Clinician Reviews

Last month, I described a 28-year-old patient with a history of injection drug use who presented with pain in his left forearm. His history showed that, within the past 2 years, he’d been seen for cutaneous infections multiple times as an outpatient and in the emergency department. His records indicated that he was diagnosed with a penicillin allergy as a child when he developed a rash after receiving amoxicillin. I believed the next course of action should be to test for a penicillin allergy with an oral amoxicillin challenge.
 

Thank you for your excellent questions regarding this case. Great to hear the enthusiasm for testing for penicillin allergy!

One question focused on the course of action in the case of a mild or moderate IgE-mediated reaction after a single dose test with amoxicillin. Treatment for these reactions should include an antihistamine. I would reserve intravenous antihistamines for more severe cases, which also require treatment with a course of corticosteroids. However, the risk for a moderate to severe reaction to amoxicillin on retesting is quite low.

Clinicians need to exercise caution in the use of systemic corticosteroids. These drugs can be lifesaving, but even short courses of corticosteroids are associated with potentially serious adverse events. In a review of adverse events associated with short-course systemic corticosteroids among children, the rate of vomiting was 5.4%; behavioral change, 4.7%; and sleep disturbance, 4.3%. One child died after contracting herpes zoster, more than one-third of children developed elevated blood pressure, and 81.1% had evidence of suppression of the hypothalamic-pituitary-adrenal axis.

Among adults, short courses of systemic corticosteroids are associated with acute increases in the risks for gastrointestinal bleeding and hypertension. Cumulative exposure to short courses of corticosteroids over time results in higher risks for obesity, type 2 diabetes, and osteoporosis.

Another question prompted by this young man’s case focused on the durability of IgE reactions against penicillin. The IgE response to penicillin does indeed wane over time; 80% of patients with a previous true penicillin allergy can tolerate the antibiotic after 10 years. Thus, about 95% of patients with a remote history of penicillin allergy are tolerant of penicillin, and testing can be performed using the algorithm described.

Clinicians should avoid applying current guidelines for the evaluation of patients with penicillin allergy to other common drug allergies. The overall prevalence of sulfonamide allergy is 3%-8%, and the vast majority of these reactions follow treatment with trimethoprim-sulfamethoxazole. Sulfa allergy is even more common among persons living with HIV infection. The natural history of sulfa allergy is not as well established as penicillin allergy. Allergy testing is encouraged in these cases. Graded oral challenge testing is best reserved for patients who are unlikely to have a true sulfa allergy based on their history.

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

Last month, I described a 28-year-old patient with a history of injection drug use who presented with pain in his left forearm. His history showed that, within the past 2 years, he’d been seen for cutaneous infections multiple times as an outpatient and in the emergency department. His records indicated that he was diagnosed with a penicillin allergy as a child when he developed a rash after receiving amoxicillin. I believed the next course of action should be to test for a penicillin allergy with an oral amoxicillin challenge.
 

Thank you for your excellent questions regarding this case. Great to hear the enthusiasm for testing for penicillin allergy!

One question focused on the course of action in the case of a mild or moderate IgE-mediated reaction after a single dose test with amoxicillin. Treatment for these reactions should include an antihistamine. I would reserve intravenous antihistamines for more severe cases, which also require treatment with a course of corticosteroids. However, the risk for a moderate to severe reaction to amoxicillin on retesting is quite low.

Clinicians need to exercise caution in the use of systemic corticosteroids. These drugs can be lifesaving, but even short courses of corticosteroids are associated with potentially serious adverse events. In a review of adverse events associated with short-course systemic corticosteroids among children, the rate of vomiting was 5.4%; behavioral change, 4.7%; and sleep disturbance, 4.3%. One child died after contracting herpes zoster, more than one-third of children developed elevated blood pressure, and 81.1% had evidence of suppression of the hypothalamic-pituitary-adrenal axis.

Among adults, short courses of systemic corticosteroids are associated with acute increases in the risks for gastrointestinal bleeding and hypertension. Cumulative exposure to short courses of corticosteroids over time results in higher risks for obesity, type 2 diabetes, and osteoporosis.

Another question prompted by this young man’s case focused on the durability of IgE reactions against penicillin. The IgE response to penicillin does indeed wane over time; 80% of patients with a previous true penicillin allergy can tolerate the antibiotic after 10 years. Thus, about 95% of patients with a remote history of penicillin allergy are tolerant of penicillin, and testing can be performed using the algorithm described.

Clinicians should avoid applying current guidelines for the evaluation of patients with penicillin allergy to other common drug allergies. The overall prevalence of sulfonamide allergy is 3%-8%, and the vast majority of these reactions follow treatment with trimethoprim-sulfamethoxazole. Sulfa allergy is even more common among persons living with HIV infection. The natural history of sulfa allergy is not as well established as penicillin allergy. Allergy testing is encouraged in these cases. Graded oral challenge testing is best reserved for patients who are unlikely to have a true sulfa allergy based on their history.

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

Last month, I described a 28-year-old patient with a history of injection drug use who presented with pain in his left forearm. His history showed that, within the past 2 years, he’d been seen for cutaneous infections multiple times as an outpatient and in the emergency department. His records indicated that he was diagnosed with a penicillin allergy as a child when he developed a rash after receiving amoxicillin. I believed the next course of action should be to test for a penicillin allergy with an oral amoxicillin challenge.
 

Thank you for your excellent questions regarding this case. Great to hear the enthusiasm for testing for penicillin allergy!

One question focused on the course of action in the case of a mild or moderate IgE-mediated reaction after a single dose test with amoxicillin. Treatment for these reactions should include an antihistamine. I would reserve intravenous antihistamines for more severe cases, which also require treatment with a course of corticosteroids. However, the risk for a moderate to severe reaction to amoxicillin on retesting is quite low.

Clinicians need to exercise caution in the use of systemic corticosteroids. These drugs can be lifesaving, but even short courses of corticosteroids are associated with potentially serious adverse events. In a review of adverse events associated with short-course systemic corticosteroids among children, the rate of vomiting was 5.4%; behavioral change, 4.7%; and sleep disturbance, 4.3%. One child died after contracting herpes zoster, more than one-third of children developed elevated blood pressure, and 81.1% had evidence of suppression of the hypothalamic-pituitary-adrenal axis.

Among adults, short courses of systemic corticosteroids are associated with acute increases in the risks for gastrointestinal bleeding and hypertension. Cumulative exposure to short courses of corticosteroids over time results in higher risks for obesity, type 2 diabetes, and osteoporosis.

Another question prompted by this young man’s case focused on the durability of IgE reactions against penicillin. The IgE response to penicillin does indeed wane over time; 80% of patients with a previous true penicillin allergy can tolerate the antibiotic after 10 years. Thus, about 95% of patients with a remote history of penicillin allergy are tolerant of penicillin, and testing can be performed using the algorithm described.

Clinicians should avoid applying current guidelines for the evaluation of patients with penicillin allergy to other common drug allergies. The overall prevalence of sulfonamide allergy is 3%-8%, and the vast majority of these reactions follow treatment with trimethoprim-sulfamethoxazole. Sulfa allergy is even more common among persons living with HIV infection. The natural history of sulfa allergy is not as well established as penicillin allergy. Allergy testing is encouraged in these cases. Graded oral challenge testing is best reserved for patients who are unlikely to have a true sulfa allergy based on their history.

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

Higher body mass index and changes in BMI over time may increase a person’s risk for gastrointestinal cancer, according to new data from the Prostate, Lung, Colorectal, and Ovarian (PLCO) Cancer Screening Trial.

The researchers found that being overweight or obese in early and middle adulthood was associated with an increased risk for colorectal cancer (CRC) and noncolorectal GI cancers. Maintaining or increasing BMI over time among overweight or obese individuals was also associated with an increased GI cancer risk.

Aspirin use did not significantly modify these associations, suggesting that aspirin may not be as effective for cancer prevention among overweight or obese individuals.

The results provide “relatively consistent messaging that overweight or obesity from early to later adulthood as well as BMI increases throughout adulthood were associated with increased risk of GI cancers, especially CRC,” the authors of an editorial accompanying the study wrote.

These “important findings highlight the unmet need to identify the critical time window linking adiposity and GI cancer,” said editorialists Mengyao Shi, MBBS, MPD, and Yin Cao, ScD, MPH, of Washington University in St. Louis.

The analysis was published online in JAMA Network Open. 

A growing body of evidence has revealed a strong association between obesity and GI cancers, with chronic inflammation being a likely cause. As rates of overweight and obesity continue to grow, better understanding of the association between obesity and cancer has become increasingly important.

In the analysis, Holli A. Loomans-Kropp, PhD, MPH, with Ohio State University, Columbus, and Asad Umar, PhD, DVM, with the National Cancer Institute, Rockville, Md., explored associations between BMI in early adulthood (age 20), middle adulthood (age 50) and later adulthood (age 55 and over) and GI cancer risk in 135,161 adults from the PLCO Cancer Screening Trial.

BMI was determined using self-reported height and weight at each age time point. The median age at enrollment was 62 years, and 50% of participants were women. Overweight BMI was 25.0-29.9 kg/m² and obese BMI was 30 or higher.

During as many as 21 years of follow-up, 2,803 individuals developed CRC and 2,285 developed non-CRC GI cancers (esophageal, liver, gastric, and pancreatic).

Overweight BMI in early, middle, and later adulthood was associated with an increased risk of CRC (hazard ratio, 1.23 for early and middle years; HR, 1.21 for later years). Obese BMI in middle and later adulthood was also associated with increased risk of CRC (HR, 1.55 and 1.39, respectively). 

The authors observed similar associations between BMI in middle and later adulthood and overall GI and non-CRC GI risk.

“When modeled continuously, we observed 2%-4% increased risk of both CRC and noncolorectal GI cancer with each 1-unit increase in BMI across all time points,” the researchers said.

Their data also suggest that BMI over time may be associated with GI cancer risk. Adults who exhibited no change in overweight or obese BMIs between early and later adulthood and those who exhibited increases in BMI from underweight or normal in early adulthood to overweight or obese BMI in later adulthood had a significantly higher risk for CRC and noncolorectal GI cancer.

Among frequent aspirin users, those with overweight or obese BMIs in early, middle, and later adulthood still had an increased risk for CRC and noncolorectal GI cancer (hazard ratios, 1.44, 1.45, and 1.43, respectively).

The finding that regular weekly aspirin use did not modify GI cancer risk suggests that obesity may alter the cancer-preventive effect of aspirin, the researchers suggested. Individuals with obesity may need to increase aspirin frequency or dosage to see an effect, but upping the dose comes with its own risks, including GI bleeding.

Overall, until now, most epidemiologic studies have examined BMI at one time point, “missing the opportunity to delineate the contribution of adiposity throughout the life course,” Dr. Shi and Dr. Cao wrote.

“As we continue to investigate precision-based interventions to intercept the link between obesity and cancer, it is imperative to reiterate the importance of maintaining a healthy weight and lifestyle from an early age and incorporate it widely into cancer prevention strategies at all levels with immediate implementation,” the editorialists concluded.

This study was supported in part by funds from Ohio State University and the NIH. The study authors reported no relevant financial relationships. Dr. Cao has received personal fees from Geneoscopy for consulting.

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

Higher body mass index and changes in BMI over time may increase a person’s risk for gastrointestinal cancer, according to new data from the Prostate, Lung, Colorectal, and Ovarian (PLCO) Cancer Screening Trial.

The researchers found that being overweight or obese in early and middle adulthood was associated with an increased risk for colorectal cancer (CRC) and noncolorectal GI cancers. Maintaining or increasing BMI over time among overweight or obese individuals was also associated with an increased GI cancer risk.

Aspirin use did not significantly modify these associations, suggesting that aspirin may not be as effective for cancer prevention among overweight or obese individuals.

The results provide “relatively consistent messaging that overweight or obesity from early to later adulthood as well as BMI increases throughout adulthood were associated with increased risk of GI cancers, especially CRC,” the authors of an editorial accompanying the study wrote.

These “important findings highlight the unmet need to identify the critical time window linking adiposity and GI cancer,” said editorialists Mengyao Shi, MBBS, MPD, and Yin Cao, ScD, MPH, of Washington University in St. Louis.

The analysis was published online in JAMA Network Open. 

A growing body of evidence has revealed a strong association between obesity and GI cancers, with chronic inflammation being a likely cause. As rates of overweight and obesity continue to grow, better understanding of the association between obesity and cancer has become increasingly important.

In the analysis, Holli A. Loomans-Kropp, PhD, MPH, with Ohio State University, Columbus, and Asad Umar, PhD, DVM, with the National Cancer Institute, Rockville, Md., explored associations between BMI in early adulthood (age 20), middle adulthood (age 50) and later adulthood (age 55 and over) and GI cancer risk in 135,161 adults from the PLCO Cancer Screening Trial.

BMI was determined using self-reported height and weight at each age time point. The median age at enrollment was 62 years, and 50% of participants were women. Overweight BMI was 25.0-29.9 kg/m² and obese BMI was 30 or higher.

During as many as 21 years of follow-up, 2,803 individuals developed CRC and 2,285 developed non-CRC GI cancers (esophageal, liver, gastric, and pancreatic).

Overweight BMI in early, middle, and later adulthood was associated with an increased risk of CRC (hazard ratio, 1.23 for early and middle years; HR, 1.21 for later years). Obese BMI in middle and later adulthood was also associated with increased risk of CRC (HR, 1.55 and 1.39, respectively). 

The authors observed similar associations between BMI in middle and later adulthood and overall GI and non-CRC GI risk.

“When modeled continuously, we observed 2%-4% increased risk of both CRC and noncolorectal GI cancer with each 1-unit increase in BMI across all time points,” the researchers said.

Their data also suggest that BMI over time may be associated with GI cancer risk. Adults who exhibited no change in overweight or obese BMIs between early and later adulthood and those who exhibited increases in BMI from underweight or normal in early adulthood to overweight or obese BMI in later adulthood had a significantly higher risk for CRC and noncolorectal GI cancer.

Among frequent aspirin users, those with overweight or obese BMIs in early, middle, and later adulthood still had an increased risk for CRC and noncolorectal GI cancer (hazard ratios, 1.44, 1.45, and 1.43, respectively).

The finding that regular weekly aspirin use did not modify GI cancer risk suggests that obesity may alter the cancer-preventive effect of aspirin, the researchers suggested. Individuals with obesity may need to increase aspirin frequency or dosage to see an effect, but upping the dose comes with its own risks, including GI bleeding.

Overall, until now, most epidemiologic studies have examined BMI at one time point, “missing the opportunity to delineate the contribution of adiposity throughout the life course,” Dr. Shi and Dr. Cao wrote.

“As we continue to investigate precision-based interventions to intercept the link between obesity and cancer, it is imperative to reiterate the importance of maintaining a healthy weight and lifestyle from an early age and incorporate it widely into cancer prevention strategies at all levels with immediate implementation,” the editorialists concluded.

This study was supported in part by funds from Ohio State University and the NIH. The study authors reported no relevant financial relationships. Dr. Cao has received personal fees from Geneoscopy for consulting.

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

Higher body mass index and changes in BMI over time may increase a person’s risk for gastrointestinal cancer, according to new data from the Prostate, Lung, Colorectal, and Ovarian (PLCO) Cancer Screening Trial.

The researchers found that being overweight or obese in early and middle adulthood was associated with an increased risk for colorectal cancer (CRC) and noncolorectal GI cancers. Maintaining or increasing BMI over time among overweight or obese individuals was also associated with an increased GI cancer risk.

Aspirin use did not significantly modify these associations, suggesting that aspirin may not be as effective for cancer prevention among overweight or obese individuals.

The results provide “relatively consistent messaging that overweight or obesity from early to later adulthood as well as BMI increases throughout adulthood were associated with increased risk of GI cancers, especially CRC,” the authors of an editorial accompanying the study wrote.

These “important findings highlight the unmet need to identify the critical time window linking adiposity and GI cancer,” said editorialists Mengyao Shi, MBBS, MPD, and Yin Cao, ScD, MPH, of Washington University in St. Louis.

The analysis was published online in JAMA Network Open. 

A growing body of evidence has revealed a strong association between obesity and GI cancers, with chronic inflammation being a likely cause. As rates of overweight and obesity continue to grow, better understanding of the association between obesity and cancer has become increasingly important.

In the analysis, Holli A. Loomans-Kropp, PhD, MPH, with Ohio State University, Columbus, and Asad Umar, PhD, DVM, with the National Cancer Institute, Rockville, Md., explored associations between BMI in early adulthood (age 20), middle adulthood (age 50) and later adulthood (age 55 and over) and GI cancer risk in 135,161 adults from the PLCO Cancer Screening Trial.

BMI was determined using self-reported height and weight at each age time point. The median age at enrollment was 62 years, and 50% of participants were women. Overweight BMI was 25.0-29.9 kg/m² and obese BMI was 30 or higher.

During as many as 21 years of follow-up, 2,803 individuals developed CRC and 2,285 developed non-CRC GI cancers (esophageal, liver, gastric, and pancreatic).

Overweight BMI in early, middle, and later adulthood was associated with an increased risk of CRC (hazard ratio, 1.23 for early and middle years; HR, 1.21 for later years). Obese BMI in middle and later adulthood was also associated with increased risk of CRC (HR, 1.55 and 1.39, respectively). 

The authors observed similar associations between BMI in middle and later adulthood and overall GI and non-CRC GI risk.

“When modeled continuously, we observed 2%-4% increased risk of both CRC and noncolorectal GI cancer with each 1-unit increase in BMI across all time points,” the researchers said.

Their data also suggest that BMI over time may be associated with GI cancer risk. Adults who exhibited no change in overweight or obese BMIs between early and later adulthood and those who exhibited increases in BMI from underweight or normal in early adulthood to overweight or obese BMI in later adulthood had a significantly higher risk for CRC and noncolorectal GI cancer.

Among frequent aspirin users, those with overweight or obese BMIs in early, middle, and later adulthood still had an increased risk for CRC and noncolorectal GI cancer (hazard ratios, 1.44, 1.45, and 1.43, respectively).

The finding that regular weekly aspirin use did not modify GI cancer risk suggests that obesity may alter the cancer-preventive effect of aspirin, the researchers suggested. Individuals with obesity may need to increase aspirin frequency or dosage to see an effect, but upping the dose comes with its own risks, including GI bleeding.

Overall, until now, most epidemiologic studies have examined BMI at one time point, “missing the opportunity to delineate the contribution of adiposity throughout the life course,” Dr. Shi and Dr. Cao wrote.

“As we continue to investigate precision-based interventions to intercept the link between obesity and cancer, it is imperative to reiterate the importance of maintaining a healthy weight and lifestyle from an early age and incorporate it widely into cancer prevention strategies at all levels with immediate implementation,” the editorialists concluded.

This study was supported in part by funds from Ohio State University and the NIH. The study authors reported no relevant financial relationships. Dr. Cao has received personal fees from Geneoscopy for consulting.

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

Stroke is a “disease of disparities,” with racial and ethnic inequities in incidence, prevalence, treatment, and outcomes, and research is needed to identify structural or “upstream” interventions to address the problem, the American Heart Association says in a new scientific statement.

“There are enormous inequities in stroke care, which lead to significant gaps in functional outcomes after stroke for people from historically disenfranchised racial and ethnic groups, including Black, Hispanic, and Indigenous peoples,” writing group chair Amytis Towfighi, MD, professor of neurology, University of Southern California, Los Angeles, says in a news release.

“While research has historically focused on describing these inequities, it is critical to develop and test interventions to address them,” Dr. Towfighi adds.

The scientific statement was published online in the journal Stroke.

It follows a 2020 AHA presidential advisory that declared structural racism a fundamental driver of poor health and early death from heart disease and stroke.

Dr. Towfighi and colleagues reviewed the literature on interventions to address racial and ethnic inequities to identify gaps and areas for future research.

They note that various interventions have shown promise in reducing inequities across the stroke continuum of care.

For example, data suggest that careful attention to stroke preparedness among patients, caregivers, and emergency medical services can reduce inequities in getting people suspected of having a stroke to the emergency department quickly, with delivery of prompt treatment.

However, insufficient research attention has been paid to reducing inequities in rehabilitation, recovery, and social reintegration, the writing group says.

In addition, most studies have addressed patient-level factors, such as medication adherence, health literacy, and health behaviors, but not upstream social factors such as structural racism, housing, income, food security, and access to care, which also affect stroke incidence, care, and outcomes.

“Combating the effects of systemic racism will involve upstream interventions, including policy changes, place-based interventions, and engaging with the health care systems that serve predominantly historically disenfranchised populations and the communities they serve, understanding the barriers, and collaboratively developing solutions to address barriers,” the writing group says.

Further research is needed across the stroke continuum of care to tackle racial and ethnic inequities in stroke care and improve outcomes, they say.

“It’s critical for historically disenfranchised communities to participate in research so that researchers may collaborate in addressing the communities’ needs and concerns,” Bernadette Boden-Albala, DrPH, MPH, vice chair of the writing group, says in the news release.

“Opportunities include working with community stakeholder groups and community organizations to advocate for partnerships with hospitals, academic medical centers, local colleges and universities; or joining community advisory boards and volunteering with the American Heart Association,” Dr. Boden-Albala adds.

Dr. Towfighi encourages health care professionals to “think outside the ‘stroke box.’ Sustainable, effective interventions to address inequities will likely require collaboration with patients, their communities, policymakers, and other sectors.”

The scientific statement was prepared by the volunteer writing group on behalf of the AHA Stroke Council, the Council on Cardiovascular and Stroke Nursing, the Council on Cardiovascular Radiology and Intervention, the Council on Clinical Cardiology, the Council on Hypertension, the Council on the Kidney in Cardiovascular Disease, and the Council on Peripheral Vascular Disease.

The research had no commercial funding.
 

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

Stroke is a “disease of disparities,” with racial and ethnic inequities in incidence, prevalence, treatment, and outcomes, and research is needed to identify structural or “upstream” interventions to address the problem, the American Heart Association says in a new scientific statement.

“There are enormous inequities in stroke care, which lead to significant gaps in functional outcomes after stroke for people from historically disenfranchised racial and ethnic groups, including Black, Hispanic, and Indigenous peoples,” writing group chair Amytis Towfighi, MD, professor of neurology, University of Southern California, Los Angeles, says in a news release.

“While research has historically focused on describing these inequities, it is critical to develop and test interventions to address them,” Dr. Towfighi adds.

The scientific statement was published online in the journal Stroke.

It follows a 2020 AHA presidential advisory that declared structural racism a fundamental driver of poor health and early death from heart disease and stroke.

Dr. Towfighi and colleagues reviewed the literature on interventions to address racial and ethnic inequities to identify gaps and areas for future research.

They note that various interventions have shown promise in reducing inequities across the stroke continuum of care.

For example, data suggest that careful attention to stroke preparedness among patients, caregivers, and emergency medical services can reduce inequities in getting people suspected of having a stroke to the emergency department quickly, with delivery of prompt treatment.

However, insufficient research attention has been paid to reducing inequities in rehabilitation, recovery, and social reintegration, the writing group says.

In addition, most studies have addressed patient-level factors, such as medication adherence, health literacy, and health behaviors, but not upstream social factors such as structural racism, housing, income, food security, and access to care, which also affect stroke incidence, care, and outcomes.

“Combating the effects of systemic racism will involve upstream interventions, including policy changes, place-based interventions, and engaging with the health care systems that serve predominantly historically disenfranchised populations and the communities they serve, understanding the barriers, and collaboratively developing solutions to address barriers,” the writing group says.

Further research is needed across the stroke continuum of care to tackle racial and ethnic inequities in stroke care and improve outcomes, they say.

“It’s critical for historically disenfranchised communities to participate in research so that researchers may collaborate in addressing the communities’ needs and concerns,” Bernadette Boden-Albala, DrPH, MPH, vice chair of the writing group, says in the news release.

“Opportunities include working with community stakeholder groups and community organizations to advocate for partnerships with hospitals, academic medical centers, local colleges and universities; or joining community advisory boards and volunteering with the American Heart Association,” Dr. Boden-Albala adds.

Dr. Towfighi encourages health care professionals to “think outside the ‘stroke box.’ Sustainable, effective interventions to address inequities will likely require collaboration with patients, their communities, policymakers, and other sectors.”

The scientific statement was prepared by the volunteer writing group on behalf of the AHA Stroke Council, the Council on Cardiovascular and Stroke Nursing, the Council on Cardiovascular Radiology and Intervention, the Council on Clinical Cardiology, the Council on Hypertension, the Council on the Kidney in Cardiovascular Disease, and the Council on Peripheral Vascular Disease.

The research had no commercial funding.
 

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

Stroke is a “disease of disparities,” with racial and ethnic inequities in incidence, prevalence, treatment, and outcomes, and research is needed to identify structural or “upstream” interventions to address the problem, the American Heart Association says in a new scientific statement.

“There are enormous inequities in stroke care, which lead to significant gaps in functional outcomes after stroke for people from historically disenfranchised racial and ethnic groups, including Black, Hispanic, and Indigenous peoples,” writing group chair Amytis Towfighi, MD, professor of neurology, University of Southern California, Los Angeles, says in a news release.

“While research has historically focused on describing these inequities, it is critical to develop and test interventions to address them,” Dr. Towfighi adds.

The scientific statement was published online in the journal Stroke.

It follows a 2020 AHA presidential advisory that declared structural racism a fundamental driver of poor health and early death from heart disease and stroke.

Dr. Towfighi and colleagues reviewed the literature on interventions to address racial and ethnic inequities to identify gaps and areas for future research.

They note that various interventions have shown promise in reducing inequities across the stroke continuum of care.

For example, data suggest that careful attention to stroke preparedness among patients, caregivers, and emergency medical services can reduce inequities in getting people suspected of having a stroke to the emergency department quickly, with delivery of prompt treatment.

However, insufficient research attention has been paid to reducing inequities in rehabilitation, recovery, and social reintegration, the writing group says.

In addition, most studies have addressed patient-level factors, such as medication adherence, health literacy, and health behaviors, but not upstream social factors such as structural racism, housing, income, food security, and access to care, which also affect stroke incidence, care, and outcomes.

“Combating the effects of systemic racism will involve upstream interventions, including policy changes, place-based interventions, and engaging with the health care systems that serve predominantly historically disenfranchised populations and the communities they serve, understanding the barriers, and collaboratively developing solutions to address barriers,” the writing group says.

Further research is needed across the stroke continuum of care to tackle racial and ethnic inequities in stroke care and improve outcomes, they say.

“It’s critical for historically disenfranchised communities to participate in research so that researchers may collaborate in addressing the communities’ needs and concerns,” Bernadette Boden-Albala, DrPH, MPH, vice chair of the writing group, says in the news release.

“Opportunities include working with community stakeholder groups and community organizations to advocate for partnerships with hospitals, academic medical centers, local colleges and universities; or joining community advisory boards and volunteering with the American Heart Association,” Dr. Boden-Albala adds.

Dr. Towfighi encourages health care professionals to “think outside the ‘stroke box.’ Sustainable, effective interventions to address inequities will likely require collaboration with patients, their communities, policymakers, and other sectors.”

The scientific statement was prepared by the volunteer writing group on behalf of the AHA Stroke Council, the Council on Cardiovascular and Stroke Nursing, the Council on Cardiovascular Radiology and Intervention, the Council on Clinical Cardiology, the Council on Hypertension, the Council on the Kidney in Cardiovascular Disease, and the Council on Peripheral Vascular Disease.

The research had no commercial funding.
 

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

A broad shave biopsy was performed at the base of the lesion and the results were consistent with a thick nodular melanoma with a Breslow depth of 5.5 mm.

Melanoma is the deadliest skin cancer in the United States with mortality risk corresponding with the depth of the tumor.¹ Nodular melanomas grow faster than all other types of melanoma. For this reason, a concerning raised lesion with a risk of melanoma should not be observed for change over time; it should be biopsied promptly. In this case, a depth of 5.5 mm was cause for quick action. Patients with tumors > 1 mm in depth (and some tumors > 0.8 mm) should be offered sentinel lymph node biopsy (SLNB) along with wide local excision to evaluate for lymphatic spread. Patients with thinner tumors may undergo wide local excision without SLNB.

In this case, National Comprehensive Cancer Network guidelines would dictate a 2-cm margin for a wide local incision; the patient underwent a modified version of this with Surgical Oncology to accommodate maintenance of hand function. This patient’s SLNB was negative, so the melanoma was classified as Stage IIC.

In the recent past, there were no additional treatments for patients with late Stage II disease (thick tumors without evidence of metastasis). However, in December 2021, the US Food and Drug Administration approved the use of immunotherapy with pembrolizumab in patients with node-negative late Stage II melanoma after demonstration of improved recurrence-free survival in the KEYNOTE trial.² Evidence of improved long-term survival is mixed with adjuvant therapy, and studies evaluating the best role of adjuvant therapy are ongoing.

This patient was started on a regimen of pembrolizumab 200 mg IV every 3 weeks, which he will continue for as long as 1 year. He has tolerated this regimen without difficulty and has no evidence of disease.

‌

Photos and text for Photo Rounds Friday courtesy of Jonathan Karnes, MD (copyright retained). Dr. Karnes is the medical director of MDFMR Dermatology Services, Augusta, ME.

A broad shave biopsy was performed at the base of the lesion and the results were consistent with a thick nodular melanoma with a Breslow depth of 5.5 mm.

Melanoma is the deadliest skin cancer in the United States with mortality risk corresponding with the depth of the tumor.¹ Nodular melanomas grow faster than all other types of melanoma. For this reason, a concerning raised lesion with a risk of melanoma should not be observed for change over time; it should be biopsied promptly. In this case, a depth of 5.5 mm was cause for quick action. Patients with tumors > 1 mm in depth (and some tumors > 0.8 mm) should be offered sentinel lymph node biopsy (SLNB) along with wide local excision to evaluate for lymphatic spread. Patients with thinner tumors may undergo wide local excision without SLNB.

In this case, National Comprehensive Cancer Network guidelines would dictate a 2-cm margin for a wide local incision; the patient underwent a modified version of this with Surgical Oncology to accommodate maintenance of hand function. This patient’s SLNB was negative, so the melanoma was classified as Stage IIC.

In the recent past, there were no additional treatments for patients with late Stage II disease (thick tumors without evidence of metastasis). However, in December 2021, the US Food and Drug Administration approved the use of immunotherapy with pembrolizumab in patients with node-negative late Stage II melanoma after demonstration of improved recurrence-free survival in the KEYNOTE trial.² Evidence of improved long-term survival is mixed with adjuvant therapy, and studies evaluating the best role of adjuvant therapy are ongoing.

This patient was started on a regimen of pembrolizumab 200 mg IV every 3 weeks, which he will continue for as long as 1 year. He has tolerated this regimen without difficulty and has no evidence of disease.

‌

Photos and text for Photo Rounds Friday courtesy of Jonathan Karnes, MD (copyright retained). Dr. Karnes is the medical director of MDFMR Dermatology Services, Augusta, ME.

A broad shave biopsy was performed at the base of the lesion and the results were consistent with a thick nodular melanoma with a Breslow depth of 5.5 mm.

Melanoma is the deadliest skin cancer in the United States with mortality risk corresponding with the depth of the tumor.¹ Nodular melanomas grow faster than all other types of melanoma. For this reason, a concerning raised lesion with a risk of melanoma should not be observed for change over time; it should be biopsied promptly. In this case, a depth of 5.5 mm was cause for quick action. Patients with tumors > 1 mm in depth (and some tumors > 0.8 mm) should be offered sentinel lymph node biopsy (SLNB) along with wide local excision to evaluate for lymphatic spread. Patients with thinner tumors may undergo wide local excision without SLNB.

In this case, National Comprehensive Cancer Network guidelines would dictate a 2-cm margin for a wide local incision; the patient underwent a modified version of this with Surgical Oncology to accommodate maintenance of hand function. This patient’s SLNB was negative, so the melanoma was classified as Stage IIC.

In the recent past, there were no additional treatments for patients with late Stage II disease (thick tumors without evidence of metastasis). However, in December 2021, the US Food and Drug Administration approved the use of immunotherapy with pembrolizumab in patients with node-negative late Stage II melanoma after demonstration of improved recurrence-free survival in the KEYNOTE trial.² Evidence of improved long-term survival is mixed with adjuvant therapy, and studies evaluating the best role of adjuvant therapy are ongoing.

This patient was started on a regimen of pembrolizumab 200 mg IV every 3 weeks, which he will continue for as long as 1 year. He has tolerated this regimen without difficulty and has no evidence of disease.

‌

Photos and text for Photo Rounds Friday courtesy of Jonathan Karnes, MD (copyright retained). Dr. Karnes is the medical director of MDFMR Dermatology Services, Augusta, ME.

The biopsy revealed abundant lymphocytes, neutrophils, and eosinophils consistent with a diagnosis of cutaneous B cell pseudolymphoma. The pseudolymphoma was caused by an exaggerated response to a tick bite.

As the name implies, B cell pseudolymphomas clinically and histologically mimic the various patterns of cutaneous lymphoma, often appearing as a firm, pink to dark violet nodule. A biopsy is mandatory to distinguish between pseudolymphoma and true lymphoma. There is an association between pseudolymphomas and Borrelia burgdorferi, the organism responsible for Lyme disease. Thus, testing for Lyme disease is recommended for patients with pseudolymphomas who live in endemic areas. Patients who test positive should be treated with doxycycline 100 mg bid for 10 days.

In the absence of Lyme disease, a pseudolymphoma may resolve spontaneously over weeks or months. Resolution can be hastened with topical superpotent steroids, intralesional steroids, or systemic steroids. Treatment can begin with topical clobetasol 0.05% bid. If the lesion does not resolve, the next step would be intralesional triamcinolone 10 mg/mL injected directly into the nodule until it blanches slightly. Injections should be repeated every 3 to 4 weeks for a total of 2 to 3 injections.

The patient in this case had negative Lyme serology and was treated with 2 injections of triamcinolone 10 mg/mL administered 3 weeks apart. She experienced complete resolution.

‌

Photos and text for Photo Rounds Friday courtesy of Jonathan Karnes, MD (copyright retained). Dr. Karnes is the medical director of MDFMR Dermatology Services, Augusta, ME.

The biopsy revealed abundant lymphocytes, neutrophils, and eosinophils consistent with a diagnosis of cutaneous B cell pseudolymphoma. The pseudolymphoma was caused by an exaggerated response to a tick bite.

As the name implies, B cell pseudolymphomas clinically and histologically mimic the various patterns of cutaneous lymphoma, often appearing as a firm, pink to dark violet nodule. A biopsy is mandatory to distinguish between pseudolymphoma and true lymphoma. There is an association between pseudolymphomas and Borrelia burgdorferi, the organism responsible for Lyme disease. Thus, testing for Lyme disease is recommended for patients with pseudolymphomas who live in endemic areas. Patients who test positive should be treated with doxycycline 100 mg bid for 10 days.

In the absence of Lyme disease, a pseudolymphoma may resolve spontaneously over weeks or months. Resolution can be hastened with topical superpotent steroids, intralesional steroids, or systemic steroids. Treatment can begin with topical clobetasol 0.05% bid. If the lesion does not resolve, the next step would be intralesional triamcinolone 10 mg/mL injected directly into the nodule until it blanches slightly. Injections should be repeated every 3 to 4 weeks for a total of 2 to 3 injections.

The patient in this case had negative Lyme serology and was treated with 2 injections of triamcinolone 10 mg/mL administered 3 weeks apart. She experienced complete resolution.

‌

Photos and text for Photo Rounds Friday courtesy of Jonathan Karnes, MD (copyright retained). Dr. Karnes is the medical director of MDFMR Dermatology Services, Augusta, ME.

The biopsy revealed abundant lymphocytes, neutrophils, and eosinophils consistent with a diagnosis of cutaneous B cell pseudolymphoma. The pseudolymphoma was caused by an exaggerated response to a tick bite.

As the name implies, B cell pseudolymphomas clinically and histologically mimic the various patterns of cutaneous lymphoma, often appearing as a firm, pink to dark violet nodule. A biopsy is mandatory to distinguish between pseudolymphoma and true lymphoma. There is an association between pseudolymphomas and Borrelia burgdorferi, the organism responsible for Lyme disease. Thus, testing for Lyme disease is recommended for patients with pseudolymphomas who live in endemic areas. Patients who test positive should be treated with doxycycline 100 mg bid for 10 days.

In the absence of Lyme disease, a pseudolymphoma may resolve spontaneously over weeks or months. Resolution can be hastened with topical superpotent steroids, intralesional steroids, or systemic steroids. Treatment can begin with topical clobetasol 0.05% bid. If the lesion does not resolve, the next step would be intralesional triamcinolone 10 mg/mL injected directly into the nodule until it blanches slightly. Injections should be repeated every 3 to 4 weeks for a total of 2 to 3 injections.

The patient in this case had negative Lyme serology and was treated with 2 injections of triamcinolone 10 mg/mL administered 3 weeks apart. She experienced complete resolution.

‌

Photos and text for Photo Rounds Friday courtesy of Jonathan Karnes, MD (copyright retained). Dr. Karnes is the medical director of MDFMR Dermatology Services, Augusta, ME.

Women who experienced gestational hypertension or preeclampsia are at increased risk of developing nonischemic heart failure (HF) and especially ischemic HF over the next decade or two, an observational study suggests.

The risks were most pronounced, jumping more than sixfold in the case of ischemic HF, during the first 6 years after the pregnancy. They then receded to plateau at a lower, still significantly elevated level of risk that persisted even years later, in the analysis of women in a Swedish medical birth registry.

Jupiterimages/Thinkstock.com

The case-matching study compared women with no history of cardiovascular (CV) disease and a first successful pregnancy during which they either developed or did not experience gestational hypertension or preeclampsia.

It’s among the first studies to explore the impact of pregnancy-induced hypertensive disease on subsequent HF risk separately for both ischemic and nonischemic HF and to find that the severity of such risk differs for the two HF etiologies, according to a report published in JACC: Heart Failure.

The adjusted risk for any HF during a median of 13 years after the pregnancy rose 70% for those who had developed gestational hypertension or preeclampsia. Their risk of nonischemic HF went up 60%, and their risk of ischemic HF more than doubled.

Hypertensive disorders of pregnancy “are so much more than short-term disorders confined to the pregnancy period. They have long-term implications throughout a lifetime,” lead author Ängla Mantel, MD, PhD, said in an interview.

Obstetric history doesn’t figure into any formal HF risk scoring systems, observed Dr. Mantel of Karolinska Institutet, Stockholm. Still, women who develop gestational hypertension, preeclampsia, or other pregnancy complications “should be considered a high-risk population even after the pregnancy and monitored for cardiovascular risk factors regularly throughout life.”

In many studies, she said, “knowledge of women-specific risk factors for cardiovascular disease is poor among both clinicians and patients.” The current findings should help raise awareness about such obstetric risk factors for HF, “especially” in patients with HF with preserved ejection fraction (HFpEF), which isn’t closely related to a number of traditional CV risk factors.

Even though pregnancy complications such as gestational hypertension and preeclampsia don’t feature in risk calculators, “they are actually risk enhancers per the 2019 primary prevention guidelines,” Natalie A. Bello, MD, MPH, who was not involved in the current study, said in an interview.

“We’re working to educate physicians and cardiovascular team members to take a pregnancy history” for risk stratification of women in primary prevention,” said Dr. Bello, director of hypertension research at the Smidt Heart Institute, Cedars-Sinai Medical Center, Los Angeles.

The current study, she said, “is an important step” for its finding that hypertensive disorders of pregnancy are associated separately with both ischemic and nonischemic HF.

She pointed out, however, that because the study excluded women with peripartum cardiomyopathy, a form of nonischemic HF, it may “underestimate the impact of hypertensive disorders on the short-term risk of nonischemic heart failure.” Women who had peripartum cardiomyopathy were excluded to avoid misclassification of other HF outcomes, the authors stated.

Also, Dr. Bello said, the study’s inclusion of patients with either gestational hypertension or preeclampsia may complicate its interpretation. Compared with the former condition, she said, preeclampsia “involves more inflammation and more endothelial dysfunction. It may cause a different impact on the heart and the vasculature.”

In the analysis, about 79,000 women with gestational hypertension or preeclampsia were identified among more than 1.4 million primiparous women who entered the Swedish Medical Birth Register over a period of about 30 years. They were matched with about 396,000 women in the registry who had normotensive pregnancies.

Excluded, besides women with peripartum cardiomyopathy, were women with a prepregnancy history of HF, hypertension, ischemic heart disease, atrial fibrillation, or valvular heart disease.

Hazard ratios (HRs) for HF, ischemic HF, and nonischemic HF were significantly elevated over among the women with gestational hypertension or preeclampsia compared to those with normotensive pregnancies:

• Any HF: HR, 1.70 (95% confidence interval [CI], 1.51-1.91)
• Nonischemic HF: HR, 1.60 (95% CI, 1.40-1.83)
• Ischemic HF: HR, 2.28 (95% CI, 1.74-2.98)

The analyses were adjusted for maternal age at delivery, year of delivery, prepregnancy comorbidities, maternal education level, smoking status, and body mass index.

Sharper risk increases were seen among women with gestational hypertension or preeclampsia who delivered prior to gestational week 34:

• Any HF: HR, 2.46 (95% CI, 1.82-3.32)
• Nonischemic HF: HR, 2.33 (95% CI, 1.65-3.31)
• Ischemic HF: HR, 3.64 (95% CI, 1.97-6.74)

Risks for HF developing within 6 years of pregnancy characterized by gestational hypertension or preeclampsia were far more pronounced for ischemic HF than for nonischemic HF:

• Any HF: HR, 2.09 (95% CI, 1.52-2.89)
• Nonischemic HF: HR, 1.86 (95% CI, 1.32-2.61)
• Ischemic HF: HR, 6.52 (95% CI, 2.00-12.34).

The study couldn’t directly explore potential mechanisms for the associations between pregnancy-induced hypertensive disorders and different forms of HF, but it may have provided clues, Dr. Mantel said.

The hypertensive disorders and ischemic HF appear to share risk factors that could lead to both conditions, she noted. Also, hypertension itself is a risk factor for ischemic heart disease.

In contrast, “the risk of nonischemic heart failure might be driven by other factors, such as the inflammatory profile, endothelial dysfunction, and cardiac remodeling induced by preeclampsia or gestational hypertension.”

Those disorders, moreover, are associated with cardiac structural changes that are also seen in HFpEF, Dr. Mantel said. And both HFpEF and preeclampsia are characterized by systemic inflammation and endothelial dysfunction.

“These pathophysiological similarities,” she proposed, “might explain the link between pregnancy-induced hypertensive disorder and HFpEF.”

The authors have disclosed no relevant financial relationships. Dr. Bello has received grants from the National Institutes of Health.
 

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

Women who experienced gestational hypertension or preeclampsia are at increased risk of developing nonischemic heart failure (HF) and especially ischemic HF over the next decade or two, an observational study suggests.

The risks were most pronounced, jumping more than sixfold in the case of ischemic HF, during the first 6 years after the pregnancy. They then receded to plateau at a lower, still significantly elevated level of risk that persisted even years later, in the analysis of women in a Swedish medical birth registry.

Jupiterimages/Thinkstock.com

The case-matching study compared women with no history of cardiovascular (CV) disease and a first successful pregnancy during which they either developed or did not experience gestational hypertension or preeclampsia.

It’s among the first studies to explore the impact of pregnancy-induced hypertensive disease on subsequent HF risk separately for both ischemic and nonischemic HF and to find that the severity of such risk differs for the two HF etiologies, according to a report published in JACC: Heart Failure.

The adjusted risk for any HF during a median of 13 years after the pregnancy rose 70% for those who had developed gestational hypertension or preeclampsia. Their risk of nonischemic HF went up 60%, and their risk of ischemic HF more than doubled.

Hypertensive disorders of pregnancy “are so much more than short-term disorders confined to the pregnancy period. They have long-term implications throughout a lifetime,” lead author Ängla Mantel, MD, PhD, said in an interview.

Obstetric history doesn’t figure into any formal HF risk scoring systems, observed Dr. Mantel of Karolinska Institutet, Stockholm. Still, women who develop gestational hypertension, preeclampsia, or other pregnancy complications “should be considered a high-risk population even after the pregnancy and monitored for cardiovascular risk factors regularly throughout life.”

In many studies, she said, “knowledge of women-specific risk factors for cardiovascular disease is poor among both clinicians and patients.” The current findings should help raise awareness about such obstetric risk factors for HF, “especially” in patients with HF with preserved ejection fraction (HFpEF), which isn’t closely related to a number of traditional CV risk factors.

Even though pregnancy complications such as gestational hypertension and preeclampsia don’t feature in risk calculators, “they are actually risk enhancers per the 2019 primary prevention guidelines,” Natalie A. Bello, MD, MPH, who was not involved in the current study, said in an interview.

“We’re working to educate physicians and cardiovascular team members to take a pregnancy history” for risk stratification of women in primary prevention,” said Dr. Bello, director of hypertension research at the Smidt Heart Institute, Cedars-Sinai Medical Center, Los Angeles.

The current study, she said, “is an important step” for its finding that hypertensive disorders of pregnancy are associated separately with both ischemic and nonischemic HF.

She pointed out, however, that because the study excluded women with peripartum cardiomyopathy, a form of nonischemic HF, it may “underestimate the impact of hypertensive disorders on the short-term risk of nonischemic heart failure.” Women who had peripartum cardiomyopathy were excluded to avoid misclassification of other HF outcomes, the authors stated.

Also, Dr. Bello said, the study’s inclusion of patients with either gestational hypertension or preeclampsia may complicate its interpretation. Compared with the former condition, she said, preeclampsia “involves more inflammation and more endothelial dysfunction. It may cause a different impact on the heart and the vasculature.”

In the analysis, about 79,000 women with gestational hypertension or preeclampsia were identified among more than 1.4 million primiparous women who entered the Swedish Medical Birth Register over a period of about 30 years. They were matched with about 396,000 women in the registry who had normotensive pregnancies.

Excluded, besides women with peripartum cardiomyopathy, were women with a prepregnancy history of HF, hypertension, ischemic heart disease, atrial fibrillation, or valvular heart disease.

Hazard ratios (HRs) for HF, ischemic HF, and nonischemic HF were significantly elevated over among the women with gestational hypertension or preeclampsia compared to those with normotensive pregnancies:

• Any HF: HR, 1.70 (95% confidence interval [CI], 1.51-1.91)
• Nonischemic HF: HR, 1.60 (95% CI, 1.40-1.83)
• Ischemic HF: HR, 2.28 (95% CI, 1.74-2.98)

The analyses were adjusted for maternal age at delivery, year of delivery, prepregnancy comorbidities, maternal education level, smoking status, and body mass index.

Sharper risk increases were seen among women with gestational hypertension or preeclampsia who delivered prior to gestational week 34:

• Any HF: HR, 2.46 (95% CI, 1.82-3.32)
• Nonischemic HF: HR, 2.33 (95% CI, 1.65-3.31)
• Ischemic HF: HR, 3.64 (95% CI, 1.97-6.74)

Risks for HF developing within 6 years of pregnancy characterized by gestational hypertension or preeclampsia were far more pronounced for ischemic HF than for nonischemic HF:

• Any HF: HR, 2.09 (95% CI, 1.52-2.89)
• Nonischemic HF: HR, 1.86 (95% CI, 1.32-2.61)
• Ischemic HF: HR, 6.52 (95% CI, 2.00-12.34).

The study couldn’t directly explore potential mechanisms for the associations between pregnancy-induced hypertensive disorders and different forms of HF, but it may have provided clues, Dr. Mantel said.

The hypertensive disorders and ischemic HF appear to share risk factors that could lead to both conditions, she noted. Also, hypertension itself is a risk factor for ischemic heart disease.

In contrast, “the risk of nonischemic heart failure might be driven by other factors, such as the inflammatory profile, endothelial dysfunction, and cardiac remodeling induced by preeclampsia or gestational hypertension.”

Those disorders, moreover, are associated with cardiac structural changes that are also seen in HFpEF, Dr. Mantel said. And both HFpEF and preeclampsia are characterized by systemic inflammation and endothelial dysfunction.

“These pathophysiological similarities,” she proposed, “might explain the link between pregnancy-induced hypertensive disorder and HFpEF.”

The authors have disclosed no relevant financial relationships. Dr. Bello has received grants from the National Institutes of Health.
 

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

Women who experienced gestational hypertension or preeclampsia are at increased risk of developing nonischemic heart failure (HF) and especially ischemic HF over the next decade or two, an observational study suggests.

The risks were most pronounced, jumping more than sixfold in the case of ischemic HF, during the first 6 years after the pregnancy. They then receded to plateau at a lower, still significantly elevated level of risk that persisted even years later, in the analysis of women in a Swedish medical birth registry.

Jupiterimages/Thinkstock.com

The case-matching study compared women with no history of cardiovascular (CV) disease and a first successful pregnancy during which they either developed or did not experience gestational hypertension or preeclampsia.

It’s among the first studies to explore the impact of pregnancy-induced hypertensive disease on subsequent HF risk separately for both ischemic and nonischemic HF and to find that the severity of such risk differs for the two HF etiologies, according to a report published in JACC: Heart Failure.

The adjusted risk for any HF during a median of 13 years after the pregnancy rose 70% for those who had developed gestational hypertension or preeclampsia. Their risk of nonischemic HF went up 60%, and their risk of ischemic HF more than doubled.

Hypertensive disorders of pregnancy “are so much more than short-term disorders confined to the pregnancy period. They have long-term implications throughout a lifetime,” lead author Ängla Mantel, MD, PhD, said in an interview.

Obstetric history doesn’t figure into any formal HF risk scoring systems, observed Dr. Mantel of Karolinska Institutet, Stockholm. Still, women who develop gestational hypertension, preeclampsia, or other pregnancy complications “should be considered a high-risk population even after the pregnancy and monitored for cardiovascular risk factors regularly throughout life.”

In many studies, she said, “knowledge of women-specific risk factors for cardiovascular disease is poor among both clinicians and patients.” The current findings should help raise awareness about such obstetric risk factors for HF, “especially” in patients with HF with preserved ejection fraction (HFpEF), which isn’t closely related to a number of traditional CV risk factors.

Even though pregnancy complications such as gestational hypertension and preeclampsia don’t feature in risk calculators, “they are actually risk enhancers per the 2019 primary prevention guidelines,” Natalie A. Bello, MD, MPH, who was not involved in the current study, said in an interview.

“We’re working to educate physicians and cardiovascular team members to take a pregnancy history” for risk stratification of women in primary prevention,” said Dr. Bello, director of hypertension research at the Smidt Heart Institute, Cedars-Sinai Medical Center, Los Angeles.

The current study, she said, “is an important step” for its finding that hypertensive disorders of pregnancy are associated separately with both ischemic and nonischemic HF.

She pointed out, however, that because the study excluded women with peripartum cardiomyopathy, a form of nonischemic HF, it may “underestimate the impact of hypertensive disorders on the short-term risk of nonischemic heart failure.” Women who had peripartum cardiomyopathy were excluded to avoid misclassification of other HF outcomes, the authors stated.

Also, Dr. Bello said, the study’s inclusion of patients with either gestational hypertension or preeclampsia may complicate its interpretation. Compared with the former condition, she said, preeclampsia “involves more inflammation and more endothelial dysfunction. It may cause a different impact on the heart and the vasculature.”

In the analysis, about 79,000 women with gestational hypertension or preeclampsia were identified among more than 1.4 million primiparous women who entered the Swedish Medical Birth Register over a period of about 30 years. They were matched with about 396,000 women in the registry who had normotensive pregnancies.

Excluded, besides women with peripartum cardiomyopathy, were women with a prepregnancy history of HF, hypertension, ischemic heart disease, atrial fibrillation, or valvular heart disease.

Hazard ratios (HRs) for HF, ischemic HF, and nonischemic HF were significantly elevated over among the women with gestational hypertension or preeclampsia compared to those with normotensive pregnancies:

• Any HF: HR, 1.70 (95% confidence interval [CI], 1.51-1.91)
• Nonischemic HF: HR, 1.60 (95% CI, 1.40-1.83)
• Ischemic HF: HR, 2.28 (95% CI, 1.74-2.98)

The analyses were adjusted for maternal age at delivery, year of delivery, prepregnancy comorbidities, maternal education level, smoking status, and body mass index.

Sharper risk increases were seen among women with gestational hypertension or preeclampsia who delivered prior to gestational week 34:

• Any HF: HR, 2.46 (95% CI, 1.82-3.32)
• Nonischemic HF: HR, 2.33 (95% CI, 1.65-3.31)
• Ischemic HF: HR, 3.64 (95% CI, 1.97-6.74)

Risks for HF developing within 6 years of pregnancy characterized by gestational hypertension or preeclampsia were far more pronounced for ischemic HF than for nonischemic HF:

• Any HF: HR, 2.09 (95% CI, 1.52-2.89)
• Nonischemic HF: HR, 1.86 (95% CI, 1.32-2.61)
• Ischemic HF: HR, 6.52 (95% CI, 2.00-12.34).

The study couldn’t directly explore potential mechanisms for the associations between pregnancy-induced hypertensive disorders and different forms of HF, but it may have provided clues, Dr. Mantel said.

The hypertensive disorders and ischemic HF appear to share risk factors that could lead to both conditions, she noted. Also, hypertension itself is a risk factor for ischemic heart disease.

In contrast, “the risk of nonischemic heart failure might be driven by other factors, such as the inflammatory profile, endothelial dysfunction, and cardiac remodeling induced by preeclampsia or gestational hypertension.”

Those disorders, moreover, are associated with cardiac structural changes that are also seen in HFpEF, Dr. Mantel said. And both HFpEF and preeclampsia are characterized by systemic inflammation and endothelial dysfunction.

“These pathophysiological similarities,” she proposed, “might explain the link between pregnancy-induced hypertensive disorder and HFpEF.”

The authors have disclosed no relevant financial relationships. Dr. Bello has received grants from the National Institutes of Health.
 

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

Patients with long COVID-19 – where the effects of an initial COVID infection last more than 12 weeks – had lower levels of 25(OH) vitamin D than other patients who survived COVID-19, in a retrospective, case-matched study.

The lower levels of vitamin D in patients with long COVID were most notable in those with brain fog.

Reasonable to test vitamin D levels, consider supplementation

Invited to comment, Amiel Dror, MD, PhD, who led a related study that showed that people with a vitamin D deficiency were more likely to have severe COVID-19, agreed.

“The novelty and significance of this [new] study lie in the fact that it expands on our current understanding of the interplay between vitamin D and COVID-19, taking it beyond the acute phase of the disease,” said Dr. Dror, from Bar-Ilan University, Safed, Israel.

“It’s striking to see how vitamin D levels continue to influence patients’ health even after recovery from the initial infection,” he noted. 

“The findings certainly add weight to the argument for conducting a randomized control trial [RCT],” he continued, which “would enable us to conclusively determine whether vitamin D supplementation can effectively reduce the risk or severity of long COVID.”

“In the interim,” Dr. Dror said, “given the safety profile of vitamin D and its broad health benefits, it could be reasonable to test for vitamin D levels in patients admitted with COVID-19. If levels are found to be low, supplementation could be considered.”

“However, it’s important to note that this should be done under medical supervision,” he cautioned, “and further studies are needed to establish the optimal timing and dosage of supplementation.”

“I anticipate that we’ll see more RCTs [of this] in the future,” he speculated.
 

Low vitamin D and risk of long COVID

Long COVID is an emerging syndrome that affects 50%-70% of COVID-19 survivors.

Low levels of vitamin D have been associated with increased likelihood of needing mechanical ventilation and worse survival in patients hospitalized with COVID-19, but the risk of long COVID associated with vitamin D has not been known.

Researchers analyzed data from adults aged 18 and older hospitalized at San Raffaele Hospital with a confirmed diagnosis of COVID-19 and discharged during the first pandemic wave, from March to May 2020, and then seen 6-months later for follow-up.

Patients were excluded if they had been admitted to the intensive care unit during hospitalization or had missing medical data or blood samples available to determine (OH) vitamin D levels, at admission and the 6-month follow-up.

Long COVID-19 was defined based on the U.K. National Institute for Health and Care Excellence guidelines as the concomitant presence of at least two or more of 17 signs and symptoms that were absent prior to the COVID-19 infection and could only be attributed to that acute disease.

Researchers identified 50 patients with long COVID at the 6-month follow-up and matched them with 50 patients without long COVID at that time point, based on age, sex, concomitant comorbidities, need for noninvasive mechanical ventilation, and week of evaluation.

Patients were a mean age of 61 years (range, 51-73) and 56% were men; 28% had been on a ventilator during hospitalization for COVID-19.

The most frequent signs and symptoms at 6 months in the patients with long COVID were asthenia (weakness, 38% of patients), dysgeusia (bad taste in the mouth, 34%), dyspnea (shortness of breath, 34%), and anosmia (loss of sense of smell, 24%).

Most symptoms were related to the cardiorespiratory system (42%), the feeling of well-being (42%), or the senses (36%), and fewer patients had symptoms related to neurocognitive impairment (headache or brain fog, 14%), or ear, nose, and throat (12%), or gastrointestinal system (4%).

Patients with long COVID had lower mean 25(OH) vitamin D levels than patients without long COVID (20.1 vs 23.2 ng/mL; P = .03). However, actual vitamin D deficiency levels were similar in both groups.

Two-thirds of patients with low vitamin D levels at hospital admission still presented with low levels at the 6-month follow-up.

Vitamin D levels were significantly lower in patients with neurocognitive symptoms at follow-up (n = 7) than in those without such symptoms (n = 93) (14.6 vs. 20.6 ng/mL; P = .042).

In patients with vitamin D deficiency (< 20 ng/mL) at admission and at follow-up (n = 42), those with long COVID (n = 22) had lower vitamin D levels at follow-up than those without long COVID (n = 20) (12.7 vs. 15.2 ng/mL; P = .041).

And in multiple regression analyses, a lower 25(OH) vitamin D level at follow-up was the only variable that was significantly associated with long COVID (odds ratio, 1.09; 95% confidence interval, 1.01-1.16; P = .008).

The findings “strongly reinforce the clinical usefulness of 25(OH) vitamin D evaluation as a possible modifiable pathophysiological factor underlying this emerging worldwide critical health issue,” the researchers concluded.

The study was supported by Abiogen Pharma. One study author is an employee at Abiogen. Dr. Giustina has reported being a consultant for Abiogen and Takeda and receiving a research grant to his institution from Takeda. Dr. Di Filippo and the other authors reported no relevant financial relationships.

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

Patients with long COVID-19 – where the effects of an initial COVID infection last more than 12 weeks – had lower levels of 25(OH) vitamin D than other patients who survived COVID-19, in a retrospective, case-matched study.

The lower levels of vitamin D in patients with long COVID were most notable in those with brain fog.

Reasonable to test vitamin D levels, consider supplementation

Invited to comment, Amiel Dror, MD, PhD, who led a related study that showed that people with a vitamin D deficiency were more likely to have severe COVID-19, agreed.

“The novelty and significance of this [new] study lie in the fact that it expands on our current understanding of the interplay between vitamin D and COVID-19, taking it beyond the acute phase of the disease,” said Dr. Dror, from Bar-Ilan University, Safed, Israel.

“It’s striking to see how vitamin D levels continue to influence patients’ health even after recovery from the initial infection,” he noted. 

“The findings certainly add weight to the argument for conducting a randomized control trial [RCT],” he continued, which “would enable us to conclusively determine whether vitamin D supplementation can effectively reduce the risk or severity of long COVID.”

“In the interim,” Dr. Dror said, “given the safety profile of vitamin D and its broad health benefits, it could be reasonable to test for vitamin D levels in patients admitted with COVID-19. If levels are found to be low, supplementation could be considered.”

“However, it’s important to note that this should be done under medical supervision,” he cautioned, “and further studies are needed to establish the optimal timing and dosage of supplementation.”

“I anticipate that we’ll see more RCTs [of this] in the future,” he speculated.
 

Low vitamin D and risk of long COVID

Long COVID is an emerging syndrome that affects 50%-70% of COVID-19 survivors.

Low levels of vitamin D have been associated with increased likelihood of needing mechanical ventilation and worse survival in patients hospitalized with COVID-19, but the risk of long COVID associated with vitamin D has not been known.

Researchers analyzed data from adults aged 18 and older hospitalized at San Raffaele Hospital with a confirmed diagnosis of COVID-19 and discharged during the first pandemic wave, from March to May 2020, and then seen 6-months later for follow-up.

Patients were excluded if they had been admitted to the intensive care unit during hospitalization or had missing medical data or blood samples available to determine (OH) vitamin D levels, at admission and the 6-month follow-up.

Long COVID-19 was defined based on the U.K. National Institute for Health and Care Excellence guidelines as the concomitant presence of at least two or more of 17 signs and symptoms that were absent prior to the COVID-19 infection and could only be attributed to that acute disease.

Researchers identified 50 patients with long COVID at the 6-month follow-up and matched them with 50 patients without long COVID at that time point, based on age, sex, concomitant comorbidities, need for noninvasive mechanical ventilation, and week of evaluation.

Patients were a mean age of 61 years (range, 51-73) and 56% were men; 28% had been on a ventilator during hospitalization for COVID-19.

The most frequent signs and symptoms at 6 months in the patients with long COVID were asthenia (weakness, 38% of patients), dysgeusia (bad taste in the mouth, 34%), dyspnea (shortness of breath, 34%), and anosmia (loss of sense of smell, 24%).

Most symptoms were related to the cardiorespiratory system (42%), the feeling of well-being (42%), or the senses (36%), and fewer patients had symptoms related to neurocognitive impairment (headache or brain fog, 14%), or ear, nose, and throat (12%), or gastrointestinal system (4%).

Patients with long COVID had lower mean 25(OH) vitamin D levels than patients without long COVID (20.1 vs 23.2 ng/mL; P = .03). However, actual vitamin D deficiency levels were similar in both groups.

Two-thirds of patients with low vitamin D levels at hospital admission still presented with low levels at the 6-month follow-up.

Vitamin D levels were significantly lower in patients with neurocognitive symptoms at follow-up (n = 7) than in those without such symptoms (n = 93) (14.6 vs. 20.6 ng/mL; P = .042).

In patients with vitamin D deficiency (< 20 ng/mL) at admission and at follow-up (n = 42), those with long COVID (n = 22) had lower vitamin D levels at follow-up than those without long COVID (n = 20) (12.7 vs. 15.2 ng/mL; P = .041).

And in multiple regression analyses, a lower 25(OH) vitamin D level at follow-up was the only variable that was significantly associated with long COVID (odds ratio, 1.09; 95% confidence interval, 1.01-1.16; P = .008).

The findings “strongly reinforce the clinical usefulness of 25(OH) vitamin D evaluation as a possible modifiable pathophysiological factor underlying this emerging worldwide critical health issue,” the researchers concluded.

The study was supported by Abiogen Pharma. One study author is an employee at Abiogen. Dr. Giustina has reported being a consultant for Abiogen and Takeda and receiving a research grant to his institution from Takeda. Dr. Di Filippo and the other authors reported no relevant financial relationships.

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

Patients with long COVID-19 – where the effects of an initial COVID infection last more than 12 weeks – had lower levels of 25(OH) vitamin D than other patients who survived COVID-19, in a retrospective, case-matched study.

The lower levels of vitamin D in patients with long COVID were most notable in those with brain fog.

Reasonable to test vitamin D levels, consider supplementation

Invited to comment, Amiel Dror, MD, PhD, who led a related study that showed that people with a vitamin D deficiency were more likely to have severe COVID-19, agreed.

“The novelty and significance of this [new] study lie in the fact that it expands on our current understanding of the interplay between vitamin D and COVID-19, taking it beyond the acute phase of the disease,” said Dr. Dror, from Bar-Ilan University, Safed, Israel.

“It’s striking to see how vitamin D levels continue to influence patients’ health even after recovery from the initial infection,” he noted. 

“The findings certainly add weight to the argument for conducting a randomized control trial [RCT],” he continued, which “would enable us to conclusively determine whether vitamin D supplementation can effectively reduce the risk or severity of long COVID.”

“In the interim,” Dr. Dror said, “given the safety profile of vitamin D and its broad health benefits, it could be reasonable to test for vitamin D levels in patients admitted with COVID-19. If levels are found to be low, supplementation could be considered.”

“However, it’s important to note that this should be done under medical supervision,” he cautioned, “and further studies are needed to establish the optimal timing and dosage of supplementation.”

“I anticipate that we’ll see more RCTs [of this] in the future,” he speculated.
 

Low vitamin D and risk of long COVID

Long COVID is an emerging syndrome that affects 50%-70% of COVID-19 survivors.

Low levels of vitamin D have been associated with increased likelihood of needing mechanical ventilation and worse survival in patients hospitalized with COVID-19, but the risk of long COVID associated with vitamin D has not been known.

Researchers analyzed data from adults aged 18 and older hospitalized at San Raffaele Hospital with a confirmed diagnosis of COVID-19 and discharged during the first pandemic wave, from March to May 2020, and then seen 6-months later for follow-up.

Patients were excluded if they had been admitted to the intensive care unit during hospitalization or had missing medical data or blood samples available to determine (OH) vitamin D levels, at admission and the 6-month follow-up.

Long COVID-19 was defined based on the U.K. National Institute for Health and Care Excellence guidelines as the concomitant presence of at least two or more of 17 signs and symptoms that were absent prior to the COVID-19 infection and could only be attributed to that acute disease.

Researchers identified 50 patients with long COVID at the 6-month follow-up and matched them with 50 patients without long COVID at that time point, based on age, sex, concomitant comorbidities, need for noninvasive mechanical ventilation, and week of evaluation.

Patients were a mean age of 61 years (range, 51-73) and 56% were men; 28% had been on a ventilator during hospitalization for COVID-19.

The most frequent signs and symptoms at 6 months in the patients with long COVID were asthenia (weakness, 38% of patients), dysgeusia (bad taste in the mouth, 34%), dyspnea (shortness of breath, 34%), and anosmia (loss of sense of smell, 24%).

Most symptoms were related to the cardiorespiratory system (42%), the feeling of well-being (42%), or the senses (36%), and fewer patients had symptoms related to neurocognitive impairment (headache or brain fog, 14%), or ear, nose, and throat (12%), or gastrointestinal system (4%).

Patients with long COVID had lower mean 25(OH) vitamin D levels than patients without long COVID (20.1 vs 23.2 ng/mL; P = .03). However, actual vitamin D deficiency levels were similar in both groups.

Two-thirds of patients with low vitamin D levels at hospital admission still presented with low levels at the 6-month follow-up.

Vitamin D levels were significantly lower in patients with neurocognitive symptoms at follow-up (n = 7) than in those without such symptoms (n = 93) (14.6 vs. 20.6 ng/mL; P = .042).

In patients with vitamin D deficiency (< 20 ng/mL) at admission and at follow-up (n = 42), those with long COVID (n = 22) had lower vitamin D levels at follow-up than those without long COVID (n = 20) (12.7 vs. 15.2 ng/mL; P = .041).

And in multiple regression analyses, a lower 25(OH) vitamin D level at follow-up was the only variable that was significantly associated with long COVID (odds ratio, 1.09; 95% confidence interval, 1.01-1.16; P = .008).

The findings “strongly reinforce the clinical usefulness of 25(OH) vitamin D evaluation as a possible modifiable pathophysiological factor underlying this emerging worldwide critical health issue,” the researchers concluded.

The study was supported by Abiogen Pharma. One study author is an employee at Abiogen. Dr. Giustina has reported being a consultant for Abiogen and Takeda and receiving a research grant to his institution from Takeda. Dr. Di Filippo and the other authors reported no relevant financial relationships.

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

According to the Centers for Disease Control and Prevention National Diabetes Statistic Report, there are more than 37 million adults aged 18 years or older with diabetes in the United States, representing 14.7% of the adult population. Approximately 90%-95% of people diagnosed with diabetes have type 2 diabetes (T2D). An increasing aging population with T2D and a disparate incidence and burden of disease in African American and Hispanic populations raise important care considerations in effective disease assessment and management, especially in primary care, where the majority of diabetes management occurs.

This extends to the need for quality patient education in an effort to give persons with diabetes a better understanding of what it’s like to live with the disease.

Here are five things to know about nonpharmacologic therapies for effective T2D management.

1. Understand and treat the person before the disease.

Diabetes is a complex and unrelenting disease of self-management, requiring an individualized care approach to achieve optimal health outcomes and quality of life for persons living with this condition. Over 90% of care is provided by the person with diabetes, therefore understanding the lived world of the person with diabetes and its connected impact on self-care is critical to establishing effective treatment recommendations, especially for people from racial and ethnic minority groups and lower socioeconomic status where diabetes disparities are highest. Disease prevalence, cost of care, and disease burden are driven by social determinants of health (SDOH) factors that need to be assessed, and strategies addressing causative factors need to be implemented. SDOH factors, including the built environment, safety, financial status, education, food access, health care access, and social support, directly affect the ability of a person with diabetes to effectively implement treatment recommendations, including access to new medications. The adoption of a shared decision-making approach is key to person-centered care. Shared decision-making promotes a positive communication feedback loop, therapeutic patient-care team relationship, and collaborative plan of care between the person with diabetes and the care team. It also supports the establishment of mutual respect between the person with diabetes and the care team members. This cultivates the strong, open, and authentic partnership needed for effective chronic disease management.

2. Quality diabetes education is the foundation for effective self-care.

Diabetes self-management education and support (DSMES) is a fundamental component of diabetes care and ensures patients have the knowledge, skills, motivation, and resources necessary for effectively managing this condition. Despite treatment advances and the evidence base for DSMES, less than 5% of Medicare beneficiaries and 6.8% of privately insured beneficiaries have utilized its services, and this is a likely contributor to the lack of improvement for achieving national diabetes clinical targets. The Association of Diabetes Care and Education Specialists (ADCES7) Self-Care Behaviors provides an evidence-based framework for an optimal DSMES curriculum, incorporating the self-care behaviors of healthy coping (e.g., having a positive attitude toward diabetes self-management), nutritious eating, being active, taking medication, monitoring, reducing risk, and problem-solving.

There are four core times to implement and adapt referral for DSMES: (1) at diagnosis, (2) annually or when not meeting targets, (3) when complications arise, and (4) with transitions in life and care. DSMES referrals should be made for programs accredited by the ADCES or American Diabetes Association (ADA) and led by expert Certified Diabetes Care and Education Specialists (CDCES). The multidisciplinary composition and clinical skill level of CDCES make them a highly valued member of the diabetes care team. CDCES have demonstrated not only diabetes education expertise but are involved in broader health care roles to include population health management, technology integration, mitigation of therapeutic inertia, quality improvement activity, and delivery of cost-effective care.

3. Establish a strong foundation in lifestyle medicine.

Lifestyle medicine encompasses healthy eating, physical activity, restorative sleep, stress management, avoidance of risky behaviors, and positive social connections. It has also been strongly connected as a primary modality to prevent and treat chronic conditions like T2D. Lifestyle modifications have been noted in reducing the incidence of developing diabetes, reversing disease, improving clinical markers such as A1c and lipids, weight reduction, reducing use of medications, and improving quality of life. The multidisciplinary care team and CDCES can support the empowerment of individuals with T2D to develop the life skills and knowledge needed to establish positive self-care behaviors and successfully achieve health goals. Lifestyle medicine is not a replacement for pharmacologic interventions but rather serves as an adjunct when medication management is required.

4. Harness technology in diabetes treatment and care delivery.

Diabetes technology is advancing swiftly and includes glucose monitors, medication delivery devices, data-sharing platforms, and disease self-management applications. Combined with education and support, diabetes technology has been shown to have a positive clinical and personal impact on disease outcomes and quality of life. Regardless of its benefits, at times technology can seem overwhelming for the person with diabetes and the care team. Diabetes Care and Education Specialists (DCES) can support the care team and people living with diabetes to effectively identify, implement, and evaluate patient-centered diabetes technologies, as well as implement processes to drive clinical efficiencies and sustainability. Patient-generated health data reports can provide the care team with effective and proficient evaluation of diabetes care and needed treatment changes.

The expansion of telehealth during the COVID-19 pandemic, including real-time and asynchronous approaches, coupled with in-person care team visits, has resulted in improved access to diabetes care and education. Moreover, there continues to be an expanding health system focus on improving access to care beyond traditional brick and mortar solutions. Telehealth poses one possible access solution for people living with diabetes for whom factors such as transportation, remote geographies, and physical limitations affect their ability to attend in-person care visits.

5. Assess and address diabetes-related distress.

The persistent nature of diabetes self-care expectations and the impact on lifestyle behaviors, medication adherence, and glycemic control demands the need for assessment and treatment of diabetes-related distress (DRD). DRD can be expressed as shame, guilt, anger, fear, and frustration in combination with the everyday context of life priorities and stressors. An assessment of diabetes distress, utilizing a simple scale, should be included as part of an annual therapeutic diabetes care plan. The ADA Standards of Care in Diabetes recommends assessing patients’ psychological and social situations as an ongoing part of medical management, including an annual screening for depression and other psychological problems. The prevalence of depression is nearly twice as high in people with T2D than in the general population and can significantly influence patients’ ability to self-manage their diabetes and achieve healthy outcomes. Assessment and treatment of psychosocial components of care can result in significant improvements in A1c and other positive outcomes, including quality of life.

Kellie M. Rodriguez, director of the global diabetes program at Parkland Health, Dallas, Tex., disclosed ties with the Association of Diabetes Care and Education Specialists.

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

According to the Centers for Disease Control and Prevention National Diabetes Statistic Report, there are more than 37 million adults aged 18 years or older with diabetes in the United States, representing 14.7% of the adult population. Approximately 90%-95% of people diagnosed with diabetes have type 2 diabetes (T2D). An increasing aging population with T2D and a disparate incidence and burden of disease in African American and Hispanic populations raise important care considerations in effective disease assessment and management, especially in primary care, where the majority of diabetes management occurs.

This extends to the need for quality patient education in an effort to give persons with diabetes a better understanding of what it’s like to live with the disease.

Here are five things to know about nonpharmacologic therapies for effective T2D management.

1. Understand and treat the person before the disease.

Diabetes is a complex and unrelenting disease of self-management, requiring an individualized care approach to achieve optimal health outcomes and quality of life for persons living with this condition. Over 90% of care is provided by the person with diabetes, therefore understanding the lived world of the person with diabetes and its connected impact on self-care is critical to establishing effective treatment recommendations, especially for people from racial and ethnic minority groups and lower socioeconomic status where diabetes disparities are highest. Disease prevalence, cost of care, and disease burden are driven by social determinants of health (SDOH) factors that need to be assessed, and strategies addressing causative factors need to be implemented. SDOH factors, including the built environment, safety, financial status, education, food access, health care access, and social support, directly affect the ability of a person with diabetes to effectively implement treatment recommendations, including access to new medications. The adoption of a shared decision-making approach is key to person-centered care. Shared decision-making promotes a positive communication feedback loop, therapeutic patient-care team relationship, and collaborative plan of care between the person with diabetes and the care team. It also supports the establishment of mutual respect between the person with diabetes and the care team members. This cultivates the strong, open, and authentic partnership needed for effective chronic disease management.

2. Quality diabetes education is the foundation for effective self-care.

Diabetes self-management education and support (DSMES) is a fundamental component of diabetes care and ensures patients have the knowledge, skills, motivation, and resources necessary for effectively managing this condition. Despite treatment advances and the evidence base for DSMES, less than 5% of Medicare beneficiaries and 6.8% of privately insured beneficiaries have utilized its services, and this is a likely contributor to the lack of improvement for achieving national diabetes clinical targets. The Association of Diabetes Care and Education Specialists (ADCES7) Self-Care Behaviors provides an evidence-based framework for an optimal DSMES curriculum, incorporating the self-care behaviors of healthy coping (e.g., having a positive attitude toward diabetes self-management), nutritious eating, being active, taking medication, monitoring, reducing risk, and problem-solving.

There are four core times to implement and adapt referral for DSMES: (1) at diagnosis, (2) annually or when not meeting targets, (3) when complications arise, and (4) with transitions in life and care. DSMES referrals should be made for programs accredited by the ADCES or American Diabetes Association (ADA) and led by expert Certified Diabetes Care and Education Specialists (CDCES). The multidisciplinary composition and clinical skill level of CDCES make them a highly valued member of the diabetes care team. CDCES have demonstrated not only diabetes education expertise but are involved in broader health care roles to include population health management, technology integration, mitigation of therapeutic inertia, quality improvement activity, and delivery of cost-effective care.

3. Establish a strong foundation in lifestyle medicine.

Lifestyle medicine encompasses healthy eating, physical activity, restorative sleep, stress management, avoidance of risky behaviors, and positive social connections. It has also been strongly connected as a primary modality to prevent and treat chronic conditions like T2D. Lifestyle modifications have been noted in reducing the incidence of developing diabetes, reversing disease, improving clinical markers such as A1c and lipids, weight reduction, reducing use of medications, and improving quality of life. The multidisciplinary care team and CDCES can support the empowerment of individuals with T2D to develop the life skills and knowledge needed to establish positive self-care behaviors and successfully achieve health goals. Lifestyle medicine is not a replacement for pharmacologic interventions but rather serves as an adjunct when medication management is required.

4. Harness technology in diabetes treatment and care delivery.

Diabetes technology is advancing swiftly and includes glucose monitors, medication delivery devices, data-sharing platforms, and disease self-management applications. Combined with education and support, diabetes technology has been shown to have a positive clinical and personal impact on disease outcomes and quality of life. Regardless of its benefits, at times technology can seem overwhelming for the person with diabetes and the care team. Diabetes Care and Education Specialists (DCES) can support the care team and people living with diabetes to effectively identify, implement, and evaluate patient-centered diabetes technologies, as well as implement processes to drive clinical efficiencies and sustainability. Patient-generated health data reports can provide the care team with effective and proficient evaluation of diabetes care and needed treatment changes.

The expansion of telehealth during the COVID-19 pandemic, including real-time and asynchronous approaches, coupled with in-person care team visits, has resulted in improved access to diabetes care and education. Moreover, there continues to be an expanding health system focus on improving access to care beyond traditional brick and mortar solutions. Telehealth poses one possible access solution for people living with diabetes for whom factors such as transportation, remote geographies, and physical limitations affect their ability to attend in-person care visits.

5. Assess and address diabetes-related distress.

The persistent nature of diabetes self-care expectations and the impact on lifestyle behaviors, medication adherence, and glycemic control demands the need for assessment and treatment of diabetes-related distress (DRD). DRD can be expressed as shame, guilt, anger, fear, and frustration in combination with the everyday context of life priorities and stressors. An assessment of diabetes distress, utilizing a simple scale, should be included as part of an annual therapeutic diabetes care plan. The ADA Standards of Care in Diabetes recommends assessing patients’ psychological and social situations as an ongoing part of medical management, including an annual screening for depression and other psychological problems. The prevalence of depression is nearly twice as high in people with T2D than in the general population and can significantly influence patients’ ability to self-manage their diabetes and achieve healthy outcomes. Assessment and treatment of psychosocial components of care can result in significant improvements in A1c and other positive outcomes, including quality of life.

Kellie M. Rodriguez, director of the global diabetes program at Parkland Health, Dallas, Tex., disclosed ties with the Association of Diabetes Care and Education Specialists.

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

According to the Centers for Disease Control and Prevention National Diabetes Statistic Report, there are more than 37 million adults aged 18 years or older with diabetes in the United States, representing 14.7% of the adult population. Approximately 90%-95% of people diagnosed with diabetes have type 2 diabetes (T2D). An increasing aging population with T2D and a disparate incidence and burden of disease in African American and Hispanic populations raise important care considerations in effective disease assessment and management, especially in primary care, where the majority of diabetes management occurs.

This extends to the need for quality patient education in an effort to give persons with diabetes a better understanding of what it’s like to live with the disease.

Here are five things to know about nonpharmacologic therapies for effective T2D management.

1. Understand and treat the person before the disease.

Diabetes is a complex and unrelenting disease of self-management, requiring an individualized care approach to achieve optimal health outcomes and quality of life for persons living with this condition. Over 90% of care is provided by the person with diabetes, therefore understanding the lived world of the person with diabetes and its connected impact on self-care is critical to establishing effective treatment recommendations, especially for people from racial and ethnic minority groups and lower socioeconomic status where diabetes disparities are highest. Disease prevalence, cost of care, and disease burden are driven by social determinants of health (SDOH) factors that need to be assessed, and strategies addressing causative factors need to be implemented. SDOH factors, including the built environment, safety, financial status, education, food access, health care access, and social support, directly affect the ability of a person with diabetes to effectively implement treatment recommendations, including access to new medications. The adoption of a shared decision-making approach is key to person-centered care. Shared decision-making promotes a positive communication feedback loop, therapeutic patient-care team relationship, and collaborative plan of care between the person with diabetes and the care team. It also supports the establishment of mutual respect between the person with diabetes and the care team members. This cultivates the strong, open, and authentic partnership needed for effective chronic disease management.

2. Quality diabetes education is the foundation for effective self-care.

Diabetes self-management education and support (DSMES) is a fundamental component of diabetes care and ensures patients have the knowledge, skills, motivation, and resources necessary for effectively managing this condition. Despite treatment advances and the evidence base for DSMES, less than 5% of Medicare beneficiaries and 6.8% of privately insured beneficiaries have utilized its services, and this is a likely contributor to the lack of improvement for achieving national diabetes clinical targets. The Association of Diabetes Care and Education Specialists (ADCES7) Self-Care Behaviors provides an evidence-based framework for an optimal DSMES curriculum, incorporating the self-care behaviors of healthy coping (e.g., having a positive attitude toward diabetes self-management), nutritious eating, being active, taking medication, monitoring, reducing risk, and problem-solving.

There are four core times to implement and adapt referral for DSMES: (1) at diagnosis, (2) annually or when not meeting targets, (3) when complications arise, and (4) with transitions in life and care. DSMES referrals should be made for programs accredited by the ADCES or American Diabetes Association (ADA) and led by expert Certified Diabetes Care and Education Specialists (CDCES). The multidisciplinary composition and clinical skill level of CDCES make them a highly valued member of the diabetes care team. CDCES have demonstrated not only diabetes education expertise but are involved in broader health care roles to include population health management, technology integration, mitigation of therapeutic inertia, quality improvement activity, and delivery of cost-effective care.

3. Establish a strong foundation in lifestyle medicine.

Lifestyle medicine encompasses healthy eating, physical activity, restorative sleep, stress management, avoidance of risky behaviors, and positive social connections. It has also been strongly connected as a primary modality to prevent and treat chronic conditions like T2D. Lifestyle modifications have been noted in reducing the incidence of developing diabetes, reversing disease, improving clinical markers such as A1c and lipids, weight reduction, reducing use of medications, and improving quality of life. The multidisciplinary care team and CDCES can support the empowerment of individuals with T2D to develop the life skills and knowledge needed to establish positive self-care behaviors and successfully achieve health goals. Lifestyle medicine is not a replacement for pharmacologic interventions but rather serves as an adjunct when medication management is required.

4. Harness technology in diabetes treatment and care delivery.

Diabetes technology is advancing swiftly and includes glucose monitors, medication delivery devices, data-sharing platforms, and disease self-management applications. Combined with education and support, diabetes technology has been shown to have a positive clinical and personal impact on disease outcomes and quality of life. Regardless of its benefits, at times technology can seem overwhelming for the person with diabetes and the care team. Diabetes Care and Education Specialists (DCES) can support the care team and people living with diabetes to effectively identify, implement, and evaluate patient-centered diabetes technologies, as well as implement processes to drive clinical efficiencies and sustainability. Patient-generated health data reports can provide the care team with effective and proficient evaluation of diabetes care and needed treatment changes.

The expansion of telehealth during the COVID-19 pandemic, including real-time and asynchronous approaches, coupled with in-person care team visits, has resulted in improved access to diabetes care and education. Moreover, there continues to be an expanding health system focus on improving access to care beyond traditional brick and mortar solutions. Telehealth poses one possible access solution for people living with diabetes for whom factors such as transportation, remote geographies, and physical limitations affect their ability to attend in-person care visits.

5. Assess and address diabetes-related distress.

The persistent nature of diabetes self-care expectations and the impact on lifestyle behaviors, medication adherence, and glycemic control demands the need for assessment and treatment of diabetes-related distress (DRD). DRD can be expressed as shame, guilt, anger, fear, and frustration in combination with the everyday context of life priorities and stressors. An assessment of diabetes distress, utilizing a simple scale, should be included as part of an annual therapeutic diabetes care plan. The ADA Standards of Care in Diabetes recommends assessing patients’ psychological and social situations as an ongoing part of medical management, including an annual screening for depression and other psychological problems. The prevalence of depression is nearly twice as high in people with T2D than in the general population and can significantly influence patients’ ability to self-manage their diabetes and achieve healthy outcomes. Assessment and treatment of psychosocial components of care can result in significant improvements in A1c and other positive outcomes, including quality of life.

Kellie M. Rodriguez, director of the global diabetes program at Parkland Health, Dallas, Tex., disclosed ties with the Association of Diabetes Care and Education Specialists.

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

Sores on the feet can signal problems with the eyes in patients with diabetes.

Prior research and anecdotal experience show that diabetic foot ulcers and diabetic retinopathy frequently co-occur. New research further clarifies this link and shows that patients with foot ulcers may receive fewer treatments to protect their sight.

David J. Ramsey, MD, PhD, MPH, director of ophthalmic research at Lahey Hospital & Medical Center, Burlington, Mass., said when clinicians detect either condition, they should involve a team that can intervene to help protect a patient’s vision and mobility.

For example, they should ensure patients receive comprehensive eye and foot evaluations and help them optimize diabetes management.

The new study, presented at the annual meeting of the Association for Research in Vision and Ophthalmology, “adds an important dimension” to understanding the association between the conditions, said Dr. Ramsey, who recently reviewed correlations between diabetic foot ulcers and diabetic retinopathy and their underlying causes.

“Patients with diabetic foot ulcers appear to receive less attention to their diabetic retinopathy and may receive fewer treatments with eye injections targeting vascular endothelial growth factor (VEGF), an important driver of progression of diabetic retinopathy,” said Dr. Ramsey, who is also an associate professor of ophthalmology at Tufts University School of Medicine, Boston. He was not involved in the study presented at ARVO 2023.

In the new study, Christopher T. Zhu, a medical student at UT Health San Antonio, and colleagues analyzed data from 426 eyes of 213 patients with type 2 diabetes who had had at least two eye exams between 2012 and 2022; 72 of the patients had diabetic foot ulcers. Patients were followed for about 4 years on average.

Patients with diabetic foot ulcers had a higher percentage of eyes with macular edema on their initial exam (32.6% vs. 28%). By the final exam, the percentage of eyes with macular edema was significantly greater in the group with diabetic foot ulcers (64.6% vs. 37.6%; P < .0001), Mr. Zhu’s group reported.

Eyes with nonproliferative diabetic retinopathy progressed to proliferative diabetic retinopathy, the worst grade, at a higher rate in the group with foot ulcers (50.6% vs. 35.6%; P = .03). In addition, patients with foot ulcers were more likely to experience vitreous hemorrhage (55.6% vs. 38.7%), the researchers found.

Despite patients with foot ulcers tending to have worse disease, they received fewer treatments for retinopathy. Those without ulcers received an average of 6.9 anti-VEGF injections per eye, while those with ulcers averaged 4.3.

Foot ulcers may hinder the ability of patients to get to appointments to receive the injections, Mr. Zhu and colleagues wrote. “For many patients in our part of the country [South Texas], a lack of transportation is a particular barrier to health care access,” Mr. Zhu told this news organization.

Mr. Zhu’s team conducted their study after noticing that patients with diabetes and foot ulcers who presented to their eye clinics “appeared to progress faster to worse grades of retinopathy” than patients with diabetes who did not have ulcers.

“Similar to how foot ulcers develop due to a severe disruption in blood flow [vascular] and a loss of sensation [neurologic], diabetic retinopathy may have a relation to microvascular disease, neurologic degeneration, and inflammation,” he said.

The findings confirm “that poor perfusion of the eye and foot are linked and can cause ischemic retinopathy leading to the development of proliferative diabetic retinopathy and vitreous hemorrhages, both serious, vision-threatening conditions,” Dr. Ramsey said.

To some extent, fewer treatments with anti-VEGF agents may account for why patients with foot ulcers have more eye complications, Dr. Ramsey added. “Additional research needs to be done to further dissect the cause and the effect, but it’s a very important finding that we need to increase awareness about,” he said.

Dr. Ramsey and Mr. Zhu reported no relevant financial relationships.

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

Sores on the feet can signal problems with the eyes in patients with diabetes.

Prior research and anecdotal experience show that diabetic foot ulcers and diabetic retinopathy frequently co-occur. New research further clarifies this link and shows that patients with foot ulcers may receive fewer treatments to protect their sight.

David J. Ramsey, MD, PhD, MPH, director of ophthalmic research at Lahey Hospital & Medical Center, Burlington, Mass., said when clinicians detect either condition, they should involve a team that can intervene to help protect a patient’s vision and mobility.

For example, they should ensure patients receive comprehensive eye and foot evaluations and help them optimize diabetes management.

The new study, presented at the annual meeting of the Association for Research in Vision and Ophthalmology, “adds an important dimension” to understanding the association between the conditions, said Dr. Ramsey, who recently reviewed correlations between diabetic foot ulcers and diabetic retinopathy and their underlying causes.

“Patients with diabetic foot ulcers appear to receive less attention to their diabetic retinopathy and may receive fewer treatments with eye injections targeting vascular endothelial growth factor (VEGF), an important driver of progression of diabetic retinopathy,” said Dr. Ramsey, who is also an associate professor of ophthalmology at Tufts University School of Medicine, Boston. He was not involved in the study presented at ARVO 2023.

In the new study, Christopher T. Zhu, a medical student at UT Health San Antonio, and colleagues analyzed data from 426 eyes of 213 patients with type 2 diabetes who had had at least two eye exams between 2012 and 2022; 72 of the patients had diabetic foot ulcers. Patients were followed for about 4 years on average.

Patients with diabetic foot ulcers had a higher percentage of eyes with macular edema on their initial exam (32.6% vs. 28%). By the final exam, the percentage of eyes with macular edema was significantly greater in the group with diabetic foot ulcers (64.6% vs. 37.6%; P < .0001), Mr. Zhu’s group reported.

Eyes with nonproliferative diabetic retinopathy progressed to proliferative diabetic retinopathy, the worst grade, at a higher rate in the group with foot ulcers (50.6% vs. 35.6%; P = .03). In addition, patients with foot ulcers were more likely to experience vitreous hemorrhage (55.6% vs. 38.7%), the researchers found.

Despite patients with foot ulcers tending to have worse disease, they received fewer treatments for retinopathy. Those without ulcers received an average of 6.9 anti-VEGF injections per eye, while those with ulcers averaged 4.3.

Foot ulcers may hinder the ability of patients to get to appointments to receive the injections, Mr. Zhu and colleagues wrote. “For many patients in our part of the country [South Texas], a lack of transportation is a particular barrier to health care access,” Mr. Zhu told this news organization.

Mr. Zhu’s team conducted their study after noticing that patients with diabetes and foot ulcers who presented to their eye clinics “appeared to progress faster to worse grades of retinopathy” than patients with diabetes who did not have ulcers.

“Similar to how foot ulcers develop due to a severe disruption in blood flow [vascular] and a loss of sensation [neurologic], diabetic retinopathy may have a relation to microvascular disease, neurologic degeneration, and inflammation,” he said.

The findings confirm “that poor perfusion of the eye and foot are linked and can cause ischemic retinopathy leading to the development of proliferative diabetic retinopathy and vitreous hemorrhages, both serious, vision-threatening conditions,” Dr. Ramsey said.

To some extent, fewer treatments with anti-VEGF agents may account for why patients with foot ulcers have more eye complications, Dr. Ramsey added. “Additional research needs to be done to further dissect the cause and the effect, but it’s a very important finding that we need to increase awareness about,” he said.

Dr. Ramsey and Mr. Zhu reported no relevant financial relationships.

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

Sores on the feet can signal problems with the eyes in patients with diabetes.

Prior research and anecdotal experience show that diabetic foot ulcers and diabetic retinopathy frequently co-occur. New research further clarifies this link and shows that patients with foot ulcers may receive fewer treatments to protect their sight.

David J. Ramsey, MD, PhD, MPH, director of ophthalmic research at Lahey Hospital & Medical Center, Burlington, Mass., said when clinicians detect either condition, they should involve a team that can intervene to help protect a patient’s vision and mobility.

For example, they should ensure patients receive comprehensive eye and foot evaluations and help them optimize diabetes management.

The new study, presented at the annual meeting of the Association for Research in Vision and Ophthalmology, “adds an important dimension” to understanding the association between the conditions, said Dr. Ramsey, who recently reviewed correlations between diabetic foot ulcers and diabetic retinopathy and their underlying causes.

“Patients with diabetic foot ulcers appear to receive less attention to their diabetic retinopathy and may receive fewer treatments with eye injections targeting vascular endothelial growth factor (VEGF), an important driver of progression of diabetic retinopathy,” said Dr. Ramsey, who is also an associate professor of ophthalmology at Tufts University School of Medicine, Boston. He was not involved in the study presented at ARVO 2023.

In the new study, Christopher T. Zhu, a medical student at UT Health San Antonio, and colleagues analyzed data from 426 eyes of 213 patients with type 2 diabetes who had had at least two eye exams between 2012 and 2022; 72 of the patients had diabetic foot ulcers. Patients were followed for about 4 years on average.

Patients with diabetic foot ulcers had a higher percentage of eyes with macular edema on their initial exam (32.6% vs. 28%). By the final exam, the percentage of eyes with macular edema was significantly greater in the group with diabetic foot ulcers (64.6% vs. 37.6%; P < .0001), Mr. Zhu’s group reported.

Eyes with nonproliferative diabetic retinopathy progressed to proliferative diabetic retinopathy, the worst grade, at a higher rate in the group with foot ulcers (50.6% vs. 35.6%; P = .03). In addition, patients with foot ulcers were more likely to experience vitreous hemorrhage (55.6% vs. 38.7%), the researchers found.

Despite patients with foot ulcers tending to have worse disease, they received fewer treatments for retinopathy. Those without ulcers received an average of 6.9 anti-VEGF injections per eye, while those with ulcers averaged 4.3.

Foot ulcers may hinder the ability of patients to get to appointments to receive the injections, Mr. Zhu and colleagues wrote. “For many patients in our part of the country [South Texas], a lack of transportation is a particular barrier to health care access,” Mr. Zhu told this news organization.

Mr. Zhu’s team conducted their study after noticing that patients with diabetes and foot ulcers who presented to their eye clinics “appeared to progress faster to worse grades of retinopathy” than patients with diabetes who did not have ulcers.

“Similar to how foot ulcers develop due to a severe disruption in blood flow [vascular] and a loss of sensation [neurologic], diabetic retinopathy may have a relation to microvascular disease, neurologic degeneration, and inflammation,” he said.

The findings confirm “that poor perfusion of the eye and foot are linked and can cause ischemic retinopathy leading to the development of proliferative diabetic retinopathy and vitreous hemorrhages, both serious, vision-threatening conditions,” Dr. Ramsey said.

To some extent, fewer treatments with anti-VEGF agents may account for why patients with foot ulcers have more eye complications, Dr. Ramsey added. “Additional research needs to be done to further dissect the cause and the effect, but it’s a very important finding that we need to increase awareness about,” he said.

Dr. Ramsey and Mr. Zhu reported no relevant financial relationships.

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

Disappointment – “I failed this exam, my life is ruined” or regret – “I am getting a divorce, I wasted so much of my life.” Patients present with a wide variety of complaints that can be understood as a form of death anxiety.

Fundamentally, patients come to see us to understand and explain their lives. One can reinterpret this as a patient asking, “If I died today, would my life have been good enough?” or “When I die, how will I look back at this moment in time and judge the choices I made?”

Other patients come to us attempting to use the same maladaptive defenses that did not serve them well in the past in the hopes of achieving a new outcome that will validate their lives. While it may be understandable that a child dissociates when facing abuse, hoping that this defense mechanism – as an adult – will work, it is unlikely to be fruitful and will certainly not validate or repair the past. This hope to repair one’s past can be interpreted as a fear of death – “I cannot die without correcting this.” This psychic conflict can intensify if one does not adopt a more adaptive understanding of his or her life.

Courtesy Dr. Neha Akkoor

Death anxiety is the feeling associated with the finality of life. Not only is life final, but a constant reminder of that fact is the idea that any one moment is final. Other than in science fiction, one cannot return to a prior moment and repair the past in the hope of a better future. Time goes only in one direction and death is the natural outcome of all life.

Death may have some evolutionary purpose that encourages the promotion of newer and more fitter genes, but one doesn’t have to consider its origin and reason to admit death’s constancy throughout humanity. People die and that is an anxiety-provoking fact of life. Death anxiety can feel especially tangible in our connected world. In a world of constant news, it can feel – for many people – that if your house wasn’t displaced because of global warming or that you are not a war refugee, you don’t deserve to be seen and heard.

This can be a particularly strong feeling for and among physicians, who don’t think that the mental health challenges generated by their own tough circumstances deserve to be labeled a mental disorder, so they designate themselves as having “burnout”¹ – as they don’t deserve the sympathy of having the clinically significant impairments of “depression.” Our traumas don’t seem important enough to deserve notice, and thus we may feel like we could die without ever having truly mattered.

This can also be applied in the reverse fashion. Certain individuals, like celebrities, live such extravagant lives that our simpler achievements can feel futile in comparison. While the neighbor’s grass has always felt greener, we are now constantly exposed to perfectly manicured lawns on social media. When compounded, the idea that our successes and our pains are both simultaneously irrelevant can lead one to have very palpable death anxiety – my life will never matter if none of the things I do matter, or my life will never matter because I will never achieve the requisite number of “likes” or “views” on social media required to believe that one’s life was worth living.

A way of alleviating death anxiety can be through the concept of legacy, or what we leave behind. How will people remember me? Will people remember me, or will I disappear like a shadow into the distant memory of my near and dear ones? The idea of being forgotten or lost to memory is intolerable to some and can be a strong driving force to “make a name” for oneself. For those who crave fame, whether a celebrity or a generous alumnus, part of this is likely related to remaining well known after death. After all, one can argue that you are not truly dead as long as you continue to live in the memory and/or genes of others.

Legacy thus serves as a form of posthumous transitional object; a way of calming our fears about how we will be remembered. For many, reconciling their feelings towards their legacy is an avenue to tame death anxiety.
 

A case study

The case of Mr. B illustrates this. As a 72-year-old male with a long history of generalized anxiety, he once had a nightmare as a child, similar to the plot of Sleeping Beauty. In his dream, he walks up a spiral staircase in a castle and touches the spindle on a spinning wheel, thus ending his life. The dream was vivid and marked him.

His fear of death has subsequently reared its head throughout his life. In more recent years, he has suffered from cardiovascular disease. Although he is now quite stable on his current cardiac medications, he is constantly fearful that he will experience a cardiac event while asleep and suddenly die. He is so anxious about not waking up in the morning that falling asleep is nearly impossible.

Mr. B is single, with no close family besides a sister who lives in another state. He has a dog and few friends. He worries about what will happen to his dog if he doesn’t wake up in the morning, but perhaps most distressing to him is “there’s so much left for me to do, I have so much to write!” As an accomplished author, he continues to write, and hopes to publish many more novels in his lifetime. It is unsurprising that someone without a strong social network may fear death and feel pressured to somehow make a mark on the world before the curtain falls. It is scary to think that even without us, life goes on.

By bringing to Mr. B’s attention that his ever-present anxiety is rooted in fear of death, he was able to gain more insight into his own defensive behaviors. By confronting his death anxiety and processing his definition of a life well lived together in therapy, he’s acknowledged his lack of social connection as demoralizing, and has made significant strides to remedy this. He’s been able to focus on a more fulfilling life day to day, with less emphasis on his to-do list and aspirations. Instead, he’s connected more with his faith and members of his church. He’s gotten close to several neighbors and enjoys long dinners with them on his back patio.

At a recent meeting, he confessed that he feels “lighter” and not as fearful about sudden cardiac death, and thus has noticed that his overall anxiety has diminished greatly. He concluded that experiencing meaningful relationships in the present moment would give him greater joy than spending his remaining time engaged in preserving a future identity for himself. It seems elementary, but if we look within, we may find that we all suffer similarly: How much of our daily actions, thoughts, and fears are tied to the looming threat of death?
 

Conclusion

While modern psychiatry continues to advance with better understandings of our neurobiology, improved knowledge of pathophysiological processes of mental illness, and expanding discovery of novel pharmacotherapeutics, the modern psychiatrist should not forget fundamental truths of behavior and humanity that were once the staple of psychiatry.

Death anxiety is one of those truths; it is the ultimate stressor that we will all face and should be regular study and practice for psychiatrists. In this article, we explored some of those facets most meaningful to us but recommend you expand your study to the many more available.

Death anxiety is a constant reminder that life is final, and it is natural to feel anxious when thinking about it. Patients often come to physicians seeking validation of their lives or trying to use the same maladaptive defense mechanisms that did not serve them well in the past to achieve a better outcome.

In today’s world, death anxiety can feel palpable due to the constant exposure to global news and social media that can make us feel irrelevant. However, legacy, or what we leave behind, can serve as a way to alleviate death anxiety. For many, reconciling their feelings toward their legacy is an avenue to tame death anxiety. Therapy can help individuals gain insight into their defensive behaviors and process their definition of a life well lived. By focusing on a life worth living, individuals can alleviate their death anxiety and gain a sense of fulfillment.

Dr. Akkoor is a psychiatry resident at the University of California, San Diego. She is interested in immigrant mental health, ethics, consultation-liaison psychiatry, and medical education. Dr. Badre is a clinical and forensic psychiatrist in San Diego. He holds teaching positions at the University of California, San Diego, and the University of San Diego. He teaches medical education, psychopharmacology, ethics in psychiatry, and correctional care. Dr. Badre can be reached at his website, BadreMD.com. Dr. Badre and Dr. Akkoor have no conflicts of interest.

Reference

1. Badre N. Burnout: A concept that rebrands mental illness for professionals. Clinical Psychiatry News. 2020 Mar 5.

Disappointment – “I failed this exam, my life is ruined” or regret – “I am getting a divorce, I wasted so much of my life.” Patients present with a wide variety of complaints that can be understood as a form of death anxiety.

Fundamentally, patients come to see us to understand and explain their lives. One can reinterpret this as a patient asking, “If I died today, would my life have been good enough?” or “When I die, how will I look back at this moment in time and judge the choices I made?”

Other patients come to us attempting to use the same maladaptive defenses that did not serve them well in the past in the hopes of achieving a new outcome that will validate their lives. While it may be understandable that a child dissociates when facing abuse, hoping that this defense mechanism – as an adult – will work, it is unlikely to be fruitful and will certainly not validate or repair the past. This hope to repair one’s past can be interpreted as a fear of death – “I cannot die without correcting this.” This psychic conflict can intensify if one does not adopt a more adaptive understanding of his or her life.

Courtesy Dr. Neha Akkoor

Death anxiety is the feeling associated with the finality of life. Not only is life final, but a constant reminder of that fact is the idea that any one moment is final. Other than in science fiction, one cannot return to a prior moment and repair the past in the hope of a better future. Time goes only in one direction and death is the natural outcome of all life.

Death may have some evolutionary purpose that encourages the promotion of newer and more fitter genes, but one doesn’t have to consider its origin and reason to admit death’s constancy throughout humanity. People die and that is an anxiety-provoking fact of life. Death anxiety can feel especially tangible in our connected world. In a world of constant news, it can feel – for many people – that if your house wasn’t displaced because of global warming or that you are not a war refugee, you don’t deserve to be seen and heard.

This can be a particularly strong feeling for and among physicians, who don’t think that the mental health challenges generated by their own tough circumstances deserve to be labeled a mental disorder, so they designate themselves as having “burnout”¹ – as they don’t deserve the sympathy of having the clinically significant impairments of “depression.” Our traumas don’t seem important enough to deserve notice, and thus we may feel like we could die without ever having truly mattered.

This can also be applied in the reverse fashion. Certain individuals, like celebrities, live such extravagant lives that our simpler achievements can feel futile in comparison. While the neighbor’s grass has always felt greener, we are now constantly exposed to perfectly manicured lawns on social media. When compounded, the idea that our successes and our pains are both simultaneously irrelevant can lead one to have very palpable death anxiety – my life will never matter if none of the things I do matter, or my life will never matter because I will never achieve the requisite number of “likes” or “views” on social media required to believe that one’s life was worth living.

A way of alleviating death anxiety can be through the concept of legacy, or what we leave behind. How will people remember me? Will people remember me, or will I disappear like a shadow into the distant memory of my near and dear ones? The idea of being forgotten or lost to memory is intolerable to some and can be a strong driving force to “make a name” for oneself. For those who crave fame, whether a celebrity or a generous alumnus, part of this is likely related to remaining well known after death. After all, one can argue that you are not truly dead as long as you continue to live in the memory and/or genes of others.

Legacy thus serves as a form of posthumous transitional object; a way of calming our fears about how we will be remembered. For many, reconciling their feelings towards their legacy is an avenue to tame death anxiety.
 

A case study

The case of Mr. B illustrates this. As a 72-year-old male with a long history of generalized anxiety, he once had a nightmare as a child, similar to the plot of Sleeping Beauty. In his dream, he walks up a spiral staircase in a castle and touches the spindle on a spinning wheel, thus ending his life. The dream was vivid and marked him.

His fear of death has subsequently reared its head throughout his life. In more recent years, he has suffered from cardiovascular disease. Although he is now quite stable on his current cardiac medications, he is constantly fearful that he will experience a cardiac event while asleep and suddenly die. He is so anxious about not waking up in the morning that falling asleep is nearly impossible.

Mr. B is single, with no close family besides a sister who lives in another state. He has a dog and few friends. He worries about what will happen to his dog if he doesn’t wake up in the morning, but perhaps most distressing to him is “there’s so much left for me to do, I have so much to write!” As an accomplished author, he continues to write, and hopes to publish many more novels in his lifetime. It is unsurprising that someone without a strong social network may fear death and feel pressured to somehow make a mark on the world before the curtain falls. It is scary to think that even without us, life goes on.

By bringing to Mr. B’s attention that his ever-present anxiety is rooted in fear of death, he was able to gain more insight into his own defensive behaviors. By confronting his death anxiety and processing his definition of a life well lived together in therapy, he’s acknowledged his lack of social connection as demoralizing, and has made significant strides to remedy this. He’s been able to focus on a more fulfilling life day to day, with less emphasis on his to-do list and aspirations. Instead, he’s connected more with his faith and members of his church. He’s gotten close to several neighbors and enjoys long dinners with them on his back patio.

At a recent meeting, he confessed that he feels “lighter” and not as fearful about sudden cardiac death, and thus has noticed that his overall anxiety has diminished greatly. He concluded that experiencing meaningful relationships in the present moment would give him greater joy than spending his remaining time engaged in preserving a future identity for himself. It seems elementary, but if we look within, we may find that we all suffer similarly: How much of our daily actions, thoughts, and fears are tied to the looming threat of death?
 

Conclusion

While modern psychiatry continues to advance with better understandings of our neurobiology, improved knowledge of pathophysiological processes of mental illness, and expanding discovery of novel pharmacotherapeutics, the modern psychiatrist should not forget fundamental truths of behavior and humanity that were once the staple of psychiatry.

Death anxiety is one of those truths; it is the ultimate stressor that we will all face and should be regular study and practice for psychiatrists. In this article, we explored some of those facets most meaningful to us but recommend you expand your study to the many more available.

Death anxiety is a constant reminder that life is final, and it is natural to feel anxious when thinking about it. Patients often come to physicians seeking validation of their lives or trying to use the same maladaptive defense mechanisms that did not serve them well in the past to achieve a better outcome.

In today’s world, death anxiety can feel palpable due to the constant exposure to global news and social media that can make us feel irrelevant. However, legacy, or what we leave behind, can serve as a way to alleviate death anxiety. For many, reconciling their feelings toward their legacy is an avenue to tame death anxiety. Therapy can help individuals gain insight into their defensive behaviors and process their definition of a life well lived. By focusing on a life worth living, individuals can alleviate their death anxiety and gain a sense of fulfillment.

Dr. Akkoor is a psychiatry resident at the University of California, San Diego. She is interested in immigrant mental health, ethics, consultation-liaison psychiatry, and medical education. Dr. Badre is a clinical and forensic psychiatrist in San Diego. He holds teaching positions at the University of California, San Diego, and the University of San Diego. He teaches medical education, psychopharmacology, ethics in psychiatry, and correctional care. Dr. Badre can be reached at his website, BadreMD.com. Dr. Badre and Dr. Akkoor have no conflicts of interest.

Reference

1. Badre N. Burnout: A concept that rebrands mental illness for professionals. Clinical Psychiatry News. 2020 Mar 5.

Disappointment – “I failed this exam, my life is ruined” or regret – “I am getting a divorce, I wasted so much of my life.” Patients present with a wide variety of complaints that can be understood as a form of death anxiety.

Fundamentally, patients come to see us to understand and explain their lives. One can reinterpret this as a patient asking, “If I died today, would my life have been good enough?” or “When I die, how will I look back at this moment in time and judge the choices I made?”

Other patients come to us attempting to use the same maladaptive defenses that did not serve them well in the past in the hopes of achieving a new outcome that will validate their lives. While it may be understandable that a child dissociates when facing abuse, hoping that this defense mechanism – as an adult – will work, it is unlikely to be fruitful and will certainly not validate or repair the past. This hope to repair one’s past can be interpreted as a fear of death – “I cannot die without correcting this.” This psychic conflict can intensify if one does not adopt a more adaptive understanding of his or her life.

Courtesy Dr. Neha Akkoor

Death anxiety is the feeling associated with the finality of life. Not only is life final, but a constant reminder of that fact is the idea that any one moment is final. Other than in science fiction, one cannot return to a prior moment and repair the past in the hope of a better future. Time goes only in one direction and death is the natural outcome of all life.

Death may have some evolutionary purpose that encourages the promotion of newer and more fitter genes, but one doesn’t have to consider its origin and reason to admit death’s constancy throughout humanity. People die and that is an anxiety-provoking fact of life. Death anxiety can feel especially tangible in our connected world. In a world of constant news, it can feel – for many people – that if your house wasn’t displaced because of global warming or that you are not a war refugee, you don’t deserve to be seen and heard.

This can be a particularly strong feeling for and among physicians, who don’t think that the mental health challenges generated by their own tough circumstances deserve to be labeled a mental disorder, so they designate themselves as having “burnout”¹ – as they don’t deserve the sympathy of having the clinically significant impairments of “depression.” Our traumas don’t seem important enough to deserve notice, and thus we may feel like we could die without ever having truly mattered.

This can also be applied in the reverse fashion. Certain individuals, like celebrities, live such extravagant lives that our simpler achievements can feel futile in comparison. While the neighbor’s grass has always felt greener, we are now constantly exposed to perfectly manicured lawns on social media. When compounded, the idea that our successes and our pains are both simultaneously irrelevant can lead one to have very palpable death anxiety – my life will never matter if none of the things I do matter, or my life will never matter because I will never achieve the requisite number of “likes” or “views” on social media required to believe that one’s life was worth living.

A way of alleviating death anxiety can be through the concept of legacy, or what we leave behind. How will people remember me? Will people remember me, or will I disappear like a shadow into the distant memory of my near and dear ones? The idea of being forgotten or lost to memory is intolerable to some and can be a strong driving force to “make a name” for oneself. For those who crave fame, whether a celebrity or a generous alumnus, part of this is likely related to remaining well known after death. After all, one can argue that you are not truly dead as long as you continue to live in the memory and/or genes of others.

Legacy thus serves as a form of posthumous transitional object; a way of calming our fears about how we will be remembered. For many, reconciling their feelings towards their legacy is an avenue to tame death anxiety.
 

A case study

The case of Mr. B illustrates this. As a 72-year-old male with a long history of generalized anxiety, he once had a nightmare as a child, similar to the plot of Sleeping Beauty. In his dream, he walks up a spiral staircase in a castle and touches the spindle on a spinning wheel, thus ending his life. The dream was vivid and marked him.

His fear of death has subsequently reared its head throughout his life. In more recent years, he has suffered from cardiovascular disease. Although he is now quite stable on his current cardiac medications, he is constantly fearful that he will experience a cardiac event while asleep and suddenly die. He is so anxious about not waking up in the morning that falling asleep is nearly impossible.

Mr. B is single, with no close family besides a sister who lives in another state. He has a dog and few friends. He worries about what will happen to his dog if he doesn’t wake up in the morning, but perhaps most distressing to him is “there’s so much left for me to do, I have so much to write!” As an accomplished author, he continues to write, and hopes to publish many more novels in his lifetime. It is unsurprising that someone without a strong social network may fear death and feel pressured to somehow make a mark on the world before the curtain falls. It is scary to think that even without us, life goes on.

By bringing to Mr. B’s attention that his ever-present anxiety is rooted in fear of death, he was able to gain more insight into his own defensive behaviors. By confronting his death anxiety and processing his definition of a life well lived together in therapy, he’s acknowledged his lack of social connection as demoralizing, and has made significant strides to remedy this. He’s been able to focus on a more fulfilling life day to day, with less emphasis on his to-do list and aspirations. Instead, he’s connected more with his faith and members of his church. He’s gotten close to several neighbors and enjoys long dinners with them on his back patio.

At a recent meeting, he confessed that he feels “lighter” and not as fearful about sudden cardiac death, and thus has noticed that his overall anxiety has diminished greatly. He concluded that experiencing meaningful relationships in the present moment would give him greater joy than spending his remaining time engaged in preserving a future identity for himself. It seems elementary, but if we look within, we may find that we all suffer similarly: How much of our daily actions, thoughts, and fears are tied to the looming threat of death?
 

Conclusion

While modern psychiatry continues to advance with better understandings of our neurobiology, improved knowledge of pathophysiological processes of mental illness, and expanding discovery of novel pharmacotherapeutics, the modern psychiatrist should not forget fundamental truths of behavior and humanity that were once the staple of psychiatry.

Death anxiety is one of those truths; it is the ultimate stressor that we will all face and should be regular study and practice for psychiatrists. In this article, we explored some of those facets most meaningful to us but recommend you expand your study to the many more available.

Death anxiety is a constant reminder that life is final, and it is natural to feel anxious when thinking about it. Patients often come to physicians seeking validation of their lives or trying to use the same maladaptive defense mechanisms that did not serve them well in the past to achieve a better outcome.

In today’s world, death anxiety can feel palpable due to the constant exposure to global news and social media that can make us feel irrelevant. However, legacy, or what we leave behind, can serve as a way to alleviate death anxiety. For many, reconciling their feelings toward their legacy is an avenue to tame death anxiety. Therapy can help individuals gain insight into their defensive behaviors and process their definition of a life well lived. By focusing on a life worth living, individuals can alleviate their death anxiety and gain a sense of fulfillment.

Dr. Akkoor is a psychiatry resident at the University of California, San Diego. She is interested in immigrant mental health, ethics, consultation-liaison psychiatry, and medical education. Dr. Badre is a clinical and forensic psychiatrist in San Diego. He holds teaching positions at the University of California, San Diego, and the University of San Diego. He teaches medical education, psychopharmacology, ethics in psychiatry, and correctional care. Dr. Badre can be reached at his website, BadreMD.com. Dr. Badre and Dr. Akkoor have no conflicts of interest.

Reference

1. Badre N. Burnout: A concept that rebrands mental illness for professionals. Clinical Psychiatry News. 2020 Mar 5.