Commentary

Medical case reports are as old as the healing profession itself.¹ These ancient medical stories have a modern definition: “A case report is a narrative that describes, for medical, scientific or educational purposes, a medical problem experienced by one or more patients.”² Case report experts describe the 3-fold purposes of this type of research: as a mainstay of education; a harbinger of emerging illnesses; and an appraiser of new interventions. Case-based education has long been a pillar of health professions education: Nurses, doctors, and allied health professionals are taught and learn through reading and discussing with their teachers and each other about cases of their own patients and of those in the literature.³ Case reports also have helped identify and raise awareness of new diseases and rare conditions, such as HIV.⁴ Finally, case reports have alerted regulatory agencies and the medical community about medication adverse effects, such as birth defects from thalidomide.⁵

Case reports also have been criticized on both scientific and ethical grounds. Critics argue that many case reports often lack the rigor and consistency of other types of research.⁶ Three recent trends in medical publication have strengthened the validity of these criticisms: the increase in the popularity of case reports; the corresponding increase in submissions to journals, including Federal Practitioner; and the rise of predatory publishers.^7,8

The ethical scrutiny of case reports discussed in this column focuses on the tension between providing readers with adequate, accurate information to fulfil the goals of case reports while also protecting patient confidentiality. The latter issue during most of the history of medicine was not considered by health care professionals when the prevailing paternalism supported a professional-oriented approach to health care. The rise of bioethics in the 1960s and 1970s began the shift toward patient autonomy in medical decision making and patient rights to control their protected health information that rendered case reports ethically problematic.

To address both changes in ethical standards and scientific limitations, a committee of clinicians, researchers, and journal editors formed the Case Report (CARE) group.^2,8 The group undertook an effort to improve the quality of case reports. From 2011 to 2012, they developed the CARE guidelines for clinical case reporting. The guidance took the form of a Statement and Checklist presented at the 2013 International Congress on Peer Review and Biomedical Publication. Since their presentation, multiple prestigious medical journals in many countries have implemented these recommendations.

As part of an overall effort to raise the ethical caliber of our own journal, Federal Practitioner will begin to implement the CARE guidelines for case reports for all future submissions. Use of the CARE recommendations will help prospective authors enhance the scientific value and ethical caliber of case reports submitted to the journal as well as assist the Federal Practitioner editorial team, editorial board, and peer reviewers to evaluate submissions more judiciously.

An essential part of the CARE guidelines is that the patient who is the subject of the case report provide informed consent for the publication of their personal narrative. The CARE group considers this an “ethical duty” of authors and editors alike. In “exceptional circumstances” such as if the patient is a minor or permanently incapacitated, a guardian or relative may grant consent. In the rare event that even with exhaustive attempts, if informed consent cannot be obtained from a patient or their representative, then the authors of the case report must submit a statement to this effect.⁴ Some journals may require that the authors obtain the approval of an institutional review board or the permission of an ethics or other institutional committee or a privacy officer.²

Requesting the patient’s consent is an extension of the shared decision making that is now a best practice in clinical care into the arena of research, making the patient or their representative a partner in the work. Ethicists have recommended inviting patients or relatives to read a draft of the case report and agree to its publication or request specific modifications to the manuscript. The CARE group rightly points out that with the rise of open notes in medical documentation, patients increasingly have access to their charts in near or real time.² Gone are the days of Sir William Osler when only doctors read medical journals and all of these technical developments as well as standards of research and social changes in the practitioner-patient relationship make it imperative that writers and editors join together to make case reports more transparent, accurate, and consistent.⁷

An additional step to protect patient privacy is the requirement that authors either de-identify potentially identifiable health information, such as age, birth, death, admission, and discharge dates, or in some instances obtain separate consent for the release of that protected data.⁸ These restrictions constitute a challenge to case report authors who in some instances may consider these same facts critical to the integrity of the case presentation that have made some scholars doubt their continued viability. After all, the contribution of the case to the medical literature often lies in its very particularity. Conversely, no matter how frustrated we might become during writing a case report, we would not want to see our own protected health information or that of our family on a website or in print without our knowledge or approval. Indeed, the International Committee of Medical Journal Editors states that “If identifying characteristics are de-identified, authors should provide assurance, and editors should so note, that such changes do not distort scientific meaning.”⁹

However, the exponential growth of the internet, the spread of social media, and the ubiquity of a plethora of electronic devices, which prior generations of writers and readers could not even imagine, make these limitations necessary to protect patient privacy and the public’s trust in health care professionals. The CARE guidelines can help authors of case reports hone the art of anonymizing the protected health information of subjects of case reports, such as ethnicity and occupation, while accurately conveying the clinical specifics of the case that make it valuable to students and colleagues.

We at Federal Practitioner recognize there is a real tension between truth-telling in case report publication and respect for patient confidentiality that will never be perfectly achieved, but is one that is important for medical knowledge, making it worthy of the continuous efforts of authors and editors to negotiate.

Medical case reports are as old as the healing profession itself.¹ These ancient medical stories have a modern definition: “A case report is a narrative that describes, for medical, scientific or educational purposes, a medical problem experienced by one or more patients.”² Case report experts describe the 3-fold purposes of this type of research: as a mainstay of education; a harbinger of emerging illnesses; and an appraiser of new interventions. Case-based education has long been a pillar of health professions education: Nurses, doctors, and allied health professionals are taught and learn through reading and discussing with their teachers and each other about cases of their own patients and of those in the literature.³ Case reports also have helped identify and raise awareness of new diseases and rare conditions, such as HIV.⁴ Finally, case reports have alerted regulatory agencies and the medical community about medication adverse effects, such as birth defects from thalidomide.⁵

Case reports also have been criticized on both scientific and ethical grounds. Critics argue that many case reports often lack the rigor and consistency of other types of research.⁶ Three recent trends in medical publication have strengthened the validity of these criticisms: the increase in the popularity of case reports; the corresponding increase in submissions to journals, including Federal Practitioner; and the rise of predatory publishers.^7,8

The ethical scrutiny of case reports discussed in this column focuses on the tension between providing readers with adequate, accurate information to fulfil the goals of case reports while also protecting patient confidentiality. The latter issue during most of the history of medicine was not considered by health care professionals when the prevailing paternalism supported a professional-oriented approach to health care. The rise of bioethics in the 1960s and 1970s began the shift toward patient autonomy in medical decision making and patient rights to control their protected health information that rendered case reports ethically problematic.

To address both changes in ethical standards and scientific limitations, a committee of clinicians, researchers, and journal editors formed the Case Report (CARE) group.^2,8 The group undertook an effort to improve the quality of case reports. From 2011 to 2012, they developed the CARE guidelines for clinical case reporting. The guidance took the form of a Statement and Checklist presented at the 2013 International Congress on Peer Review and Biomedical Publication. Since their presentation, multiple prestigious medical journals in many countries have implemented these recommendations.

As part of an overall effort to raise the ethical caliber of our own journal, Federal Practitioner will begin to implement the CARE guidelines for case reports for all future submissions. Use of the CARE recommendations will help prospective authors enhance the scientific value and ethical caliber of case reports submitted to the journal as well as assist the Federal Practitioner editorial team, editorial board, and peer reviewers to evaluate submissions more judiciously.

An essential part of the CARE guidelines is that the patient who is the subject of the case report provide informed consent for the publication of their personal narrative. The CARE group considers this an “ethical duty” of authors and editors alike. In “exceptional circumstances” such as if the patient is a minor or permanently incapacitated, a guardian or relative may grant consent. In the rare event that even with exhaustive attempts, if informed consent cannot be obtained from a patient or their representative, then the authors of the case report must submit a statement to this effect.⁴ Some journals may require that the authors obtain the approval of an institutional review board or the permission of an ethics or other institutional committee or a privacy officer.²

Requesting the patient’s consent is an extension of the shared decision making that is now a best practice in clinical care into the arena of research, making the patient or their representative a partner in the work. Ethicists have recommended inviting patients or relatives to read a draft of the case report and agree to its publication or request specific modifications to the manuscript. The CARE group rightly points out that with the rise of open notes in medical documentation, patients increasingly have access to their charts in near or real time.² Gone are the days of Sir William Osler when only doctors read medical journals and all of these technical developments as well as standards of research and social changes in the practitioner-patient relationship make it imperative that writers and editors join together to make case reports more transparent, accurate, and consistent.⁷

An additional step to protect patient privacy is the requirement that authors either de-identify potentially identifiable health information, such as age, birth, death, admission, and discharge dates, or in some instances obtain separate consent for the release of that protected data.⁸ These restrictions constitute a challenge to case report authors who in some instances may consider these same facts critical to the integrity of the case presentation that have made some scholars doubt their continued viability. After all, the contribution of the case to the medical literature often lies in its very particularity. Conversely, no matter how frustrated we might become during writing a case report, we would not want to see our own protected health information or that of our family on a website or in print without our knowledge or approval. Indeed, the International Committee of Medical Journal Editors states that “If identifying characteristics are de-identified, authors should provide assurance, and editors should so note, that such changes do not distort scientific meaning.”⁹

However, the exponential growth of the internet, the spread of social media, and the ubiquity of a plethora of electronic devices, which prior generations of writers and readers could not even imagine, make these limitations necessary to protect patient privacy and the public’s trust in health care professionals. The CARE guidelines can help authors of case reports hone the art of anonymizing the protected health information of subjects of case reports, such as ethnicity and occupation, while accurately conveying the clinical specifics of the case that make it valuable to students and colleagues.

We at Federal Practitioner recognize there is a real tension between truth-telling in case report publication and respect for patient confidentiality that will never be perfectly achieved, but is one that is important for medical knowledge, making it worthy of the continuous efforts of authors and editors to negotiate.

Medical case reports are as old as the healing profession itself.¹ These ancient medical stories have a modern definition: “A case report is a narrative that describes, for medical, scientific or educational purposes, a medical problem experienced by one or more patients.”² Case report experts describe the 3-fold purposes of this type of research: as a mainstay of education; a harbinger of emerging illnesses; and an appraiser of new interventions. Case-based education has long been a pillar of health professions education: Nurses, doctors, and allied health professionals are taught and learn through reading and discussing with their teachers and each other about cases of their own patients and of those in the literature.³ Case reports also have helped identify and raise awareness of new diseases and rare conditions, such as HIV.⁴ Finally, case reports have alerted regulatory agencies and the medical community about medication adverse effects, such as birth defects from thalidomide.⁵

Case reports also have been criticized on both scientific and ethical grounds. Critics argue that many case reports often lack the rigor and consistency of other types of research.⁶ Three recent trends in medical publication have strengthened the validity of these criticisms: the increase in the popularity of case reports; the corresponding increase in submissions to journals, including Federal Practitioner; and the rise of predatory publishers.^7,8

The ethical scrutiny of case reports discussed in this column focuses on the tension between providing readers with adequate, accurate information to fulfil the goals of case reports while also protecting patient confidentiality. The latter issue during most of the history of medicine was not considered by health care professionals when the prevailing paternalism supported a professional-oriented approach to health care. The rise of bioethics in the 1960s and 1970s began the shift toward patient autonomy in medical decision making and patient rights to control their protected health information that rendered case reports ethically problematic.

To address both changes in ethical standards and scientific limitations, a committee of clinicians, researchers, and journal editors formed the Case Report (CARE) group.^2,8 The group undertook an effort to improve the quality of case reports. From 2011 to 2012, they developed the CARE guidelines for clinical case reporting. The guidance took the form of a Statement and Checklist presented at the 2013 International Congress on Peer Review and Biomedical Publication. Since their presentation, multiple prestigious medical journals in many countries have implemented these recommendations.

As part of an overall effort to raise the ethical caliber of our own journal, Federal Practitioner will begin to implement the CARE guidelines for case reports for all future submissions. Use of the CARE recommendations will help prospective authors enhance the scientific value and ethical caliber of case reports submitted to the journal as well as assist the Federal Practitioner editorial team, editorial board, and peer reviewers to evaluate submissions more judiciously.

An essential part of the CARE guidelines is that the patient who is the subject of the case report provide informed consent for the publication of their personal narrative. The CARE group considers this an “ethical duty” of authors and editors alike. In “exceptional circumstances” such as if the patient is a minor or permanently incapacitated, a guardian or relative may grant consent. In the rare event that even with exhaustive attempts, if informed consent cannot be obtained from a patient or their representative, then the authors of the case report must submit a statement to this effect.⁴ Some journals may require that the authors obtain the approval of an institutional review board or the permission of an ethics or other institutional committee or a privacy officer.²

Requesting the patient’s consent is an extension of the shared decision making that is now a best practice in clinical care into the arena of research, making the patient or their representative a partner in the work. Ethicists have recommended inviting patients or relatives to read a draft of the case report and agree to its publication or request specific modifications to the manuscript. The CARE group rightly points out that with the rise of open notes in medical documentation, patients increasingly have access to their charts in near or real time.² Gone are the days of Sir William Osler when only doctors read medical journals and all of these technical developments as well as standards of research and social changes in the practitioner-patient relationship make it imperative that writers and editors join together to make case reports more transparent, accurate, and consistent.⁷

An additional step to protect patient privacy is the requirement that authors either de-identify potentially identifiable health information, such as age, birth, death, admission, and discharge dates, or in some instances obtain separate consent for the release of that protected data.⁸ These restrictions constitute a challenge to case report authors who in some instances may consider these same facts critical to the integrity of the case presentation that have made some scholars doubt their continued viability. After all, the contribution of the case to the medical literature often lies in its very particularity. Conversely, no matter how frustrated we might become during writing a case report, we would not want to see our own protected health information or that of our family on a website or in print without our knowledge or approval. Indeed, the International Committee of Medical Journal Editors states that “If identifying characteristics are de-identified, authors should provide assurance, and editors should so note, that such changes do not distort scientific meaning.”⁹

However, the exponential growth of the internet, the spread of social media, and the ubiquity of a plethora of electronic devices, which prior generations of writers and readers could not even imagine, make these limitations necessary to protect patient privacy and the public’s trust in health care professionals. The CARE guidelines can help authors of case reports hone the art of anonymizing the protected health information of subjects of case reports, such as ethnicity and occupation, while accurately conveying the clinical specifics of the case that make it valuable to students and colleagues.

We at Federal Practitioner recognize there is a real tension between truth-telling in case report publication and respect for patient confidentiality that will never be perfectly achieved, but is one that is important for medical knowledge, making it worthy of the continuous efforts of authors and editors to negotiate.

When I finished my dermatology training in 1986, the only moving parts in the skin that I recall were keratinocytes moving upward from the basal layer of the epidermis until they were desquamated 4 or 5 weeks later and hairs growing within their follicles until they were shed. Now we are learning about countless cytokines, chemokines, interleukins, antibodies, receptors, enzymes, and cell types, as well as their associated pathways, at an endless pace. Every day I am looking in my inbox to sign up for the “Cytokine of the Month” club! Despite the challenges of sorting through what is relevant clinically, it is a very exciting time. Coupled with this myriad of fundamental science is the emergence of newer therapies that are more directly targeting specific disease states and dramatically changing the lives of patients. We see prominent examples of these therapeutic results every day in patients we treat, especially with psoriasis and atopic dermatitis. Importantly, there also is hope for patients with notoriously refractory skin disorders, such as hidradenitis suppurativa, alopecia areata, and vitiligo, as newer therapies are being thoroughly studied in clinical trials.

Despite the best advances in therapy that we currently have available and those anticipated in the foreseeable future, patients with chronic dermatoses such as psoriasis and atopic dermatitis still require prolonged constant or frequently used intermittent therapies to adequately control their disease. Fortunately, as dermatologists we understand the importance of proper skin care and topical medications as well as how to incorporate them in the management plan. To date, specifically with psoriasis, we have a variety of brand and generic topical corticosteroids, calcipotriene (vitamin D analogue), and tazarotene (retinoid), as well as combination formulations, in our toolbox to help manage localized areas of involvement.¹ This includes both patients with more limited psoriasis and those responding favorably to systemic therapy but who still develop some new or persistent areas of localized psoriatic lesions. New data with the brand formulation of calcipotriene–betamethasone dipropionate (Cal-BDP) foam applied once daily shows that after adequate control is achieved, continued application to the affected sites twice weekly is superior to vehicle in preventing relapse of psoriasis.² A highly cosmetically acceptable Cal-BDP cream incorporating a unique vehicle technology has been US Food and Drug Administration (FDA) approved for once-daily use for plaque psoriasis, overcoming the compatibility difficulties encountered in combining both active ingredients in an aqueous-based formulation and also optimizing the delivery of the active ingredients into the skin. This Cal-BDP cream demonstrated efficacy superior to a brand Cal-BDP suspension, rapid reduction in pruritus, and favorable tolerability and safety.³ Another combination formulation that is FDA approved for plaque psoriasis with once-daily application that has been shown to be effective and safe is halobetasol propionate–tazarotene lotion. This formulation contains lower concentrations of both active ingredients than those normally used in a barrier-friendly polymeric emulsion vehicle, allowing for augmented delivery of both active ingredients into the skin than with the individual agents applied separately and sequentially.^4,5 In the best of circumstances, most patients with psoriasis still require use of topical therapy and appreciate its availability. Just like on any menu, it is good to have multiple good options.

What else does this psoriasis management story need? A pipeline! I am happy to tell you that with topical therapy, 2 nonsteroidal agents are under development with completion of phase 2 and phase 3 trials submitted to the FDA to evaluate for approval for psoriasis. They are tapinarof cream, an aryl hydrocarbon receptor agonist, and roflumilast cream, a phosphodiesterase 4 (PDE4) inhibitor. Both of these modes of action involve intracellular pathways that are highly conserved in humans and are ubiquitously present in structural and hematopoietic cells.

Topical application of tapinarof cream once daily has been shown to be effective and safe for plaque psoriasis, is well tolerated with some reports of folliculitis observed that did not typically interfere with use, exhibits a remittive effect in patients achieving clearance on therapy, and is devoid of any systemic safety signals with both short-term and long-term use.^6-8 It also is currently under evaluation for atopic dermatitis. Topical roflumilast cream once daily has been shown to be effective and safe for plaque psoriasis as well as intertriginous psoriasis; is well tolerated including negligible rates of skin tolerability reactions such as stinging and burning; and is devoid of systemic safety signals, including those often observed with oral PDE4 inhibitor therapy (apremilast).^9,10 In addition, roflumilast has been shown to be more inherently potent in PDE4 inhibition activity than crisaborole and apremilast.¹¹ Roflumilast cream also is being studied for atopic dermatitis and a foam formulation is being evaluated for seborrheic dermatitis. Importantly, both tapinarof and roflumilast are not corticosteroids and are not associated with adverse effects observed with topical corticosteroid therapy, such as atrophy, striae, telangiectasia, and hypothalamic-pituitary-adrenal axis suppression. This provides a sense of comfort for clinicians and patients, as potential side effects associated with more prolonged topical corticosteroid therapy are common and lingering concerns.

To summarize, topical therapy for psoriasis is here to stay, just like all the rock and roll we have more access to than ever through expanded modern-day radio access and several music streaming sources, most of which are on demand. Also available to us are some viable current options, including a few newer brand formulations. New nonsteroidal agents with favorable data thus far are on the horizon, providing their own inherent efficacy and safety, which appear to be advantageous thus far. As the late Ric Ocasek of the Cars sang, “Let the good times roll.”

When I finished my dermatology training in 1986, the only moving parts in the skin that I recall were keratinocytes moving upward from the basal layer of the epidermis until they were desquamated 4 or 5 weeks later and hairs growing within their follicles until they were shed. Now we are learning about countless cytokines, chemokines, interleukins, antibodies, receptors, enzymes, and cell types, as well as their associated pathways, at an endless pace. Every day I am looking in my inbox to sign up for the “Cytokine of the Month” club! Despite the challenges of sorting through what is relevant clinically, it is a very exciting time. Coupled with this myriad of fundamental science is the emergence of newer therapies that are more directly targeting specific disease states and dramatically changing the lives of patients. We see prominent examples of these therapeutic results every day in patients we treat, especially with psoriasis and atopic dermatitis. Importantly, there also is hope for patients with notoriously refractory skin disorders, such as hidradenitis suppurativa, alopecia areata, and vitiligo, as newer therapies are being thoroughly studied in clinical trials.

Despite the best advances in therapy that we currently have available and those anticipated in the foreseeable future, patients with chronic dermatoses such as psoriasis and atopic dermatitis still require prolonged constant or frequently used intermittent therapies to adequately control their disease. Fortunately, as dermatologists we understand the importance of proper skin care and topical medications as well as how to incorporate them in the management plan. To date, specifically with psoriasis, we have a variety of brand and generic topical corticosteroids, calcipotriene (vitamin D analogue), and tazarotene (retinoid), as well as combination formulations, in our toolbox to help manage localized areas of involvement.¹ This includes both patients with more limited psoriasis and those responding favorably to systemic therapy but who still develop some new or persistent areas of localized psoriatic lesions. New data with the brand formulation of calcipotriene–betamethasone dipropionate (Cal-BDP) foam applied once daily shows that after adequate control is achieved, continued application to the affected sites twice weekly is superior to vehicle in preventing relapse of psoriasis.² A highly cosmetically acceptable Cal-BDP cream incorporating a unique vehicle technology has been US Food and Drug Administration (FDA) approved for once-daily use for plaque psoriasis, overcoming the compatibility difficulties encountered in combining both active ingredients in an aqueous-based formulation and also optimizing the delivery of the active ingredients into the skin. This Cal-BDP cream demonstrated efficacy superior to a brand Cal-BDP suspension, rapid reduction in pruritus, and favorable tolerability and safety.³ Another combination formulation that is FDA approved for plaque psoriasis with once-daily application that has been shown to be effective and safe is halobetasol propionate–tazarotene lotion. This formulation contains lower concentrations of both active ingredients than those normally used in a barrier-friendly polymeric emulsion vehicle, allowing for augmented delivery of both active ingredients into the skin than with the individual agents applied separately and sequentially.^4,5 In the best of circumstances, most patients with psoriasis still require use of topical therapy and appreciate its availability. Just like on any menu, it is good to have multiple good options.

What else does this psoriasis management story need? A pipeline! I am happy to tell you that with topical therapy, 2 nonsteroidal agents are under development with completion of phase 2 and phase 3 trials submitted to the FDA to evaluate for approval for psoriasis. They are tapinarof cream, an aryl hydrocarbon receptor agonist, and roflumilast cream, a phosphodiesterase 4 (PDE4) inhibitor. Both of these modes of action involve intracellular pathways that are highly conserved in humans and are ubiquitously present in structural and hematopoietic cells.

Topical application of tapinarof cream once daily has been shown to be effective and safe for plaque psoriasis, is well tolerated with some reports of folliculitis observed that did not typically interfere with use, exhibits a remittive effect in patients achieving clearance on therapy, and is devoid of any systemic safety signals with both short-term and long-term use.^6-8 It also is currently under evaluation for atopic dermatitis. Topical roflumilast cream once daily has been shown to be effective and safe for plaque psoriasis as well as intertriginous psoriasis; is well tolerated including negligible rates of skin tolerability reactions such as stinging and burning; and is devoid of systemic safety signals, including those often observed with oral PDE4 inhibitor therapy (apremilast).^9,10 In addition, roflumilast has been shown to be more inherently potent in PDE4 inhibition activity than crisaborole and apremilast.¹¹ Roflumilast cream also is being studied for atopic dermatitis and a foam formulation is being evaluated for seborrheic dermatitis. Importantly, both tapinarof and roflumilast are not corticosteroids and are not associated with adverse effects observed with topical corticosteroid therapy, such as atrophy, striae, telangiectasia, and hypothalamic-pituitary-adrenal axis suppression. This provides a sense of comfort for clinicians and patients, as potential side effects associated with more prolonged topical corticosteroid therapy are common and lingering concerns.

To summarize, topical therapy for psoriasis is here to stay, just like all the rock and roll we have more access to than ever through expanded modern-day radio access and several music streaming sources, most of which are on demand. Also available to us are some viable current options, including a few newer brand formulations. New nonsteroidal agents with favorable data thus far are on the horizon, providing their own inherent efficacy and safety, which appear to be advantageous thus far. As the late Ric Ocasek of the Cars sang, “Let the good times roll.”

When I finished my dermatology training in 1986, the only moving parts in the skin that I recall were keratinocytes moving upward from the basal layer of the epidermis until they were desquamated 4 or 5 weeks later and hairs growing within their follicles until they were shed. Now we are learning about countless cytokines, chemokines, interleukins, antibodies, receptors, enzymes, and cell types, as well as their associated pathways, at an endless pace. Every day I am looking in my inbox to sign up for the “Cytokine of the Month” club! Despite the challenges of sorting through what is relevant clinically, it is a very exciting time. Coupled with this myriad of fundamental science is the emergence of newer therapies that are more directly targeting specific disease states and dramatically changing the lives of patients. We see prominent examples of these therapeutic results every day in patients we treat, especially with psoriasis and atopic dermatitis. Importantly, there also is hope for patients with notoriously refractory skin disorders, such as hidradenitis suppurativa, alopecia areata, and vitiligo, as newer therapies are being thoroughly studied in clinical trials.

Despite the best advances in therapy that we currently have available and those anticipated in the foreseeable future, patients with chronic dermatoses such as psoriasis and atopic dermatitis still require prolonged constant or frequently used intermittent therapies to adequately control their disease. Fortunately, as dermatologists we understand the importance of proper skin care and topical medications as well as how to incorporate them in the management plan. To date, specifically with psoriasis, we have a variety of brand and generic topical corticosteroids, calcipotriene (vitamin D analogue), and tazarotene (retinoid), as well as combination formulations, in our toolbox to help manage localized areas of involvement.¹ This includes both patients with more limited psoriasis and those responding favorably to systemic therapy but who still develop some new or persistent areas of localized psoriatic lesions. New data with the brand formulation of calcipotriene–betamethasone dipropionate (Cal-BDP) foam applied once daily shows that after adequate control is achieved, continued application to the affected sites twice weekly is superior to vehicle in preventing relapse of psoriasis.² A highly cosmetically acceptable Cal-BDP cream incorporating a unique vehicle technology has been US Food and Drug Administration (FDA) approved for once-daily use for plaque psoriasis, overcoming the compatibility difficulties encountered in combining both active ingredients in an aqueous-based formulation and also optimizing the delivery of the active ingredients into the skin. This Cal-BDP cream demonstrated efficacy superior to a brand Cal-BDP suspension, rapid reduction in pruritus, and favorable tolerability and safety.³ Another combination formulation that is FDA approved for plaque psoriasis with once-daily application that has been shown to be effective and safe is halobetasol propionate–tazarotene lotion. This formulation contains lower concentrations of both active ingredients than those normally used in a barrier-friendly polymeric emulsion vehicle, allowing for augmented delivery of both active ingredients into the skin than with the individual agents applied separately and sequentially.^4,5 In the best of circumstances, most patients with psoriasis still require use of topical therapy and appreciate its availability. Just like on any menu, it is good to have multiple good options.

What else does this psoriasis management story need? A pipeline! I am happy to tell you that with topical therapy, 2 nonsteroidal agents are under development with completion of phase 2 and phase 3 trials submitted to the FDA to evaluate for approval for psoriasis. They are tapinarof cream, an aryl hydrocarbon receptor agonist, and roflumilast cream, a phosphodiesterase 4 (PDE4) inhibitor. Both of these modes of action involve intracellular pathways that are highly conserved in humans and are ubiquitously present in structural and hematopoietic cells.

Topical application of tapinarof cream once daily has been shown to be effective and safe for plaque psoriasis, is well tolerated with some reports of folliculitis observed that did not typically interfere with use, exhibits a remittive effect in patients achieving clearance on therapy, and is devoid of any systemic safety signals with both short-term and long-term use.^6-8 It also is currently under evaluation for atopic dermatitis. Topical roflumilast cream once daily has been shown to be effective and safe for plaque psoriasis as well as intertriginous psoriasis; is well tolerated including negligible rates of skin tolerability reactions such as stinging and burning; and is devoid of systemic safety signals, including those often observed with oral PDE4 inhibitor therapy (apremilast).^9,10 In addition, roflumilast has been shown to be more inherently potent in PDE4 inhibition activity than crisaborole and apremilast.¹¹ Roflumilast cream also is being studied for atopic dermatitis and a foam formulation is being evaluated for seborrheic dermatitis. Importantly, both tapinarof and roflumilast are not corticosteroids and are not associated with adverse effects observed with topical corticosteroid therapy, such as atrophy, striae, telangiectasia, and hypothalamic-pituitary-adrenal axis suppression. This provides a sense of comfort for clinicians and patients, as potential side effects associated with more prolonged topical corticosteroid therapy are common and lingering concerns.

To summarize, topical therapy for psoriasis is here to stay, just like all the rock and roll we have more access to than ever through expanded modern-day radio access and several music streaming sources, most of which are on demand. Also available to us are some viable current options, including a few newer brand formulations. New nonsteroidal agents with favorable data thus far are on the horizon, providing their own inherent efficacy and safety, which appear to be advantageous thus far. As the late Ric Ocasek of the Cars sang, “Let the good times roll.”

You have a 16-year-old patient who has been doing poorly in school. He has withdrawn from his social group and quit the sports in which he excelled. He admits to using marijuana “maybe once or twice a week.” But you and his parents suspect that it is much more often and contributing to the change in his behavior and school performance.

They would prefer he not use marijuana at all but could maybe be comfortable with some arrangement in which their son could demonstrate that his usage was indeed limited to once or twice on the weekends. They ask for your help with crafting a contract that might include “some urine or blood test” that would allow them to be sure their son was adhering to the contract.

You explain to them that there are hazards associated with setting up contracts such as the one they are proposing. One revolving around the issue of trust. Another being that he may be addicted to the point that a compromise that includes scaling back his usage is unlikely to succeed. And, finally, you tell them that because of marijuana’s pharmacokinetics, their son’s urine tests will always be positive and not reflective of the how much he is using or whether he is intoxicated.

Scenarios similar to this are increasingly common for those of us living in states that have legalized recreational cannabis use. The absence of a laboratory test that can determine when a person is impaired by marijuana has made life difficult for law enforcement officers accustomed to relying on breath and blood tests for alcohol to confirm their suspicion that a driver is under the influence.

In addition, because marijuana is still detectable days after it is used, many well-paying jobs go unfilled when potential applicants are hesitant to submit to a required drug test. The quirky pharmacokinetics of cannabis are well-known to the recreational users and they see no reason to risk failing a urine test regardless of how good the job may be.

This lack of a reliable indicator of cannabis intoxication has not gone unnoticed, and in a recent study published in the journal Neuropharmacology, researchers at Massachusetts General Hospital in Boston report some hopeful results using fNIRS brain scanning. The investigators observed an increase in the level of oxygenated hemoglobin concentration (HbO), which is a type of neural activity signature, in the prefrontal cortex region of the volunteers who reported being impaired.

While a brain scan may sound like an unwieldy tool to use on roadside sobriety stops, the researchers report that portable scanners – some using skull cap sensors – could be easily adapted for use by law enforcement in the field. This technology also could be used by employers on the job site to test truck drivers and heavy machine operators at the beginning of each shift, thereby allaying the fears of responsible cannabis users.

This technology might be helpful to you in advising the parents of the 16-year-old you suspect of heavy usage. It would certainly help in confirming the suspicion that he is using more often than he claims. However, the contract the parents propose still may not work. If this young man demonstrates on multiple attempts that his word can’t be trusted, technology isn’t going to be the answer.

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Other than a Littman stethoscope he accepted as a first-year medical student in 1966, Dr. Wilkoff reports having nothing to disclose. Email him at [email protected].

You have a 16-year-old patient who has been doing poorly in school. He has withdrawn from his social group and quit the sports in which he excelled. He admits to using marijuana “maybe once or twice a week.” But you and his parents suspect that it is much more often and contributing to the change in his behavior and school performance.

They would prefer he not use marijuana at all but could maybe be comfortable with some arrangement in which their son could demonstrate that his usage was indeed limited to once or twice on the weekends. They ask for your help with crafting a contract that might include “some urine or blood test” that would allow them to be sure their son was adhering to the contract.

You explain to them that there are hazards associated with setting up contracts such as the one they are proposing. One revolving around the issue of trust. Another being that he may be addicted to the point that a compromise that includes scaling back his usage is unlikely to succeed. And, finally, you tell them that because of marijuana’s pharmacokinetics, their son’s urine tests will always be positive and not reflective of the how much he is using or whether he is intoxicated.

Scenarios similar to this are increasingly common for those of us living in states that have legalized recreational cannabis use. The absence of a laboratory test that can determine when a person is impaired by marijuana has made life difficult for law enforcement officers accustomed to relying on breath and blood tests for alcohol to confirm their suspicion that a driver is under the influence.

In addition, because marijuana is still detectable days after it is used, many well-paying jobs go unfilled when potential applicants are hesitant to submit to a required drug test. The quirky pharmacokinetics of cannabis are well-known to the recreational users and they see no reason to risk failing a urine test regardless of how good the job may be.

This lack of a reliable indicator of cannabis intoxication has not gone unnoticed, and in a recent study published in the journal Neuropharmacology, researchers at Massachusetts General Hospital in Boston report some hopeful results using fNIRS brain scanning. The investigators observed an increase in the level of oxygenated hemoglobin concentration (HbO), which is a type of neural activity signature, in the prefrontal cortex region of the volunteers who reported being impaired.

While a brain scan may sound like an unwieldy tool to use on roadside sobriety stops, the researchers report that portable scanners – some using skull cap sensors – could be easily adapted for use by law enforcement in the field. This technology also could be used by employers on the job site to test truck drivers and heavy machine operators at the beginning of each shift, thereby allaying the fears of responsible cannabis users.

This technology might be helpful to you in advising the parents of the 16-year-old you suspect of heavy usage. It would certainly help in confirming the suspicion that he is using more often than he claims. However, the contract the parents propose still may not work. If this young man demonstrates on multiple attempts that his word can’t be trusted, technology isn’t going to be the answer.

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Other than a Littman stethoscope he accepted as a first-year medical student in 1966, Dr. Wilkoff reports having nothing to disclose. Email him at [email protected].

You have a 16-year-old patient who has been doing poorly in school. He has withdrawn from his social group and quit the sports in which he excelled. He admits to using marijuana “maybe once or twice a week.” But you and his parents suspect that it is much more often and contributing to the change in his behavior and school performance.

They would prefer he not use marijuana at all but could maybe be comfortable with some arrangement in which their son could demonstrate that his usage was indeed limited to once or twice on the weekends. They ask for your help with crafting a contract that might include “some urine or blood test” that would allow them to be sure their son was adhering to the contract.

You explain to them that there are hazards associated with setting up contracts such as the one they are proposing. One revolving around the issue of trust. Another being that he may be addicted to the point that a compromise that includes scaling back his usage is unlikely to succeed. And, finally, you tell them that because of marijuana’s pharmacokinetics, their son’s urine tests will always be positive and not reflective of the how much he is using or whether he is intoxicated.

Scenarios similar to this are increasingly common for those of us living in states that have legalized recreational cannabis use. The absence of a laboratory test that can determine when a person is impaired by marijuana has made life difficult for law enforcement officers accustomed to relying on breath and blood tests for alcohol to confirm their suspicion that a driver is under the influence.

In addition, because marijuana is still detectable days after it is used, many well-paying jobs go unfilled when potential applicants are hesitant to submit to a required drug test. The quirky pharmacokinetics of cannabis are well-known to the recreational users and they see no reason to risk failing a urine test regardless of how good the job may be.

This lack of a reliable indicator of cannabis intoxication has not gone unnoticed, and in a recent study published in the journal Neuropharmacology, researchers at Massachusetts General Hospital in Boston report some hopeful results using fNIRS brain scanning. The investigators observed an increase in the level of oxygenated hemoglobin concentration (HbO), which is a type of neural activity signature, in the prefrontal cortex region of the volunteers who reported being impaired.

While a brain scan may sound like an unwieldy tool to use on roadside sobriety stops, the researchers report that portable scanners – some using skull cap sensors – could be easily adapted for use by law enforcement in the field. This technology also could be used by employers on the job site to test truck drivers and heavy machine operators at the beginning of each shift, thereby allaying the fears of responsible cannabis users.

This technology might be helpful to you in advising the parents of the 16-year-old you suspect of heavy usage. It would certainly help in confirming the suspicion that he is using more often than he claims. However, the contract the parents propose still may not work. If this young man demonstrates on multiple attempts that his word can’t be trusted, technology isn’t going to be the answer.

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Other than a Littman stethoscope he accepted as a first-year medical student in 1966, Dr. Wilkoff reports having nothing to disclose. Email him at [email protected].

This transcript has been edited for clarity. The transcript and an accompanying video first appeared on Medscape.com.

This is Mark Kris from chilly New York and Memorial Sloan Kettering. Today I want to talk about a recent article in the Journal of Clinical Oncology that reported a study of a new neurokinin-1 antagonist called fosnetupitant. This was a well-conducted trial that demonstrates the noninferiority of IV fosnetupitant when compared with IV fosaprepitant. By their study criteria, fosnetupitant was not inferior.

But my reason for discussing this is that the paper and the trial miss the point for the field right now. Although the authors talk about the prevention of nausea and vomiting in the introduction, in the paper itself and in the abstract results section, there’s not a single mention about the medication’s ability to control nausea, which is the critical issue for our patients today. You have to go into the supplementary data to find it mentioned, and what you find is that the prevention of nausea is 50% for both the control and this new drug. We control nausea in only half of the patients who receive cisplatin in 2022. That is a huge issue.

When you ask patients what are the effects of cancer treatment that they fear most, that concerns them most, it’s nausea and emesis; indeed, nausea has replaced emesis as the biggest concern. And although this trial used emesis as the main endpoint, and it was useful in defining the drug, it was not useful in coming up with a new treatment that addresses a huge need. Further, the authors talk about an advantage to fosnetupitant based on infusion reactions, but it is a difference of 0.3% vs. 3%. They talk about that sort of thing in the abstract and in the discussion section but don’t include nausea as part of the key endpoint of this trial. Again, you had to dig deeply to find out that, frankly, fosnetupitant was no better than the drugs we already have.

The other concerning point is that we do have another drug that works well. If you go to the American Society of Clinical Oncology or National Comprehensive Cancer Network guidelines for patients receiving high dosages of cisplatin, you find a four-drug regimen, including olanzapine, and that was not used here. Why is olanzapine so critical? It’s an available drug, it’s an inexpensive drug, it’s a safe drug, and it improves nausea by 15%.

So they did this huge trial to show noninferiority, and they neglected to give a drug that could deal with the most serious side effect of cancer therapy – nausea – and improve things by 15%.

A challenge to people in this field: We have to do better. Nausea is a big problem. While noninferiority trials can be helpful for drug development, they’re not really helpful for the field. With a problem of this magnitude, we need better drugs to control nausea. In the meantime, I urge you all to follow the guidelines for high doses of cisplatin. Please use the four-drug regimen that is recommended in the guidelines and widely used in the United States. Going forward, make sure that when we expend huge amounts of energy to develop new agents and report them in our medical journals, that we look for ways to advance care where there are significant gaps in our ability to deliver what we want. Delivering better control of nausea is something we all need to be committed to. It’s a huge unmet need, and I hope future trials will address that need. Our patients will be better for it and we’ll be better in that we’re delivering what patients deserve, what they need, and what they ask for.

Mark G. Kris, MD, is chief of the thoracic oncology service and the William and Joy Ruane Chair in Thoracic Oncology at Memorial Sloan Kettering Cancer Center in New York City. He reported serving as a director, officer, partner, employee, adviser, consultant, or trustee for AstraZeneca, Roche/Genentech, and Ariad Pharmaceuticals, and has received research grants from Pfizer, PUMA, and Roche/Genentech.

This transcript has been edited for clarity. The transcript and an accompanying video first appeared on Medscape.com.

This is Mark Kris from chilly New York and Memorial Sloan Kettering. Today I want to talk about a recent article in the Journal of Clinical Oncology that reported a study of a new neurokinin-1 antagonist called fosnetupitant. This was a well-conducted trial that demonstrates the noninferiority of IV fosnetupitant when compared with IV fosaprepitant. By their study criteria, fosnetupitant was not inferior.

But my reason for discussing this is that the paper and the trial miss the point for the field right now. Although the authors talk about the prevention of nausea and vomiting in the introduction, in the paper itself and in the abstract results section, there’s not a single mention about the medication’s ability to control nausea, which is the critical issue for our patients today. You have to go into the supplementary data to find it mentioned, and what you find is that the prevention of nausea is 50% for both the control and this new drug. We control nausea in only half of the patients who receive cisplatin in 2022. That is a huge issue.

When you ask patients what are the effects of cancer treatment that they fear most, that concerns them most, it’s nausea and emesis; indeed, nausea has replaced emesis as the biggest concern. And although this trial used emesis as the main endpoint, and it was useful in defining the drug, it was not useful in coming up with a new treatment that addresses a huge need. Further, the authors talk about an advantage to fosnetupitant based on infusion reactions, but it is a difference of 0.3% vs. 3%. They talk about that sort of thing in the abstract and in the discussion section but don’t include nausea as part of the key endpoint of this trial. Again, you had to dig deeply to find out that, frankly, fosnetupitant was no better than the drugs we already have.

The other concerning point is that we do have another drug that works well. If you go to the American Society of Clinical Oncology or National Comprehensive Cancer Network guidelines for patients receiving high dosages of cisplatin, you find a four-drug regimen, including olanzapine, and that was not used here. Why is olanzapine so critical? It’s an available drug, it’s an inexpensive drug, it’s a safe drug, and it improves nausea by 15%.

So they did this huge trial to show noninferiority, and they neglected to give a drug that could deal with the most serious side effect of cancer therapy – nausea – and improve things by 15%.

A challenge to people in this field: We have to do better. Nausea is a big problem. While noninferiority trials can be helpful for drug development, they’re not really helpful for the field. With a problem of this magnitude, we need better drugs to control nausea. In the meantime, I urge you all to follow the guidelines for high doses of cisplatin. Please use the four-drug regimen that is recommended in the guidelines and widely used in the United States. Going forward, make sure that when we expend huge amounts of energy to develop new agents and report them in our medical journals, that we look for ways to advance care where there are significant gaps in our ability to deliver what we want. Delivering better control of nausea is something we all need to be committed to. It’s a huge unmet need, and I hope future trials will address that need. Our patients will be better for it and we’ll be better in that we’re delivering what patients deserve, what they need, and what they ask for.

Mark G. Kris, MD, is chief of the thoracic oncology service and the William and Joy Ruane Chair in Thoracic Oncology at Memorial Sloan Kettering Cancer Center in New York City. He reported serving as a director, officer, partner, employee, adviser, consultant, or trustee for AstraZeneca, Roche/Genentech, and Ariad Pharmaceuticals, and has received research grants from Pfizer, PUMA, and Roche/Genentech.

This transcript has been edited for clarity. The transcript and an accompanying video first appeared on Medscape.com.

This is Mark Kris from chilly New York and Memorial Sloan Kettering. Today I want to talk about a recent article in the Journal of Clinical Oncology that reported a study of a new neurokinin-1 antagonist called fosnetupitant. This was a well-conducted trial that demonstrates the noninferiority of IV fosnetupitant when compared with IV fosaprepitant. By their study criteria, fosnetupitant was not inferior.

But my reason for discussing this is that the paper and the trial miss the point for the field right now. Although the authors talk about the prevention of nausea and vomiting in the introduction, in the paper itself and in the abstract results section, there’s not a single mention about the medication’s ability to control nausea, which is the critical issue for our patients today. You have to go into the supplementary data to find it mentioned, and what you find is that the prevention of nausea is 50% for both the control and this new drug. We control nausea in only half of the patients who receive cisplatin in 2022. That is a huge issue.

When you ask patients what are the effects of cancer treatment that they fear most, that concerns them most, it’s nausea and emesis; indeed, nausea has replaced emesis as the biggest concern. And although this trial used emesis as the main endpoint, and it was useful in defining the drug, it was not useful in coming up with a new treatment that addresses a huge need. Further, the authors talk about an advantage to fosnetupitant based on infusion reactions, but it is a difference of 0.3% vs. 3%. They talk about that sort of thing in the abstract and in the discussion section but don’t include nausea as part of the key endpoint of this trial. Again, you had to dig deeply to find out that, frankly, fosnetupitant was no better than the drugs we already have.

The other concerning point is that we do have another drug that works well. If you go to the American Society of Clinical Oncology or National Comprehensive Cancer Network guidelines for patients receiving high dosages of cisplatin, you find a four-drug regimen, including olanzapine, and that was not used here. Why is olanzapine so critical? It’s an available drug, it’s an inexpensive drug, it’s a safe drug, and it improves nausea by 15%.

So they did this huge trial to show noninferiority, and they neglected to give a drug that could deal with the most serious side effect of cancer therapy – nausea – and improve things by 15%.

A challenge to people in this field: We have to do better. Nausea is a big problem. While noninferiority trials can be helpful for drug development, they’re not really helpful for the field. With a problem of this magnitude, we need better drugs to control nausea. In the meantime, I urge you all to follow the guidelines for high doses of cisplatin. Please use the four-drug regimen that is recommended in the guidelines and widely used in the United States. Going forward, make sure that when we expend huge amounts of energy to develop new agents and report them in our medical journals, that we look for ways to advance care where there are significant gaps in our ability to deliver what we want. Delivering better control of nausea is something we all need to be committed to. It’s a huge unmet need, and I hope future trials will address that need. Our patients will be better for it and we’ll be better in that we’re delivering what patients deserve, what they need, and what they ask for.

Mark G. Kris, MD, is chief of the thoracic oncology service and the William and Joy Ruane Chair in Thoracic Oncology at Memorial Sloan Kettering Cancer Center in New York City. He reported serving as a director, officer, partner, employee, adviser, consultant, or trustee for AstraZeneca, Roche/Genentech, and Ariad Pharmaceuticals, and has received research grants from Pfizer, PUMA, and Roche/Genentech.

An otherwise healthy 55-year-old male, with no previous psychiatric or medical history, sought care with a family medicine physician for the first time in decades.

Medical symptoms began Oct. 9, 2021, with “some leg weakness and mild sniffles.” Since he was going to be at a public event, he decided to take a PCR test for the SARS-CoV-2 virus on Oct. 13. The patient tested positive.

His symptoms continued to worsen, and he experienced severe body fatigue, sleep disturbance, and lethargy. “A few days after my positive test, the cognitive and physical symptoms dramatically ramped up,” the patient recalled.

Because of those worsening symptoms, on Oct. 20, the patient obtained a new patient appointment with a family medicine physician. After a telemedicine evaluation, the family medicine physician began a multifaceted early outpatient COVID-19 treatment protocol,¹ as I (C.M.W.) and colleagues wrote about late last year. However, this treatment began late in the course because of the patient’s initial resistance to seek care.

This early outpatient treatment protocol for COVID-19 included vitamin D3 125 mcg (5,000 ICU), N-acetylcysteine (NAC) 600 mg every day x 30 days; acetylsalicylic acid 325 mg every day x 30 days; azithromycin 250 mg b.i.d. before every meal x 10 days; hydroxychloroquine sulfate 200 mg b.i.d. x 10 days; ivermectin 3 mg, 5 pills daily x 10 days; zinc sulfate 220 mg (50 mg elemental) every day x 30 days; and a prednisone taper (30 mg daily x 3 days, tapering down 5 mg every 3 days). Hydroxyzine 50 mg at bedtime as needed was added for sleep. The patient did not comment to the family physician on any of the psychological or psychiatric symptoms and responded appropriately to questions during the Oct. 20 initial evaluation.

However, he later described that around the time the PCR was positive, “COVID twisted my brain. I could not think straight. Every thought required 50 times the effort.” For example, he was watching a simple YouTube video for work and “everything was confusing me ... it rattled me, and I couldn’t understand it.” He described his COVID-19 mind as: “The words in my head would come out in a jumbled order, like the message from the words in my brain to my mouth would get crossed. I had trouble spelling and texting. Total cognitive breakdown. I couldn’t do simple mathematics.”

Despite his physical exhaustion, he endured a 3-day period of sleep deprivation. During this time, he recalled looking up at the roof and thinking, “I need to jump off the roof” or thinking, “I might want to throw myself under a bus.” He did not initially reveal his suicidal thoughts to his family medicine physician. After beginning COVID-19 treatment, the patient had two nights of sleep and felt notably improved, and his physical symptoms began to remit. However, the sleeplessness quickly returned “with a vengeance” along with “silly suicidal thoughts.” The thoughts took on a more obsessional quality. For example, he repeatedly thought of jumping out of his second-story bedroom to the living room below and was preoccupied by continually looking at people’s roofs and thinking about jumping. Those thoughts intensified and culminated in his “going missing,” leading his wife to call the police. It was discovered that he had driven to a local bridge and was contemplating jumping off.

After that “going missing” incident, the patient and his wife reached out to their family medicine physician. He reevaluated the patient and, given the new information about the psychiatric symptoms, strongly recommended stat crisis and psychiatric consultation. After discussing the case on the same day, both the family medicine physician and the psychiatrist recommended stat hospital emergency department (ED) assessment on Oct. 29. In the ED, a head CT without contrast at the recommendation of both psychiatrist and family physician, routine electrolytes, CBC with differential, and EKG all were within normal limits. The ED initially discharged him home after crisis evaluation, deciding he was not an imminent risk to himself or others.

The next day, the psychiatrist spoke on the phone with the patient, family medicine physician, and the patient’s wife to arrange an initial assessment. At that time, it remained unclear to all whether the obsessional thoughts had resolved to such a degree that the patient could resist acting upon them. Further, the patient’s sleep architecture had not returned to normal. All agreed another emergency ED assessment was indicated. Ultimately, after voluntary re-evaluation and a difficult hold in the crisis unit, the patient was admitted for psychiatric hospitalization on Oct. 29 and discharged on Nov. 4.

In the psychiatric hospital, venlafaxine XR was started and titrated to 75 mg. The patient was discovered to be hypertensive, and hydrochlorothiazide was started. The discharge diagnosis was major depressive disorder, single episode, severe, without psychotic features.
 

Posthospitalization course

The patient’s clinical course cleared remarkably. He was seen for his initial psychiatric outpatient assessment postpsychiatric hospitalization on Nov. 9, as he had not yet been formally evaluated by the psychiatrist because of the emergency situation.

Gabapentin 300 mg by mouth at bedtime was started, and his sleep architecture was restored. The initial plan to titrate venlafaxine XR into dual selective norepinephrine reuptake inhibitor dose range was terminated, and his psychiatrist considered tapering and discontinuing the venlafaxine XR. A clinical examination, additional history, and collateral data no longer necessarily pointed to an active major depressive disorder or even unspecified depressive disorder, though to be sure, the patient was taking 75 mg of venlafaxine XR. While there were seasonal stressors, historically, nothing had risen to the level of MDD.

The obsessions driving his thoughts to jump off buildings and bridges had completely remitted. His cognitive ability returned to baseline with an ability to focus and perform the complicated tasks of his high-intensity work by the Dec. 8 psychiatric examination, where he was accompanied by his wife. He described feeling like, “I snapped back to like I was before this crazy stuff happened.” His mood was reported as, “Very good; like my old self” and this was confirmed by his wife. His affect was calmer and less tense. He was now using gabapentin sparingly for sleep. We continued to entertain discontinuing the venlafaxine XR, considering this recent severe episode likely driven by the COVID-19 virus. The decision was made to continue venlafaxine XR through the winter rather than discontinuing, remaining on the conservative side of treatment. The patient’s diagnosis was changed from “MDD, single episode,” to “mood disorder due to known physiologic condition (COVID-19) (F06.31) with depressive features; resolving.” At the patient’s follow-up examination on Jan. 5, 2022, he was continuing to do well, stating, “The whole series of crazy events happened to someone else.” The hydrochlorothiazide had been discontinued, and the patient’s blood pressure and pulse were normal at 119/81 and 69, respectively. He had made strategic changes at work to lessen stressors during the typically difficult months.
 

Discussion

Literature has discussed neuropsychiatric sequelae of COVID-19.² The cited example questions whether psychiatric symptoms are tied directly to the viral infection or to the “host’s immune response.” We believe our case represents a direct neurocognitive/neuropsychiatric insult due to the COVID-19 infection.

This case presents a 55-year-old male with no previous psychiatric or medical history with new onset significant and debilitating cognitive impairment and obsessive thoughts of throwing himself from his bedroom balcony ending up at a bridge struggling with an irrational thought of jumping; ultimately requiring psychiatric hospitalization for acute suicidal thoughts. The patient’s psychiatric symptoms arose prior to any and all medication treatment. The obsessive thoughts correlated both with the onset of SARS-CoV-2 infection and a period of sleep deprivation subsequent to the infection. A course of steroid treatment and taper were started after the onset of neurocognitive-psychiatric symptoms, though there is close timing. We submit that the patient experienced, as part of the initial neurocognitive psychiatric initiating cascade, a COVID-19–induced sleep deprivation that was not etiologic but part of the process; since, even when sleep returned to normal, it was still several weeks before full cognitive function returned to baseline.

An argument could be made for possible MDD or unspecified depressive disorder, as historically there had been work-related stressors for the patient at this time of year because of the chronological nature of his work; though previously nothing presented with obsessional suicidal thinking and nothing with any cognitive impairment – let alone to this incapacitating degree.

The patient describes his seasonal work much like an accountant’s work at the beginning of each year. In the patient’s case, the months of September and October are historically “nonstop, working days,” which then slow down in the winter months for a period of recuperation. In gathering his past history of symptoms, he denied neurovegetative symptoms to meet full diagnostic criteria for MDD or unspecified depressive disorder, absent this episode in the presence of SARS-CoV-2 infection.

We could also consider a contributory negative “organic push” by the viral load and prednisone helping to express an underlying unspecified depression or MDD, but for the profound and unusual presentation. There was little prodrome of depressive symptoms (again, he reported his “typical” extraordinary work burden for this time of year, which is common in his industry).

In this patient, the symptoms have remitted completely. However, the patient is currently taking venlafaxine XR 75 mg. We have considered tapering and discontinuing the venlafaxine – since it is not entirely clear that he needs to be on this medication – so this question remains an open one. We did decide, however, to continue the venlafaxine until after the winter months and to reassess at that time.
 

Conclusion

The patient presented with new onset psychological and psychiatric symptoms in addition to physiologic symptoms; the former symptoms were not revealed prior to initial family medicine evaluation. As the symptoms worsened, he and his wife sought additional consultation with family physician, psychiatrists, and ED. Steroid treatment may have played a part in exacerbation of symptoms, but the neuropsychiatric cognitive symptoms were present prior to initiation of all pharmacologic and medical treatment. The successful outcome of this case was based upon quick action and collaboration between the family medicine physician, the psychiatrist, and the ED physician. The value of communication, assessment, and action via phone call and text cannot be overstated. Future considerations include further large-scale evaluation of multifaceted early treatment of patients with COVID-19 within the first 72 hours of symptoms to prevent not only hospitalization, morbidity, and mortality, but newly recognized psychological and psychiatric syndromes.^3,4

Lastly, fluvoxamine might have been a better choice for adjunctive early treatment of COVID-19.⁵ As a matter of distinction, if a lingering mood disorder or obsessive-compulsive disorder remain a result of SARS-CoV-2 or if one were to start an antidepressant during the course of illness, it would be reasonable to consider fluvoxamine as a potential first-line agent.

Dr. Kohanski is a fellowship trained forensic psychiatrist and a diplomate of the American Board of Psychiatry & Neurology. She maintains a private practice in Somerset, N.J., and is a frequent media commentator and medical podcaster. Dr. Kohanski has no conflicts of interest. Dr. Wax is a residency-trained osteopathic family medicine physician in independent private practice in Mullica Hill, N.J. He has authored multiple papers over 2 decades on topics such as SARS-CoV-2 and COVID-19 early treatment. He has been a speaker and media host over 2 decades and served on the National Physicians Council on Healthcare Policy’s congressional subcommittee. Dr. Wax has no conflicts of interest.

References

1. Rev Cardiovasc Med. 2020 Dec 30;21(4):517-30.

2. Brain Behav Immun. 2020 Jul;87:34-9.

3. Trav Med Infect Dis. 2020 May-Jun 35;10738.

4. Kirsch S. “Early treatment for COVID is key to better outcomes.” Times of India. 2021 May 21.

5. Lancet. 2022 Jan 1;10(1):E42-E51.

An otherwise healthy 55-year-old male, with no previous psychiatric or medical history, sought care with a family medicine physician for the first time in decades.

Medical symptoms began Oct. 9, 2021, with “some leg weakness and mild sniffles.” Since he was going to be at a public event, he decided to take a PCR test for the SARS-CoV-2 virus on Oct. 13. The patient tested positive.

His symptoms continued to worsen, and he experienced severe body fatigue, sleep disturbance, and lethargy. “A few days after my positive test, the cognitive and physical symptoms dramatically ramped up,” the patient recalled.

Because of those worsening symptoms, on Oct. 20, the patient obtained a new patient appointment with a family medicine physician. After a telemedicine evaluation, the family medicine physician began a multifaceted early outpatient COVID-19 treatment protocol,¹ as I (C.M.W.) and colleagues wrote about late last year. However, this treatment began late in the course because of the patient’s initial resistance to seek care.

This early outpatient treatment protocol for COVID-19 included vitamin D3 125 mcg (5,000 ICU), N-acetylcysteine (NAC) 600 mg every day x 30 days; acetylsalicylic acid 325 mg every day x 30 days; azithromycin 250 mg b.i.d. before every meal x 10 days; hydroxychloroquine sulfate 200 mg b.i.d. x 10 days; ivermectin 3 mg, 5 pills daily x 10 days; zinc sulfate 220 mg (50 mg elemental) every day x 30 days; and a prednisone taper (30 mg daily x 3 days, tapering down 5 mg every 3 days). Hydroxyzine 50 mg at bedtime as needed was added for sleep. The patient did not comment to the family physician on any of the psychological or psychiatric symptoms and responded appropriately to questions during the Oct. 20 initial evaluation.

However, he later described that around the time the PCR was positive, “COVID twisted my brain. I could not think straight. Every thought required 50 times the effort.” For example, he was watching a simple YouTube video for work and “everything was confusing me ... it rattled me, and I couldn’t understand it.” He described his COVID-19 mind as: “The words in my head would come out in a jumbled order, like the message from the words in my brain to my mouth would get crossed. I had trouble spelling and texting. Total cognitive breakdown. I couldn’t do simple mathematics.”

Despite his physical exhaustion, he endured a 3-day period of sleep deprivation. During this time, he recalled looking up at the roof and thinking, “I need to jump off the roof” or thinking, “I might want to throw myself under a bus.” He did not initially reveal his suicidal thoughts to his family medicine physician. After beginning COVID-19 treatment, the patient had two nights of sleep and felt notably improved, and his physical symptoms began to remit. However, the sleeplessness quickly returned “with a vengeance” along with “silly suicidal thoughts.” The thoughts took on a more obsessional quality. For example, he repeatedly thought of jumping out of his second-story bedroom to the living room below and was preoccupied by continually looking at people’s roofs and thinking about jumping. Those thoughts intensified and culminated in his “going missing,” leading his wife to call the police. It was discovered that he had driven to a local bridge and was contemplating jumping off.

After that “going missing” incident, the patient and his wife reached out to their family medicine physician. He reevaluated the patient and, given the new information about the psychiatric symptoms, strongly recommended stat crisis and psychiatric consultation. After discussing the case on the same day, both the family medicine physician and the psychiatrist recommended stat hospital emergency department (ED) assessment on Oct. 29. In the ED, a head CT without contrast at the recommendation of both psychiatrist and family physician, routine electrolytes, CBC with differential, and EKG all were within normal limits. The ED initially discharged him home after crisis evaluation, deciding he was not an imminent risk to himself or others.

The next day, the psychiatrist spoke on the phone with the patient, family medicine physician, and the patient’s wife to arrange an initial assessment. At that time, it remained unclear to all whether the obsessional thoughts had resolved to such a degree that the patient could resist acting upon them. Further, the patient’s sleep architecture had not returned to normal. All agreed another emergency ED assessment was indicated. Ultimately, after voluntary re-evaluation and a difficult hold in the crisis unit, the patient was admitted for psychiatric hospitalization on Oct. 29 and discharged on Nov. 4.

In the psychiatric hospital, venlafaxine XR was started and titrated to 75 mg. The patient was discovered to be hypertensive, and hydrochlorothiazide was started. The discharge diagnosis was major depressive disorder, single episode, severe, without psychotic features.
 

Posthospitalization course

The patient’s clinical course cleared remarkably. He was seen for his initial psychiatric outpatient assessment postpsychiatric hospitalization on Nov. 9, as he had not yet been formally evaluated by the psychiatrist because of the emergency situation.

Gabapentin 300 mg by mouth at bedtime was started, and his sleep architecture was restored. The initial plan to titrate venlafaxine XR into dual selective norepinephrine reuptake inhibitor dose range was terminated, and his psychiatrist considered tapering and discontinuing the venlafaxine XR. A clinical examination, additional history, and collateral data no longer necessarily pointed to an active major depressive disorder or even unspecified depressive disorder, though to be sure, the patient was taking 75 mg of venlafaxine XR. While there were seasonal stressors, historically, nothing had risen to the level of MDD.

The obsessions driving his thoughts to jump off buildings and bridges had completely remitted. His cognitive ability returned to baseline with an ability to focus and perform the complicated tasks of his high-intensity work by the Dec. 8 psychiatric examination, where he was accompanied by his wife. He described feeling like, “I snapped back to like I was before this crazy stuff happened.” His mood was reported as, “Very good; like my old self” and this was confirmed by his wife. His affect was calmer and less tense. He was now using gabapentin sparingly for sleep. We continued to entertain discontinuing the venlafaxine XR, considering this recent severe episode likely driven by the COVID-19 virus. The decision was made to continue venlafaxine XR through the winter rather than discontinuing, remaining on the conservative side of treatment. The patient’s diagnosis was changed from “MDD, single episode,” to “mood disorder due to known physiologic condition (COVID-19) (F06.31) with depressive features; resolving.” At the patient’s follow-up examination on Jan. 5, 2022, he was continuing to do well, stating, “The whole series of crazy events happened to someone else.” The hydrochlorothiazide had been discontinued, and the patient’s blood pressure and pulse were normal at 119/81 and 69, respectively. He had made strategic changes at work to lessen stressors during the typically difficult months.
 

Discussion

Literature has discussed neuropsychiatric sequelae of COVID-19.² The cited example questions whether psychiatric symptoms are tied directly to the viral infection or to the “host’s immune response.” We believe our case represents a direct neurocognitive/neuropsychiatric insult due to the COVID-19 infection.

This case presents a 55-year-old male with no previous psychiatric or medical history with new onset significant and debilitating cognitive impairment and obsessive thoughts of throwing himself from his bedroom balcony ending up at a bridge struggling with an irrational thought of jumping; ultimately requiring psychiatric hospitalization for acute suicidal thoughts. The patient’s psychiatric symptoms arose prior to any and all medication treatment. The obsessive thoughts correlated both with the onset of SARS-CoV-2 infection and a period of sleep deprivation subsequent to the infection. A course of steroid treatment and taper were started after the onset of neurocognitive-psychiatric symptoms, though there is close timing. We submit that the patient experienced, as part of the initial neurocognitive psychiatric initiating cascade, a COVID-19–induced sleep deprivation that was not etiologic but part of the process; since, even when sleep returned to normal, it was still several weeks before full cognitive function returned to baseline.

An argument could be made for possible MDD or unspecified depressive disorder, as historically there had been work-related stressors for the patient at this time of year because of the chronological nature of his work; though previously nothing presented with obsessional suicidal thinking and nothing with any cognitive impairment – let alone to this incapacitating degree.

The patient describes his seasonal work much like an accountant’s work at the beginning of each year. In the patient’s case, the months of September and October are historically “nonstop, working days,” which then slow down in the winter months for a period of recuperation. In gathering his past history of symptoms, he denied neurovegetative symptoms to meet full diagnostic criteria for MDD or unspecified depressive disorder, absent this episode in the presence of SARS-CoV-2 infection.

We could also consider a contributory negative “organic push” by the viral load and prednisone helping to express an underlying unspecified depression or MDD, but for the profound and unusual presentation. There was little prodrome of depressive symptoms (again, he reported his “typical” extraordinary work burden for this time of year, which is common in his industry).

In this patient, the symptoms have remitted completely. However, the patient is currently taking venlafaxine XR 75 mg. We have considered tapering and discontinuing the venlafaxine – since it is not entirely clear that he needs to be on this medication – so this question remains an open one. We did decide, however, to continue the venlafaxine until after the winter months and to reassess at that time.
 

Conclusion

The patient presented with new onset psychological and psychiatric symptoms in addition to physiologic symptoms; the former symptoms were not revealed prior to initial family medicine evaluation. As the symptoms worsened, he and his wife sought additional consultation with family physician, psychiatrists, and ED. Steroid treatment may have played a part in exacerbation of symptoms, but the neuropsychiatric cognitive symptoms were present prior to initiation of all pharmacologic and medical treatment. The successful outcome of this case was based upon quick action and collaboration between the family medicine physician, the psychiatrist, and the ED physician. The value of communication, assessment, and action via phone call and text cannot be overstated. Future considerations include further large-scale evaluation of multifaceted early treatment of patients with COVID-19 within the first 72 hours of symptoms to prevent not only hospitalization, morbidity, and mortality, but newly recognized psychological and psychiatric syndromes.^3,4

Lastly, fluvoxamine might have been a better choice for adjunctive early treatment of COVID-19.⁵ As a matter of distinction, if a lingering mood disorder or obsessive-compulsive disorder remain a result of SARS-CoV-2 or if one were to start an antidepressant during the course of illness, it would be reasonable to consider fluvoxamine as a potential first-line agent.

Dr. Kohanski is a fellowship trained forensic psychiatrist and a diplomate of the American Board of Psychiatry & Neurology. She maintains a private practice in Somerset, N.J., and is a frequent media commentator and medical podcaster. Dr. Kohanski has no conflicts of interest. Dr. Wax is a residency-trained osteopathic family medicine physician in independent private practice in Mullica Hill, N.J. He has authored multiple papers over 2 decades on topics such as SARS-CoV-2 and COVID-19 early treatment. He has been a speaker and media host over 2 decades and served on the National Physicians Council on Healthcare Policy’s congressional subcommittee. Dr. Wax has no conflicts of interest.

References

1. Rev Cardiovasc Med. 2020 Dec 30;21(4):517-30.

2. Brain Behav Immun. 2020 Jul;87:34-9.

3. Trav Med Infect Dis. 2020 May-Jun 35;10738.

4. Kirsch S. “Early treatment for COVID is key to better outcomes.” Times of India. 2021 May 21.

5. Lancet. 2022 Jan 1;10(1):E42-E51.

An otherwise healthy 55-year-old male, with no previous psychiatric or medical history, sought care with a family medicine physician for the first time in decades.

Medical symptoms began Oct. 9, 2021, with “some leg weakness and mild sniffles.” Since he was going to be at a public event, he decided to take a PCR test for the SARS-CoV-2 virus on Oct. 13. The patient tested positive.

His symptoms continued to worsen, and he experienced severe body fatigue, sleep disturbance, and lethargy. “A few days after my positive test, the cognitive and physical symptoms dramatically ramped up,” the patient recalled.

Because of those worsening symptoms, on Oct. 20, the patient obtained a new patient appointment with a family medicine physician. After a telemedicine evaluation, the family medicine physician began a multifaceted early outpatient COVID-19 treatment protocol,¹ as I (C.M.W.) and colleagues wrote about late last year. However, this treatment began late in the course because of the patient’s initial resistance to seek care.

This early outpatient treatment protocol for COVID-19 included vitamin D3 125 mcg (5,000 ICU), N-acetylcysteine (NAC) 600 mg every day x 30 days; acetylsalicylic acid 325 mg every day x 30 days; azithromycin 250 mg b.i.d. before every meal x 10 days; hydroxychloroquine sulfate 200 mg b.i.d. x 10 days; ivermectin 3 mg, 5 pills daily x 10 days; zinc sulfate 220 mg (50 mg elemental) every day x 30 days; and a prednisone taper (30 mg daily x 3 days, tapering down 5 mg every 3 days). Hydroxyzine 50 mg at bedtime as needed was added for sleep. The patient did not comment to the family physician on any of the psychological or psychiatric symptoms and responded appropriately to questions during the Oct. 20 initial evaluation.

However, he later described that around the time the PCR was positive, “COVID twisted my brain. I could not think straight. Every thought required 50 times the effort.” For example, he was watching a simple YouTube video for work and “everything was confusing me ... it rattled me, and I couldn’t understand it.” He described his COVID-19 mind as: “The words in my head would come out in a jumbled order, like the message from the words in my brain to my mouth would get crossed. I had trouble spelling and texting. Total cognitive breakdown. I couldn’t do simple mathematics.”

Despite his physical exhaustion, he endured a 3-day period of sleep deprivation. During this time, he recalled looking up at the roof and thinking, “I need to jump off the roof” or thinking, “I might want to throw myself under a bus.” He did not initially reveal his suicidal thoughts to his family medicine physician. After beginning COVID-19 treatment, the patient had two nights of sleep and felt notably improved, and his physical symptoms began to remit. However, the sleeplessness quickly returned “with a vengeance” along with “silly suicidal thoughts.” The thoughts took on a more obsessional quality. For example, he repeatedly thought of jumping out of his second-story bedroom to the living room below and was preoccupied by continually looking at people’s roofs and thinking about jumping. Those thoughts intensified and culminated in his “going missing,” leading his wife to call the police. It was discovered that he had driven to a local bridge and was contemplating jumping off.

After that “going missing” incident, the patient and his wife reached out to their family medicine physician. He reevaluated the patient and, given the new information about the psychiatric symptoms, strongly recommended stat crisis and psychiatric consultation. After discussing the case on the same day, both the family medicine physician and the psychiatrist recommended stat hospital emergency department (ED) assessment on Oct. 29. In the ED, a head CT without contrast at the recommendation of both psychiatrist and family physician, routine electrolytes, CBC with differential, and EKG all were within normal limits. The ED initially discharged him home after crisis evaluation, deciding he was not an imminent risk to himself or others.

The next day, the psychiatrist spoke on the phone with the patient, family medicine physician, and the patient’s wife to arrange an initial assessment. At that time, it remained unclear to all whether the obsessional thoughts had resolved to such a degree that the patient could resist acting upon them. Further, the patient’s sleep architecture had not returned to normal. All agreed another emergency ED assessment was indicated. Ultimately, after voluntary re-evaluation and a difficult hold in the crisis unit, the patient was admitted for psychiatric hospitalization on Oct. 29 and discharged on Nov. 4.

In the psychiatric hospital, venlafaxine XR was started and titrated to 75 mg. The patient was discovered to be hypertensive, and hydrochlorothiazide was started. The discharge diagnosis was major depressive disorder, single episode, severe, without psychotic features.
 

Posthospitalization course

The patient’s clinical course cleared remarkably. He was seen for his initial psychiatric outpatient assessment postpsychiatric hospitalization on Nov. 9, as he had not yet been formally evaluated by the psychiatrist because of the emergency situation.

Gabapentin 300 mg by mouth at bedtime was started, and his sleep architecture was restored. The initial plan to titrate venlafaxine XR into dual selective norepinephrine reuptake inhibitor dose range was terminated, and his psychiatrist considered tapering and discontinuing the venlafaxine XR. A clinical examination, additional history, and collateral data no longer necessarily pointed to an active major depressive disorder or even unspecified depressive disorder, though to be sure, the patient was taking 75 mg of venlafaxine XR. While there were seasonal stressors, historically, nothing had risen to the level of MDD.

The obsessions driving his thoughts to jump off buildings and bridges had completely remitted. His cognitive ability returned to baseline with an ability to focus and perform the complicated tasks of his high-intensity work by the Dec. 8 psychiatric examination, where he was accompanied by his wife. He described feeling like, “I snapped back to like I was before this crazy stuff happened.” His mood was reported as, “Very good; like my old self” and this was confirmed by his wife. His affect was calmer and less tense. He was now using gabapentin sparingly for sleep. We continued to entertain discontinuing the venlafaxine XR, considering this recent severe episode likely driven by the COVID-19 virus. The decision was made to continue venlafaxine XR through the winter rather than discontinuing, remaining on the conservative side of treatment. The patient’s diagnosis was changed from “MDD, single episode,” to “mood disorder due to known physiologic condition (COVID-19) (F06.31) with depressive features; resolving.” At the patient’s follow-up examination on Jan. 5, 2022, he was continuing to do well, stating, “The whole series of crazy events happened to someone else.” The hydrochlorothiazide had been discontinued, and the patient’s blood pressure and pulse were normal at 119/81 and 69, respectively. He had made strategic changes at work to lessen stressors during the typically difficult months.
 

Discussion

Literature has discussed neuropsychiatric sequelae of COVID-19.² The cited example questions whether psychiatric symptoms are tied directly to the viral infection or to the “host’s immune response.” We believe our case represents a direct neurocognitive/neuropsychiatric insult due to the COVID-19 infection.

This case presents a 55-year-old male with no previous psychiatric or medical history with new onset significant and debilitating cognitive impairment and obsessive thoughts of throwing himself from his bedroom balcony ending up at a bridge struggling with an irrational thought of jumping; ultimately requiring psychiatric hospitalization for acute suicidal thoughts. The patient’s psychiatric symptoms arose prior to any and all medication treatment. The obsessive thoughts correlated both with the onset of SARS-CoV-2 infection and a period of sleep deprivation subsequent to the infection. A course of steroid treatment and taper were started after the onset of neurocognitive-psychiatric symptoms, though there is close timing. We submit that the patient experienced, as part of the initial neurocognitive psychiatric initiating cascade, a COVID-19–induced sleep deprivation that was not etiologic but part of the process; since, even when sleep returned to normal, it was still several weeks before full cognitive function returned to baseline.

An argument could be made for possible MDD or unspecified depressive disorder, as historically there had been work-related stressors for the patient at this time of year because of the chronological nature of his work; though previously nothing presented with obsessional suicidal thinking and nothing with any cognitive impairment – let alone to this incapacitating degree.

The patient describes his seasonal work much like an accountant’s work at the beginning of each year. In the patient’s case, the months of September and October are historically “nonstop, working days,” which then slow down in the winter months for a period of recuperation. In gathering his past history of symptoms, he denied neurovegetative symptoms to meet full diagnostic criteria for MDD or unspecified depressive disorder, absent this episode in the presence of SARS-CoV-2 infection.

We could also consider a contributory negative “organic push” by the viral load and prednisone helping to express an underlying unspecified depression or MDD, but for the profound and unusual presentation. There was little prodrome of depressive symptoms (again, he reported his “typical” extraordinary work burden for this time of year, which is common in his industry).

In this patient, the symptoms have remitted completely. However, the patient is currently taking venlafaxine XR 75 mg. We have considered tapering and discontinuing the venlafaxine – since it is not entirely clear that he needs to be on this medication – so this question remains an open one. We did decide, however, to continue the venlafaxine until after the winter months and to reassess at that time.
 

Conclusion

The patient presented with new onset psychological and psychiatric symptoms in addition to physiologic symptoms; the former symptoms were not revealed prior to initial family medicine evaluation. As the symptoms worsened, he and his wife sought additional consultation with family physician, psychiatrists, and ED. Steroid treatment may have played a part in exacerbation of symptoms, but the neuropsychiatric cognitive symptoms were present prior to initiation of all pharmacologic and medical treatment. The successful outcome of this case was based upon quick action and collaboration between the family medicine physician, the psychiatrist, and the ED physician. The value of communication, assessment, and action via phone call and text cannot be overstated. Future considerations include further large-scale evaluation of multifaceted early treatment of patients with COVID-19 within the first 72 hours of symptoms to prevent not only hospitalization, morbidity, and mortality, but newly recognized psychological and psychiatric syndromes.^3,4

Lastly, fluvoxamine might have been a better choice for adjunctive early treatment of COVID-19.⁵ As a matter of distinction, if a lingering mood disorder or obsessive-compulsive disorder remain a result of SARS-CoV-2 or if one were to start an antidepressant during the course of illness, it would be reasonable to consider fluvoxamine as a potential first-line agent.

Dr. Kohanski is a fellowship trained forensic psychiatrist and a diplomate of the American Board of Psychiatry & Neurology. She maintains a private practice in Somerset, N.J., and is a frequent media commentator and medical podcaster. Dr. Kohanski has no conflicts of interest. Dr. Wax is a residency-trained osteopathic family medicine physician in independent private practice in Mullica Hill, N.J. He has authored multiple papers over 2 decades on topics such as SARS-CoV-2 and COVID-19 early treatment. He has been a speaker and media host over 2 decades and served on the National Physicians Council on Healthcare Policy’s congressional subcommittee. Dr. Wax has no conflicts of interest.

References

1. Rev Cardiovasc Med. 2020 Dec 30;21(4):517-30.

2. Brain Behav Immun. 2020 Jul;87:34-9.

3. Trav Med Infect Dis. 2020 May-Jun 35;10738.

4. Kirsch S. “Early treatment for COVID is key to better outcomes.” Times of India. 2021 May 21.

5. Lancet. 2022 Jan 1;10(1):E42-E51.

All else being equal, I’d prefer to do nothing. Whether this is nihilism, laziness, or experience is a matter of debate. The American College of Chest Physicians (CHEST) Guidelines on therapy for venous thromboembolism (VTE) opened a door for withholding treatment for isolated subsegmental pulmonary embolism (ISSPE) in 2016 and kept it open in 2021. I was happy to walk through it and withhold therapy if it wasn’t indicated.

ISSPE is truly a conundrum. With advances in technology, the distal vessels in the lung became visible on commercial CT a little more than 10 years ago. The subsegmental branches are located after the fourth bifurcation of the pulmonary arterial system, and the new technology offered resolution adequate to identify clot in these vessels. But the new technology told us nothing about how to manage clot isolated to the subsegmental vasculature.

Autopsy data say clot in these vessels is common, even in patients who were never diagnosed with VTE while they were alive. To some degree then, the pulmonary arterial system is thought to serve as a filter to prevent clot from crossing to the systemic circulation and causing stroke. This led some to speculate that the subsegmental pulmonary arteries are supposed to contain clot and that we simply couldn’t see it before now. If this theory is correct, the practice of providing anticoagulation for ISSPE could increase bleeding without reducing the risk for VTE recurrence.

Management studies generally supported this concept. In 2007, a trial that was published in JAMA randomized patients to two different diagnostic strategies: ventilation-perfusion (VQ) and CT. CT detected more clot than VQ did, so more anticoagulation was given in the CT arm. Yet, the VTE rate during follow-up was not significantly different between arms. The implication? Some of the clots detected by CT were of lesser clinical significance and didn’t need to be treated.

Meta-analytic data from management trials also suggested that some pulmonary emboli (PE) need not be treated. Data also show when compared with patients who have more proximal PE, those with ISSPE have lower pretest probability for VTE, are less symptomatic, and have a lower burden of coexistent lower extremity thrombosis (deep vein thrombosis [DVT]).

In response to this data, the CHEST Guidelines began cautiously providing the option for withholding therapy in patients who were diagnosed with ISSPE in 2016. Their recommendations stated that patients should be stratified for recurrence risk and have lower extremity ultrasonography performed to rule out DVT. A patient with ISSPE, a low recurrence risk, and a negative ultrasound can have anticoagulation withheld. This made perfect sense to me based on what I thought I knew at the time.

Recently published data cast doubt on my nihilism. The first prospective study designed specifically to assess the safety of withholding therapy for ISSPE suggests that this practice could be dangerous. How did this happen? The trial was very well done, and the authors enrolled the right population. All of the patients had ISSPE, low recurrence risk, and negative lower extremity ultrasound. The authors were anticipating a 1% VTE rate at 90 days based on prior data but instead found a rate of 3.1% (1.6%-6.1%). They point out that this rate is not different from those seen in patients with more proximal PE who are treated with anticoagulation. However, they acknowledge that it is higher than what’s considered acceptable and warrants therapeutic anticoagulation.

So what should we do now? We treat ISSPE, that’s what. All the arguments for withholding therapy remain valid, the recurrence rate is reasonably low, and none of the recurrent VTEs in the new study were fatal. There’s still no doubt that some patients with PE won’t benefit from anticoagulation. Unfortunately, we currently lack the tools to identify them. The risk-benefit ratio for recurrence versus bleeding will be tighter with ISSPE, particularly when there’s only one clot. Unless the bleeding risk is elevated though, the ratio still favors treatment.

Aaron B. Holley, MD, is an associate professor of medicine at Uniformed Services University and program director of pulmonary and critical care medicine at Walter Reed National Military Medical Center.

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

All else being equal, I’d prefer to do nothing. Whether this is nihilism, laziness, or experience is a matter of debate. The American College of Chest Physicians (CHEST) Guidelines on therapy for venous thromboembolism (VTE) opened a door for withholding treatment for isolated subsegmental pulmonary embolism (ISSPE) in 2016 and kept it open in 2021. I was happy to walk through it and withhold therapy if it wasn’t indicated.

ISSPE is truly a conundrum. With advances in technology, the distal vessels in the lung became visible on commercial CT a little more than 10 years ago. The subsegmental branches are located after the fourth bifurcation of the pulmonary arterial system, and the new technology offered resolution adequate to identify clot in these vessels. But the new technology told us nothing about how to manage clot isolated to the subsegmental vasculature.

Autopsy data say clot in these vessels is common, even in patients who were never diagnosed with VTE while they were alive. To some degree then, the pulmonary arterial system is thought to serve as a filter to prevent clot from crossing to the systemic circulation and causing stroke. This led some to speculate that the subsegmental pulmonary arteries are supposed to contain clot and that we simply couldn’t see it before now. If this theory is correct, the practice of providing anticoagulation for ISSPE could increase bleeding without reducing the risk for VTE recurrence.

Management studies generally supported this concept. In 2007, a trial that was published in JAMA randomized patients to two different diagnostic strategies: ventilation-perfusion (VQ) and CT. CT detected more clot than VQ did, so more anticoagulation was given in the CT arm. Yet, the VTE rate during follow-up was not significantly different between arms. The implication? Some of the clots detected by CT were of lesser clinical significance and didn’t need to be treated.

Meta-analytic data from management trials also suggested that some pulmonary emboli (PE) need not be treated. Data also show when compared with patients who have more proximal PE, those with ISSPE have lower pretest probability for VTE, are less symptomatic, and have a lower burden of coexistent lower extremity thrombosis (deep vein thrombosis [DVT]).

In response to this data, the CHEST Guidelines began cautiously providing the option for withholding therapy in patients who were diagnosed with ISSPE in 2016. Their recommendations stated that patients should be stratified for recurrence risk and have lower extremity ultrasonography performed to rule out DVT. A patient with ISSPE, a low recurrence risk, and a negative ultrasound can have anticoagulation withheld. This made perfect sense to me based on what I thought I knew at the time.

Recently published data cast doubt on my nihilism. The first prospective study designed specifically to assess the safety of withholding therapy for ISSPE suggests that this practice could be dangerous. How did this happen? The trial was very well done, and the authors enrolled the right population. All of the patients had ISSPE, low recurrence risk, and negative lower extremity ultrasound. The authors were anticipating a 1% VTE rate at 90 days based on prior data but instead found a rate of 3.1% (1.6%-6.1%). They point out that this rate is not different from those seen in patients with more proximal PE who are treated with anticoagulation. However, they acknowledge that it is higher than what’s considered acceptable and warrants therapeutic anticoagulation.

So what should we do now? We treat ISSPE, that’s what. All the arguments for withholding therapy remain valid, the recurrence rate is reasonably low, and none of the recurrent VTEs in the new study were fatal. There’s still no doubt that some patients with PE won’t benefit from anticoagulation. Unfortunately, we currently lack the tools to identify them. The risk-benefit ratio for recurrence versus bleeding will be tighter with ISSPE, particularly when there’s only one clot. Unless the bleeding risk is elevated though, the ratio still favors treatment.

Aaron B. Holley, MD, is an associate professor of medicine at Uniformed Services University and program director of pulmonary and critical care medicine at Walter Reed National Military Medical Center.

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

All else being equal, I’d prefer to do nothing. Whether this is nihilism, laziness, or experience is a matter of debate. The American College of Chest Physicians (CHEST) Guidelines on therapy for venous thromboembolism (VTE) opened a door for withholding treatment for isolated subsegmental pulmonary embolism (ISSPE) in 2016 and kept it open in 2021. I was happy to walk through it and withhold therapy if it wasn’t indicated.

ISSPE is truly a conundrum. With advances in technology, the distal vessels in the lung became visible on commercial CT a little more than 10 years ago. The subsegmental branches are located after the fourth bifurcation of the pulmonary arterial system, and the new technology offered resolution adequate to identify clot in these vessels. But the new technology told us nothing about how to manage clot isolated to the subsegmental vasculature.

Autopsy data say clot in these vessels is common, even in patients who were never diagnosed with VTE while they were alive. To some degree then, the pulmonary arterial system is thought to serve as a filter to prevent clot from crossing to the systemic circulation and causing stroke. This led some to speculate that the subsegmental pulmonary arteries are supposed to contain clot and that we simply couldn’t see it before now. If this theory is correct, the practice of providing anticoagulation for ISSPE could increase bleeding without reducing the risk for VTE recurrence.

Management studies generally supported this concept. In 2007, a trial that was published in JAMA randomized patients to two different diagnostic strategies: ventilation-perfusion (VQ) and CT. CT detected more clot than VQ did, so more anticoagulation was given in the CT arm. Yet, the VTE rate during follow-up was not significantly different between arms. The implication? Some of the clots detected by CT were of lesser clinical significance and didn’t need to be treated.

Meta-analytic data from management trials also suggested that some pulmonary emboli (PE) need not be treated. Data also show when compared with patients who have more proximal PE, those with ISSPE have lower pretest probability for VTE, are less symptomatic, and have a lower burden of coexistent lower extremity thrombosis (deep vein thrombosis [DVT]).

In response to this data, the CHEST Guidelines began cautiously providing the option for withholding therapy in patients who were diagnosed with ISSPE in 2016. Their recommendations stated that patients should be stratified for recurrence risk and have lower extremity ultrasonography performed to rule out DVT. A patient with ISSPE, a low recurrence risk, and a negative ultrasound can have anticoagulation withheld. This made perfect sense to me based on what I thought I knew at the time.

Recently published data cast doubt on my nihilism. The first prospective study designed specifically to assess the safety of withholding therapy for ISSPE suggests that this practice could be dangerous. How did this happen? The trial was very well done, and the authors enrolled the right population. All of the patients had ISSPE, low recurrence risk, and negative lower extremity ultrasound. The authors were anticipating a 1% VTE rate at 90 days based on prior data but instead found a rate of 3.1% (1.6%-6.1%). They point out that this rate is not different from those seen in patients with more proximal PE who are treated with anticoagulation. However, they acknowledge that it is higher than what’s considered acceptable and warrants therapeutic anticoagulation.

So what should we do now? We treat ISSPE, that’s what. All the arguments for withholding therapy remain valid, the recurrence rate is reasonably low, and none of the recurrent VTEs in the new study were fatal. There’s still no doubt that some patients with PE won’t benefit from anticoagulation. Unfortunately, we currently lack the tools to identify them. The risk-benefit ratio for recurrence versus bleeding will be tighter with ISSPE, particularly when there’s only one clot. Unless the bleeding risk is elevated though, the ratio still favors treatment.

Aaron B. Holley, MD, is an associate professor of medicine at Uniformed Services University and program director of pulmonary and critical care medicine at Walter Reed National Military Medical Center.

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

One clinic morning in an office visit, I stood next to the door talking, hand on the doorknob ready to exit. My elderly patient was sitting in the chair next to the door, family member in another, as I attempted my exit. Suddenly, as if looking for something, my patient locked her gaze to my abdomen and began to slowly advance herself forward, eyes squinting for a better view. She had found something. Poke, poke, poke. Three pokes in quick succession into my apparently protruding abdomen stoked an internal horror that I dared not release onto my face. How in the hell could she know? My heart sank – the signs were still there. 

“There’s something in there,” she said with a seasoned certainty.

“No there’s not,” I said trying hard to hide any emotion. 

“Yes, there is,” she said flatly. 

“Grannie, no there isn’t,” her family member interrupted, unknowingly saving me. I thanked them again and quickly left the room. 

My patient had the ongoings of slowly progressing dementia. Little did she know she was right. Maybe she had known something in another time and space. Either way, I wasn’t prepared to tell the story. She wasn’t prepared to fully understand. 

I tried to forge on to see the next patient. Tears began welling in both eyes. I tilted my head back slightly to prevent the water from falling. I wanted to feel offended, but she couldn’t have known the war my body was fighting at the time. I had not yet shared the pregnancy news with this particular patient, and yet her knowing was telling in a sense. I’m learning that the old folks always know. 

I was at work, actively having yet another miscarriage. This was the second of two. This most recent time, we found out at 9 weeks that our baby had stopped growing about a week or so earlier. Cue the denial. Cue the rage. Cue the devastation. 

Thinking back, with each pregnancy discovery, we did not wait the customary 3 months before telling anyone. Just about everyone knew. We were immediately excited to start sharing with friends, family, coworkers, and even patients early on. We knew the risks in my 40-something age group but were quintessentially optimistic. 

I am a family medicine physician with expert-level knowledge and clinical experiences in women’s health counseling, contraception, conception, and pregnancy. In my training, I’ve delivered babies, been elbow-deep searching for wayward tissue from bleeding uteri, and sutured gaping vaginal lacerations. I’ve cried with new mothers at the end of long labors. I’ve been bear-hugged by doting new fathers. I have an abundance of medical knowledge, and yet the pain and struggle of miscarriage over the past 2.5 years has twice reduced me to absolute pieces. There was no course to teach me how to navigate loss within my own body, no textbook to study so that I could test out of the experience. Life hit us dead-on, and I was broken.

I can say that the experience of a miscarriage does not get easier with each subsequent loss. At least for me, the emotions were always raw and tender. Each one was a new gash to my emotional and physical health. My sanity bled out. I was physically exhausted. The struggles of being a health care worker in the midst of a global pandemic I’m sure did not help the situation. My first miscarriage was just before the start of the pandemic. I was in New York visiting family and after dinner at Tavern on the Green, of all places, when I began showing signs. Two days later, I was at the coffee station in our clinic cafeteria adding my cream and sugar when my ob.gyn.’s office called. The hCG levels were probably too low; a miscarriage was likely. I kept my composure, walked out of the cafeteria, got my car keys, went to my car, and proceeded to scream at the top of my lungs for a few minutes. Afterward, I went back to finish up my work and canceled my clinic for the rest of the day. 

For my second miscarriage, I was laying in my doctor’s office getting an ultrasound. I had started bleeding the previous day but thought that the subchorionic hemorrhage noted on the last ultrasound might be the culprit. The bleeding was light. That’s the thing about being a pregnant physician: We know too much. The image on the screen looked abnormal, the remnants a ghost of its former self. I knew something was wrong but held out some hope. She searched and turned and pressed the transducer into my belly for a seemingly better view. She apologized for not finding the heartbeat. How is this happening again?

So how does one get through the loss of multiple pregnancies? I know my husband and I worked hard to get through each loss. We did all the right things a good therapist would recommend: Be present in the moment, go with your feelings, allow yourself to feel everything. There were no wrong emotions. Little by little we grieved and healed, grieved and healed. Having a successful pregnancy did help. Miracles are not promised but I believe we were sent one, and her name is Giavonna Barbara. Bookended by miscarriages, she has made me realize just how precious and delicate life really is. She is our absolute world and joy. 

I’ve learned twice now that men mourn differently than women. Not any less, just in a different way. There is a pain in the silence that often goes unvocalized, but it is of no less value. My husband and I allowed each other to heal in our own unique ways, and that has made all of the difference. I think I knew I was doing okay when one day I found something funny and I let out the heartiest laugh my belly could muster. A different purpose was renewed. Tears were harder to come by. Hope for the future again sprung eternal. Life went on and so did we. 

Looking back, I realize that having a miscarriage and working as a physician in the middle of a global pandemic pushed me to my emotional and physical limits. There is a second-guessing of sorts that occurs. Did the miscarriage happen because I was under so much stress at work? It had happened in the past, was this going to continue to happen? 

I can say that I was great at compartmentalizing emotions. I’d try and box them away until I got off of work and then turn them on like a switch once I hit the driver’s seat. It’s easy as a busy physician with so many patients to see, messages to return, notes to write, students and residents to teach, and programs to run to completely tune out the thought of mourning. Temporarily anyway. Work was actually a welcome distraction at times. A purpose. The journey to healing is individualized and can’t be rushed. I like to think that I heal a little bit more every day thinking about the losses and gains that I’ve had. I’m grateful for the experience and growth. 

In 2022, I’m looking forward to continuing my healing journey among the twists and turns of the pandemic. I now bring a different level of understanding and empathy to my patients who are undergoing or who have undergone a miscarriage. There will always be a piece of me that viscerally mourns with them. We have a hidden shared experience. I believe I am a better physician because of those lessons learned from my own personal tragedy. Now, I look forward to sharing big belly laughs with my family and friends and savoring the small, quiet moments with my husband and daughter. 

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

One clinic morning in an office visit, I stood next to the door talking, hand on the doorknob ready to exit. My elderly patient was sitting in the chair next to the door, family member in another, as I attempted my exit. Suddenly, as if looking for something, my patient locked her gaze to my abdomen and began to slowly advance herself forward, eyes squinting for a better view. She had found something. Poke, poke, poke. Three pokes in quick succession into my apparently protruding abdomen stoked an internal horror that I dared not release onto my face. How in the hell could she know? My heart sank – the signs were still there. 

“There’s something in there,” she said with a seasoned certainty.

“No there’s not,” I said trying hard to hide any emotion. 

“Yes, there is,” she said flatly. 

“Grannie, no there isn’t,” her family member interrupted, unknowingly saving me. I thanked them again and quickly left the room. 

My patient had the ongoings of slowly progressing dementia. Little did she know she was right. Maybe she had known something in another time and space. Either way, I wasn’t prepared to tell the story. She wasn’t prepared to fully understand. 

I tried to forge on to see the next patient. Tears began welling in both eyes. I tilted my head back slightly to prevent the water from falling. I wanted to feel offended, but she couldn’t have known the war my body was fighting at the time. I had not yet shared the pregnancy news with this particular patient, and yet her knowing was telling in a sense. I’m learning that the old folks always know. 

I was at work, actively having yet another miscarriage. This was the second of two. This most recent time, we found out at 9 weeks that our baby had stopped growing about a week or so earlier. Cue the denial. Cue the rage. Cue the devastation. 

Thinking back, with each pregnancy discovery, we did not wait the customary 3 months before telling anyone. Just about everyone knew. We were immediately excited to start sharing with friends, family, coworkers, and even patients early on. We knew the risks in my 40-something age group but were quintessentially optimistic. 

I am a family medicine physician with expert-level knowledge and clinical experiences in women’s health counseling, contraception, conception, and pregnancy. In my training, I’ve delivered babies, been elbow-deep searching for wayward tissue from bleeding uteri, and sutured gaping vaginal lacerations. I’ve cried with new mothers at the end of long labors. I’ve been bear-hugged by doting new fathers. I have an abundance of medical knowledge, and yet the pain and struggle of miscarriage over the past 2.5 years has twice reduced me to absolute pieces. There was no course to teach me how to navigate loss within my own body, no textbook to study so that I could test out of the experience. Life hit us dead-on, and I was broken.

I can say that the experience of a miscarriage does not get easier with each subsequent loss. At least for me, the emotions were always raw and tender. Each one was a new gash to my emotional and physical health. My sanity bled out. I was physically exhausted. The struggles of being a health care worker in the midst of a global pandemic I’m sure did not help the situation. My first miscarriage was just before the start of the pandemic. I was in New York visiting family and after dinner at Tavern on the Green, of all places, when I began showing signs. Two days later, I was at the coffee station in our clinic cafeteria adding my cream and sugar when my ob.gyn.’s office called. The hCG levels were probably too low; a miscarriage was likely. I kept my composure, walked out of the cafeteria, got my car keys, went to my car, and proceeded to scream at the top of my lungs for a few minutes. Afterward, I went back to finish up my work and canceled my clinic for the rest of the day. 

For my second miscarriage, I was laying in my doctor’s office getting an ultrasound. I had started bleeding the previous day but thought that the subchorionic hemorrhage noted on the last ultrasound might be the culprit. The bleeding was light. That’s the thing about being a pregnant physician: We know too much. The image on the screen looked abnormal, the remnants a ghost of its former self. I knew something was wrong but held out some hope. She searched and turned and pressed the transducer into my belly for a seemingly better view. She apologized for not finding the heartbeat. How is this happening again?

So how does one get through the loss of multiple pregnancies? I know my husband and I worked hard to get through each loss. We did all the right things a good therapist would recommend: Be present in the moment, go with your feelings, allow yourself to feel everything. There were no wrong emotions. Little by little we grieved and healed, grieved and healed. Having a successful pregnancy did help. Miracles are not promised but I believe we were sent one, and her name is Giavonna Barbara. Bookended by miscarriages, she has made me realize just how precious and delicate life really is. She is our absolute world and joy. 

I’ve learned twice now that men mourn differently than women. Not any less, just in a different way. There is a pain in the silence that often goes unvocalized, but it is of no less value. My husband and I allowed each other to heal in our own unique ways, and that has made all of the difference. I think I knew I was doing okay when one day I found something funny and I let out the heartiest laugh my belly could muster. A different purpose was renewed. Tears were harder to come by. Hope for the future again sprung eternal. Life went on and so did we. 

Looking back, I realize that having a miscarriage and working as a physician in the middle of a global pandemic pushed me to my emotional and physical limits. There is a second-guessing of sorts that occurs. Did the miscarriage happen because I was under so much stress at work? It had happened in the past, was this going to continue to happen? 

I can say that I was great at compartmentalizing emotions. I’d try and box them away until I got off of work and then turn them on like a switch once I hit the driver’s seat. It’s easy as a busy physician with so many patients to see, messages to return, notes to write, students and residents to teach, and programs to run to completely tune out the thought of mourning. Temporarily anyway. Work was actually a welcome distraction at times. A purpose. The journey to healing is individualized and can’t be rushed. I like to think that I heal a little bit more every day thinking about the losses and gains that I’ve had. I’m grateful for the experience and growth. 

In 2022, I’m looking forward to continuing my healing journey among the twists and turns of the pandemic. I now bring a different level of understanding and empathy to my patients who are undergoing or who have undergone a miscarriage. There will always be a piece of me that viscerally mourns with them. We have a hidden shared experience. I believe I am a better physician because of those lessons learned from my own personal tragedy. Now, I look forward to sharing big belly laughs with my family and friends and savoring the small, quiet moments with my husband and daughter. 

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

One clinic morning in an office visit, I stood next to the door talking, hand on the doorknob ready to exit. My elderly patient was sitting in the chair next to the door, family member in another, as I attempted my exit. Suddenly, as if looking for something, my patient locked her gaze to my abdomen and began to slowly advance herself forward, eyes squinting for a better view. She had found something. Poke, poke, poke. Three pokes in quick succession into my apparently protruding abdomen stoked an internal horror that I dared not release onto my face. How in the hell could she know? My heart sank – the signs were still there. 

“There’s something in there,” she said with a seasoned certainty.

“No there’s not,” I said trying hard to hide any emotion. 

“Yes, there is,” she said flatly. 

“Grannie, no there isn’t,” her family member interrupted, unknowingly saving me. I thanked them again and quickly left the room. 

My patient had the ongoings of slowly progressing dementia. Little did she know she was right. Maybe she had known something in another time and space. Either way, I wasn’t prepared to tell the story. She wasn’t prepared to fully understand. 

I tried to forge on to see the next patient. Tears began welling in both eyes. I tilted my head back slightly to prevent the water from falling. I wanted to feel offended, but she couldn’t have known the war my body was fighting at the time. I had not yet shared the pregnancy news with this particular patient, and yet her knowing was telling in a sense. I’m learning that the old folks always know. 

I was at work, actively having yet another miscarriage. This was the second of two. This most recent time, we found out at 9 weeks that our baby had stopped growing about a week or so earlier. Cue the denial. Cue the rage. Cue the devastation. 

Thinking back, with each pregnancy discovery, we did not wait the customary 3 months before telling anyone. Just about everyone knew. We were immediately excited to start sharing with friends, family, coworkers, and even patients early on. We knew the risks in my 40-something age group but were quintessentially optimistic. 

I am a family medicine physician with expert-level knowledge and clinical experiences in women’s health counseling, contraception, conception, and pregnancy. In my training, I’ve delivered babies, been elbow-deep searching for wayward tissue from bleeding uteri, and sutured gaping vaginal lacerations. I’ve cried with new mothers at the end of long labors. I’ve been bear-hugged by doting new fathers. I have an abundance of medical knowledge, and yet the pain and struggle of miscarriage over the past 2.5 years has twice reduced me to absolute pieces. There was no course to teach me how to navigate loss within my own body, no textbook to study so that I could test out of the experience. Life hit us dead-on, and I was broken.

I can say that the experience of a miscarriage does not get easier with each subsequent loss. At least for me, the emotions were always raw and tender. Each one was a new gash to my emotional and physical health. My sanity bled out. I was physically exhausted. The struggles of being a health care worker in the midst of a global pandemic I’m sure did not help the situation. My first miscarriage was just before the start of the pandemic. I was in New York visiting family and after dinner at Tavern on the Green, of all places, when I began showing signs. Two days later, I was at the coffee station in our clinic cafeteria adding my cream and sugar when my ob.gyn.’s office called. The hCG levels were probably too low; a miscarriage was likely. I kept my composure, walked out of the cafeteria, got my car keys, went to my car, and proceeded to scream at the top of my lungs for a few minutes. Afterward, I went back to finish up my work and canceled my clinic for the rest of the day. 

For my second miscarriage, I was laying in my doctor’s office getting an ultrasound. I had started bleeding the previous day but thought that the subchorionic hemorrhage noted on the last ultrasound might be the culprit. The bleeding was light. That’s the thing about being a pregnant physician: We know too much. The image on the screen looked abnormal, the remnants a ghost of its former self. I knew something was wrong but held out some hope. She searched and turned and pressed the transducer into my belly for a seemingly better view. She apologized for not finding the heartbeat. How is this happening again?

So how does one get through the loss of multiple pregnancies? I know my husband and I worked hard to get through each loss. We did all the right things a good therapist would recommend: Be present in the moment, go with your feelings, allow yourself to feel everything. There were no wrong emotions. Little by little we grieved and healed, grieved and healed. Having a successful pregnancy did help. Miracles are not promised but I believe we were sent one, and her name is Giavonna Barbara. Bookended by miscarriages, she has made me realize just how precious and delicate life really is. She is our absolute world and joy. 

I’ve learned twice now that men mourn differently than women. Not any less, just in a different way. There is a pain in the silence that often goes unvocalized, but it is of no less value. My husband and I allowed each other to heal in our own unique ways, and that has made all of the difference. I think I knew I was doing okay when one day I found something funny and I let out the heartiest laugh my belly could muster. A different purpose was renewed. Tears were harder to come by. Hope for the future again sprung eternal. Life went on and so did we. 

Looking back, I realize that having a miscarriage and working as a physician in the middle of a global pandemic pushed me to my emotional and physical limits. There is a second-guessing of sorts that occurs. Did the miscarriage happen because I was under so much stress at work? It had happened in the past, was this going to continue to happen? 

I can say that I was great at compartmentalizing emotions. I’d try and box them away until I got off of work and then turn them on like a switch once I hit the driver’s seat. It’s easy as a busy physician with so many patients to see, messages to return, notes to write, students and residents to teach, and programs to run to completely tune out the thought of mourning. Temporarily anyway. Work was actually a welcome distraction at times. A purpose. The journey to healing is individualized and can’t be rushed. I like to think that I heal a little bit more every day thinking about the losses and gains that I’ve had. I’m grateful for the experience and growth. 

In 2022, I’m looking forward to continuing my healing journey among the twists and turns of the pandemic. I now bring a different level of understanding and empathy to my patients who are undergoing or who have undergone a miscarriage. There will always be a piece of me that viscerally mourns with them. We have a hidden shared experience. I believe I am a better physician because of those lessons learned from my own personal tragedy. Now, I look forward to sharing big belly laughs with my family and friends and savoring the small, quiet moments with my husband and daughter. 

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

“I believe that this nation should commit itself to achieving the goal, before the decade is out, of landing a man on the Moon and returning him safely to Earth.”

President John F. Kennedy, May 25, 1961

Despite significant progress, there remain many unmet needs in psychiatry. These include a granular understanding of the neurobiology of various psychopathologies, an objective and valid diagnostic schema, and disease-modifying treatments for chronic and disabling psychiatric disorders. Several moonshots are needed to address those festering needs.

A “moonshot” is an extremely ambitious, dramatic, imaginative, and inspiring goal. Landing on the Moon was generally believed to be impossible when President Kennedy boldly set that as a goal for the United States in 1961. Yet, 8 short years later, on July 20, 1969, Neil Armstrong stepped off the lunar module ladder onto the Moon’s surface, a feat that captured the imagination of the nation and the world. I distinctly remember watching it on television with amazement as a young boy. It was a surreal experience. That’s what achieving a moonshot feels like.

Successful organizations should always have 1 or more moonshots (American Psychiatric Association and National Institute of Mental Health [NIMH], are you listening?). Setting lofty goals that require monumental determination and effort to accomplish will have a transformative, long-lasting impact. The construction of the Panama Canal to connect 2 oceans and the Manhattan Project to develop the first nuclear bomb, which ended World War II, are examples of moonshots that continue to reverberate. A more recent moonshot is the driverless car, which in the past was a laughable idea but is now a reality that will change society and the world in many ways. Innovative billionaire moguls now speak loudly about colonizing Mars, which sounds improbable and highly risky, but it’s a moonshot that may be achieved within a few years. Establishing world peace is a moonshot that requires collective Kennedy-esque vision and motivation among world leaders, which currently is sadly lacking.

So, for contemporary psychiatry, what is the equivalent of landing on the Moon? Here is the list that pops in my brain’s mind (let us know which of these would be your top 3 moonshots by taking our survey at https://bit.ly/3qkKqTa):

• A cure for schizophrenia (across positive, negative, and cognitive symptom domains)
• A cure for mood disorders, unipolar and bipolar (including suicide)
• A cure for anxiety disorders
• A cure for obsessive-compulsive disorder
• A cure for posttraumatic stress disorder
• A cure for alcoholism/addiction
• A cure for autism
• A cure for Alzheimer’s disease and other dementias
• A cure for personality disorders, especially antisocial and borderline
• A cure for the visceral hatred across political parties that permeates our society (obviously not a psychiatric category, but perhaps it should be added to DSM because it is so destructive).

Those moonshots may be regarded as absurd, and totally unachievable, but so was landing on the Moon, until it was accomplished. Psychiatry must stop thinking small and being content with tiny advances (which is like changing the chairs to more comfortable sofas on the deck of the Titanic and calling it “progress…”). Psychiatry needs to be unified under the flag of “moonshot thinking” by several visionary and transformative leaders to start believing in a miraculously better future for our patients. But to pave the way for moonshots in psychiatry, the leading organizations must collaborate closely to open the door for unprecedented scientific and medical breakthroughs of a moonshot by:

1. Lobbying effectively to secure massive funding for research from federal, state, corporate, and foundation sources (perhaps convincing the Gates Foundation that schizophrenia is as devastating worldwide as malaria may bring a few badly needed billions into psychiatric brain research).
2. Reminding members of Congress that in the United States, costs associated with psychiatric brain disorders total an estimated $700 billion annually,¹ and that this must be addressed by boosting the meager NIMH budget by at least an order of magnitude. The NIMH should disproportionately invest its resources on severe brain disorders such as schizophrenia because breakthrough advances in its neurobiology will provide unprecedented insights to the pathophysiology of other severe psychiatric brain disorders.
3. Partnering intimately with the pharmaceutical industry in a powerful public-private coalition to exploit the extensive research infrastructure of this industry.
4. Creating the necessary army of researchers (physician-scientists) by providing huge incentives to medical students and psychiatric residents to pursue careers in neuroscience research. Incentives can include paying for an individual’s entire medical education and research training, and providing generous salaries that match or exceed the income of a very successful clinical practice.
5. Convincing all psychiatric clinicians to support research by referring patients to research projects. Clinical psychiatrists are badly needed to care for the population, but they must be reminded that every treatment they are using today was a research project in the past, and that the research of today will evolve into the treatments (or cures) of tomorrow.

Pursuing lofty moonshots via innovative research is very likely to enhance serendipity and lead to unexpected discoveries along the way. As Louis Pasteur said, “chance only favors the prepared mind.”² Moonshot thinking in psychiatry today is more feasible than ever before because of the many advances in research methods (neuroimaging, pluripotent cells, optogenetics, CRISPR, etc) and complex data management technologies (big data, machine learning, artificial intelligence), each of which qualifies as a preparatory moonshot in its own right.

Given the tragic consequences of psychiatric brain disorders, it is imperative that we “think big.” Humanity expects us to do that. We must envision the future of psychiatry as dramatically different from the present. Moonshot thinking is the indispensable vehicle to take us there.

“I believe that this nation should commit itself to achieving the goal, before the decade is out, of landing a man on the Moon and returning him safely to Earth.”

President John F. Kennedy, May 25, 1961

Despite significant progress, there remain many unmet needs in psychiatry. These include a granular understanding of the neurobiology of various psychopathologies, an objective and valid diagnostic schema, and disease-modifying treatments for chronic and disabling psychiatric disorders. Several moonshots are needed to address those festering needs.

A “moonshot” is an extremely ambitious, dramatic, imaginative, and inspiring goal. Landing on the Moon was generally believed to be impossible when President Kennedy boldly set that as a goal for the United States in 1961. Yet, 8 short years later, on July 20, 1969, Neil Armstrong stepped off the lunar module ladder onto the Moon’s surface, a feat that captured the imagination of the nation and the world. I distinctly remember watching it on television with amazement as a young boy. It was a surreal experience. That’s what achieving a moonshot feels like.

Successful organizations should always have 1 or more moonshots (American Psychiatric Association and National Institute of Mental Health [NIMH], are you listening?). Setting lofty goals that require monumental determination and effort to accomplish will have a transformative, long-lasting impact. The construction of the Panama Canal to connect 2 oceans and the Manhattan Project to develop the first nuclear bomb, which ended World War II, are examples of moonshots that continue to reverberate. A more recent moonshot is the driverless car, which in the past was a laughable idea but is now a reality that will change society and the world in many ways. Innovative billionaire moguls now speak loudly about colonizing Mars, which sounds improbable and highly risky, but it’s a moonshot that may be achieved within a few years. Establishing world peace is a moonshot that requires collective Kennedy-esque vision and motivation among world leaders, which currently is sadly lacking.

So, for contemporary psychiatry, what is the equivalent of landing on the Moon? Here is the list that pops in my brain’s mind (let us know which of these would be your top 3 moonshots by taking our survey at https://bit.ly/3qkKqTa):

• A cure for schizophrenia (across positive, negative, and cognitive symptom domains)
• A cure for mood disorders, unipolar and bipolar (including suicide)
• A cure for anxiety disorders
• A cure for obsessive-compulsive disorder
• A cure for posttraumatic stress disorder
• A cure for alcoholism/addiction
• A cure for autism
• A cure for Alzheimer’s disease and other dementias
• A cure for personality disorders, especially antisocial and borderline
• A cure for the visceral hatred across political parties that permeates our society (obviously not a psychiatric category, but perhaps it should be added to DSM because it is so destructive).

Those moonshots may be regarded as absurd, and totally unachievable, but so was landing on the Moon, until it was accomplished. Psychiatry must stop thinking small and being content with tiny advances (which is like changing the chairs to more comfortable sofas on the deck of the Titanic and calling it “progress…”). Psychiatry needs to be unified under the flag of “moonshot thinking” by several visionary and transformative leaders to start believing in a miraculously better future for our patients. But to pave the way for moonshots in psychiatry, the leading organizations must collaborate closely to open the door for unprecedented scientific and medical breakthroughs of a moonshot by:

1. Lobbying effectively to secure massive funding for research from federal, state, corporate, and foundation sources (perhaps convincing the Gates Foundation that schizophrenia is as devastating worldwide as malaria may bring a few badly needed billions into psychiatric brain research).
2. Reminding members of Congress that in the United States, costs associated with psychiatric brain disorders total an estimated $700 billion annually,¹ and that this must be addressed by boosting the meager NIMH budget by at least an order of magnitude. The NIMH should disproportionately invest its resources on severe brain disorders such as schizophrenia because breakthrough advances in its neurobiology will provide unprecedented insights to the pathophysiology of other severe psychiatric brain disorders.
3. Partnering intimately with the pharmaceutical industry in a powerful public-private coalition to exploit the extensive research infrastructure of this industry.
4. Creating the necessary army of researchers (physician-scientists) by providing huge incentives to medical students and psychiatric residents to pursue careers in neuroscience research. Incentives can include paying for an individual’s entire medical education and research training, and providing generous salaries that match or exceed the income of a very successful clinical practice.
5. Convincing all psychiatric clinicians to support research by referring patients to research projects. Clinical psychiatrists are badly needed to care for the population, but they must be reminded that every treatment they are using today was a research project in the past, and that the research of today will evolve into the treatments (or cures) of tomorrow.

Pursuing lofty moonshots via innovative research is very likely to enhance serendipity and lead to unexpected discoveries along the way. As Louis Pasteur said, “chance only favors the prepared mind.”² Moonshot thinking in psychiatry today is more feasible than ever before because of the many advances in research methods (neuroimaging, pluripotent cells, optogenetics, CRISPR, etc) and complex data management technologies (big data, machine learning, artificial intelligence), each of which qualifies as a preparatory moonshot in its own right.

Given the tragic consequences of psychiatric brain disorders, it is imperative that we “think big.” Humanity expects us to do that. We must envision the future of psychiatry as dramatically different from the present. Moonshot thinking is the indispensable vehicle to take us there.

“I believe that this nation should commit itself to achieving the goal, before the decade is out, of landing a man on the Moon and returning him safely to Earth.”

President John F. Kennedy, May 25, 1961

Despite significant progress, there remain many unmet needs in psychiatry. These include a granular understanding of the neurobiology of various psychopathologies, an objective and valid diagnostic schema, and disease-modifying treatments for chronic and disabling psychiatric disorders. Several moonshots are needed to address those festering needs.

A “moonshot” is an extremely ambitious, dramatic, imaginative, and inspiring goal. Landing on the Moon was generally believed to be impossible when President Kennedy boldly set that as a goal for the United States in 1961. Yet, 8 short years later, on July 20, 1969, Neil Armstrong stepped off the lunar module ladder onto the Moon’s surface, a feat that captured the imagination of the nation and the world. I distinctly remember watching it on television with amazement as a young boy. It was a surreal experience. That’s what achieving a moonshot feels like.

Successful organizations should always have 1 or more moonshots (American Psychiatric Association and National Institute of Mental Health [NIMH], are you listening?). Setting lofty goals that require monumental determination and effort to accomplish will have a transformative, long-lasting impact. The construction of the Panama Canal to connect 2 oceans and the Manhattan Project to develop the first nuclear bomb, which ended World War II, are examples of moonshots that continue to reverberate. A more recent moonshot is the driverless car, which in the past was a laughable idea but is now a reality that will change society and the world in many ways. Innovative billionaire moguls now speak loudly about colonizing Mars, which sounds improbable and highly risky, but it’s a moonshot that may be achieved within a few years. Establishing world peace is a moonshot that requires collective Kennedy-esque vision and motivation among world leaders, which currently is sadly lacking.

So, for contemporary psychiatry, what is the equivalent of landing on the Moon? Here is the list that pops in my brain’s mind (let us know which of these would be your top 3 moonshots by taking our survey at https://bit.ly/3qkKqTa):

• A cure for schizophrenia (across positive, negative, and cognitive symptom domains)
• A cure for mood disorders, unipolar and bipolar (including suicide)
• A cure for anxiety disorders
• A cure for obsessive-compulsive disorder
• A cure for posttraumatic stress disorder
• A cure for alcoholism/addiction
• A cure for autism
• A cure for Alzheimer’s disease and other dementias
• A cure for personality disorders, especially antisocial and borderline
• A cure for the visceral hatred across political parties that permeates our society (obviously not a psychiatric category, but perhaps it should be added to DSM because it is so destructive).

Those moonshots may be regarded as absurd, and totally unachievable, but so was landing on the Moon, until it was accomplished. Psychiatry must stop thinking small and being content with tiny advances (which is like changing the chairs to more comfortable sofas on the deck of the Titanic and calling it “progress…”). Psychiatry needs to be unified under the flag of “moonshot thinking” by several visionary and transformative leaders to start believing in a miraculously better future for our patients. But to pave the way for moonshots in psychiatry, the leading organizations must collaborate closely to open the door for unprecedented scientific and medical breakthroughs of a moonshot by:

1. Lobbying effectively to secure massive funding for research from federal, state, corporate, and foundation sources (perhaps convincing the Gates Foundation that schizophrenia is as devastating worldwide as malaria may bring a few badly needed billions into psychiatric brain research).
2. Reminding members of Congress that in the United States, costs associated with psychiatric brain disorders total an estimated $700 billion annually,¹ and that this must be addressed by boosting the meager NIMH budget by at least an order of magnitude. The NIMH should disproportionately invest its resources on severe brain disorders such as schizophrenia because breakthrough advances in its neurobiology will provide unprecedented insights to the pathophysiology of other severe psychiatric brain disorders.
3. Partnering intimately with the pharmaceutical industry in a powerful public-private coalition to exploit the extensive research infrastructure of this industry.
4. Creating the necessary army of researchers (physician-scientists) by providing huge incentives to medical students and psychiatric residents to pursue careers in neuroscience research. Incentives can include paying for an individual’s entire medical education and research training, and providing generous salaries that match or exceed the income of a very successful clinical practice.
5. Convincing all psychiatric clinicians to support research by referring patients to research projects. Clinical psychiatrists are badly needed to care for the population, but they must be reminded that every treatment they are using today was a research project in the past, and that the research of today will evolve into the treatments (or cures) of tomorrow.

Pursuing lofty moonshots via innovative research is very likely to enhance serendipity and lead to unexpected discoveries along the way. As Louis Pasteur said, “chance only favors the prepared mind.”² Moonshot thinking in psychiatry today is more feasible than ever before because of the many advances in research methods (neuroimaging, pluripotent cells, optogenetics, CRISPR, etc) and complex data management technologies (big data, machine learning, artificial intelligence), each of which qualifies as a preparatory moonshot in its own right.

Given the tragic consequences of psychiatric brain disorders, it is imperative that we “think big.” Humanity expects us to do that. We must envision the future of psychiatry as dramatically different from the present. Moonshot thinking is the indispensable vehicle to take us there.

February is National Cancer Prevention Month. With approximately 4.8 million new cases and 3.4 million deaths worldwide annually, GI cancers represent roughly a quarter of the global cancer incidence and over a third of all cancer-related deaths, according to one study.

In this month’s issue of GI & Hepatology News, we feature timely content relevant to prevention and early detection of GI cancers, which remains a central focus of our clinical and endoscopic practice as gastroenterologists. This includes important studies that demonstrate the value of upper endoscopy in reducing GI cancer mortality, illustrate the potential promise of artificial intelligence in improving early detection of gastric cancer, and link adenoma detection rate to long-term survival in patients who undergo CRC screening with flexible sigmoidoscopy. We also report on a focused update from the U.S. Multi-Society Task Force on colorectal cancer, which thoughtfully reviews the data supporting a shift in the age of initiation of average-risk CRC screening from 50 to 45 years.

On the policy front, AGA and its partners have worked tirelessly for many years to eliminate financial barriers to colorectal cancer (CRC) screening through national advocacy efforts. These efforts resulted in closure of the so-called Medicare “colonoscopy loophole” through legislation included in the COVID-19 relief bill – as a result, out-of-pocket costs for patients undergoing a screening colonoscopy that results in polypectomy are disallowed as of January 2022. The Biden Administration recently issued guidance in January in response to multisociety advocacy efforts: Private insurers must provide coverage without cost sharing for a follow-up colonoscopy after a positive stool-based CRC screening test for plan or policy years starting on or after May 31, 2022. Removing these financial barriers to care is particularly critical to efforts to improve CRC screening rates among medically underserved communities.

These achievements highlight the power of physician advocacy in inspiring policy changes that directly improve the health and well-being of our patients. I encourage you to visit the AGA website to learn how you can contribute to ongoing advocacy efforts.

Megan A. Adams, MD, JD, MSc
Editor in Chief

February is National Cancer Prevention Month. With approximately 4.8 million new cases and 3.4 million deaths worldwide annually, GI cancers represent roughly a quarter of the global cancer incidence and over a third of all cancer-related deaths, according to one study.

In this month’s issue of GI & Hepatology News, we feature timely content relevant to prevention and early detection of GI cancers, which remains a central focus of our clinical and endoscopic practice as gastroenterologists. This includes important studies that demonstrate the value of upper endoscopy in reducing GI cancer mortality, illustrate the potential promise of artificial intelligence in improving early detection of gastric cancer, and link adenoma detection rate to long-term survival in patients who undergo CRC screening with flexible sigmoidoscopy. We also report on a focused update from the U.S. Multi-Society Task Force on colorectal cancer, which thoughtfully reviews the data supporting a shift in the age of initiation of average-risk CRC screening from 50 to 45 years.

On the policy front, AGA and its partners have worked tirelessly for many years to eliminate financial barriers to colorectal cancer (CRC) screening through national advocacy efforts. These efforts resulted in closure of the so-called Medicare “colonoscopy loophole” through legislation included in the COVID-19 relief bill – as a result, out-of-pocket costs for patients undergoing a screening colonoscopy that results in polypectomy are disallowed as of January 2022. The Biden Administration recently issued guidance in January in response to multisociety advocacy efforts: Private insurers must provide coverage without cost sharing for a follow-up colonoscopy after a positive stool-based CRC screening test for plan or policy years starting on or after May 31, 2022. Removing these financial barriers to care is particularly critical to efforts to improve CRC screening rates among medically underserved communities.

These achievements highlight the power of physician advocacy in inspiring policy changes that directly improve the health and well-being of our patients. I encourage you to visit the AGA website to learn how you can contribute to ongoing advocacy efforts.

Megan A. Adams, MD, JD, MSc
Editor in Chief

February is National Cancer Prevention Month. With approximately 4.8 million new cases and 3.4 million deaths worldwide annually, GI cancers represent roughly a quarter of the global cancer incidence and over a third of all cancer-related deaths, according to one study.

In this month’s issue of GI & Hepatology News, we feature timely content relevant to prevention and early detection of GI cancers, which remains a central focus of our clinical and endoscopic practice as gastroenterologists. This includes important studies that demonstrate the value of upper endoscopy in reducing GI cancer mortality, illustrate the potential promise of artificial intelligence in improving early detection of gastric cancer, and link adenoma detection rate to long-term survival in patients who undergo CRC screening with flexible sigmoidoscopy. We also report on a focused update from the U.S. Multi-Society Task Force on colorectal cancer, which thoughtfully reviews the data supporting a shift in the age of initiation of average-risk CRC screening from 50 to 45 years.

On the policy front, AGA and its partners have worked tirelessly for many years to eliminate financial barriers to colorectal cancer (CRC) screening through national advocacy efforts. These efforts resulted in closure of the so-called Medicare “colonoscopy loophole” through legislation included in the COVID-19 relief bill – as a result, out-of-pocket costs for patients undergoing a screening colonoscopy that results in polypectomy are disallowed as of January 2022. The Biden Administration recently issued guidance in January in response to multisociety advocacy efforts: Private insurers must provide coverage without cost sharing for a follow-up colonoscopy after a positive stool-based CRC screening test for plan or policy years starting on or after May 31, 2022. Removing these financial barriers to care is particularly critical to efforts to improve CRC screening rates among medically underserved communities.

These achievements highlight the power of physician advocacy in inspiring policy changes that directly improve the health and well-being of our patients. I encourage you to visit the AGA website to learn how you can contribute to ongoing advocacy efforts.

Megan A. Adams, MD, JD, MSc
Editor in Chief