue to: The role of blood transfusion...

The role of blood transfusion

Blood transfusion is expensive and potentially hazardous, so its use is limited to treatment of acute blood loss or severe anemia.

A one-time red blood cell transfusion does not impact diagnostic criteria to assess for iron deficiency with ferritin, and it does not improve underlying iron deficiency.²⁸Patients with acute blood loss anemia superimposed on chronic blood loss should be screened and treated for iron deficiency even after receiving a transfusion.

Since ferritin levels can rise significantly as an acute phase reactant, even following a hemorrhage, iron deficiency during inflammation is defined as ferritin less than 70 ng/mL.

The potential for iron overload

Since iron is never metabolized or excreted, it is possible to have iron overload following accidental overdose, transfusion dependency, and disorders of iron transport, such as hemochromatosis and thalassemia.

While a low ferritin level always indicates iron deficiency, high ferritin levels can be an acute phase reactant. Ferritin levels greater than 150 ng/mL in healthy menstruating individuals and greater than 500 ng/mL in unhealthy individuals should raise concern for excess iron and should prompt discontinuation of iron intake or workup for conditions at risk for overload.⁵

Oral iron supplements should be stored away from small children, who are at particular risk of toxicity.

How long to treat?

Treatment duration depends on the individual’s degree of iron deficiency, whether anemia is present, and the amount of ongoing blood loss. The main treatment goal is normalization and maintenance of serum ferritin.

Successful treatment should be confirmed with a complete blood count and ferritin level. Hemoglobin levels improve 2 g/dL after 3 weeks of oral iron therapy, but repletion may take 4 to 6 months.^23,29 The American College of Obstetricians and Gynecologists recommends 3 to 6 months of continued iron therapy after resolution of HMB.¹⁹

In a comparative study of treatment for HMB with the 52-mg LNG IUD versus hysterectomy, hemoglobin levels increased in both treatment groups but stayed lower in those with initial anemia.⁸ Ferritin levels normalized only after 5 years and were still lower in individuals with initial anemia.

Increase in hemoglobin is faster after intravenous iron administration but is equivalent to oral therapy by 12 weeks. If management to reduce menstrual losses is discontinued, periodic or maintenance iron repletion will be necessary.

CASE Management plan initiated

This 17-year-old patient with iron deficiency resulting from HMB requests management to reduce menstrual iron losses with a preference for predictable menses. We have already completed a basic workup, which could also include assessment for hypermobility with a Beighton score, as connective tissue disorders also are associated with HMB.³⁰ We discuss the options of cyclic hormonal therapy, antifibrinolytic treatment, and an LNG IUD. The patient is concerned about adherence and wants to avoid unscheduled bleeding, so she opts for a trial of tranexamic acid 1,300 mg 3 times daily for 5 days during menses. This regimen results in a 50% reduction in bleeding amount, which the patient finds satisfactory. Iron repletion with oral ferrous sulfate 325 mg (containing 65 mg of elemental iron) is administered on alternating days with vitamin C taken 1 hour prior to dinner. Repeat laboratory test results at 3 weeks show improvement to a hemoglobin level of 14.2 g/dL and a ferritin level of 12 ng/mL. By 3 months, her ferritin levels are greater than 30 ng/mL and oral iron is administered only during menses.

Summing up

Chronic HMB results in a progressive net loss of iron and eventual anemia. Screening with complete blood count and ferritin and early treatment of low iron storage when ferritin is less than 30 ng/mL will help avoid symptoms. Any amount of reduction of menstrual blood loss can be beneficial, allowing a variety of effective hormonal and nonhormonal treatment options. ●

NEW ORLEANS – Assessing underlying mechanisms for the effects of age, mean platelet volume (MPV), and tryptase may help identify pediatric patients with chronic spontaneous urticaria (CSU) who will respond to different treatment options, results from a single-center prospective study showed.

“Given that the majority of CSU cases in adults are due to autoimmunity and there being very [few] studies on biomarkers for CSU in children, our study furthers our current understanding of the role of different biomarkers in treatment response,” lead study author Alex Nguyen, MsC, said in an interview at the annual meeting of the American Academy of Dermatology, where the study was presented during a poster session.

NEW ORLEANS – Assessing underlying mechanisms for the effects of age, mean platelet volume (MPV), and tryptase may help identify pediatric patients with chronic spontaneous urticaria (CSU) who will respond to different treatment options, results from a single-center prospective study showed.

“Given that the majority of CSU cases in adults are due to autoimmunity and there being very [few] studies on biomarkers for CSU in children, our study furthers our current understanding of the role of different biomarkers in treatment response,” lead study author Alex Nguyen, MsC, said in an interview at the annual meeting of the American Academy of Dermatology, where the study was presented during a poster session.

NEW ORLEANS – Assessing underlying mechanisms for the effects of age, mean platelet volume (MPV), and tryptase may help identify pediatric patients with chronic spontaneous urticaria (CSU) who will respond to different treatment options, results from a single-center prospective study showed.

“Given that the majority of CSU cases in adults are due to autoimmunity and there being very [few] studies on biomarkers for CSU in children, our study furthers our current understanding of the role of different biomarkers in treatment response,” lead study author Alex Nguyen, MsC, said in an interview at the annual meeting of the American Academy of Dermatology, where the study was presented during a poster session.

NEW ORLEANS – All but one Janus kinase (JAK) inhibitor with dermatologic indications carries a boxed warning that lists multiple risks for drugs in this class, including the risk of major adverse cardiac events (MACE), even though the basis for all the risks is a rheumatoid arthritis study, according to a critical review at the annual meeting of the American Academy of Dermatology.  

Given the fact that the postmarketing RA study was specifically enriched with high-risk patients by requiring an age at enrollment of at least 50 years and the presence of at least one cardiovascular risk factor, the extrapolation of these risks to dermatologic indications is “not necessarily data-driven,” said Brett A. King, MD, PhD, associate professor of dermatology, Yale University, New Haven, Conn.

The recently approved deucravacitinib is the only JAK inhibitor that has so far been exempt from these warnings. Instead, based on the ORAL Surveillance study, published in the New England Journal of Medicine, the Food and Drug Administration requires a boxed warning in nearly identical language for all the other JAK inhibitors. Relative to tofacitinib, the JAK inhibitor tested in ORAL Surveillance, many of these drugs differ by JAK selectivity and other characteristics that are likely relevant to risk of adverse events, Dr. King said. The same language has even been applied to topical ruxolitinib cream. 
 

Basis of boxed warnings

In ORAL Surveillance, about 4,300 high-risk patients with RA were randomized to one of two doses of tofacitinib (5 mg or 10 mg) twice daily or a tumor necrosis factor (TNF) inhibitor. All patients in the trial were taking methotrexate, and almost 60% were taking concomitant corticosteroids. The average body mass index of the study population was about 30 kg/m².

After a median 4 years of follow-up (about 5,000 patient-years), the incidence of many of the adverse events tracked in the study were higher in the tofacitinib groups, including serious infections, MACE, thromboembolic events, and cancer. Dr. King did not challenge the importance of these data, but he questioned whether they are reasonably extrapolated to dermatologic indications, particularly as many of those treated are younger than those common to an RA population.

In fact, despite a study enriched for a higher risk of many events tracked, most adverse events were only slightly elevated, Dr. King pointed out. For example, the incidence of MACE over the 4 years of follow-up was 3.4% among those taking any dose of tofacitinib versus 2.5% of those randomized to TNF inhibitor. Rates of cancer were 4.2% versus 2.9%, respectively. There were also absolute increases in the number of serious infections and thromboembolic events for tofacitinib relative to TNF inhibitor.

Dr. King acknowledged that the numbers in ORAL Surveillance associated tofacitinib with a higher risk of serious events than TNF inhibitor in patients with RA, but he believes that “JAK inhibitor safety is almost certainly not the same in dermatology as it is in rheumatology patients.”
 

Evidence of difference in dermatology

There is some evidence to back this up. Dr. King cited a recently published study in RMD Open that evaluated the safety profile of the JAK inhibitor upadacitinib in nearly 7,000 patients over 15,000 patient-years of follow-up. Drug safety data were evaluated with up to 5.5 years of follow-up from 12 clinical trials of the four diseases for which upadacitinib is now indicated. Three were rheumatologic (RA, psoriatic arthritis, and ankylosing spondylitis), and the fourth was atopic dermatitis (AD). Fourteen outcomes, including numerous types of infection, MACE, hepatic complications, and malignancy, were compared with methotrexate and the TNF inhibitor adalimumab.

For the RA diseases, upadacitinib was associated with a greater risk than comparators for several outcomes, including serious infections. But in AD, there was a smaller increased risk of adverse outcomes for the JAK inhibitor relative to comparators.

When evaluated by risk of adverse events across indications, for MACE, the exposure-adjusted event rates for upadacitinib were less than 0.1 in patients treated for AD over the observation period versus 0.3 and 0.4 for RA and psoriatic arthritis, respectively. Similarly, for venous thromboembolism, the rates for upadacitinib were again less than 0.1 in patients with AD versus 0.4 and 0.2 in RA and psoriatic arthritis, respectively.

Referring back to the postmarketing study, Dr. King emphasized that it is essential to consider how the boxed warning for JAK inhibitors was generated before applying them to dermatologic indications.

“Is a 30-year-old patient with a dermatologic disorder possibly at the same risk as the patients in the study from which we got the boxed warning? The answer is simply no,” he said.

Like the tofacitinib data in the ORAL Surveillance study, the upadacitinib clinical trial data are not necessarily relevant to other JAK inhibitors. In fact, Dr. King pointed out that the safety profiles of the available JAK inhibitors are not identical, an observation that is consistent with differences in JAK inhibitor selectivity that has implications for off-target events.  

Dr. King does not dismiss the potential risks outlined in the current regulatory cautions about the use of JAK inhibitors, but he believes that dermatologists should be cognizant of “where the black box warning comes from.”

“We need to think carefully about the risk-to-benefit ratio in older patients or patients with risk factors, such as obesity and diabetes,” he said. But the safety profile of JAK inhibitors “is almost certainly better” than the profile suggested in boxed warnings applied to JAK inhibitors for dermatologic indications, he advised.
 

Risk-benefit considerations in dermatology

This position was supported by numerous other experts when asked for their perspectives. “I fully agree,” said Emma Guttman-Yassky, MD, PhD, system chair of dermatology and immunology, Icahn School of Medicine, Mount Sinai, New York.

Like Dr. King, Dr. Guttman-Yassky did not dismiss the potential risks of JAK inhibitors when treating dermatologic diseases.

“While JAK inhibitors need monitoring as advised, adopting a boxed warning from an RA study for patients who are older [is problematic],” she commented. A study with the nonselective tofacitinib in this population “cannot be compared to more selective inhibitors in a much younger population, such as those treated [for] alopecia areata or atopic dermatitis.”

George Z. Han, MD, PhD, an associate professor of dermatology, Zucker School of Medicine, Hofstra, Northwell Medical Center, New Hyde Park, New York, also agreed but added some caveats.

“The comments about the ORAL Surveillance study are salient,” he said in an interview. “This kind of data should not directly be extrapolated to other patient types or to other medications.” However, one of Dr. Han’s most important caveats involves long-term use.

“JAK inhibitors are still relatively narrow-therapeutic-window drugs that in a dose-dependent fashion could lead to negative effects, including thromboembolic events, abnormalities in red blood cells, white blood cells, platelets, and lipids,” he said. While doses used in dermatology “are generally below the level of any major concern,” Dr. Han cautioned that “we lack definitive data” on long-term use, and this is important for understanding “any potential small risk of rare events, such as malignancy or thromboembolism.”

Saakshi Khattri, MD, a colleague of Dr. Guttman-Yassky at Mount Sinai, said the risks of JAK inhibitors should not be underestimated, but she also agreed that risk “needs to be delivered in the right context.” Dr. Khattri, who is board certified in both dermatology and rheumatology, noted the safety profiles of available JAK inhibitors differ and that extrapolating safety from an RA study to dermatologic indications does not make sense. “Different diseases, different age groups,” she said.

Dr. King has reported financial relationships with more than 15 pharmaceutical companies, including companies that make JAK inhibitors. Dr. Guttman-Yassky has reported financial relationships with more than 20 pharmaceutical companies, including companies that make JAK inhibitors. Dr. Han reports financial relationships with Amgen, Athenex, Boehringer Ingelheim, Bond Avillion, Bristol-Myers Squibb, Celgene, Janssen, Lilly, Novartis, PellePharm, Pfizer, and UCB. Dr. Khattri has reported financial relationships with AbbVie, Arcutis, Bristol-Myers Squibb, Janssen, Leo, Lilly, Novartis, Pfizer, and UCB.

A version of this article originally appeared on Medscape.com.

NEW ORLEANS – All but one Janus kinase (JAK) inhibitor with dermatologic indications carries a boxed warning that lists multiple risks for drugs in this class, including the risk of major adverse cardiac events (MACE), even though the basis for all the risks is a rheumatoid arthritis study, according to a critical review at the annual meeting of the American Academy of Dermatology.  

Given the fact that the postmarketing RA study was specifically enriched with high-risk patients by requiring an age at enrollment of at least 50 years and the presence of at least one cardiovascular risk factor, the extrapolation of these risks to dermatologic indications is “not necessarily data-driven,” said Brett A. King, MD, PhD, associate professor of dermatology, Yale University, New Haven, Conn.

The recently approved deucravacitinib is the only JAK inhibitor that has so far been exempt from these warnings. Instead, based on the ORAL Surveillance study, published in the New England Journal of Medicine, the Food and Drug Administration requires a boxed warning in nearly identical language for all the other JAK inhibitors. Relative to tofacitinib, the JAK inhibitor tested in ORAL Surveillance, many of these drugs differ by JAK selectivity and other characteristics that are likely relevant to risk of adverse events, Dr. King said. The same language has even been applied to topical ruxolitinib cream. 
 

Basis of boxed warnings

In ORAL Surveillance, about 4,300 high-risk patients with RA were randomized to one of two doses of tofacitinib (5 mg or 10 mg) twice daily or a tumor necrosis factor (TNF) inhibitor. All patients in the trial were taking methotrexate, and almost 60% were taking concomitant corticosteroids. The average body mass index of the study population was about 30 kg/m².

After a median 4 years of follow-up (about 5,000 patient-years), the incidence of many of the adverse events tracked in the study were higher in the tofacitinib groups, including serious infections, MACE, thromboembolic events, and cancer. Dr. King did not challenge the importance of these data, but he questioned whether they are reasonably extrapolated to dermatologic indications, particularly as many of those treated are younger than those common to an RA population.

In fact, despite a study enriched for a higher risk of many events tracked, most adverse events were only slightly elevated, Dr. King pointed out. For example, the incidence of MACE over the 4 years of follow-up was 3.4% among those taking any dose of tofacitinib versus 2.5% of those randomized to TNF inhibitor. Rates of cancer were 4.2% versus 2.9%, respectively. There were also absolute increases in the number of serious infections and thromboembolic events for tofacitinib relative to TNF inhibitor.

Dr. King acknowledged that the numbers in ORAL Surveillance associated tofacitinib with a higher risk of serious events than TNF inhibitor in patients with RA, but he believes that “JAK inhibitor safety is almost certainly not the same in dermatology as it is in rheumatology patients.”
 

Evidence of difference in dermatology

There is some evidence to back this up. Dr. King cited a recently published study in RMD Open that evaluated the safety profile of the JAK inhibitor upadacitinib in nearly 7,000 patients over 15,000 patient-years of follow-up. Drug safety data were evaluated with up to 5.5 years of follow-up from 12 clinical trials of the four diseases for which upadacitinib is now indicated. Three were rheumatologic (RA, psoriatic arthritis, and ankylosing spondylitis), and the fourth was atopic dermatitis (AD). Fourteen outcomes, including numerous types of infection, MACE, hepatic complications, and malignancy, were compared with methotrexate and the TNF inhibitor adalimumab.

For the RA diseases, upadacitinib was associated with a greater risk than comparators for several outcomes, including serious infections. But in AD, there was a smaller increased risk of adverse outcomes for the JAK inhibitor relative to comparators.

When evaluated by risk of adverse events across indications, for MACE, the exposure-adjusted event rates for upadacitinib were less than 0.1 in patients treated for AD over the observation period versus 0.3 and 0.4 for RA and psoriatic arthritis, respectively. Similarly, for venous thromboembolism, the rates for upadacitinib were again less than 0.1 in patients with AD versus 0.4 and 0.2 in RA and psoriatic arthritis, respectively.

Referring back to the postmarketing study, Dr. King emphasized that it is essential to consider how the boxed warning for JAK inhibitors was generated before applying them to dermatologic indications.

“Is a 30-year-old patient with a dermatologic disorder possibly at the same risk as the patients in the study from which we got the boxed warning? The answer is simply no,” he said.

Like the tofacitinib data in the ORAL Surveillance study, the upadacitinib clinical trial data are not necessarily relevant to other JAK inhibitors. In fact, Dr. King pointed out that the safety profiles of the available JAK inhibitors are not identical, an observation that is consistent with differences in JAK inhibitor selectivity that has implications for off-target events.  

Dr. King does not dismiss the potential risks outlined in the current regulatory cautions about the use of JAK inhibitors, but he believes that dermatologists should be cognizant of “where the black box warning comes from.”

“We need to think carefully about the risk-to-benefit ratio in older patients or patients with risk factors, such as obesity and diabetes,” he said. But the safety profile of JAK inhibitors “is almost certainly better” than the profile suggested in boxed warnings applied to JAK inhibitors for dermatologic indications, he advised.
 

Risk-benefit considerations in dermatology

This position was supported by numerous other experts when asked for their perspectives. “I fully agree,” said Emma Guttman-Yassky, MD, PhD, system chair of dermatology and immunology, Icahn School of Medicine, Mount Sinai, New York.

Like Dr. King, Dr. Guttman-Yassky did not dismiss the potential risks of JAK inhibitors when treating dermatologic diseases.

“While JAK inhibitors need monitoring as advised, adopting a boxed warning from an RA study for patients who are older [is problematic],” she commented. A study with the nonselective tofacitinib in this population “cannot be compared to more selective inhibitors in a much younger population, such as those treated [for] alopecia areata or atopic dermatitis.”

George Z. Han, MD, PhD, an associate professor of dermatology, Zucker School of Medicine, Hofstra, Northwell Medical Center, New Hyde Park, New York, also agreed but added some caveats.

“The comments about the ORAL Surveillance study are salient,” he said in an interview. “This kind of data should not directly be extrapolated to other patient types or to other medications.” However, one of Dr. Han’s most important caveats involves long-term use.

“JAK inhibitors are still relatively narrow-therapeutic-window drugs that in a dose-dependent fashion could lead to negative effects, including thromboembolic events, abnormalities in red blood cells, white blood cells, platelets, and lipids,” he said. While doses used in dermatology “are generally below the level of any major concern,” Dr. Han cautioned that “we lack definitive data” on long-term use, and this is important for understanding “any potential small risk of rare events, such as malignancy or thromboembolism.”

Saakshi Khattri, MD, a colleague of Dr. Guttman-Yassky at Mount Sinai, said the risks of JAK inhibitors should not be underestimated, but she also agreed that risk “needs to be delivered in the right context.” Dr. Khattri, who is board certified in both dermatology and rheumatology, noted the safety profiles of available JAK inhibitors differ and that extrapolating safety from an RA study to dermatologic indications does not make sense. “Different diseases, different age groups,” she said.

Dr. King has reported financial relationships with more than 15 pharmaceutical companies, including companies that make JAK inhibitors. Dr. Guttman-Yassky has reported financial relationships with more than 20 pharmaceutical companies, including companies that make JAK inhibitors. Dr. Han reports financial relationships with Amgen, Athenex, Boehringer Ingelheim, Bond Avillion, Bristol-Myers Squibb, Celgene, Janssen, Lilly, Novartis, PellePharm, Pfizer, and UCB. Dr. Khattri has reported financial relationships with AbbVie, Arcutis, Bristol-Myers Squibb, Janssen, Leo, Lilly, Novartis, Pfizer, and UCB.

A version of this article originally appeared on Medscape.com.

NEW ORLEANS – All but one Janus kinase (JAK) inhibitor with dermatologic indications carries a boxed warning that lists multiple risks for drugs in this class, including the risk of major adverse cardiac events (MACE), even though the basis for all the risks is a rheumatoid arthritis study, according to a critical review at the annual meeting of the American Academy of Dermatology.  

Given the fact that the postmarketing RA study was specifically enriched with high-risk patients by requiring an age at enrollment of at least 50 years and the presence of at least one cardiovascular risk factor, the extrapolation of these risks to dermatologic indications is “not necessarily data-driven,” said Brett A. King, MD, PhD, associate professor of dermatology, Yale University, New Haven, Conn.

The recently approved deucravacitinib is the only JAK inhibitor that has so far been exempt from these warnings. Instead, based on the ORAL Surveillance study, published in the New England Journal of Medicine, the Food and Drug Administration requires a boxed warning in nearly identical language for all the other JAK inhibitors. Relative to tofacitinib, the JAK inhibitor tested in ORAL Surveillance, many of these drugs differ by JAK selectivity and other characteristics that are likely relevant to risk of adverse events, Dr. King said. The same language has even been applied to topical ruxolitinib cream. 
 

Basis of boxed warnings

In ORAL Surveillance, about 4,300 high-risk patients with RA were randomized to one of two doses of tofacitinib (5 mg or 10 mg) twice daily or a tumor necrosis factor (TNF) inhibitor. All patients in the trial were taking methotrexate, and almost 60% were taking concomitant corticosteroids. The average body mass index of the study population was about 30 kg/m².

After a median 4 years of follow-up (about 5,000 patient-years), the incidence of many of the adverse events tracked in the study were higher in the tofacitinib groups, including serious infections, MACE, thromboembolic events, and cancer. Dr. King did not challenge the importance of these data, but he questioned whether they are reasonably extrapolated to dermatologic indications, particularly as many of those treated are younger than those common to an RA population.

In fact, despite a study enriched for a higher risk of many events tracked, most adverse events were only slightly elevated, Dr. King pointed out. For example, the incidence of MACE over the 4 years of follow-up was 3.4% among those taking any dose of tofacitinib versus 2.5% of those randomized to TNF inhibitor. Rates of cancer were 4.2% versus 2.9%, respectively. There were also absolute increases in the number of serious infections and thromboembolic events for tofacitinib relative to TNF inhibitor.

Dr. King acknowledged that the numbers in ORAL Surveillance associated tofacitinib with a higher risk of serious events than TNF inhibitor in patients with RA, but he believes that “JAK inhibitor safety is almost certainly not the same in dermatology as it is in rheumatology patients.”
 

Evidence of difference in dermatology

There is some evidence to back this up. Dr. King cited a recently published study in RMD Open that evaluated the safety profile of the JAK inhibitor upadacitinib in nearly 7,000 patients over 15,000 patient-years of follow-up. Drug safety data were evaluated with up to 5.5 years of follow-up from 12 clinical trials of the four diseases for which upadacitinib is now indicated. Three were rheumatologic (RA, psoriatic arthritis, and ankylosing spondylitis), and the fourth was atopic dermatitis (AD). Fourteen outcomes, including numerous types of infection, MACE, hepatic complications, and malignancy, were compared with methotrexate and the TNF inhibitor adalimumab.

For the RA diseases, upadacitinib was associated with a greater risk than comparators for several outcomes, including serious infections. But in AD, there was a smaller increased risk of adverse outcomes for the JAK inhibitor relative to comparators.

When evaluated by risk of adverse events across indications, for MACE, the exposure-adjusted event rates for upadacitinib were less than 0.1 in patients treated for AD over the observation period versus 0.3 and 0.4 for RA and psoriatic arthritis, respectively. Similarly, for venous thromboembolism, the rates for upadacitinib were again less than 0.1 in patients with AD versus 0.4 and 0.2 in RA and psoriatic arthritis, respectively.

Referring back to the postmarketing study, Dr. King emphasized that it is essential to consider how the boxed warning for JAK inhibitors was generated before applying them to dermatologic indications.

“Is a 30-year-old patient with a dermatologic disorder possibly at the same risk as the patients in the study from which we got the boxed warning? The answer is simply no,” he said.

Like the tofacitinib data in the ORAL Surveillance study, the upadacitinib clinical trial data are not necessarily relevant to other JAK inhibitors. In fact, Dr. King pointed out that the safety profiles of the available JAK inhibitors are not identical, an observation that is consistent with differences in JAK inhibitor selectivity that has implications for off-target events.  

Dr. King does not dismiss the potential risks outlined in the current regulatory cautions about the use of JAK inhibitors, but he believes that dermatologists should be cognizant of “where the black box warning comes from.”

“We need to think carefully about the risk-to-benefit ratio in older patients or patients with risk factors, such as obesity and diabetes,” he said. But the safety profile of JAK inhibitors “is almost certainly better” than the profile suggested in boxed warnings applied to JAK inhibitors for dermatologic indications, he advised.
 

Risk-benefit considerations in dermatology

This position was supported by numerous other experts when asked for their perspectives. “I fully agree,” said Emma Guttman-Yassky, MD, PhD, system chair of dermatology and immunology, Icahn School of Medicine, Mount Sinai, New York.

Like Dr. King, Dr. Guttman-Yassky did not dismiss the potential risks of JAK inhibitors when treating dermatologic diseases.

“While JAK inhibitors need monitoring as advised, adopting a boxed warning from an RA study for patients who are older [is problematic],” she commented. A study with the nonselective tofacitinib in this population “cannot be compared to more selective inhibitors in a much younger population, such as those treated [for] alopecia areata or atopic dermatitis.”

George Z. Han, MD, PhD, an associate professor of dermatology, Zucker School of Medicine, Hofstra, Northwell Medical Center, New Hyde Park, New York, also agreed but added some caveats.

“The comments about the ORAL Surveillance study are salient,” he said in an interview. “This kind of data should not directly be extrapolated to other patient types or to other medications.” However, one of Dr. Han’s most important caveats involves long-term use.

“JAK inhibitors are still relatively narrow-therapeutic-window drugs that in a dose-dependent fashion could lead to negative effects, including thromboembolic events, abnormalities in red blood cells, white blood cells, platelets, and lipids,” he said. While doses used in dermatology “are generally below the level of any major concern,” Dr. Han cautioned that “we lack definitive data” on long-term use, and this is important for understanding “any potential small risk of rare events, such as malignancy or thromboembolism.”

Saakshi Khattri, MD, a colleague of Dr. Guttman-Yassky at Mount Sinai, said the risks of JAK inhibitors should not be underestimated, but she also agreed that risk “needs to be delivered in the right context.” Dr. Khattri, who is board certified in both dermatology and rheumatology, noted the safety profiles of available JAK inhibitors differ and that extrapolating safety from an RA study to dermatologic indications does not make sense. “Different diseases, different age groups,” she said.

Dr. King has reported financial relationships with more than 15 pharmaceutical companies, including companies that make JAK inhibitors. Dr. Guttman-Yassky has reported financial relationships with more than 20 pharmaceutical companies, including companies that make JAK inhibitors. Dr. Han reports financial relationships with Amgen, Athenex, Boehringer Ingelheim, Bond Avillion, Bristol-Myers Squibb, Celgene, Janssen, Lilly, Novartis, PellePharm, Pfizer, and UCB. Dr. Khattri has reported financial relationships with AbbVie, Arcutis, Bristol-Myers Squibb, Janssen, Leo, Lilly, Novartis, Pfizer, and UCB.

A version of this article originally appeared on Medscape.com.

The only true wisdom is in knowing you know nothing. – Socrates

At what age is one supposed to be wise? I feel like I’m falling behind. I’ve crossed the middle of life and can check the prerequisite experiences: Joy, tragedy, love, adventure, love again. I lived a jetsetter life with an overnight bag always packed. I’ve sported the “Dad AF” tee with a fully loaded dad-pack. I’ve seen the 50 states and had my picture wrapped on a city bus (super-weird when you pull up next to one). Yet, when a moment arrives to pop in pithy advice for a resident or drop a few reassuring lines for a grieving friend, I’m often unable to find the words. If life were a video game, I’ve not earned the wisdom level yet.

Who are the wise men and women in your life? It’s difficult to list them. This is because it’s a complex attribute and hard to explain. It’s also because the wise who walk among us are rare. Wise is more than being brilliant at bullous diseases or knowing how to sleep train a baby. Nor is wise the buddy who purchased $1,000 of Bitcoin in 2010 (although stay close with him, he probably owns a jet). Neither content experts nor lucky friends rise to the appellation. To be wise you have to not only make good decisions, but also offer good advice. You need both knowledge and insight. Both experience and empathy.

Public domain/Wikimedia Commons

The ancients considered wisdom to be one of the vital virtues. It was personified in high-profile gods like Apollo and Athena. It’s rare and important enough to be seen as spiritual. It features heavily in the Bible, the Bhagavad Gita, the Meditations of Marcus Aurelius. In some cultures the wise are called elders or sages. In all cultures they are helpful, respected, sought after, appreciated. We need more wise people in this game of life. I want to be one. But there’s no Coursera for it.

To become wise you have to pass through many levels, put in a lot of reps, suffer through many sleepless nights. Like the third molar, also known as the wisdom tooth, it takes years. You also have to emerge stronger and smarter through those experiences. FDR would not have become one of the wisest presidents in history had it not been for his trials, and victories, over polio. Osler missed Cushing syndrome multiple times before he got it right. It seems you have to go to the mountain, like Batman, and fight a few battles to realize your full wisdom potential.

You must also reflect on your experiences and hone your insight. The management sage Peter Drucker would write what he expected to happen after a decision. Then he’d return to it to hone his intuition and judgment.

Lastly, you have to use your powers for good. Using insight to win your NCAA bracket pool isn’t wisdom. Helping a friend whose marriage is falling apart or colleague whose patient is suing them or a resident whose excision hit an arteriole surely is.

I’ve got a ways to go before anyone puts me on their wise friend list. I’m working on it though. Perhaps you will too – we are desperately short-staffed in this area. For now, I can start with writing better condolences.



“Who maintains that it is not a heavy blow? But it is part of being human.” – Seneca

Dr. Benabio is director of Healthcare Transformation and chief of dermatology at Kaiser Permanente San Diego. The opinions expressed in this column are his own and do not represent those of Kaiser Permanente. Dr. Benabio is @Dermdoc on Twitter. Write to him at [email protected].

The only true wisdom is in knowing you know nothing. – Socrates

At what age is one supposed to be wise? I feel like I’m falling behind. I’ve crossed the middle of life and can check the prerequisite experiences: Joy, tragedy, love, adventure, love again. I lived a jetsetter life with an overnight bag always packed. I’ve sported the “Dad AF” tee with a fully loaded dad-pack. I’ve seen the 50 states and had my picture wrapped on a city bus (super-weird when you pull up next to one). Yet, when a moment arrives to pop in pithy advice for a resident or drop a few reassuring lines for a grieving friend, I’m often unable to find the words. If life were a video game, I’ve not earned the wisdom level yet.

Who are the wise men and women in your life? It’s difficult to list them. This is because it’s a complex attribute and hard to explain. It’s also because the wise who walk among us are rare. Wise is more than being brilliant at bullous diseases or knowing how to sleep train a baby. Nor is wise the buddy who purchased $1,000 of Bitcoin in 2010 (although stay close with him, he probably owns a jet). Neither content experts nor lucky friends rise to the appellation. To be wise you have to not only make good decisions, but also offer good advice. You need both knowledge and insight. Both experience and empathy.

Public domain/Wikimedia Commons

The ancients considered wisdom to be one of the vital virtues. It was personified in high-profile gods like Apollo and Athena. It’s rare and important enough to be seen as spiritual. It features heavily in the Bible, the Bhagavad Gita, the Meditations of Marcus Aurelius. In some cultures the wise are called elders or sages. In all cultures they are helpful, respected, sought after, appreciated. We need more wise people in this game of life. I want to be one. But there’s no Coursera for it.

To become wise you have to pass through many levels, put in a lot of reps, suffer through many sleepless nights. Like the third molar, also known as the wisdom tooth, it takes years. You also have to emerge stronger and smarter through those experiences. FDR would not have become one of the wisest presidents in history had it not been for his trials, and victories, over polio. Osler missed Cushing syndrome multiple times before he got it right. It seems you have to go to the mountain, like Batman, and fight a few battles to realize your full wisdom potential.

You must also reflect on your experiences and hone your insight. The management sage Peter Drucker would write what he expected to happen after a decision. Then he’d return to it to hone his intuition and judgment.

Lastly, you have to use your powers for good. Using insight to win your NCAA bracket pool isn’t wisdom. Helping a friend whose marriage is falling apart or colleague whose patient is suing them or a resident whose excision hit an arteriole surely is.

I’ve got a ways to go before anyone puts me on their wise friend list. I’m working on it though. Perhaps you will too – we are desperately short-staffed in this area. For now, I can start with writing better condolences.



“Who maintains that it is not a heavy blow? But it is part of being human.” – Seneca

Dr. Benabio is director of Healthcare Transformation and chief of dermatology at Kaiser Permanente San Diego. The opinions expressed in this column are his own and do not represent those of Kaiser Permanente. Dr. Benabio is @Dermdoc on Twitter. Write to him at [email protected].

The only true wisdom is in knowing you know nothing. – Socrates

At what age is one supposed to be wise? I feel like I’m falling behind. I’ve crossed the middle of life and can check the prerequisite experiences: Joy, tragedy, love, adventure, love again. I lived a jetsetter life with an overnight bag always packed. I’ve sported the “Dad AF” tee with a fully loaded dad-pack. I’ve seen the 50 states and had my picture wrapped on a city bus (super-weird when you pull up next to one). Yet, when a moment arrives to pop in pithy advice for a resident or drop a few reassuring lines for a grieving friend, I’m often unable to find the words. If life were a video game, I’ve not earned the wisdom level yet.

Who are the wise men and women in your life? It’s difficult to list them. This is because it’s a complex attribute and hard to explain. It’s also because the wise who walk among us are rare. Wise is more than being brilliant at bullous diseases or knowing how to sleep train a baby. Nor is wise the buddy who purchased $1,000 of Bitcoin in 2010 (although stay close with him, he probably owns a jet). Neither content experts nor lucky friends rise to the appellation. To be wise you have to not only make good decisions, but also offer good advice. You need both knowledge and insight. Both experience and empathy.

Public domain/Wikimedia Commons

The ancients considered wisdom to be one of the vital virtues. It was personified in high-profile gods like Apollo and Athena. It’s rare and important enough to be seen as spiritual. It features heavily in the Bible, the Bhagavad Gita, the Meditations of Marcus Aurelius. In some cultures the wise are called elders or sages. In all cultures they are helpful, respected, sought after, appreciated. We need more wise people in this game of life. I want to be one. But there’s no Coursera for it.

To become wise you have to pass through many levels, put in a lot of reps, suffer through many sleepless nights. Like the third molar, also known as the wisdom tooth, it takes years. You also have to emerge stronger and smarter through those experiences. FDR would not have become one of the wisest presidents in history had it not been for his trials, and victories, over polio. Osler missed Cushing syndrome multiple times before he got it right. It seems you have to go to the mountain, like Batman, and fight a few battles to realize your full wisdom potential.

You must also reflect on your experiences and hone your insight. The management sage Peter Drucker would write what he expected to happen after a decision. Then he’d return to it to hone his intuition and judgment.

Lastly, you have to use your powers for good. Using insight to win your NCAA bracket pool isn’t wisdom. Helping a friend whose marriage is falling apart or colleague whose patient is suing them or a resident whose excision hit an arteriole surely is.

I’ve got a ways to go before anyone puts me on their wise friend list. I’m working on it though. Perhaps you will too – we are desperately short-staffed in this area. For now, I can start with writing better condolences.



“Who maintains that it is not a heavy blow? But it is part of being human.” – Seneca

Dr. Benabio is director of Healthcare Transformation and chief of dermatology at Kaiser Permanente San Diego. The opinions expressed in this column are his own and do not represent those of Kaiser Permanente. Dr. Benabio is @Dermdoc on Twitter. Write to him at [email protected].

Lanolin, known mainly for its emollient properties, has been named by the American Contact Dermatitis Society as the Contact Allergen of the Year for 2023.

Lanolin is a complex and varying mixture of high molecular weight esters, aliphatic alcohols, sterols, fatty acids, and hydrocarbons, but the allergic components are mainly the free lanolin alcohols, especially alkanediols, said Donald V. Belsito, MD, professor of dermatology, Columbia University, New York, who announced the Allergen of the Year at the society’s annual meeting.

Criteria for selection can include a known allergen with a new twist or increasing frequency or a newly reported allergen with mini-epidemics that may have been missed for years, Dr. Belsito said.

“The prevalence and severity of allergy to ‘lanolin’ have been hotly debated” since a potential case was first reported in the 1920s, wrote Dr. Belsito and Blair A. Jenkins, MD, PhD, a dermatology resident at New York–Presbyterian Hospital, Columbia Campus, in a review published in Dermatitis.

“ ‘Lanolin’ is indeed a paradox allergen,” wrote Dr. Jenkins and Dr. Belsito. “The most appropriate patch test preparation(s) for detecting allergy remain disputed. Detection of lanolin-induced contact dermatitis in diseased skin by patch testing on normal skin may lead to false negative results.”

And those who test positive for a lanolin allergy on diseased skin may be able to use lanolin products on normal skin, they wrote.

“From my perspective, this was a timely year to think about lanolin, as there is significant ongoing controversy about whether it is allergenic,” Dr. Jenkins said in an interview. “Numerous companies market lanolin-containing topicals as safe and effective emollients,” she said.
 

Medical grade and highly purified anhydrous lanolin, which contain less than 2.5% and less than 1.5% of free alcohols, respectively, can still elicit or induce a contact allergy, Dr. Belsito said in his presentation. Hydrogenated lanolin has shown more allergenicity than lanolin alcohol, while lanolin wax, lanolin acid, and lanolin esters possess lower allergenicity than lanolin alcohol, he said.

Notably, modern wool textiles do not contain lanolin, and lanolin-allergic patients need not avoid wool, Dr. Belsito added.

Amerchol L-101, a common trade name on products containing lanolin, contains 10% wool wax alcohols obtained from the hydrolysis of wool fat dissolved in mineral oil at a 1:1 ratio, said Dr. Belsito. He recommended testing lanolin alcohols (in 30% petrolatum) and Amerchol L-101 (in 50% petrolatum) simultaneously with or without other lanolin derivatives and/or the patient’s products in cases of possible allergy, he said.
 

Consider high-risk groups

Current evidence suggests that the prevalence of contact allergy in the western European population is 0.4%, wrote Dr. Jenkins and Dr. Belsito.

Although the frequency of lanolin allergy is relatively low, certain conditions convey greater risk, such as stasis dermatitis, leg ulcers, perianal/genital dermatitis, and atopic dermatitis, they wrote. Older adults and children are at increased risk because they are more likely to have these conditions. Demographic data also suggest that lanolin allergy is more common in non-Hispanic Whites than in non-Hispanic Blacks, they wrote.

Looking ahead, “I think further exploration of allergy across different skin types and ethnicities is warranted,” Dr. Jenkins said. “Further investigation of ideal [lanolin] allergens for patch testing is also needed.”

Dr. Jenkins and Dr. Belsito said they had no relevant financial conflicts to disclose.

Lanolin, known mainly for its emollient properties, has been named by the American Contact Dermatitis Society as the Contact Allergen of the Year for 2023.

Lanolin is a complex and varying mixture of high molecular weight esters, aliphatic alcohols, sterols, fatty acids, and hydrocarbons, but the allergic components are mainly the free lanolin alcohols, especially alkanediols, said Donald V. Belsito, MD, professor of dermatology, Columbia University, New York, who announced the Allergen of the Year at the society’s annual meeting.

Criteria for selection can include a known allergen with a new twist or increasing frequency or a newly reported allergen with mini-epidemics that may have been missed for years, Dr. Belsito said.

“The prevalence and severity of allergy to ‘lanolin’ have been hotly debated” since a potential case was first reported in the 1920s, wrote Dr. Belsito and Blair A. Jenkins, MD, PhD, a dermatology resident at New York–Presbyterian Hospital, Columbia Campus, in a review published in Dermatitis.

“ ‘Lanolin’ is indeed a paradox allergen,” wrote Dr. Jenkins and Dr. Belsito. “The most appropriate patch test preparation(s) for detecting allergy remain disputed. Detection of lanolin-induced contact dermatitis in diseased skin by patch testing on normal skin may lead to false negative results.”

And those who test positive for a lanolin allergy on diseased skin may be able to use lanolin products on normal skin, they wrote.

“From my perspective, this was a timely year to think about lanolin, as there is significant ongoing controversy about whether it is allergenic,” Dr. Jenkins said in an interview. “Numerous companies market lanolin-containing topicals as safe and effective emollients,” she said.
 

Medical grade and highly purified anhydrous lanolin, which contain less than 2.5% and less than 1.5% of free alcohols, respectively, can still elicit or induce a contact allergy, Dr. Belsito said in his presentation. Hydrogenated lanolin has shown more allergenicity than lanolin alcohol, while lanolin wax, lanolin acid, and lanolin esters possess lower allergenicity than lanolin alcohol, he said.

Notably, modern wool textiles do not contain lanolin, and lanolin-allergic patients need not avoid wool, Dr. Belsito added.

Amerchol L-101, a common trade name on products containing lanolin, contains 10% wool wax alcohols obtained from the hydrolysis of wool fat dissolved in mineral oil at a 1:1 ratio, said Dr. Belsito. He recommended testing lanolin alcohols (in 30% petrolatum) and Amerchol L-101 (in 50% petrolatum) simultaneously with or without other lanolin derivatives and/or the patient’s products in cases of possible allergy, he said.
 

Consider high-risk groups

Current evidence suggests that the prevalence of contact allergy in the western European population is 0.4%, wrote Dr. Jenkins and Dr. Belsito.

Although the frequency of lanolin allergy is relatively low, certain conditions convey greater risk, such as stasis dermatitis, leg ulcers, perianal/genital dermatitis, and atopic dermatitis, they wrote. Older adults and children are at increased risk because they are more likely to have these conditions. Demographic data also suggest that lanolin allergy is more common in non-Hispanic Whites than in non-Hispanic Blacks, they wrote.

Looking ahead, “I think further exploration of allergy across different skin types and ethnicities is warranted,” Dr. Jenkins said. “Further investigation of ideal [lanolin] allergens for patch testing is also needed.”

Dr. Jenkins and Dr. Belsito said they had no relevant financial conflicts to disclose.

Lanolin, known mainly for its emollient properties, has been named by the American Contact Dermatitis Society as the Contact Allergen of the Year for 2023.

Lanolin is a complex and varying mixture of high molecular weight esters, aliphatic alcohols, sterols, fatty acids, and hydrocarbons, but the allergic components are mainly the free lanolin alcohols, especially alkanediols, said Donald V. Belsito, MD, professor of dermatology, Columbia University, New York, who announced the Allergen of the Year at the society’s annual meeting.

Criteria for selection can include a known allergen with a new twist or increasing frequency or a newly reported allergen with mini-epidemics that may have been missed for years, Dr. Belsito said.

“The prevalence and severity of allergy to ‘lanolin’ have been hotly debated” since a potential case was first reported in the 1920s, wrote Dr. Belsito and Blair A. Jenkins, MD, PhD, a dermatology resident at New York–Presbyterian Hospital, Columbia Campus, in a review published in Dermatitis.

“ ‘Lanolin’ is indeed a paradox allergen,” wrote Dr. Jenkins and Dr. Belsito. “The most appropriate patch test preparation(s) for detecting allergy remain disputed. Detection of lanolin-induced contact dermatitis in diseased skin by patch testing on normal skin may lead to false negative results.”

And those who test positive for a lanolin allergy on diseased skin may be able to use lanolin products on normal skin, they wrote.

“From my perspective, this was a timely year to think about lanolin, as there is significant ongoing controversy about whether it is allergenic,” Dr. Jenkins said in an interview. “Numerous companies market lanolin-containing topicals as safe and effective emollients,” she said.
 

Medical grade and highly purified anhydrous lanolin, which contain less than 2.5% and less than 1.5% of free alcohols, respectively, can still elicit or induce a contact allergy, Dr. Belsito said in his presentation. Hydrogenated lanolin has shown more allergenicity than lanolin alcohol, while lanolin wax, lanolin acid, and lanolin esters possess lower allergenicity than lanolin alcohol, he said.

Notably, modern wool textiles do not contain lanolin, and lanolin-allergic patients need not avoid wool, Dr. Belsito added.

Amerchol L-101, a common trade name on products containing lanolin, contains 10% wool wax alcohols obtained from the hydrolysis of wool fat dissolved in mineral oil at a 1:1 ratio, said Dr. Belsito. He recommended testing lanolin alcohols (in 30% petrolatum) and Amerchol L-101 (in 50% petrolatum) simultaneously with or without other lanolin derivatives and/or the patient’s products in cases of possible allergy, he said.
 

Consider high-risk groups

Current evidence suggests that the prevalence of contact allergy in the western European population is 0.4%, wrote Dr. Jenkins and Dr. Belsito.

Although the frequency of lanolin allergy is relatively low, certain conditions convey greater risk, such as stasis dermatitis, leg ulcers, perianal/genital dermatitis, and atopic dermatitis, they wrote. Older adults and children are at increased risk because they are more likely to have these conditions. Demographic data also suggest that lanolin allergy is more common in non-Hispanic Whites than in non-Hispanic Blacks, they wrote.

Looking ahead, “I think further exploration of allergy across different skin types and ethnicities is warranted,” Dr. Jenkins said. “Further investigation of ideal [lanolin] allergens for patch testing is also needed.”

Dr. Jenkins and Dr. Belsito said they had no relevant financial conflicts to disclose.

NEW ORLEANS – Among the 10 most viewed YouTube videos regarding topical steroid withdrawal, patient testimonials had the poorest quality and reliability of all information sources, results from a novel analysis showed.

“Video-sharing platforms such as YouTube are a great place for patients to connect and find community with others dealing with the same conditions,” senior author Adam Friedman, MD, professor and chair of dermatology at George Washington University, Washington, said in an interview in advance of the annual meeting of the American Academy of Dermatology, where the study was presented during an e-poster session. “There is no doubt tremendous value in viewing the shared experience; however, it is important that medical advice be evidence based and validated. Seeking said advice from a medical professional such as a board-certified dermatologist will no doubt increase the likelihood that said guidance is supported by the literature and most importantly, will do no harm.”

Noting a trend of increased user-created content on social media and Internet sites about topical steroid withdrawal in recent years, Dr. Friedman, first author Erika McCormick, a fourth-year medical student at George Washington University, and colleagues used the keywords “topical steroid withdrawal” on YouTube to search for and analyze the top 10 most viewed videos on the subject.

Two independent reviewers used the modified DISCERN (mDISCERN) tool and the Global Quality Scale (GQS) to assess reliability and quality/scientific accuracy of videos, respectively. Average scores were generated for each video and the researchers used one way ANOVA, unpaired t-tests, and linear regression to analyze the ratings. For mDISCERN criteria, a point is given per each of five criteria for a possible score between 0 and 5. Examples of criteria included “Are the aims clear and achieved?” and “Is the information presented both balanced and unbiased”? For GQS, a score from 1 to 5 is designated based on criteria ranging from “poor quality, poor flow, most information missing” to “excellent quality and flow, very useful for patients.”

The researchers found that the mean combined mDISCERN score of the 10 videos was a 2, which indicates poor reliability and shortcomings. Similarly, the combined mean GQS score was 2.5, which suggests poor to moderate quality of videos, missing discussion of important topics, and limited use to patients. The researchers found no correlation between mDISCERN or GQS scores and length of video, duration on YouTube, or number of views, subscribers, or likes.

“We were disheartened that patient testimonial videos had the poorest quality and reliability of the information sources,” Ms. McCormick said in an interview. “Videos that included medical research and information from dermatologists had significantly higher quality and reliability scores than the remainder of videos.” Accurate information online is essential to help patients recognize topical steroid withdrawal and seek medical care, she continued.

Conversely, wide viewership of unreliable information “may contribute to fear of topical corticosteroids and dissuade use in patients with primary skin diseases that may benefit from this common treatment,” Dr. Friedman said. “Dermatologists must be aware of the content patients are consuming online, should guide patients in appraising quality and reliability of online resources, and must provide valid sources of additional information for their patients.” One such resource he recommended is the National Eczema Association, which has created online content for patients about topical steroid withdrawal.

Doris Day, MD, a New York–based dermatologist who was asked to comment on the study, said that many patients rely on YouTube as a go-to resource, with videos that can be watched at times of their choosing. “Oftentimes, the person on the video is relatable and has some general knowledge but is lacking the information that would be relevant and important for the individual patient,” said Dr. Day, who was not involved with the study. “The downside of this is that the person who takes that advice may not use the prescription properly or for the correct amount of time, which can lead to either undertreating or, even worse, overtreatment, which can have permanent consequences.”

One possible solution is for more doctors to create videos for YouTube, she added, “but that doesn’t guarantee that those would be the ones patients would choose to watch.” Another solution “is to have YouTube add qualifiers indicating that the information being discussed is not medical,” she suggested. “Ideally, patients will get all the information they need while they are in the office and also have clear written instructions and even a video they can review at a later time, made by the office, to help them feel they are getting personalized care and the attention they need.”

Ms. McCormick’s research is funded by a grant from Galderma. Dr. Friedman and Dr. Day had no relevant disclosures to report.

NEW ORLEANS – Among the 10 most viewed YouTube videos regarding topical steroid withdrawal, patient testimonials had the poorest quality and reliability of all information sources, results from a novel analysis showed.

“Video-sharing platforms such as YouTube are a great place for patients to connect and find community with others dealing with the same conditions,” senior author Adam Friedman, MD, professor and chair of dermatology at George Washington University, Washington, said in an interview in advance of the annual meeting of the American Academy of Dermatology, where the study was presented during an e-poster session. “There is no doubt tremendous value in viewing the shared experience; however, it is important that medical advice be evidence based and validated. Seeking said advice from a medical professional such as a board-certified dermatologist will no doubt increase the likelihood that said guidance is supported by the literature and most importantly, will do no harm.”

Noting a trend of increased user-created content on social media and Internet sites about topical steroid withdrawal in recent years, Dr. Friedman, first author Erika McCormick, a fourth-year medical student at George Washington University, and colleagues used the keywords “topical steroid withdrawal” on YouTube to search for and analyze the top 10 most viewed videos on the subject.

Two independent reviewers used the modified DISCERN (mDISCERN) tool and the Global Quality Scale (GQS) to assess reliability and quality/scientific accuracy of videos, respectively. Average scores were generated for each video and the researchers used one way ANOVA, unpaired t-tests, and linear regression to analyze the ratings. For mDISCERN criteria, a point is given per each of five criteria for a possible score between 0 and 5. Examples of criteria included “Are the aims clear and achieved?” and “Is the information presented both balanced and unbiased”? For GQS, a score from 1 to 5 is designated based on criteria ranging from “poor quality, poor flow, most information missing” to “excellent quality and flow, very useful for patients.”

The researchers found that the mean combined mDISCERN score of the 10 videos was a 2, which indicates poor reliability and shortcomings. Similarly, the combined mean GQS score was 2.5, which suggests poor to moderate quality of videos, missing discussion of important topics, and limited use to patients. The researchers found no correlation between mDISCERN or GQS scores and length of video, duration on YouTube, or number of views, subscribers, or likes.

“We were disheartened that patient testimonial videos had the poorest quality and reliability of the information sources,” Ms. McCormick said in an interview. “Videos that included medical research and information from dermatologists had significantly higher quality and reliability scores than the remainder of videos.” Accurate information online is essential to help patients recognize topical steroid withdrawal and seek medical care, she continued.

Conversely, wide viewership of unreliable information “may contribute to fear of topical corticosteroids and dissuade use in patients with primary skin diseases that may benefit from this common treatment,” Dr. Friedman said. “Dermatologists must be aware of the content patients are consuming online, should guide patients in appraising quality and reliability of online resources, and must provide valid sources of additional information for their patients.” One such resource he recommended is the National Eczema Association, which has created online content for patients about topical steroid withdrawal.

Doris Day, MD, a New York–based dermatologist who was asked to comment on the study, said that many patients rely on YouTube as a go-to resource, with videos that can be watched at times of their choosing. “Oftentimes, the person on the video is relatable and has some general knowledge but is lacking the information that would be relevant and important for the individual patient,” said Dr. Day, who was not involved with the study. “The downside of this is that the person who takes that advice may not use the prescription properly or for the correct amount of time, which can lead to either undertreating or, even worse, overtreatment, which can have permanent consequences.”

One possible solution is for more doctors to create videos for YouTube, she added, “but that doesn’t guarantee that those would be the ones patients would choose to watch.” Another solution “is to have YouTube add qualifiers indicating that the information being discussed is not medical,” she suggested. “Ideally, patients will get all the information they need while they are in the office and also have clear written instructions and even a video they can review at a later time, made by the office, to help them feel they are getting personalized care and the attention they need.”

Ms. McCormick’s research is funded by a grant from Galderma. Dr. Friedman and Dr. Day had no relevant disclosures to report.

NEW ORLEANS – Among the 10 most viewed YouTube videos regarding topical steroid withdrawal, patient testimonials had the poorest quality and reliability of all information sources, results from a novel analysis showed.

“Video-sharing platforms such as YouTube are a great place for patients to connect and find community with others dealing with the same conditions,” senior author Adam Friedman, MD, professor and chair of dermatology at George Washington University, Washington, said in an interview in advance of the annual meeting of the American Academy of Dermatology, where the study was presented during an e-poster session. “There is no doubt tremendous value in viewing the shared experience; however, it is important that medical advice be evidence based and validated. Seeking said advice from a medical professional such as a board-certified dermatologist will no doubt increase the likelihood that said guidance is supported by the literature and most importantly, will do no harm.”

Noting a trend of increased user-created content on social media and Internet sites about topical steroid withdrawal in recent years, Dr. Friedman, first author Erika McCormick, a fourth-year medical student at George Washington University, and colleagues used the keywords “topical steroid withdrawal” on YouTube to search for and analyze the top 10 most viewed videos on the subject.

Two independent reviewers used the modified DISCERN (mDISCERN) tool and the Global Quality Scale (GQS) to assess reliability and quality/scientific accuracy of videos, respectively. Average scores were generated for each video and the researchers used one way ANOVA, unpaired t-tests, and linear regression to analyze the ratings. For mDISCERN criteria, a point is given per each of five criteria for a possible score between 0 and 5. Examples of criteria included “Are the aims clear and achieved?” and “Is the information presented both balanced and unbiased”? For GQS, a score from 1 to 5 is designated based on criteria ranging from “poor quality, poor flow, most information missing” to “excellent quality and flow, very useful for patients.”

The researchers found that the mean combined mDISCERN score of the 10 videos was a 2, which indicates poor reliability and shortcomings. Similarly, the combined mean GQS score was 2.5, which suggests poor to moderate quality of videos, missing discussion of important topics, and limited use to patients. The researchers found no correlation between mDISCERN or GQS scores and length of video, duration on YouTube, or number of views, subscribers, or likes.

“We were disheartened that patient testimonial videos had the poorest quality and reliability of the information sources,” Ms. McCormick said in an interview. “Videos that included medical research and information from dermatologists had significantly higher quality and reliability scores than the remainder of videos.” Accurate information online is essential to help patients recognize topical steroid withdrawal and seek medical care, she continued.

Conversely, wide viewership of unreliable information “may contribute to fear of topical corticosteroids and dissuade use in patients with primary skin diseases that may benefit from this common treatment,” Dr. Friedman said. “Dermatologists must be aware of the content patients are consuming online, should guide patients in appraising quality and reliability of online resources, and must provide valid sources of additional information for their patients.” One such resource he recommended is the National Eczema Association, which has created online content for patients about topical steroid withdrawal.

Doris Day, MD, a New York–based dermatologist who was asked to comment on the study, said that many patients rely on YouTube as a go-to resource, with videos that can be watched at times of their choosing. “Oftentimes, the person on the video is relatable and has some general knowledge but is lacking the information that would be relevant and important for the individual patient,” said Dr. Day, who was not involved with the study. “The downside of this is that the person who takes that advice may not use the prescription properly or for the correct amount of time, which can lead to either undertreating or, even worse, overtreatment, which can have permanent consequences.”

One possible solution is for more doctors to create videos for YouTube, she added, “but that doesn’t guarantee that those would be the ones patients would choose to watch.” Another solution “is to have YouTube add qualifiers indicating that the information being discussed is not medical,” she suggested. “Ideally, patients will get all the information they need while they are in the office and also have clear written instructions and even a video they can review at a later time, made by the office, to help them feel they are getting personalized care and the attention they need.”

Ms. McCormick’s research is funded by a grant from Galderma. Dr. Friedman and Dr. Day had no relevant disclosures to report.

A common chemical that is used in correction fluid, paint removers, gun cleaners, aerosol cleaning products, and dry cleaning may be the key culprit behind the dramatic increase in Parkinson’s disease (PD), researchers say.

An international team of researchers reviewed previous research and cited data that suggest the chemical trichloroethylene (TCE) is associated with as much as a 500% increased risk for Parkinson’s disease (PD).

Lead investigator Ray Dorsey, MD, professor of neurology, University of Rochester, N.Y., called PD “the world’s fastest-growing brain disease,” and told this news organization that it “may be largely preventable.”

“Countless people have died over generations from cancer and other disease linked to TCE [and] Parkinson’s may be the latest,” he said. “Banning these chemicals, containing contaminated sites, and protecting homes, schools, and buildings at risk may all create a world where Parkinson’s is increasingly rare, not common.”

The paper was published online in the Journal of Parkinson’s Disease.
 

Invisible, ubiquitous

TCE was first synthesized in a lab in 1864, with commercial production beginning in 1920, the researchers noted.

“Because of its unique properties, TCE has had countless industrial, commercial, military, and medical applications,” including producing refrigerants, cleaning electronics, and degreasing engine parts.

In addition, it’s been used in dry cleaning, although a similar chemical (perchloroethylene [PCE]) is currently more widely used for that purpose. Nevertheless, the authors noted, in anaerobic conditions, perchloroethylene often transforms into TCE “and their toxicity may be similar.”

Consumer products in which TCE is found include typewriter correction fluid, paint removers, gun cleaners, and aerosol cleaning products. Up until the 1970s, it was used to decaffeinate coffee.

TCE exposure isn’t confined to those who work with it. It also pollutes outdoor air, taints groundwater, and contaminates indoor air. It’s present in a substantial amount of groundwater in the United States and it “evaporates from underlying soil and groundwater and enters homes, workplaces, or schools, often undetected,” the researchers noted.

“Exposure can come via occupation or the environment and is often largely unknown at the time it occurs,” Dr. Dorsey said.

He noted that the rapid increase in PD incidence cannot be explained by genetic factors alone, which affect only about 15% of patients with PD, nor can it be explained by aging alone. “Certain pesticides ... are likely causes but would not explain the high prevalence of PD in urban areas, as is the case in the U.S.” Rather, “other factors” are involved, and “TCE is likely one such factor.”

Yet, “despite widespread contamination and increasing industrial, commercial, and military use, clinical investigations of TCE and PD have been limited.”

To fill this knowledge gap, Dr. Dorsey and his coauthors of the book, “Ending Parkinson’s Disease: A Prescription for Action,” took a deep dive into studies focusing on the potential association of TCE and PD and presented seven cases to illustrate the association.

“Like many genetic mutations (e.g., Parkin) and other environmental toxicants ... TCE damages the energy-producing parts of cells, i.e., the mitochondria,” said Dr. Dorsey.

TCE and PCE “likely mediate their toxicity through a common metabolite.” Because both are lipophilic, they “readily distribute in the brain and body tissues and appear to cause mitochondrial dysfunction at high doses,” the researchers hypothesized.

Dopaminergic neurons are particularly sensitive to mitochondrial neurotoxicants, so this might “partially explain the link to PD.”

Animal studies have shown that TCE “caused selective loss of dopaminergic neurons.” Moreover, PD-related neuropathology was found in the substantia nigra of rodents exposed to TCE over time. In addition, studies as early as 1960 were showing an association between TCE and parkinsonism.

The authors describe TCE as “ubiquitous” in the 1970s, with 10 million Americans working with the chemical or other organic solvents daily. The review details an extensive list of industries and occupations in which TCE exposure continues to occur.

People working with TCE might inhale it or touch it; but “millions more encounter the chemical unknowingly through outdoor air, contaminated groundwater, and indoor air pollution.”

They noted that TCE contaminates up to one-third of U.S. drinking water, has polluted the groundwater in more than 20 different countries on five continents, and is found in half of the 1,300 most toxic “Superfund” sites that are “part of a federal clean-up program, including 15 in California’s Silicon Valley, where TCE was used to clean electronics.”

Although the U.S. military stopped using TCE, numerous sites have been contaminated, including Marine Corps Base Camp Lejeune in North Carolina, where TCE and PCE were found in drinking water at 280 times the recommended safety standards.

The researchers highlighted seven cases of individuals who developed PD after likely exposure to TCE, including NBA basketball player Brian Grant, who developed symptoms of PD in 2006 at the age of 34.

Mr. Grant and his family had lived in Camp Lejeune when he was a child, during which time he drank, bathed, and swam in contaminated water, “unaware of its toxicity.” His father also died of esophageal cancer, “which is linked to TCE,” the authors of the study wrote. Mr. Grant has created a foundation to inspire and support patients with PD.

All of the individuals either grew up in or spent time in an area where they were extensively exposed to TCE, PCE, or other chemicals, or experienced occupational exposure.

The authors acknowledged that the role of TCE in PD, as illustrated by the cases, is “far from definitive.” For example, exposure to TCE is often combined with exposure to other toxins, or with unmeasured genetic risk factors.

They highlighted the need for more research and called for cleaning and containing contaminated sites, monitoring TCE levels, and publicly communicating risk and a ban on TCE.
 

Recall bias?

Commenting for this news organization, Rebecca Gilbert, MD, PhD, chief scientific officer, American Parkinson Disease Association (APDA), noted that the authors “are very frank about the limitations of this approach [illustrative cases] as proof of causation between PD and TCE exposure.”

Another limitation is that TCE exposure is very common, “as argued in the paper.” But “most people with exposure do not develop PD,” Dr. Gilbert pointed out. “By probing the TCE exposure of those who already have PD, there is a danger of recall bias.”

Dr. Gilbert, associate professor of neurology at NYU Langone Health, who was not involved with the study, acknowledged that the authors “present their work as hypothesis and clearly state that more work is needed to understand the connection between TCE and PD.”

In the meantime, however, there are “well-established health risks of TCE exposure, including development of various cancers,” she said. Therefore, the authors’ goals appear to be educating the public about known health risks, working to clean up known sites of contamination, and advocating to ban future use of TCE.

These goals “do not need to wait for [proof of] firm causation between TCE and PD,” she stated.

Dr. Dorsey reported he has received honoraria for speaking at the American Academy of Neurology and at multiple other societies and foundations and has received compensation for consulting services from pharmaceutical companies, foundations, medical education companies, and medical publications; he owns stock in several companies. The other authors’ disclosures can be found in the original paper. Dr. Gilbert is employed by the American Parkinson Disease Association and Bellevue Hospital Center in New York City.
 

A version of this article first appeared on Medscape.com.

A common chemical that is used in correction fluid, paint removers, gun cleaners, aerosol cleaning products, and dry cleaning may be the key culprit behind the dramatic increase in Parkinson’s disease (PD), researchers say.

An international team of researchers reviewed previous research and cited data that suggest the chemical trichloroethylene (TCE) is associated with as much as a 500% increased risk for Parkinson’s disease (PD).

Lead investigator Ray Dorsey, MD, professor of neurology, University of Rochester, N.Y., called PD “the world’s fastest-growing brain disease,” and told this news organization that it “may be largely preventable.”

“Countless people have died over generations from cancer and other disease linked to TCE [and] Parkinson’s may be the latest,” he said. “Banning these chemicals, containing contaminated sites, and protecting homes, schools, and buildings at risk may all create a world where Parkinson’s is increasingly rare, not common.”

The paper was published online in the Journal of Parkinson’s Disease.
 

Invisible, ubiquitous

TCE was first synthesized in a lab in 1864, with commercial production beginning in 1920, the researchers noted.

“Because of its unique properties, TCE has had countless industrial, commercial, military, and medical applications,” including producing refrigerants, cleaning electronics, and degreasing engine parts.

In addition, it’s been used in dry cleaning, although a similar chemical (perchloroethylene [PCE]) is currently more widely used for that purpose. Nevertheless, the authors noted, in anaerobic conditions, perchloroethylene often transforms into TCE “and their toxicity may be similar.”

Consumer products in which TCE is found include typewriter correction fluid, paint removers, gun cleaners, and aerosol cleaning products. Up until the 1970s, it was used to decaffeinate coffee.

TCE exposure isn’t confined to those who work with it. It also pollutes outdoor air, taints groundwater, and contaminates indoor air. It’s present in a substantial amount of groundwater in the United States and it “evaporates from underlying soil and groundwater and enters homes, workplaces, or schools, often undetected,” the researchers noted.

“Exposure can come via occupation or the environment and is often largely unknown at the time it occurs,” Dr. Dorsey said.

He noted that the rapid increase in PD incidence cannot be explained by genetic factors alone, which affect only about 15% of patients with PD, nor can it be explained by aging alone. “Certain pesticides ... are likely causes but would not explain the high prevalence of PD in urban areas, as is the case in the U.S.” Rather, “other factors” are involved, and “TCE is likely one such factor.”

Yet, “despite widespread contamination and increasing industrial, commercial, and military use, clinical investigations of TCE and PD have been limited.”

To fill this knowledge gap, Dr. Dorsey and his coauthors of the book, “Ending Parkinson’s Disease: A Prescription for Action,” took a deep dive into studies focusing on the potential association of TCE and PD and presented seven cases to illustrate the association.

“Like many genetic mutations (e.g., Parkin) and other environmental toxicants ... TCE damages the energy-producing parts of cells, i.e., the mitochondria,” said Dr. Dorsey.

TCE and PCE “likely mediate their toxicity through a common metabolite.” Because both are lipophilic, they “readily distribute in the brain and body tissues and appear to cause mitochondrial dysfunction at high doses,” the researchers hypothesized.

Dopaminergic neurons are particularly sensitive to mitochondrial neurotoxicants, so this might “partially explain the link to PD.”

Animal studies have shown that TCE “caused selective loss of dopaminergic neurons.” Moreover, PD-related neuropathology was found in the substantia nigra of rodents exposed to TCE over time. In addition, studies as early as 1960 were showing an association between TCE and parkinsonism.

The authors describe TCE as “ubiquitous” in the 1970s, with 10 million Americans working with the chemical or other organic solvents daily. The review details an extensive list of industries and occupations in which TCE exposure continues to occur.

People working with TCE might inhale it or touch it; but “millions more encounter the chemical unknowingly through outdoor air, contaminated groundwater, and indoor air pollution.”

They noted that TCE contaminates up to one-third of U.S. drinking water, has polluted the groundwater in more than 20 different countries on five continents, and is found in half of the 1,300 most toxic “Superfund” sites that are “part of a federal clean-up program, including 15 in California’s Silicon Valley, where TCE was used to clean electronics.”

Although the U.S. military stopped using TCE, numerous sites have been contaminated, including Marine Corps Base Camp Lejeune in North Carolina, where TCE and PCE were found in drinking water at 280 times the recommended safety standards.

The researchers highlighted seven cases of individuals who developed PD after likely exposure to TCE, including NBA basketball player Brian Grant, who developed symptoms of PD in 2006 at the age of 34.

Mr. Grant and his family had lived in Camp Lejeune when he was a child, during which time he drank, bathed, and swam in contaminated water, “unaware of its toxicity.” His father also died of esophageal cancer, “which is linked to TCE,” the authors of the study wrote. Mr. Grant has created a foundation to inspire and support patients with PD.

All of the individuals either grew up in or spent time in an area where they were extensively exposed to TCE, PCE, or other chemicals, or experienced occupational exposure.

The authors acknowledged that the role of TCE in PD, as illustrated by the cases, is “far from definitive.” For example, exposure to TCE is often combined with exposure to other toxins, or with unmeasured genetic risk factors.

They highlighted the need for more research and called for cleaning and containing contaminated sites, monitoring TCE levels, and publicly communicating risk and a ban on TCE.
 

Recall bias?

Commenting for this news organization, Rebecca Gilbert, MD, PhD, chief scientific officer, American Parkinson Disease Association (APDA), noted that the authors “are very frank about the limitations of this approach [illustrative cases] as proof of causation between PD and TCE exposure.”

Another limitation is that TCE exposure is very common, “as argued in the paper.” But “most people with exposure do not develop PD,” Dr. Gilbert pointed out. “By probing the TCE exposure of those who already have PD, there is a danger of recall bias.”

Dr. Gilbert, associate professor of neurology at NYU Langone Health, who was not involved with the study, acknowledged that the authors “present their work as hypothesis and clearly state that more work is needed to understand the connection between TCE and PD.”

In the meantime, however, there are “well-established health risks of TCE exposure, including development of various cancers,” she said. Therefore, the authors’ goals appear to be educating the public about known health risks, working to clean up known sites of contamination, and advocating to ban future use of TCE.

These goals “do not need to wait for [proof of] firm causation between TCE and PD,” she stated.

Dr. Dorsey reported he has received honoraria for speaking at the American Academy of Neurology and at multiple other societies and foundations and has received compensation for consulting services from pharmaceutical companies, foundations, medical education companies, and medical publications; he owns stock in several companies. The other authors’ disclosures can be found in the original paper. Dr. Gilbert is employed by the American Parkinson Disease Association and Bellevue Hospital Center in New York City.
 

A version of this article first appeared on Medscape.com.

A common chemical that is used in correction fluid, paint removers, gun cleaners, aerosol cleaning products, and dry cleaning may be the key culprit behind the dramatic increase in Parkinson’s disease (PD), researchers say.

An international team of researchers reviewed previous research and cited data that suggest the chemical trichloroethylene (TCE) is associated with as much as a 500% increased risk for Parkinson’s disease (PD).

Lead investigator Ray Dorsey, MD, professor of neurology, University of Rochester, N.Y., called PD “the world’s fastest-growing brain disease,” and told this news organization that it “may be largely preventable.”

“Countless people have died over generations from cancer and other disease linked to TCE [and] Parkinson’s may be the latest,” he said. “Banning these chemicals, containing contaminated sites, and protecting homes, schools, and buildings at risk may all create a world where Parkinson’s is increasingly rare, not common.”

The paper was published online in the Journal of Parkinson’s Disease.
 

Invisible, ubiquitous

TCE was first synthesized in a lab in 1864, with commercial production beginning in 1920, the researchers noted.

“Because of its unique properties, TCE has had countless industrial, commercial, military, and medical applications,” including producing refrigerants, cleaning electronics, and degreasing engine parts.

In addition, it’s been used in dry cleaning, although a similar chemical (perchloroethylene [PCE]) is currently more widely used for that purpose. Nevertheless, the authors noted, in anaerobic conditions, perchloroethylene often transforms into TCE “and their toxicity may be similar.”

Consumer products in which TCE is found include typewriter correction fluid, paint removers, gun cleaners, and aerosol cleaning products. Up until the 1970s, it was used to decaffeinate coffee.

TCE exposure isn’t confined to those who work with it. It also pollutes outdoor air, taints groundwater, and contaminates indoor air. It’s present in a substantial amount of groundwater in the United States and it “evaporates from underlying soil and groundwater and enters homes, workplaces, or schools, often undetected,” the researchers noted.

“Exposure can come via occupation or the environment and is often largely unknown at the time it occurs,” Dr. Dorsey said.

He noted that the rapid increase in PD incidence cannot be explained by genetic factors alone, which affect only about 15% of patients with PD, nor can it be explained by aging alone. “Certain pesticides ... are likely causes but would not explain the high prevalence of PD in urban areas, as is the case in the U.S.” Rather, “other factors” are involved, and “TCE is likely one such factor.”

Yet, “despite widespread contamination and increasing industrial, commercial, and military use, clinical investigations of TCE and PD have been limited.”

To fill this knowledge gap, Dr. Dorsey and his coauthors of the book, “Ending Parkinson’s Disease: A Prescription for Action,” took a deep dive into studies focusing on the potential association of TCE and PD and presented seven cases to illustrate the association.

“Like many genetic mutations (e.g., Parkin) and other environmental toxicants ... TCE damages the energy-producing parts of cells, i.e., the mitochondria,” said Dr. Dorsey.

TCE and PCE “likely mediate their toxicity through a common metabolite.” Because both are lipophilic, they “readily distribute in the brain and body tissues and appear to cause mitochondrial dysfunction at high doses,” the researchers hypothesized.

Dopaminergic neurons are particularly sensitive to mitochondrial neurotoxicants, so this might “partially explain the link to PD.”

Animal studies have shown that TCE “caused selective loss of dopaminergic neurons.” Moreover, PD-related neuropathology was found in the substantia nigra of rodents exposed to TCE over time. In addition, studies as early as 1960 were showing an association between TCE and parkinsonism.

The authors describe TCE as “ubiquitous” in the 1970s, with 10 million Americans working with the chemical or other organic solvents daily. The review details an extensive list of industries and occupations in which TCE exposure continues to occur.

People working with TCE might inhale it or touch it; but “millions more encounter the chemical unknowingly through outdoor air, contaminated groundwater, and indoor air pollution.”

They noted that TCE contaminates up to one-third of U.S. drinking water, has polluted the groundwater in more than 20 different countries on five continents, and is found in half of the 1,300 most toxic “Superfund” sites that are “part of a federal clean-up program, including 15 in California’s Silicon Valley, where TCE was used to clean electronics.”

Although the U.S. military stopped using TCE, numerous sites have been contaminated, including Marine Corps Base Camp Lejeune in North Carolina, where TCE and PCE were found in drinking water at 280 times the recommended safety standards.

The researchers highlighted seven cases of individuals who developed PD after likely exposure to TCE, including NBA basketball player Brian Grant, who developed symptoms of PD in 2006 at the age of 34.

Mr. Grant and his family had lived in Camp Lejeune when he was a child, during which time he drank, bathed, and swam in contaminated water, “unaware of its toxicity.” His father also died of esophageal cancer, “which is linked to TCE,” the authors of the study wrote. Mr. Grant has created a foundation to inspire and support patients with PD.

All of the individuals either grew up in or spent time in an area where they were extensively exposed to TCE, PCE, or other chemicals, or experienced occupational exposure.

The authors acknowledged that the role of TCE in PD, as illustrated by the cases, is “far from definitive.” For example, exposure to TCE is often combined with exposure to other toxins, or with unmeasured genetic risk factors.

They highlighted the need for more research and called for cleaning and containing contaminated sites, monitoring TCE levels, and publicly communicating risk and a ban on TCE.
 

Recall bias?

Commenting for this news organization, Rebecca Gilbert, MD, PhD, chief scientific officer, American Parkinson Disease Association (APDA), noted that the authors “are very frank about the limitations of this approach [illustrative cases] as proof of causation between PD and TCE exposure.”

Another limitation is that TCE exposure is very common, “as argued in the paper.” But “most people with exposure do not develop PD,” Dr. Gilbert pointed out. “By probing the TCE exposure of those who already have PD, there is a danger of recall bias.”

Dr. Gilbert, associate professor of neurology at NYU Langone Health, who was not involved with the study, acknowledged that the authors “present their work as hypothesis and clearly state that more work is needed to understand the connection between TCE and PD.”

In the meantime, however, there are “well-established health risks of TCE exposure, including development of various cancers,” she said. Therefore, the authors’ goals appear to be educating the public about known health risks, working to clean up known sites of contamination, and advocating to ban future use of TCE.

These goals “do not need to wait for [proof of] firm causation between TCE and PD,” she stated.

Dr. Dorsey reported he has received honoraria for speaking at the American Academy of Neurology and at multiple other societies and foundations and has received compensation for consulting services from pharmaceutical companies, foundations, medical education companies, and medical publications; he owns stock in several companies. The other authors’ disclosures can be found in the original paper. Dr. Gilbert is employed by the American Parkinson Disease Association and Bellevue Hospital Center in New York City.
 

A version of this article first appeared on Medscape.com.