Prominent female physicians are handing over their social media platforms today to black female physicians as part of a campaign called #ShareTheMicNowMed.

The social media event, which will play out on both Twitter and Instagram, is an offshoot of #ShareTheMicNow, held earlier this month. For that event, more than 90 women, including A-list celebrities like Ellen DeGeneres, Julia Roberts, and Senator Elizabeth Warren, swapped accounts with women of color, such as “I’m Still Here” author Austin Channing Brown, Olympic fencer Ibtihaj Muhammad, and #MeToo founder Tarana Burke.

The physician event will feature 10 teams of two, with one physician handing over her account to her black female counterpart for the day. The takeover will allow the black physician to share her thoughts about the successes and challenges she faces as a woman of color in medicine.

“It was such an honor to be contacted by Arghavan Salles, MD, PhD, to participate in an event that has a goal of connecting like-minded women from various backgrounds to share a diverse perspective with a different audience,” Minnesota family medicine physician Jay-Sheree Allen, MD, told Medscape Medical News. “This event is not only incredibly important but timely.”

Participants say the goal of the takeovers is to amplify the reach and voice of black women in medicine while crossing boundaries and empowering others to do the same. Only about 5% of all active physicians in 2018 identified as Black or African American, according to a report by the Association of American Medical Colleges. And of those, just over a third are female, the report found.

“I think that as we hear those small numbers we often celebrate the success of those people without looking back and understanding where all of the barriers are that are limiting talented black women from entering medicine at every stage,” another campaign participant, Chicago pediatrician Rebekah Fenton, MD, told Medscape Medical News.

Allen says that, amid continuing worldwide protests over racial injustice, prompted by the death of George Floyd while in Minneapolis police custody last month, the online event is very timely and an important way to advocate for black lives and engage in a productive conversation.

Prominent female physicians are handing over their social media platforms today to black female physicians as part of a campaign called #ShareTheMicNowMed.

The social media event, which will play out on both Twitter and Instagram, is an offshoot of #ShareTheMicNow, held earlier this month. For that event, more than 90 women, including A-list celebrities like Ellen DeGeneres, Julia Roberts, and Senator Elizabeth Warren, swapped accounts with women of color, such as “I’m Still Here” author Austin Channing Brown, Olympic fencer Ibtihaj Muhammad, and #MeToo founder Tarana Burke.

The physician event will feature 10 teams of two, with one physician handing over her account to her black female counterpart for the day. The takeover will allow the black physician to share her thoughts about the successes and challenges she faces as a woman of color in medicine.

“It was such an honor to be contacted by Arghavan Salles, MD, PhD, to participate in an event that has a goal of connecting like-minded women from various backgrounds to share a diverse perspective with a different audience,” Minnesota family medicine physician Jay-Sheree Allen, MD, told Medscape Medical News. “This event is not only incredibly important but timely.”

Participants say the goal of the takeovers is to amplify the reach and voice of black women in medicine while crossing boundaries and empowering others to do the same. Only about 5% of all active physicians in 2018 identified as Black or African American, according to a report by the Association of American Medical Colleges. And of those, just over a third are female, the report found.

“I think that as we hear those small numbers we often celebrate the success of those people without looking back and understanding where all of the barriers are that are limiting talented black women from entering medicine at every stage,” another campaign participant, Chicago pediatrician Rebekah Fenton, MD, told Medscape Medical News.

Allen says that, amid continuing worldwide protests over racial injustice, prompted by the death of George Floyd while in Minneapolis police custody last month, the online event is very timely and an important way to advocate for black lives and engage in a productive conversation.

Prominent female physicians are handing over their social media platforms today to black female physicians as part of a campaign called #ShareTheMicNowMed.

The social media event, which will play out on both Twitter and Instagram, is an offshoot of #ShareTheMicNow, held earlier this month. For that event, more than 90 women, including A-list celebrities like Ellen DeGeneres, Julia Roberts, and Senator Elizabeth Warren, swapped accounts with women of color, such as “I’m Still Here” author Austin Channing Brown, Olympic fencer Ibtihaj Muhammad, and #MeToo founder Tarana Burke.

The physician event will feature 10 teams of two, with one physician handing over her account to her black female counterpart for the day. The takeover will allow the black physician to share her thoughts about the successes and challenges she faces as a woman of color in medicine.

“It was such an honor to be contacted by Arghavan Salles, MD, PhD, to participate in an event that has a goal of connecting like-minded women from various backgrounds to share a diverse perspective with a different audience,” Minnesota family medicine physician Jay-Sheree Allen, MD, told Medscape Medical News. “This event is not only incredibly important but timely.”

Participants say the goal of the takeovers is to amplify the reach and voice of black women in medicine while crossing boundaries and empowering others to do the same. Only about 5% of all active physicians in 2018 identified as Black or African American, according to a report by the Association of American Medical Colleges. And of those, just over a third are female, the report found.

“I think that as we hear those small numbers we often celebrate the success of those people without looking back and understanding where all of the barriers are that are limiting talented black women from entering medicine at every stage,” another campaign participant, Chicago pediatrician Rebekah Fenton, MD, told Medscape Medical News.

Allen says that, amid continuing worldwide protests over racial injustice, prompted by the death of George Floyd while in Minneapolis police custody last month, the online event is very timely and an important way to advocate for black lives and engage in a productive conversation.

Here are the stories our MDedge editors across specialties think you need to know about today:

Headache may predict clinical evolution of COVID-19

Headache may be a key symptom of COVID-19 that predicts the disease’s clinical evolution, new research suggests. An observational study of more than 100 patients showed that headache onset could occur during the presymptomatic or symptomatic phase of COVID-19.

Headache itself was associated with a shorter symptomatic period, while headache and anosmia were associated with a shorter hospitalization period. 

It seems that those patients who start early on, during the asymptomatic or early symptomatic period of COVID-19, with headache have a more localized inflammatory response that may reflect the ability of the body to better control and respond to the infection,” lead investigator Patricia Pozo-Rosich, MD, PhD, said at the virtual annual meeting of the American Headache Society. Read more.

More tops news from the AHS meeting is available on our website. 

Pilot study shows apremilast effective for severe recurrent canker sores

Apremilast was highly effective in treating patients with severe recurrent aphthous stomatitis, with rapid response and an excellent safety profile, results from a small pilot study showed.

Apremilast is approved by the FDA for psoriasis and was shown in a recent phase 2 trial to be effective for Behçet’s disease aphthosis.

Dr. Alison Bruce and colleagues found that, within 4 weeks of therapy, complete clearance of RAS lesions occurred in all patients except one in whom ulcers were reported to be less severe. Remission in all patients was sustained during 16 weeks of treatment, Dr. Bruce noted at the virtual annual meeting of the American Academy of Dermatology. Read more.

For more top news from the AAD virtual conference, visit our website.

Where does dexamethasone fit in with diabetic ketoacidosis in COVID-19?

A new article in the Journal of Clinical Endocrinology & Metabolism (JCEM) addresses unique concerns and considerations regarding diabetic ketoacidosis (DKA) in the setting of COVID-19.

“Hospitals and clinicians need to be able to quickly identify and manage DKA in COVID patients to save lives. This involves determining the options for management, including when less intensive subcutaneous insulin is indicated, and understanding how to guide patients on avoiding this serious complication,” corresponding author Marie E. McDonnell, MD, said in an Endocrine Society statement.

The new article briefly touches on the fact that upward adjustments to intensive intravenous insulin therapy for DKA may be necessary in patients with COVID-19 who are receiving concomitant corticosteroids or vasopressors. But it was written prior to the June 16 announcement of the “RECOVERY” trial results with dexamethasone. The UK National Health Service immediately approved the drug’s use in the COVID-19 setting, despite the fact that there has been no published article on the findings yet.

“The peer review will be critical. It looks as if it only benefits people who need respiratory support, but I want to understand that in much more detail,” said Dr. McDonnell. Read more.

For more on COVID-19, visit our Resource Center. All of our latest news is available on MDedge.com.

Here are the stories our MDedge editors across specialties think you need to know about today:

Headache may predict clinical evolution of COVID-19

Headache may be a key symptom of COVID-19 that predicts the disease’s clinical evolution, new research suggests. An observational study of more than 100 patients showed that headache onset could occur during the presymptomatic or symptomatic phase of COVID-19.

Headache itself was associated with a shorter symptomatic period, while headache and anosmia were associated with a shorter hospitalization period. 

It seems that those patients who start early on, during the asymptomatic or early symptomatic period of COVID-19, with headache have a more localized inflammatory response that may reflect the ability of the body to better control and respond to the infection,” lead investigator Patricia Pozo-Rosich, MD, PhD, said at the virtual annual meeting of the American Headache Society. Read more.

More tops news from the AHS meeting is available on our website. 

Pilot study shows apremilast effective for severe recurrent canker sores

Apremilast was highly effective in treating patients with severe recurrent aphthous stomatitis, with rapid response and an excellent safety profile, results from a small pilot study showed.

Apremilast is approved by the FDA for psoriasis and was shown in a recent phase 2 trial to be effective for Behçet’s disease aphthosis.

Dr. Alison Bruce and colleagues found that, within 4 weeks of therapy, complete clearance of RAS lesions occurred in all patients except one in whom ulcers were reported to be less severe. Remission in all patients was sustained during 16 weeks of treatment, Dr. Bruce noted at the virtual annual meeting of the American Academy of Dermatology. Read more.

For more top news from the AAD virtual conference, visit our website.

Where does dexamethasone fit in with diabetic ketoacidosis in COVID-19?

A new article in the Journal of Clinical Endocrinology & Metabolism (JCEM) addresses unique concerns and considerations regarding diabetic ketoacidosis (DKA) in the setting of COVID-19.

“Hospitals and clinicians need to be able to quickly identify and manage DKA in COVID patients to save lives. This involves determining the options for management, including when less intensive subcutaneous insulin is indicated, and understanding how to guide patients on avoiding this serious complication,” corresponding author Marie E. McDonnell, MD, said in an Endocrine Society statement.

The new article briefly touches on the fact that upward adjustments to intensive intravenous insulin therapy for DKA may be necessary in patients with COVID-19 who are receiving concomitant corticosteroids or vasopressors. But it was written prior to the June 16 announcement of the “RECOVERY” trial results with dexamethasone. The UK National Health Service immediately approved the drug’s use in the COVID-19 setting, despite the fact that there has been no published article on the findings yet.

“The peer review will be critical. It looks as if it only benefits people who need respiratory support, but I want to understand that in much more detail,” said Dr. McDonnell. Read more.

For more on COVID-19, visit our Resource Center. All of our latest news is available on MDedge.com.

Here are the stories our MDedge editors across specialties think you need to know about today:

Headache may predict clinical evolution of COVID-19

Headache may be a key symptom of COVID-19 that predicts the disease’s clinical evolution, new research suggests. An observational study of more than 100 patients showed that headache onset could occur during the presymptomatic or symptomatic phase of COVID-19.

Headache itself was associated with a shorter symptomatic period, while headache and anosmia were associated with a shorter hospitalization period. 

It seems that those patients who start early on, during the asymptomatic or early symptomatic period of COVID-19, with headache have a more localized inflammatory response that may reflect the ability of the body to better control and respond to the infection,” lead investigator Patricia Pozo-Rosich, MD, PhD, said at the virtual annual meeting of the American Headache Society. Read more.

More tops news from the AHS meeting is available on our website. 

Pilot study shows apremilast effective for severe recurrent canker sores

Apremilast was highly effective in treating patients with severe recurrent aphthous stomatitis, with rapid response and an excellent safety profile, results from a small pilot study showed.

Apremilast is approved by the FDA for psoriasis and was shown in a recent phase 2 trial to be effective for Behçet’s disease aphthosis.

Dr. Alison Bruce and colleagues found that, within 4 weeks of therapy, complete clearance of RAS lesions occurred in all patients except one in whom ulcers were reported to be less severe. Remission in all patients was sustained during 16 weeks of treatment, Dr. Bruce noted at the virtual annual meeting of the American Academy of Dermatology. Read more.

For more top news from the AAD virtual conference, visit our website.

Where does dexamethasone fit in with diabetic ketoacidosis in COVID-19?

A new article in the Journal of Clinical Endocrinology & Metabolism (JCEM) addresses unique concerns and considerations regarding diabetic ketoacidosis (DKA) in the setting of COVID-19.

“Hospitals and clinicians need to be able to quickly identify and manage DKA in COVID patients to save lives. This involves determining the options for management, including when less intensive subcutaneous insulin is indicated, and understanding how to guide patients on avoiding this serious complication,” corresponding author Marie E. McDonnell, MD, said in an Endocrine Society statement.

The new article briefly touches on the fact that upward adjustments to intensive intravenous insulin therapy for DKA may be necessary in patients with COVID-19 who are receiving concomitant corticosteroids or vasopressors. But it was written prior to the June 16 announcement of the “RECOVERY” trial results with dexamethasone. The UK National Health Service immediately approved the drug’s use in the COVID-19 setting, despite the fact that there has been no published article on the findings yet.

“The peer review will be critical. It looks as if it only benefits people who need respiratory support, but I want to understand that in much more detail,” said Dr. McDonnell. Read more.

For more on COVID-19, visit our Resource Center. All of our latest news is available on MDedge.com.

To the Editor:

Mycosis fungoides (MF) is the most common type of primary cutaneous lymphoma, occurring in approximately 4 of 1 million individuals per year in the United States.¹ It classically occurs in patch, plaque, and tumor stages with lesions preferentially occurring on regions of the body spared from sun exposure²; however, MF is known to have variable presentations and has been reported to imitate at least 25 other dermatoses.³ This case describes MF as a morbilliform eruption mimicking a viral exanthem.

A 30-year-old man with a 12-year history of nodular sclerosing Hodgkin lymphoma (HL) presented with a widespread rash of 2 weeks’ duration. At the time of diagnosis of HL, the patient had several slightly enlarged, hyperdense, bilateral inguinal lymph nodes seen on positron emission tomography–computed tomography. He achieved complete remission 11 years prior after 6 cycles of ABVD (doxorubicin-bleomycin-vinblastine-dacarbazine) chemotherapy. He initially presented to us prior to starting chemotherapy for evaluation of what he described as eczema on the bilateral arms and legs that had been present for 10 years. Findings from a skin biopsy of an erythematous scaling patch on the left lateral thigh were consistent with MF. One year later, new lesions on the left lateral thigh were clinically and histologically consistent with lymphomatoid papulosis (LyP).

At the current presentation, the patient denied any changes in medications, which consisted of topical clobetasol, triamcinolone, and mupirocin; however, he reported that his young child had recently been diagnosed with bronchitis and impetigo. Physical examination revealed pink-orange macules and papules on the anterior and posterior trunk, medial upper arms, and bilateral legs involving 18% of the body surface area. A complete blood cell count showed no leukocytosis or left shift. A respiratory viral panel was positive for human metapneumovirus. Two weeks later, the patient noted improvement of the rash with use of topical triamcinolone.

Four months later, the rash still had not completely resolved and now involved 50% of the body surface area. A punch biopsy of the left lower abdomen demonstrated an atypical lymphoid infiltrate with focal epidermotropism and predominance of CD4 over CD8 cells (approximately 4:1 ratio), and CD30 labeled rare cells. Polymerase chain reaction analysis of the biopsy revealed monoclonal T-cell receptor gamma chain gene rearrangement. Taken together, the findings were consistent with MF. The patient started narrowband UVB phototherapy and completed a total of 25 treatments, reaching a maximum 4-minute dose, with minimal improvement.

Three months later, the patient had 90% body surface area involvement and started treatment with intramuscular interferon alfa-2b at 1 million units 3 times weekly. He noticed improvement within the first week of treatment and reported that his skin was clear until 5 months later when he woke up one morning with a morbilliform eruption on the anterior trunk, thighs, and upper arms (Figure 1). Biopsy from the right thigh showed an infiltrate of CD3⁺ lymphocytes with a predominance of CD4 over CD8 cells (approximately 6:1 ratio), both in the dermis and epidermis (Figure 2). CD30 highlighted approximately 10% of cells (Figure 3). Findings again were consistent with MF. Flow cytometry was negative for peripheral blood involvement.

Three months later, the patient reported enlargement of several left inguinal nodes. Fine needle aspiration of 1 node demonstrated an atypical lymphoid proliferation consistent with MF. Positron emission tomography–computed tomography showed several mildly enlarged inguinal lymph nodes, which were unchanged from the initial diagnosis of HL. There were no hypermetabolic lesions. One month later, the patient started extracorporeal electrophoresis in addition to interferon alfa-2b with notable improvement of the rash. The rash later recurred after completion of these treatments and continues to have a waxing and waning course. It is currently managed with triamcinolone cream only.

At the time of the initial diagnosis of MF, the patient’s lesions appeared as eczematous patches on the face, abdomen, buttocks, and legs. Based on the history of a sick child at home, viral panel positive for human metapneumovirus, and clinical appearance, a viral exanthem was considered to be a likely explanation for the patient’s new-onset morbilliform eruption rash occurring 12 years later. A drug reaction also was considered in the differential based on the appearance of the rash; however, it was deemed less likely because the patient reported no changes in his medications at the time of rash onset. Persistence of the eruption for many months was less consistent with a reactive condition. A biopsy demonstrated the rash to be histologically consistent with MF. This patient was a rare case of MF manifesting as a morbilliform eruption mimicking a viral exanthem.

Various inflammatory conditions, including drug eruptions and lichen sclerosus et atrophicus, may mimic MF, not only based on their histophenotypic findings but also occasionally clonal proliferation by molecular study.^4,5 In our patient, one consideration was the possibility of a viral infection mimicking MF; however, biopsies showed both definite histophenotypic features of MF and clonality. More importantly, subsequent biopsy also revealed similar findings by morphology, immunohistochemical study, and T-cell gene rearrangement study, confirming the diagnosis of MF.

Another interesting feature of our case was the occurrence of HL, LyP, and MF in the same patient. Lymphomatoid papulosis is a chronic condition characterized by self-healing lesions and histologic features suggestive of malignancy that lies within a spectrum of primary cutaneous CD30⁺ lymphoproliferative disorders. There is a known association between LyP and an increased incidence of lymphomas, including MF and HL.¹ In a 2016 study, lymphomas occurred in 52% of patients with LyP (N=180), with MF being the most frequently associated lymphoma.⁶ Notably, biopsies consistent with both HL and MF, respectively, in our patient were positive for the CD30 marker. Patients with HL also are at increased risk for developing other malignancies, with the risk of leukemias and non-HLs greater than that of solid tumors.⁵ There have been multiple reported cases of HL and MF occurring in the same patient and at least one prior reported case of LyP, HL, and MF occurring in the same patient.^6,7

This case highlights the myriad presentations of MF and describes an unusual case of MF manifesting as a morbilliform eruption mimicking a viral exanthem.

To the Editor:

Mycosis fungoides (MF) is the most common type of primary cutaneous lymphoma, occurring in approximately 4 of 1 million individuals per year in the United States.¹ It classically occurs in patch, plaque, and tumor stages with lesions preferentially occurring on regions of the body spared from sun exposure²; however, MF is known to have variable presentations and has been reported to imitate at least 25 other dermatoses.³ This case describes MF as a morbilliform eruption mimicking a viral exanthem.

A 30-year-old man with a 12-year history of nodular sclerosing Hodgkin lymphoma (HL) presented with a widespread rash of 2 weeks’ duration. At the time of diagnosis of HL, the patient had several slightly enlarged, hyperdense, bilateral inguinal lymph nodes seen on positron emission tomography–computed tomography. He achieved complete remission 11 years prior after 6 cycles of ABVD (doxorubicin-bleomycin-vinblastine-dacarbazine) chemotherapy. He initially presented to us prior to starting chemotherapy for evaluation of what he described as eczema on the bilateral arms and legs that had been present for 10 years. Findings from a skin biopsy of an erythematous scaling patch on the left lateral thigh were consistent with MF. One year later, new lesions on the left lateral thigh were clinically and histologically consistent with lymphomatoid papulosis (LyP).

At the current presentation, the patient denied any changes in medications, which consisted of topical clobetasol, triamcinolone, and mupirocin; however, he reported that his young child had recently been diagnosed with bronchitis and impetigo. Physical examination revealed pink-orange macules and papules on the anterior and posterior trunk, medial upper arms, and bilateral legs involving 18% of the body surface area. A complete blood cell count showed no leukocytosis or left shift. A respiratory viral panel was positive for human metapneumovirus. Two weeks later, the patient noted improvement of the rash with use of topical triamcinolone.

Four months later, the rash still had not completely resolved and now involved 50% of the body surface area. A punch biopsy of the left lower abdomen demonstrated an atypical lymphoid infiltrate with focal epidermotropism and predominance of CD4 over CD8 cells (approximately 4:1 ratio), and CD30 labeled rare cells. Polymerase chain reaction analysis of the biopsy revealed monoclonal T-cell receptor gamma chain gene rearrangement. Taken together, the findings were consistent with MF. The patient started narrowband UVB phototherapy and completed a total of 25 treatments, reaching a maximum 4-minute dose, with minimal improvement.

Three months later, the patient had 90% body surface area involvement and started treatment with intramuscular interferon alfa-2b at 1 million units 3 times weekly. He noticed improvement within the first week of treatment and reported that his skin was clear until 5 months later when he woke up one morning with a morbilliform eruption on the anterior trunk, thighs, and upper arms (Figure 1). Biopsy from the right thigh showed an infiltrate of CD3⁺ lymphocytes with a predominance of CD4 over CD8 cells (approximately 6:1 ratio), both in the dermis and epidermis (Figure 2). CD30 highlighted approximately 10% of cells (Figure 3). Findings again were consistent with MF. Flow cytometry was negative for peripheral blood involvement.

Three months later, the patient reported enlargement of several left inguinal nodes. Fine needle aspiration of 1 node demonstrated an atypical lymphoid proliferation consistent with MF. Positron emission tomography–computed tomography showed several mildly enlarged inguinal lymph nodes, which were unchanged from the initial diagnosis of HL. There were no hypermetabolic lesions. One month later, the patient started extracorporeal electrophoresis in addition to interferon alfa-2b with notable improvement of the rash. The rash later recurred after completion of these treatments and continues to have a waxing and waning course. It is currently managed with triamcinolone cream only.

At the time of the initial diagnosis of MF, the patient’s lesions appeared as eczematous patches on the face, abdomen, buttocks, and legs. Based on the history of a sick child at home, viral panel positive for human metapneumovirus, and clinical appearance, a viral exanthem was considered to be a likely explanation for the patient’s new-onset morbilliform eruption rash occurring 12 years later. A drug reaction also was considered in the differential based on the appearance of the rash; however, it was deemed less likely because the patient reported no changes in his medications at the time of rash onset. Persistence of the eruption for many months was less consistent with a reactive condition. A biopsy demonstrated the rash to be histologically consistent with MF. This patient was a rare case of MF manifesting as a morbilliform eruption mimicking a viral exanthem.

Various inflammatory conditions, including drug eruptions and lichen sclerosus et atrophicus, may mimic MF, not only based on their histophenotypic findings but also occasionally clonal proliferation by molecular study.^4,5 In our patient, one consideration was the possibility of a viral infection mimicking MF; however, biopsies showed both definite histophenotypic features of MF and clonality. More importantly, subsequent biopsy also revealed similar findings by morphology, immunohistochemical study, and T-cell gene rearrangement study, confirming the diagnosis of MF.

Another interesting feature of our case was the occurrence of HL, LyP, and MF in the same patient. Lymphomatoid papulosis is a chronic condition characterized by self-healing lesions and histologic features suggestive of malignancy that lies within a spectrum of primary cutaneous CD30⁺ lymphoproliferative disorders. There is a known association between LyP and an increased incidence of lymphomas, including MF and HL.¹ In a 2016 study, lymphomas occurred in 52% of patients with LyP (N=180), with MF being the most frequently associated lymphoma.⁶ Notably, biopsies consistent with both HL and MF, respectively, in our patient were positive for the CD30 marker. Patients with HL also are at increased risk for developing other malignancies, with the risk of leukemias and non-HLs greater than that of solid tumors.⁵ There have been multiple reported cases of HL and MF occurring in the same patient and at least one prior reported case of LyP, HL, and MF occurring in the same patient.^6,7

This case highlights the myriad presentations of MF and describes an unusual case of MF manifesting as a morbilliform eruption mimicking a viral exanthem.

To the Editor:

Mycosis fungoides (MF) is the most common type of primary cutaneous lymphoma, occurring in approximately 4 of 1 million individuals per year in the United States.¹ It classically occurs in patch, plaque, and tumor stages with lesions preferentially occurring on regions of the body spared from sun exposure²; however, MF is known to have variable presentations and has been reported to imitate at least 25 other dermatoses.³ This case describes MF as a morbilliform eruption mimicking a viral exanthem.

A 30-year-old man with a 12-year history of nodular sclerosing Hodgkin lymphoma (HL) presented with a widespread rash of 2 weeks’ duration. At the time of diagnosis of HL, the patient had several slightly enlarged, hyperdense, bilateral inguinal lymph nodes seen on positron emission tomography–computed tomography. He achieved complete remission 11 years prior after 6 cycles of ABVD (doxorubicin-bleomycin-vinblastine-dacarbazine) chemotherapy. He initially presented to us prior to starting chemotherapy for evaluation of what he described as eczema on the bilateral arms and legs that had been present for 10 years. Findings from a skin biopsy of an erythematous scaling patch on the left lateral thigh were consistent with MF. One year later, new lesions on the left lateral thigh were clinically and histologically consistent with lymphomatoid papulosis (LyP).

At the current presentation, the patient denied any changes in medications, which consisted of topical clobetasol, triamcinolone, and mupirocin; however, he reported that his young child had recently been diagnosed with bronchitis and impetigo. Physical examination revealed pink-orange macules and papules on the anterior and posterior trunk, medial upper arms, and bilateral legs involving 18% of the body surface area. A complete blood cell count showed no leukocytosis or left shift. A respiratory viral panel was positive for human metapneumovirus. Two weeks later, the patient noted improvement of the rash with use of topical triamcinolone.

Four months later, the rash still had not completely resolved and now involved 50% of the body surface area. A punch biopsy of the left lower abdomen demonstrated an atypical lymphoid infiltrate with focal epidermotropism and predominance of CD4 over CD8 cells (approximately 4:1 ratio), and CD30 labeled rare cells. Polymerase chain reaction analysis of the biopsy revealed monoclonal T-cell receptor gamma chain gene rearrangement. Taken together, the findings were consistent with MF. The patient started narrowband UVB phototherapy and completed a total of 25 treatments, reaching a maximum 4-minute dose, with minimal improvement.

Three months later, the patient had 90% body surface area involvement and started treatment with intramuscular interferon alfa-2b at 1 million units 3 times weekly. He noticed improvement within the first week of treatment and reported that his skin was clear until 5 months later when he woke up one morning with a morbilliform eruption on the anterior trunk, thighs, and upper arms (Figure 1). Biopsy from the right thigh showed an infiltrate of CD3⁺ lymphocytes with a predominance of CD4 over CD8 cells (approximately 6:1 ratio), both in the dermis and epidermis (Figure 2). CD30 highlighted approximately 10% of cells (Figure 3). Findings again were consistent with MF. Flow cytometry was negative for peripheral blood involvement.

Three months later, the patient reported enlargement of several left inguinal nodes. Fine needle aspiration of 1 node demonstrated an atypical lymphoid proliferation consistent with MF. Positron emission tomography–computed tomography showed several mildly enlarged inguinal lymph nodes, which were unchanged from the initial diagnosis of HL. There were no hypermetabolic lesions. One month later, the patient started extracorporeal electrophoresis in addition to interferon alfa-2b with notable improvement of the rash. The rash later recurred after completion of these treatments and continues to have a waxing and waning course. It is currently managed with triamcinolone cream only.

At the time of the initial diagnosis of MF, the patient’s lesions appeared as eczematous patches on the face, abdomen, buttocks, and legs. Based on the history of a sick child at home, viral panel positive for human metapneumovirus, and clinical appearance, a viral exanthem was considered to be a likely explanation for the patient’s new-onset morbilliform eruption rash occurring 12 years later. A drug reaction also was considered in the differential based on the appearance of the rash; however, it was deemed less likely because the patient reported no changes in his medications at the time of rash onset. Persistence of the eruption for many months was less consistent with a reactive condition. A biopsy demonstrated the rash to be histologically consistent with MF. This patient was a rare case of MF manifesting as a morbilliform eruption mimicking a viral exanthem.

Various inflammatory conditions, including drug eruptions and lichen sclerosus et atrophicus, may mimic MF, not only based on their histophenotypic findings but also occasionally clonal proliferation by molecular study.^4,5 In our patient, one consideration was the possibility of a viral infection mimicking MF; however, biopsies showed both definite histophenotypic features of MF and clonality. More importantly, subsequent biopsy also revealed similar findings by morphology, immunohistochemical study, and T-cell gene rearrangement study, confirming the diagnosis of MF.

Another interesting feature of our case was the occurrence of HL, LyP, and MF in the same patient. Lymphomatoid papulosis is a chronic condition characterized by self-healing lesions and histologic features suggestive of malignancy that lies within a spectrum of primary cutaneous CD30⁺ lymphoproliferative disorders. There is a known association between LyP and an increased incidence of lymphomas, including MF and HL.¹ In a 2016 study, lymphomas occurred in 52% of patients with LyP (N=180), with MF being the most frequently associated lymphoma.⁶ Notably, biopsies consistent with both HL and MF, respectively, in our patient were positive for the CD30 marker. Patients with HL also are at increased risk for developing other malignancies, with the risk of leukemias and non-HLs greater than that of solid tumors.⁵ There have been multiple reported cases of HL and MF occurring in the same patient and at least one prior reported case of LyP, HL, and MF occurring in the same patient.^6,7

This case highlights the myriad presentations of MF and describes an unusual case of MF manifesting as a morbilliform eruption mimicking a viral exanthem.

I was recently interviewed, as a gay psychiatrist treating gay patients who lived through the AIDS epidemic, about my perspectives on living through a COVID pandemic: Were there parallels and contrasts between the two? A month later, listening to patients remotely via teletherapy, I’m experiencing an unsettling similarity to serosorting, a phenomenon that emerged during the AIDS epidemic.

Serosorting is the practice of choosing a sexual partner based on their HIV serostatus. Sorting out who was positive from who was negative allowed people to give themselves permission to have unprotected sex without risk of getting HIV. However, it was not uncommon to make those decisions without really knowing a potential partner’s actual serostatus. In fact, a lot of people serosorted by guessing.

Why not just ask a potential partner, “What’s your serostatus?” Apparently, for some, introducing the subject of HIV was deemed a sexual buzzkill. Instead, assumptions were made based on outer appearances.

Did someone look healthy? Were they well built? Were they overweight, meaning not emaciated from AIDS? If so, they were presumed negative and safe to have risky, unprotected sex with them.

Some imagined age correlated with serostatus. Since anyone older than some arbitrary age – like 30, to pull a number out of a hat – was expected to be more likely to have HIV than someone under 30, they would use that guideline in choosing sexual partners. However, these decisions were made without factual knowledge, like a blood test, but using some internal reasoning process.

Which brings us to what might be called “COVID-sorting.”

Some of my patients believe they had COVID-19, although they’d not been tested to either confirm or disprove that belief. Others had positive COVID-19 antibody tests, which they believe provides immunity. Among that group, some had symptoms, others did not.

Yet regardless of what they actually know or don’t know, patients are making calculations about managing physical distancing using their own internal formulas. They make risk calculations having little to do with actual knowledge of public health precautions on preventing COVID’s spread.

For example, one patient was planning a Memorial Day weekend in a shared Fire Island house with five friends and acquaintances. All six live alone and, as far as he knows, all are physically distancing. Consequently, my patient doesn’t think house-sharing is anything to worry about, even though he doesn’t know how scrupulously others have followed distancing guidelines.

Another patient, recovering at home after being ill with COVID-19, felt safe inviting someone over for sex who had also been ill and recovered. He didn’t think they could infect each other, presuming, not altogether unreasonably, they were both immune.

Finally, there are those who don’t know whether they had COVID-19, but think they did because they experienced influenza-like symptoms. They are giving themselves permission to meet up with others who feel the same.

Yet a Mount Sinai study, which has not yet been peer-reviewed, raises fascinating issues about immunity. The study included 719 people who suspected they had COVID-19 based on some respiratory symptoms. The majority, 62%, had no antibodies. Researchers believe they mistook influenza, another viral infection, or allergies for COVID-19 (medRxiv. 2020 May 5. doi: 10.1101/2020.04.04.2008516).

The study also included 624 people who tested positive for the virus and recovered. All but three developed antibodies. Many assume those who are antibody-positive are now immune. They may be right. However, we don’t know definitively that they are, and if they are, we do not yet know how long immunity may last. Further, as reported in the New York Times, just because you test positive for antibodies, doesn’t mean you have them.

It should be underscored that COVID-sorting is not limited to gay men or psychiatric patients. Central Park, these days, is filled with many unmasked, nonsocially isolating people of all sexual orientations and genders who are making their own questionable decisions. And as many states have begun opening up restrictions on social gatherings, we are seeing an all-too-human psychological mindset with wider implications – rising numbers of cases. As we move forward, all of us will have to decide for ourselves, and not only in sexual situations, how to get on with our lives in a post–COVID-19 era.

Given how much is still unknown, it is likely each of us will come up with our own algorithm of risk assessment. It is likely that the formulas used will not necessarily be based on scientific facts, although that would be ideal. If past epidemic and recent pandemic behaviors are any indicators, people’s actions will reflect some combination of their own needs and desires, their own comfort level with risk-taking, and their relative understanding of complex subjects like virology, immunology, epidemiology, and public health. The challenge faced by public health officials today is to translate complex scientific and medical issues into messages average people can understand.

What exactly can be done? I’m not exactly sure, but I hope that improved education and communication can help. In the first 2 decades of the AIDS epidemic, efforts were made to change and tailor HIV-prevention messages to specific, at-risk demographic groups. Today, public health messages aimed at preventing COVID-19’s spread that resonate with older people can fall on a younger person’s deaf ears. One message size does not fit all. Hopefully, public health officials and government leaders will act on this sooner rather than later.
 

Dr. Drescher, a psychoanalyst, is clinical professor of psychiatry at Columbia University, and training and supervising analyst at the William A. White Institute, both in New York. He also is emeritus editor of the Journal of Gay & Lesbian Mental Health. Dr. Drescher has no other disclosures.

I was recently interviewed, as a gay psychiatrist treating gay patients who lived through the AIDS epidemic, about my perspectives on living through a COVID pandemic: Were there parallels and contrasts between the two? A month later, listening to patients remotely via teletherapy, I’m experiencing an unsettling similarity to serosorting, a phenomenon that emerged during the AIDS epidemic.

Serosorting is the practice of choosing a sexual partner based on their HIV serostatus. Sorting out who was positive from who was negative allowed people to give themselves permission to have unprotected sex without risk of getting HIV. However, it was not uncommon to make those decisions without really knowing a potential partner’s actual serostatus. In fact, a lot of people serosorted by guessing.

Why not just ask a potential partner, “What’s your serostatus?” Apparently, for some, introducing the subject of HIV was deemed a sexual buzzkill. Instead, assumptions were made based on outer appearances.

Did someone look healthy? Were they well built? Were they overweight, meaning not emaciated from AIDS? If so, they were presumed negative and safe to have risky, unprotected sex with them.

Some imagined age correlated with serostatus. Since anyone older than some arbitrary age – like 30, to pull a number out of a hat – was expected to be more likely to have HIV than someone under 30, they would use that guideline in choosing sexual partners. However, these decisions were made without factual knowledge, like a blood test, but using some internal reasoning process.

Which brings us to what might be called “COVID-sorting.”

Some of my patients believe they had COVID-19, although they’d not been tested to either confirm or disprove that belief. Others had positive COVID-19 antibody tests, which they believe provides immunity. Among that group, some had symptoms, others did not.

Yet regardless of what they actually know or don’t know, patients are making calculations about managing physical distancing using their own internal formulas. They make risk calculations having little to do with actual knowledge of public health precautions on preventing COVID’s spread.

For example, one patient was planning a Memorial Day weekend in a shared Fire Island house with five friends and acquaintances. All six live alone and, as far as he knows, all are physically distancing. Consequently, my patient doesn’t think house-sharing is anything to worry about, even though he doesn’t know how scrupulously others have followed distancing guidelines.

Another patient, recovering at home after being ill with COVID-19, felt safe inviting someone over for sex who had also been ill and recovered. He didn’t think they could infect each other, presuming, not altogether unreasonably, they were both immune.

Finally, there are those who don’t know whether they had COVID-19, but think they did because they experienced influenza-like symptoms. They are giving themselves permission to meet up with others who feel the same.

Yet a Mount Sinai study, which has not yet been peer-reviewed, raises fascinating issues about immunity. The study included 719 people who suspected they had COVID-19 based on some respiratory symptoms. The majority, 62%, had no antibodies. Researchers believe they mistook influenza, another viral infection, or allergies for COVID-19 (medRxiv. 2020 May 5. doi: 10.1101/2020.04.04.2008516).

The study also included 624 people who tested positive for the virus and recovered. All but three developed antibodies. Many assume those who are antibody-positive are now immune. They may be right. However, we don’t know definitively that they are, and if they are, we do not yet know how long immunity may last. Further, as reported in the New York Times, just because you test positive for antibodies, doesn’t mean you have them.

It should be underscored that COVID-sorting is not limited to gay men or psychiatric patients. Central Park, these days, is filled with many unmasked, nonsocially isolating people of all sexual orientations and genders who are making their own questionable decisions. And as many states have begun opening up restrictions on social gatherings, we are seeing an all-too-human psychological mindset with wider implications – rising numbers of cases. As we move forward, all of us will have to decide for ourselves, and not only in sexual situations, how to get on with our lives in a post–COVID-19 era.

Given how much is still unknown, it is likely each of us will come up with our own algorithm of risk assessment. It is likely that the formulas used will not necessarily be based on scientific facts, although that would be ideal. If past epidemic and recent pandemic behaviors are any indicators, people’s actions will reflect some combination of their own needs and desires, their own comfort level with risk-taking, and their relative understanding of complex subjects like virology, immunology, epidemiology, and public health. The challenge faced by public health officials today is to translate complex scientific and medical issues into messages average people can understand.

What exactly can be done? I’m not exactly sure, but I hope that improved education and communication can help. In the first 2 decades of the AIDS epidemic, efforts were made to change and tailor HIV-prevention messages to specific, at-risk demographic groups. Today, public health messages aimed at preventing COVID-19’s spread that resonate with older people can fall on a younger person’s deaf ears. One message size does not fit all. Hopefully, public health officials and government leaders will act on this sooner rather than later.
 

Dr. Drescher, a psychoanalyst, is clinical professor of psychiatry at Columbia University, and training and supervising analyst at the William A. White Institute, both in New York. He also is emeritus editor of the Journal of Gay & Lesbian Mental Health. Dr. Drescher has no other disclosures.

I was recently interviewed, as a gay psychiatrist treating gay patients who lived through the AIDS epidemic, about my perspectives on living through a COVID pandemic: Were there parallels and contrasts between the two? A month later, listening to patients remotely via teletherapy, I’m experiencing an unsettling similarity to serosorting, a phenomenon that emerged during the AIDS epidemic.

Serosorting is the practice of choosing a sexual partner based on their HIV serostatus. Sorting out who was positive from who was negative allowed people to give themselves permission to have unprotected sex without risk of getting HIV. However, it was not uncommon to make those decisions without really knowing a potential partner’s actual serostatus. In fact, a lot of people serosorted by guessing.

Why not just ask a potential partner, “What’s your serostatus?” Apparently, for some, introducing the subject of HIV was deemed a sexual buzzkill. Instead, assumptions were made based on outer appearances.

Did someone look healthy? Were they well built? Were they overweight, meaning not emaciated from AIDS? If so, they were presumed negative and safe to have risky, unprotected sex with them.

Some imagined age correlated with serostatus. Since anyone older than some arbitrary age – like 30, to pull a number out of a hat – was expected to be more likely to have HIV than someone under 30, they would use that guideline in choosing sexual partners. However, these decisions were made without factual knowledge, like a blood test, but using some internal reasoning process.

Which brings us to what might be called “COVID-sorting.”

Some of my patients believe they had COVID-19, although they’d not been tested to either confirm or disprove that belief. Others had positive COVID-19 antibody tests, which they believe provides immunity. Among that group, some had symptoms, others did not.

Yet regardless of what they actually know or don’t know, patients are making calculations about managing physical distancing using their own internal formulas. They make risk calculations having little to do with actual knowledge of public health precautions on preventing COVID’s spread.

For example, one patient was planning a Memorial Day weekend in a shared Fire Island house with five friends and acquaintances. All six live alone and, as far as he knows, all are physically distancing. Consequently, my patient doesn’t think house-sharing is anything to worry about, even though he doesn’t know how scrupulously others have followed distancing guidelines.

Another patient, recovering at home after being ill with COVID-19, felt safe inviting someone over for sex who had also been ill and recovered. He didn’t think they could infect each other, presuming, not altogether unreasonably, they were both immune.

Finally, there are those who don’t know whether they had COVID-19, but think they did because they experienced influenza-like symptoms. They are giving themselves permission to meet up with others who feel the same.

Yet a Mount Sinai study, which has not yet been peer-reviewed, raises fascinating issues about immunity. The study included 719 people who suspected they had COVID-19 based on some respiratory symptoms. The majority, 62%, had no antibodies. Researchers believe they mistook influenza, another viral infection, or allergies for COVID-19 (medRxiv. 2020 May 5. doi: 10.1101/2020.04.04.2008516).

The study also included 624 people who tested positive for the virus and recovered. All but three developed antibodies. Many assume those who are antibody-positive are now immune. They may be right. However, we don’t know definitively that they are, and if they are, we do not yet know how long immunity may last. Further, as reported in the New York Times, just because you test positive for antibodies, doesn’t mean you have them.

It should be underscored that COVID-sorting is not limited to gay men or psychiatric patients. Central Park, these days, is filled with many unmasked, nonsocially isolating people of all sexual orientations and genders who are making their own questionable decisions. And as many states have begun opening up restrictions on social gatherings, we are seeing an all-too-human psychological mindset with wider implications – rising numbers of cases. As we move forward, all of us will have to decide for ourselves, and not only in sexual situations, how to get on with our lives in a post–COVID-19 era.

Given how much is still unknown, it is likely each of us will come up with our own algorithm of risk assessment. It is likely that the formulas used will not necessarily be based on scientific facts, although that would be ideal. If past epidemic and recent pandemic behaviors are any indicators, people’s actions will reflect some combination of their own needs and desires, their own comfort level with risk-taking, and their relative understanding of complex subjects like virology, immunology, epidemiology, and public health. The challenge faced by public health officials today is to translate complex scientific and medical issues into messages average people can understand.

What exactly can be done? I’m not exactly sure, but I hope that improved education and communication can help. In the first 2 decades of the AIDS epidemic, efforts were made to change and tailor HIV-prevention messages to specific, at-risk demographic groups. Today, public health messages aimed at preventing COVID-19’s spread that resonate with older people can fall on a younger person’s deaf ears. One message size does not fit all. Hopefully, public health officials and government leaders will act on this sooner rather than later.
 

Dr. Drescher, a psychoanalyst, is clinical professor of psychiatry at Columbia University, and training and supervising analyst at the William A. White Institute, both in New York. He also is emeritus editor of the Journal of Gay & Lesbian Mental Health. Dr. Drescher has no other disclosures.

There is concern that the COVID-19 pandemic may be inflicting collateral damage on vulnerable patients with chronic conditions, in particular, those with COPD, according to a commentary published in CHEST (2020 May 28. doi: 10.1016/j.chest.2020.05.549) by a group of physicians who study COPD.

Not only is COPD among the most prevalent underlying diseases among hospitalized COVID-19 patients (Clin Microbiol Infect. 2020 Jun 8. doi: 10.1016/j.cmi.2020.05.041), but other unanticipated factors of treatment put these patients at extra risk. Valerie Press, MD, assistant professor of medicine and pediatrics at the University of Chicago, and colleagues aimed to alert physicians to be aware of potential negative effects, or collateral damage, that the pandemic can have on their patients with COPD, even those without a COVID-19 diagnosis.

These concerns include that patients may delay presenting to the ED with acute exacerbations of COPD and once they present they may be at later stages of the exacerbation. Further, evaluation for COVID-19 as a possible trigger of acute exacerbations of COPD (AECOPD) is essential; however, implementing proven AECOPD therapies remains challenging. For instance, routine therapy with corticosteroids for AECOPD may be delayed due to diagnostic uncertainty and hesitation to treat COVID-19 with steroids while COVID-19 testing is pending,” Dr. Press and her colleagues stated.

Shortages and scarcity of medications such as albuterol inhalers to treat COPD have been reported. In addition, patients with COPD are currently less likely to access their health care providers because of fear of COVID-19 infection. This barrier to care and the current higher threshold for presenting to the hospital may to lead to more cases of AECOPD and worsening health in these patients, according to the authors.

Dr. Press said in an interview: “Access to medications delivered through inhalers is challenging even without the pandemic due to high cost of medications. Generic medications are key to improving access for patients with chronic lung disease, so once the generic albuterol becomes available, this should help with access. In the meantime, some companies help provide medications at reduced cost, but usually only on a short time basis. In addition, some pharmacies have lower-cost albuterol inhalers, but these are often not supplied with a full month of dosing.”

In addition to all these concerns is the economic toll this pandemic is taking on patients. The association between COPD and socioeconomic status has been studied in depth (Am J Respir Crit Care Med. 2019; 199[8]:961-69) and would indicate that low-income patients with COPD would face an increased burden during an economic downturn. The authors noted, “Historic rapid job loss and unemployment in the U.S., coupled with a health system of employment-integrated health insurance coverage, makes it more likely that people with COPD will not be able to afford their medication.”

Dr. Press stressed that the COVID pandemic has highlighted critically important disparities in access to health care and disparities in health. “Many of the recommendations regarding stay-at-home and other safety mechanisms to prevent contracting and spreading COVID-19 have not been feasible for all sub-populations in the United States. Those that were essential workers did not have the ability to stay home. Further, those that rely on public transportation had less opportunities to social distance. Finally, while telemedicine opportunities have advanced for clinical care, not all patients have equal access to these capabilities and health disparities could widen in this regard as well. Clinicians have a responsibility to identify social determinants of health that increase risks to our patients’ health and limit their safety.”*

The authors offer some concrete suggestions of how physicians can address some of these concerns, including the following:

• Be alert to potential barriers to accessing medication and be aware of generic albuterol inhaler recently approved by the FDA in response to COVID-19–related shortages.
• Use telemedicine to monitor patients and improvement of home self-management. Clinicians should help patients “seek care with worsening symptoms and have clear management guidelines regarding seeking phone/video visits; implementing therapy with corticosteroids, antibiotics, or inhalers and nebulizers; COVID-19 testing recommendations; and thresholds for seeking emergent, urgent, or outpatient care in person,” Dr. Press added, “Building on the work of nurse advice lines and case management and other support services for high-risk patients with COPD may continue via telehealth and telephone visits.”
• Ensure that untried therapy for COVID-19 “does not displace proven and necessary treatments for patients with COPD, hence placing them at increased risk for poor outcomes.”

Dr. Press is also concerned about the post–COVID-19 period for patients with COPD. “It is too early to know if there are specific after effects of the COVID infection on patients with COPD, but given the damage the virus does to even healthy lungs, there is reason to have concern that COVID could cause worsening damage to the lungs of individuals with COPD.”

She noted, “Post-ICU [PICU] syndrome has been recognized in patients with ARDS generally, and patients who recover from critical illness may have long-lasting (and permanent) effects on strength, cognition, disability, and pulmonary function. Whether the PICU syndrome in patients with ARDS due to COVID-19 specifically is different from the PICU syndrome due to other causes remains unknown. But clinicians whose patients with COPD survive COVID-19 may expect long-lasting effects and slow recovery in cases where COVID-19 led to severe ARDS and a prolonged ICU stay. Assessment of overall patient recovery and functional capacity (beyond lung function and dyspnea symptoms) including deconditioning, anxiety, PTSD, weakness, and malnutrition will need to be addressed. Additionally, clinicians may help patients and their families understand the expected recovery and help facilitate family conversations about residual effects of COVID-19.”

The authors had no disclosures.

SOURCE: Press V et al. Chest. 2020 May 28. doi:10.1016/j.chest.2020.05.549.

CORRECTION: *This story was updated with further comments and clarifications from Dr. Press. 6/23/2020

There is concern that the COVID-19 pandemic may be inflicting collateral damage on vulnerable patients with chronic conditions, in particular, those with COPD, according to a commentary published in CHEST (2020 May 28. doi: 10.1016/j.chest.2020.05.549) by a group of physicians who study COPD.

Not only is COPD among the most prevalent underlying diseases among hospitalized COVID-19 patients (Clin Microbiol Infect. 2020 Jun 8. doi: 10.1016/j.cmi.2020.05.041), but other unanticipated factors of treatment put these patients at extra risk. Valerie Press, MD, assistant professor of medicine and pediatrics at the University of Chicago, and colleagues aimed to alert physicians to be aware of potential negative effects, or collateral damage, that the pandemic can have on their patients with COPD, even those without a COVID-19 diagnosis.

These concerns include that patients may delay presenting to the ED with acute exacerbations of COPD and once they present they may be at later stages of the exacerbation. Further, evaluation for COVID-19 as a possible trigger of acute exacerbations of COPD (AECOPD) is essential; however, implementing proven AECOPD therapies remains challenging. For instance, routine therapy with corticosteroids for AECOPD may be delayed due to diagnostic uncertainty and hesitation to treat COVID-19 with steroids while COVID-19 testing is pending,” Dr. Press and her colleagues stated.

Shortages and scarcity of medications such as albuterol inhalers to treat COPD have been reported. In addition, patients with COPD are currently less likely to access their health care providers because of fear of COVID-19 infection. This barrier to care and the current higher threshold for presenting to the hospital may to lead to more cases of AECOPD and worsening health in these patients, according to the authors.

Dr. Press said in an interview: “Access to medications delivered through inhalers is challenging even without the pandemic due to high cost of medications. Generic medications are key to improving access for patients with chronic lung disease, so once the generic albuterol becomes available, this should help with access. In the meantime, some companies help provide medications at reduced cost, but usually only on a short time basis. In addition, some pharmacies have lower-cost albuterol inhalers, but these are often not supplied with a full month of dosing.”

In addition to all these concerns is the economic toll this pandemic is taking on patients. The association between COPD and socioeconomic status has been studied in depth (Am J Respir Crit Care Med. 2019; 199[8]:961-69) and would indicate that low-income patients with COPD would face an increased burden during an economic downturn. The authors noted, “Historic rapid job loss and unemployment in the U.S., coupled with a health system of employment-integrated health insurance coverage, makes it more likely that people with COPD will not be able to afford their medication.”

Dr. Press stressed that the COVID pandemic has highlighted critically important disparities in access to health care and disparities in health. “Many of the recommendations regarding stay-at-home and other safety mechanisms to prevent contracting and spreading COVID-19 have not been feasible for all sub-populations in the United States. Those that were essential workers did not have the ability to stay home. Further, those that rely on public transportation had less opportunities to social distance. Finally, while telemedicine opportunities have advanced for clinical care, not all patients have equal access to these capabilities and health disparities could widen in this regard as well. Clinicians have a responsibility to identify social determinants of health that increase risks to our patients’ health and limit their safety.”*

The authors offer some concrete suggestions of how physicians can address some of these concerns, including the following:

• Be alert to potential barriers to accessing medication and be aware of generic albuterol inhaler recently approved by the FDA in response to COVID-19–related shortages.
• Use telemedicine to monitor patients and improvement of home self-management. Clinicians should help patients “seek care with worsening symptoms and have clear management guidelines regarding seeking phone/video visits; implementing therapy with corticosteroids, antibiotics, or inhalers and nebulizers; COVID-19 testing recommendations; and thresholds for seeking emergent, urgent, or outpatient care in person,” Dr. Press added, “Building on the work of nurse advice lines and case management and other support services for high-risk patients with COPD may continue via telehealth and telephone visits.”
• Ensure that untried therapy for COVID-19 “does not displace proven and necessary treatments for patients with COPD, hence placing them at increased risk for poor outcomes.”

Dr. Press is also concerned about the post–COVID-19 period for patients with COPD. “It is too early to know if there are specific after effects of the COVID infection on patients with COPD, but given the damage the virus does to even healthy lungs, there is reason to have concern that COVID could cause worsening damage to the lungs of individuals with COPD.”

She noted, “Post-ICU [PICU] syndrome has been recognized in patients with ARDS generally, and patients who recover from critical illness may have long-lasting (and permanent) effects on strength, cognition, disability, and pulmonary function. Whether the PICU syndrome in patients with ARDS due to COVID-19 specifically is different from the PICU syndrome due to other causes remains unknown. But clinicians whose patients with COPD survive COVID-19 may expect long-lasting effects and slow recovery in cases where COVID-19 led to severe ARDS and a prolonged ICU stay. Assessment of overall patient recovery and functional capacity (beyond lung function and dyspnea symptoms) including deconditioning, anxiety, PTSD, weakness, and malnutrition will need to be addressed. Additionally, clinicians may help patients and their families understand the expected recovery and help facilitate family conversations about residual effects of COVID-19.”

The authors had no disclosures.

SOURCE: Press V et al. Chest. 2020 May 28. doi:10.1016/j.chest.2020.05.549.

CORRECTION: *This story was updated with further comments and clarifications from Dr. Press. 6/23/2020

There is concern that the COVID-19 pandemic may be inflicting collateral damage on vulnerable patients with chronic conditions, in particular, those with COPD, according to a commentary published in CHEST (2020 May 28. doi: 10.1016/j.chest.2020.05.549) by a group of physicians who study COPD.

Not only is COPD among the most prevalent underlying diseases among hospitalized COVID-19 patients (Clin Microbiol Infect. 2020 Jun 8. doi: 10.1016/j.cmi.2020.05.041), but other unanticipated factors of treatment put these patients at extra risk. Valerie Press, MD, assistant professor of medicine and pediatrics at the University of Chicago, and colleagues aimed to alert physicians to be aware of potential negative effects, or collateral damage, that the pandemic can have on their patients with COPD, even those without a COVID-19 diagnosis.

These concerns include that patients may delay presenting to the ED with acute exacerbations of COPD and once they present they may be at later stages of the exacerbation. Further, evaluation for COVID-19 as a possible trigger of acute exacerbations of COPD (AECOPD) is essential; however, implementing proven AECOPD therapies remains challenging. For instance, routine therapy with corticosteroids for AECOPD may be delayed due to diagnostic uncertainty and hesitation to treat COVID-19 with steroids while COVID-19 testing is pending,” Dr. Press and her colleagues stated.

Shortages and scarcity of medications such as albuterol inhalers to treat COPD have been reported. In addition, patients with COPD are currently less likely to access their health care providers because of fear of COVID-19 infection. This barrier to care and the current higher threshold for presenting to the hospital may to lead to more cases of AECOPD and worsening health in these patients, according to the authors.

Dr. Press said in an interview: “Access to medications delivered through inhalers is challenging even without the pandemic due to high cost of medications. Generic medications are key to improving access for patients with chronic lung disease, so once the generic albuterol becomes available, this should help with access. In the meantime, some companies help provide medications at reduced cost, but usually only on a short time basis. In addition, some pharmacies have lower-cost albuterol inhalers, but these are often not supplied with a full month of dosing.”

In addition to all these concerns is the economic toll this pandemic is taking on patients. The association between COPD and socioeconomic status has been studied in depth (Am J Respir Crit Care Med. 2019; 199[8]:961-69) and would indicate that low-income patients with COPD would face an increased burden during an economic downturn. The authors noted, “Historic rapid job loss and unemployment in the U.S., coupled with a health system of employment-integrated health insurance coverage, makes it more likely that people with COPD will not be able to afford their medication.”

Dr. Press stressed that the COVID pandemic has highlighted critically important disparities in access to health care and disparities in health. “Many of the recommendations regarding stay-at-home and other safety mechanisms to prevent contracting and spreading COVID-19 have not been feasible for all sub-populations in the United States. Those that were essential workers did not have the ability to stay home. Further, those that rely on public transportation had less opportunities to social distance. Finally, while telemedicine opportunities have advanced for clinical care, not all patients have equal access to these capabilities and health disparities could widen in this regard as well. Clinicians have a responsibility to identify social determinants of health that increase risks to our patients’ health and limit their safety.”*

The authors offer some concrete suggestions of how physicians can address some of these concerns, including the following:

• Be alert to potential barriers to accessing medication and be aware of generic albuterol inhaler recently approved by the FDA in response to COVID-19–related shortages.
• Use telemedicine to monitor patients and improvement of home self-management. Clinicians should help patients “seek care with worsening symptoms and have clear management guidelines regarding seeking phone/video visits; implementing therapy with corticosteroids, antibiotics, or inhalers and nebulizers; COVID-19 testing recommendations; and thresholds for seeking emergent, urgent, or outpatient care in person,” Dr. Press added, “Building on the work of nurse advice lines and case management and other support services for high-risk patients with COPD may continue via telehealth and telephone visits.”
• Ensure that untried therapy for COVID-19 “does not displace proven and necessary treatments for patients with COPD, hence placing them at increased risk for poor outcomes.”

Dr. Press is also concerned about the post–COVID-19 period for patients with COPD. “It is too early to know if there are specific after effects of the COVID infection on patients with COPD, but given the damage the virus does to even healthy lungs, there is reason to have concern that COVID could cause worsening damage to the lungs of individuals with COPD.”

She noted, “Post-ICU [PICU] syndrome has been recognized in patients with ARDS generally, and patients who recover from critical illness may have long-lasting (and permanent) effects on strength, cognition, disability, and pulmonary function. Whether the PICU syndrome in patients with ARDS due to COVID-19 specifically is different from the PICU syndrome due to other causes remains unknown. But clinicians whose patients with COPD survive COVID-19 may expect long-lasting effects and slow recovery in cases where COVID-19 led to severe ARDS and a prolonged ICU stay. Assessment of overall patient recovery and functional capacity (beyond lung function and dyspnea symptoms) including deconditioning, anxiety, PTSD, weakness, and malnutrition will need to be addressed. Additionally, clinicians may help patients and their families understand the expected recovery and help facilitate family conversations about residual effects of COVID-19.”

The authors had no disclosures.

SOURCE: Press V et al. Chest. 2020 May 28. doi:10.1016/j.chest.2020.05.549.

CORRECTION: *This story was updated with further comments and clarifications from Dr. Press. 6/23/2020

Headache may be a key symptom of COVID-19 that predicts the disease’s clinical evolution in individual patients, new research suggests. An observational study of more than 100 patients showed that headache onset could occur during the presymptomatic or symptomatic phase of COVID-19 and could resemble tension-type or migraine headache.

Headache itself was associated with a shorter symptomatic period, while headache and anosmia were associated with a shorter hospitalization period. In a subgroup of participants, headache persisted even after the symptoms of COVID-19 had been resolved.

Investigators noted that understanding the pathophysiology of headache in COVID-19 could improve understanding of migraine and other headache disorders. “It seems that those patients who start early on, during the asymptomatic or early symptomatic period of COVID-19, with headache have a more localized inflammatory response that may reflect the ability of the body to better control and respond to the infection by SARS-CoV-2,” lead investigator Patricia Pozo-Rosich, MD, PhD, head of the headache and craniofacial pain unit at Vall d’Hebron University Hospital, Barcelona, said in an interview.

She presented the findings at the virtual annual meeting of the American Headache Society.

Systemic inflammation

Headache is one of the main symptoms of COVID-19. A recent study of 214 patients with COVID-19 showed that approximately 13% of the participants had headache and 5% had anosmia.

SARS-CoV-2 penetrates the cells through the ACE2 receptor, which is present throughout the body. “SARS-CoV-2 enters the body through the nasal cavity and it probably penetrates the nervous system in the periphery through afferent branches of the olfactory and trigeminal nerve,” Dr. Pozo-Rosich said. It travels to the lungs and, later, the bloodstream. This generates systemic inflammation that may turn into a cytokine storm. Evidence has identified cortical hyperintensities and olfactory bulb hyperintensities in patients with COVID-19, suggesting that the virus directly infects the CNS.

Interleukin-6, one of the main inflammatory molecules, has been proven to be related to COVID-19 and has become a therapeutic target. Levels of IL-6 may be lower and tend to be more stable in patients with both COVID-19 and headache than in patients with COVID-19 only.

The researchers observed 130 patients (51% women; mean age, 54 years) with COVID-19 who were attended by neurologists at Vall d’Hebron. In this group, 74.4% had headache. Patients with headache tended to be younger than those without headache (mean age, 50 years vs. 63 years, respectively) and tended to be women (58.6% vs. 29.4%).

Approximately one-third of patients with headache had a history of migraine. Most reported mild to moderate pain that resembled tension-type headache. In participants with severe pain and migraine-like features, headache more often began during the asymptomatic phase of COVID-19.

Disease evolution predictor?

The investigators followed up on 100 of the 130 patients with COVID-19, of whom 74 had headache. About 38% of these patients had ongoing headache after 6 weeks, which suggests that some patients may develop a new daily persistent headache once a 3-month period has elapsed. Half of this group had no previous headache history. Headache had been the prodromal symptom of COVID-19 for 21.4% of these patients.

Results showed that headache predicted the clinical evolution of COVID-19. The symptomatic phase of COVID-19 was 7 days shorter for patients with headache than for those without headache. In addition, the period of hospitalization was 7 days shorter for patients with headache and anosmia, compared with patients who had neither headache nor anosmia.

Most therapies, including ibuprofen, candesartan, and anti–calcitonin gene–related peptide (CGRP) monoclonal antibodies, are safe for treating headache in COVID-19, the investigators noted. “We should just try to initially avoid steroids to avoid interference with the body’s reaction to SARS-CoV-2,” Dr. Pozo-Rosich said.

Researchers at Sidney Kimmel Medical College, Philadelphia, are currently studying intranasal vazegepant, an anti-CGRP therapy, as a way to potentially blunt the severe inflammatory response in the lungs of patients with COVID-19, she noted, adding that this peptide may have a future role not only in headache, but also in COVID-19.

Historical link to viral infections

Commenting on the study, Matthew S. Robbins, MD, associate professor of neurology at Weill Cornell Medicine, New York, said the findings associating headache with a shorter symptomatic phase of COVID-19 were “interesting.”

“Headache is common with mild viral infections. More severe viral infections may simply feature more overwhelming respiratory symptoms and fever that lead to underreporting or underascertainment of headache,” said Dr. Robbins, who was not involved with the research.

He noted that the finding showing an association of headache and COVID-19 with a younger age and in women “may be related to a higher prevalence of migraine biology in such patients, and being triggered by the virus or the psychological stress associated with it.”

Dr. Robbins added that viral illnesses have long been associated with new daily persistent headache, “dating back to the early 1980s,” when it was first described in association with Epstein-Barr virus. These infections have also been implicated in the progression of migraine to chronic migraine in adolescents.

“In my view, treatment should be aimed at the symptomatic headache type for which new daily persistent headache resembles, regardless of the potential inciting factor,” Dr. Robbins said.

Dr. Pozo-Rosich has received consulting fees from Allergan, Amgen, Almirall, Biohaven, Chiesi, Eli Lilly, Medscape, Novartis, and Teva Pharmaceuticals. Dr. Robbins has disclosed no relevant financial relationships.

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

Headache may be a key symptom of COVID-19 that predicts the disease’s clinical evolution in individual patients, new research suggests. An observational study of more than 100 patients showed that headache onset could occur during the presymptomatic or symptomatic phase of COVID-19 and could resemble tension-type or migraine headache.

Headache itself was associated with a shorter symptomatic period, while headache and anosmia were associated with a shorter hospitalization period. In a subgroup of participants, headache persisted even after the symptoms of COVID-19 had been resolved.

Investigators noted that understanding the pathophysiology of headache in COVID-19 could improve understanding of migraine and other headache disorders. “It seems that those patients who start early on, during the asymptomatic or early symptomatic period of COVID-19, with headache have a more localized inflammatory response that may reflect the ability of the body to better control and respond to the infection by SARS-CoV-2,” lead investigator Patricia Pozo-Rosich, MD, PhD, head of the headache and craniofacial pain unit at Vall d’Hebron University Hospital, Barcelona, said in an interview.

She presented the findings at the virtual annual meeting of the American Headache Society.

Systemic inflammation

Headache is one of the main symptoms of COVID-19. A recent study of 214 patients with COVID-19 showed that approximately 13% of the participants had headache and 5% had anosmia.

SARS-CoV-2 penetrates the cells through the ACE2 receptor, which is present throughout the body. “SARS-CoV-2 enters the body through the nasal cavity and it probably penetrates the nervous system in the periphery through afferent branches of the olfactory and trigeminal nerve,” Dr. Pozo-Rosich said. It travels to the lungs and, later, the bloodstream. This generates systemic inflammation that may turn into a cytokine storm. Evidence has identified cortical hyperintensities and olfactory bulb hyperintensities in patients with COVID-19, suggesting that the virus directly infects the CNS.

Interleukin-6, one of the main inflammatory molecules, has been proven to be related to COVID-19 and has become a therapeutic target. Levels of IL-6 may be lower and tend to be more stable in patients with both COVID-19 and headache than in patients with COVID-19 only.

The researchers observed 130 patients (51% women; mean age, 54 years) with COVID-19 who were attended by neurologists at Vall d’Hebron. In this group, 74.4% had headache. Patients with headache tended to be younger than those without headache (mean age, 50 years vs. 63 years, respectively) and tended to be women (58.6% vs. 29.4%).

Approximately one-third of patients with headache had a history of migraine. Most reported mild to moderate pain that resembled tension-type headache. In participants with severe pain and migraine-like features, headache more often began during the asymptomatic phase of COVID-19.

Disease evolution predictor?

The investigators followed up on 100 of the 130 patients with COVID-19, of whom 74 had headache. About 38% of these patients had ongoing headache after 6 weeks, which suggests that some patients may develop a new daily persistent headache once a 3-month period has elapsed. Half of this group had no previous headache history. Headache had been the prodromal symptom of COVID-19 for 21.4% of these patients.

Results showed that headache predicted the clinical evolution of COVID-19. The symptomatic phase of COVID-19 was 7 days shorter for patients with headache than for those without headache. In addition, the period of hospitalization was 7 days shorter for patients with headache and anosmia, compared with patients who had neither headache nor anosmia.

Most therapies, including ibuprofen, candesartan, and anti–calcitonin gene–related peptide (CGRP) monoclonal antibodies, are safe for treating headache in COVID-19, the investigators noted. “We should just try to initially avoid steroids to avoid interference with the body’s reaction to SARS-CoV-2,” Dr. Pozo-Rosich said.

Researchers at Sidney Kimmel Medical College, Philadelphia, are currently studying intranasal vazegepant, an anti-CGRP therapy, as a way to potentially blunt the severe inflammatory response in the lungs of patients with COVID-19, she noted, adding that this peptide may have a future role not only in headache, but also in COVID-19.

Historical link to viral infections

Commenting on the study, Matthew S. Robbins, MD, associate professor of neurology at Weill Cornell Medicine, New York, said the findings associating headache with a shorter symptomatic phase of COVID-19 were “interesting.”

“Headache is common with mild viral infections. More severe viral infections may simply feature more overwhelming respiratory symptoms and fever that lead to underreporting or underascertainment of headache,” said Dr. Robbins, who was not involved with the research.

He noted that the finding showing an association of headache and COVID-19 with a younger age and in women “may be related to a higher prevalence of migraine biology in such patients, and being triggered by the virus or the psychological stress associated with it.”

Dr. Robbins added that viral illnesses have long been associated with new daily persistent headache, “dating back to the early 1980s,” when it was first described in association with Epstein-Barr virus. These infections have also been implicated in the progression of migraine to chronic migraine in adolescents.

“In my view, treatment should be aimed at the symptomatic headache type for which new daily persistent headache resembles, regardless of the potential inciting factor,” Dr. Robbins said.

Dr. Pozo-Rosich has received consulting fees from Allergan, Amgen, Almirall, Biohaven, Chiesi, Eli Lilly, Medscape, Novartis, and Teva Pharmaceuticals. Dr. Robbins has disclosed no relevant financial relationships.

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

Headache may be a key symptom of COVID-19 that predicts the disease’s clinical evolution in individual patients, new research suggests. An observational study of more than 100 patients showed that headache onset could occur during the presymptomatic or symptomatic phase of COVID-19 and could resemble tension-type or migraine headache.

Headache itself was associated with a shorter symptomatic period, while headache and anosmia were associated with a shorter hospitalization period. In a subgroup of participants, headache persisted even after the symptoms of COVID-19 had been resolved.

Investigators noted that understanding the pathophysiology of headache in COVID-19 could improve understanding of migraine and other headache disorders. “It seems that those patients who start early on, during the asymptomatic or early symptomatic period of COVID-19, with headache have a more localized inflammatory response that may reflect the ability of the body to better control and respond to the infection by SARS-CoV-2,” lead investigator Patricia Pozo-Rosich, MD, PhD, head of the headache and craniofacial pain unit at Vall d’Hebron University Hospital, Barcelona, said in an interview.

She presented the findings at the virtual annual meeting of the American Headache Society.

Systemic inflammation

Headache is one of the main symptoms of COVID-19. A recent study of 214 patients with COVID-19 showed that approximately 13% of the participants had headache and 5% had anosmia.

SARS-CoV-2 penetrates the cells through the ACE2 receptor, which is present throughout the body. “SARS-CoV-2 enters the body through the nasal cavity and it probably penetrates the nervous system in the periphery through afferent branches of the olfactory and trigeminal nerve,” Dr. Pozo-Rosich said. It travels to the lungs and, later, the bloodstream. This generates systemic inflammation that may turn into a cytokine storm. Evidence has identified cortical hyperintensities and olfactory bulb hyperintensities in patients with COVID-19, suggesting that the virus directly infects the CNS.

Interleukin-6, one of the main inflammatory molecules, has been proven to be related to COVID-19 and has become a therapeutic target. Levels of IL-6 may be lower and tend to be more stable in patients with both COVID-19 and headache than in patients with COVID-19 only.

The researchers observed 130 patients (51% women; mean age, 54 years) with COVID-19 who were attended by neurologists at Vall d’Hebron. In this group, 74.4% had headache. Patients with headache tended to be younger than those without headache (mean age, 50 years vs. 63 years, respectively) and tended to be women (58.6% vs. 29.4%).

Approximately one-third of patients with headache had a history of migraine. Most reported mild to moderate pain that resembled tension-type headache. In participants with severe pain and migraine-like features, headache more often began during the asymptomatic phase of COVID-19.

Disease evolution predictor?

The investigators followed up on 100 of the 130 patients with COVID-19, of whom 74 had headache. About 38% of these patients had ongoing headache after 6 weeks, which suggests that some patients may develop a new daily persistent headache once a 3-month period has elapsed. Half of this group had no previous headache history. Headache had been the prodromal symptom of COVID-19 for 21.4% of these patients.

Results showed that headache predicted the clinical evolution of COVID-19. The symptomatic phase of COVID-19 was 7 days shorter for patients with headache than for those without headache. In addition, the period of hospitalization was 7 days shorter for patients with headache and anosmia, compared with patients who had neither headache nor anosmia.

Most therapies, including ibuprofen, candesartan, and anti–calcitonin gene–related peptide (CGRP) monoclonal antibodies, are safe for treating headache in COVID-19, the investigators noted. “We should just try to initially avoid steroids to avoid interference with the body’s reaction to SARS-CoV-2,” Dr. Pozo-Rosich said.

Researchers at Sidney Kimmel Medical College, Philadelphia, are currently studying intranasal vazegepant, an anti-CGRP therapy, as a way to potentially blunt the severe inflammatory response in the lungs of patients with COVID-19, she noted, adding that this peptide may have a future role not only in headache, but also in COVID-19.

Historical link to viral infections

Commenting on the study, Matthew S. Robbins, MD, associate professor of neurology at Weill Cornell Medicine, New York, said the findings associating headache with a shorter symptomatic phase of COVID-19 were “interesting.”

“Headache is common with mild viral infections. More severe viral infections may simply feature more overwhelming respiratory symptoms and fever that lead to underreporting or underascertainment of headache,” said Dr. Robbins, who was not involved with the research.

He noted that the finding showing an association of headache and COVID-19 with a younger age and in women “may be related to a higher prevalence of migraine biology in such patients, and being triggered by the virus or the psychological stress associated with it.”

Dr. Robbins added that viral illnesses have long been associated with new daily persistent headache, “dating back to the early 1980s,” when it was first described in association with Epstein-Barr virus. These infections have also been implicated in the progression of migraine to chronic migraine in adolescents.

“In my view, treatment should be aimed at the symptomatic headache type for which new daily persistent headache resembles, regardless of the potential inciting factor,” Dr. Robbins said.

Dr. Pozo-Rosich has received consulting fees from Allergan, Amgen, Almirall, Biohaven, Chiesi, Eli Lilly, Medscape, Novartis, and Teva Pharmaceuticals. Dr. Robbins has disclosed no relevant financial relationships.

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

Here we are, faced with history in real time. A plague upon a plague. A new one and a longstanding one. COVID-19 and racial injustice. Both are plagues upon our medical house, and it’s time for some spring cleaning.

Initially, COVID-19 concerns brought news of an infection coming for anyone and everyone. Like the Black Death, it was supposedly “the great equalizer,” the “Triumph of Death,” regardless of station in life.

Yet, as the COVID-19 story unfurls, it is clear that minorities are disproportionately affected, just as they always seem to be. In Chicago, for example, African Americans make up 70% of the COVID-19 deaths, yet only 29% of the population. Similar results have been found in Milwaukee and Louisiana, and other parts of the country. As an article in the Journal of Law and the Biosciences indicated, “These racial and ethnic disparities in COVID-19 infections and deaths are a result of historical and current practices of racism that cause disparities in exposure, susceptibility and treatment.”

People of color are disproportionately affected, an outcome of racial health disparities. And these disparities are a public health crisis, sitting in the living room of our house. Disparities continue to exist in national infant mortality, maternal health, and deaths from premature heart disease and stroke. They exist in access to care and are playing out in real time during this pandemic.

COVID-19 and racial injustice, in addition to being sociological and economic crises, are both public health crises that are plaguing African American communities. Consider the case of police violence as a public health issue. Black males are three times more likely to be killed by police than are non-Hispanic white males.

This is a dying room in our medical house, with our patient lying alongside a history of medicine littered with racial injustice, telling us, “I can’t breathe.”

As professionals, we must run to that patient. Professionalism bears the pillars of our ethical principles of primacy of patient welfare, patient autonomy, and social justice. We work hard on the first two. Medical errors, quality improvement, communication, patient safety. All important. But we too often dance, or sit silently, about the third.

Here is an excerpt from “Moral choices for today’s physician”, by Donald M. Berwick, MD:

“The work of a physician as healer cannot stop at the door of an office, the threshold of an operating room, or the front gate of a hospital. The rescue of a society and the restoration of a political ethos that remembers to heal have become the physician’s jobs, too. Professional silence in the face of social injustice is wrong.”

It is chilling to see the great institutions of health care, hospitals, physician groups, and scientific bodies assume that the seat of bystander is available. That seat is gone. To try to avoid the political fray through silence is impossible because silence is now political. Either engage or assist the harm. There is no third choice.

Dr. Berwick echoed the words of Rev. Dr. Martin Luther King Jr., from 1959, in Birmingham, Ala.:

“If you fail to act now, history will have to record that the greatest tragedy of this period of social transition was not the strident clamor of the bad people, but the appalling silence of the good people.”

I have this space to write and speak up, and I urge many of you to do the same. Write to your local newspaper. Share your stories. Listen to others. Engage with your society. Create the space in your practice, your group, your hospital, your department for listening, learning, relearning, educating, and acting.

It’s not easy speaking up and speaking out. Yet, this is our foundation, our call, our professional obligation. We must remember George Floyd, Breonna Taylor, Sandra Bland, Eric Garner, Tamir Rice, Trayvon Martin, and too many others. To recognize the humanity behind the injustices, and to call out their names.

This is lesson 101 on the wards. It’s not the heart failure in bed 1 or the sepsis in bed 2, but the mother, brother, father, and sister who seek out just care. Humanity reaching out their hand, and we must grab it.

I came to medicine for the compassion, for the love, for the comforting hand offered to our patients. That compassion, by definition, requires action.

In his book “Altruism: The Power of Compassion to Change Yourself and the World,” Matthieu Ricard wrote “If compassion without wisdom is blind, compassion without action is hypocritical.”

Silence is inaction. Let’s act.

Dr. Messler is the executive director, quality initiatives, at Glytec and works as a hospitalist at Morton Plant Hospitalist group in Clearwater, Fla. This essay appeared first at SHM’s official blog The Hospital Leader.

Here we are, faced with history in real time. A plague upon a plague. A new one and a longstanding one. COVID-19 and racial injustice. Both are plagues upon our medical house, and it’s time for some spring cleaning.

Initially, COVID-19 concerns brought news of an infection coming for anyone and everyone. Like the Black Death, it was supposedly “the great equalizer,” the “Triumph of Death,” regardless of station in life.

Yet, as the COVID-19 story unfurls, it is clear that minorities are disproportionately affected, just as they always seem to be. In Chicago, for example, African Americans make up 70% of the COVID-19 deaths, yet only 29% of the population. Similar results have been found in Milwaukee and Louisiana, and other parts of the country. As an article in the Journal of Law and the Biosciences indicated, “These racial and ethnic disparities in COVID-19 infections and deaths are a result of historical and current practices of racism that cause disparities in exposure, susceptibility and treatment.”

People of color are disproportionately affected, an outcome of racial health disparities. And these disparities are a public health crisis, sitting in the living room of our house. Disparities continue to exist in national infant mortality, maternal health, and deaths from premature heart disease and stroke. They exist in access to care and are playing out in real time during this pandemic.

COVID-19 and racial injustice, in addition to being sociological and economic crises, are both public health crises that are plaguing African American communities. Consider the case of police violence as a public health issue. Black males are three times more likely to be killed by police than are non-Hispanic white males.

This is a dying room in our medical house, with our patient lying alongside a history of medicine littered with racial injustice, telling us, “I can’t breathe.”

As professionals, we must run to that patient. Professionalism bears the pillars of our ethical principles of primacy of patient welfare, patient autonomy, and social justice. We work hard on the first two. Medical errors, quality improvement, communication, patient safety. All important. But we too often dance, or sit silently, about the third.

Here is an excerpt from “Moral choices for today’s physician”, by Donald M. Berwick, MD:

“The work of a physician as healer cannot stop at the door of an office, the threshold of an operating room, or the front gate of a hospital. The rescue of a society and the restoration of a political ethos that remembers to heal have become the physician’s jobs, too. Professional silence in the face of social injustice is wrong.”

It is chilling to see the great institutions of health care, hospitals, physician groups, and scientific bodies assume that the seat of bystander is available. That seat is gone. To try to avoid the political fray through silence is impossible because silence is now political. Either engage or assist the harm. There is no third choice.

Dr. Berwick echoed the words of Rev. Dr. Martin Luther King Jr., from 1959, in Birmingham, Ala.:

“If you fail to act now, history will have to record that the greatest tragedy of this period of social transition was not the strident clamor of the bad people, but the appalling silence of the good people.”

I have this space to write and speak up, and I urge many of you to do the same. Write to your local newspaper. Share your stories. Listen to others. Engage with your society. Create the space in your practice, your group, your hospital, your department for listening, learning, relearning, educating, and acting.

It’s not easy speaking up and speaking out. Yet, this is our foundation, our call, our professional obligation. We must remember George Floyd, Breonna Taylor, Sandra Bland, Eric Garner, Tamir Rice, Trayvon Martin, and too many others. To recognize the humanity behind the injustices, and to call out their names.

This is lesson 101 on the wards. It’s not the heart failure in bed 1 or the sepsis in bed 2, but the mother, brother, father, and sister who seek out just care. Humanity reaching out their hand, and we must grab it.

I came to medicine for the compassion, for the love, for the comforting hand offered to our patients. That compassion, by definition, requires action.

In his book “Altruism: The Power of Compassion to Change Yourself and the World,” Matthieu Ricard wrote “If compassion without wisdom is blind, compassion without action is hypocritical.”

Silence is inaction. Let’s act.

Dr. Messler is the executive director, quality initiatives, at Glytec and works as a hospitalist at Morton Plant Hospitalist group in Clearwater, Fla. This essay appeared first at SHM’s official blog The Hospital Leader.

Here we are, faced with history in real time. A plague upon a plague. A new one and a longstanding one. COVID-19 and racial injustice. Both are plagues upon our medical house, and it’s time for some spring cleaning.

Initially, COVID-19 concerns brought news of an infection coming for anyone and everyone. Like the Black Death, it was supposedly “the great equalizer,” the “Triumph of Death,” regardless of station in life.

Yet, as the COVID-19 story unfurls, it is clear that minorities are disproportionately affected, just as they always seem to be. In Chicago, for example, African Americans make up 70% of the COVID-19 deaths, yet only 29% of the population. Similar results have been found in Milwaukee and Louisiana, and other parts of the country. As an article in the Journal of Law and the Biosciences indicated, “These racial and ethnic disparities in COVID-19 infections and deaths are a result of historical and current practices of racism that cause disparities in exposure, susceptibility and treatment.”

People of color are disproportionately affected, an outcome of racial health disparities. And these disparities are a public health crisis, sitting in the living room of our house. Disparities continue to exist in national infant mortality, maternal health, and deaths from premature heart disease and stroke. They exist in access to care and are playing out in real time during this pandemic.

COVID-19 and racial injustice, in addition to being sociological and economic crises, are both public health crises that are plaguing African American communities. Consider the case of police violence as a public health issue. Black males are three times more likely to be killed by police than are non-Hispanic white males.

This is a dying room in our medical house, with our patient lying alongside a history of medicine littered with racial injustice, telling us, “I can’t breathe.”

As professionals, we must run to that patient. Professionalism bears the pillars of our ethical principles of primacy of patient welfare, patient autonomy, and social justice. We work hard on the first two. Medical errors, quality improvement, communication, patient safety. All important. But we too often dance, or sit silently, about the third.

Here is an excerpt from “Moral choices for today’s physician”, by Donald M. Berwick, MD:

“The work of a physician as healer cannot stop at the door of an office, the threshold of an operating room, or the front gate of a hospital. The rescue of a society and the restoration of a political ethos that remembers to heal have become the physician’s jobs, too. Professional silence in the face of social injustice is wrong.”

It is chilling to see the great institutions of health care, hospitals, physician groups, and scientific bodies assume that the seat of bystander is available. That seat is gone. To try to avoid the political fray through silence is impossible because silence is now political. Either engage or assist the harm. There is no third choice.

Dr. Berwick echoed the words of Rev. Dr. Martin Luther King Jr., from 1959, in Birmingham, Ala.:

“If you fail to act now, history will have to record that the greatest tragedy of this period of social transition was not the strident clamor of the bad people, but the appalling silence of the good people.”

I have this space to write and speak up, and I urge many of you to do the same. Write to your local newspaper. Share your stories. Listen to others. Engage with your society. Create the space in your practice, your group, your hospital, your department for listening, learning, relearning, educating, and acting.

It’s not easy speaking up and speaking out. Yet, this is our foundation, our call, our professional obligation. We must remember George Floyd, Breonna Taylor, Sandra Bland, Eric Garner, Tamir Rice, Trayvon Martin, and too many others. To recognize the humanity behind the injustices, and to call out their names.

This is lesson 101 on the wards. It’s not the heart failure in bed 1 or the sepsis in bed 2, but the mother, brother, father, and sister who seek out just care. Humanity reaching out their hand, and we must grab it.

I came to medicine for the compassion, for the love, for the comforting hand offered to our patients. That compassion, by definition, requires action.

In his book “Altruism: The Power of Compassion to Change Yourself and the World,” Matthieu Ricard wrote “If compassion without wisdom is blind, compassion without action is hypocritical.”

Silence is inaction. Let’s act.

Dr. Messler is the executive director, quality initiatives, at Glytec and works as a hospitalist at Morton Plant Hospitalist group in Clearwater, Fla. This essay appeared first at SHM’s official blog The Hospital Leader.

Presented during the ASCO 2020 plenary session, the results of the phase 3 ADAURA trial will prove practice-changing, according to Dr. Mark Kris of Memorial Sloan Kettering Cancer Center. Over 600 patients whose resected tumors were found to have EGFR mutations were treated with osimertinib. The results more than doubled disease-free survival rates, from 44% to 90% at 2 years.

Among other adjuvant trials, the phase 2 VISION study looked at tepotinib, a once-daily, highly selective oral MET inhibitor. The study showed durable responses coupled with acceptable side effects. The drug has been given fast-track status by the US Food and Drug Administration.

Dr. Kris notes that the DESTINY study introduces trastuzumab deruxtecan, an antibody-drug conjugate, as a promising new class of drugs for lung cancer patients. Interim results presented at ASCO further support the HER2 mutation as another potential target for patients with lung cancer.

Finally, the phase 2 CITYSCAPE study provides preliminary evidence for a new checkpoint inhibitor. The monoclonal antibody tiragolumab was developed to block TIGIT. The study showed that the combination of tiragolumab and atezolizumab can improve both rates of response and time to disease recurrence — results Dr. Kris considers encouraging for patients with advanced lung cancer.

Mark G. Kris, MD

Mark G. Kris, MD, Professor, Department of Medicine, Weill Cornell Medical College; Attending Physician, Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, NY.

Presented during the ASCO 2020 plenary session, the results of the phase 3 ADAURA trial will prove practice-changing, according to Dr. Mark Kris of Memorial Sloan Kettering Cancer Center. Over 600 patients whose resected tumors were found to have EGFR mutations were treated with osimertinib. The results more than doubled disease-free survival rates, from 44% to 90% at 2 years.

Among other adjuvant trials, the phase 2 VISION study looked at tepotinib, a once-daily, highly selective oral MET inhibitor. The study showed durable responses coupled with acceptable side effects. The drug has been given fast-track status by the US Food and Drug Administration.

Dr. Kris notes that the DESTINY study introduces trastuzumab deruxtecan, an antibody-drug conjugate, as a promising new class of drugs for lung cancer patients. Interim results presented at ASCO further support the HER2 mutation as another potential target for patients with lung cancer.

Finally, the phase 2 CITYSCAPE study provides preliminary evidence for a new checkpoint inhibitor. The monoclonal antibody tiragolumab was developed to block TIGIT. The study showed that the combination of tiragolumab and atezolizumab can improve both rates of response and time to disease recurrence — results Dr. Kris considers encouraging for patients with advanced lung cancer.

Mark G. Kris, MD

Mark G. Kris, MD, Professor, Department of Medicine, Weill Cornell Medical College; Attending Physician, Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, NY.

Presented during the ASCO 2020 plenary session, the results of the phase 3 ADAURA trial will prove practice-changing, according to Dr. Mark Kris of Memorial Sloan Kettering Cancer Center. Over 600 patients whose resected tumors were found to have EGFR mutations were treated with osimertinib. The results more than doubled disease-free survival rates, from 44% to 90% at 2 years.

Among other adjuvant trials, the phase 2 VISION study looked at tepotinib, a once-daily, highly selective oral MET inhibitor. The study showed durable responses coupled with acceptable side effects. The drug has been given fast-track status by the US Food and Drug Administration.

Dr. Kris notes that the DESTINY study introduces trastuzumab deruxtecan, an antibody-drug conjugate, as a promising new class of drugs for lung cancer patients. Interim results presented at ASCO further support the HER2 mutation as another potential target for patients with lung cancer.

Finally, the phase 2 CITYSCAPE study provides preliminary evidence for a new checkpoint inhibitor. The monoclonal antibody tiragolumab was developed to block TIGIT. The study showed that the combination of tiragolumab and atezolizumab can improve both rates of response and time to disease recurrence — results Dr. Kris considers encouraging for patients with advanced lung cancer.

Mark G. Kris, MD

Mark G. Kris, MD, Professor, Department of Medicine, Weill Cornell Medical College; Attending Physician, Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, NY.

In an analysis of four phase 3 trials, the oral lipid-lowering drug bempedoic acid (Nexletol; Esperion) did not worsen glycemic control or increase the incidence of type 2 diabetes.

As previously reported, this first-in-class drug, which acts by inhibiting ATP-citrate lyase, was approved by the Food and Drug Administration in February 2020.

Lawrence A. Leiter MD, from the University of Toronto, delivered the findings of this latest analysis in an oral presentation at the virtual American Diabetes Association 80th Scientific Sessions.

“The current study is important as it shows overall consistent efficacy and safety regardless of glycemic status and no increase in new-onset diabetes,” Dr. Leiter said in an interview.

There is interest in how lipid-lowering drugs might affect glycemia because “meta-analyses have shown about a 10% increased risk of new-onset diabetes in statin users, although the absolute increased risk is 1 extra case per 255 treated patients [in whom one would expect 5.4 cardiovascular events to be prevented by the statin],” he noted.

In a comment, John R. Guyton, MD, from Duke University Medical Center, Durham, N.C., agreed that the new study demonstrates that “patients with diabetes and prediabetes respond to bempedoic acid with LDL cholesterol lowering that is similar to that in patients with normal glucose tolerance.”

Although “statins have a slight effect of worsening glucose tolerance and a modest effect of increasing cases of new-onset diabetes,” the current research shows that “bempedoic acid appears to be free of these effects,” said Dr. Guyton, who discussed this drug in another symposium at the meeting where he also discussed how the agent will “fit” into prescribing patterns.
 

How do patients with diabetes, prediabetes fare?

“Current guidelines support aggressive LDL cholesterol lowering in patients with diabetes, given the increased risk of cardiovascular morbidity and mortality,” said Dr. Leiter.

Bempedoic acid was approved as an adjunct to diet and maximally tolerated statin therapy to treat adults with atherosclerotic cardiovascular disease (ASCVD) and/or heterozygous familial hypercholesterolemia (HeFH) who require additional lowering of LDL cholesterol, although its effect on cardiovascular morbidity and mortality has not been determined, the prescribing information states.

However, it has been unknown how bempedoic acid affects LDL cholesterol or hemoglobin A1c levels in patients with diabetes, prediabetes, or normoglycemia.

To examine this, the researchers pooled data from four phase 3 trials in 3623 patients with ASCVD or HeFH who had been randomized 2:1 to bempedoic acid 180 mg/day or placebo for 12 or 24 weeks (if they were statin intolerant) or 52 weeks (if they were also on statins).

In the pooled sample, about half the patients had prediabetes (52%), and the rest had diabetes (31%) or normoglycemia (17%). Overall, 75%-84% of patients had a history of ASCVD.

Mean LDL cholesterol levels were higher in patients with normoglycemia (119 mg/dL) or prediabetes (115 mg/dL) than in patients with diabetes (110 mg/dL).

The primary outcome was percent change in LDL cholesterol from baseline to week 12.

In the two types of patients (all with ASCVD or HeFH) – those on statins and those with statin intolerance – LDL cholesterol at 12 weeks was significantly lower in patients who received bempedoic acid, compared with placebo, regardless of whether they had no diabetes, prediabetes, or diabetes (all P < .001).

Similarly, patients who received bempedoic acid also had significant reductions in total cholesterol, non–HDL cholesterol, apolipoprotein B, and high-sensitivity C-reactive protein (hsCRP) at 12 weeks, compared with patients who received placebo (all P < .01).

The safety profile of bempedoic acid was similar to placebo and did not vary by glycemic status.

“Of course, with any lipid-lowering therapy, there’s lots of interest in changes in glycemic parameters,” said Dr. Leiter. “A1c did not increase. In fact, it was significantly lower in patients with prediabetes and diabetes on bempedoic acid versus placebo.”

In addition, “statin trials have shown small increases in body weight. We did not observe this,” he reported.
 

Where does bempedoic acid ‘fit?’

“Bempedoic acid will be a useful add-on to any patient who requires additional LDL cholesterol lowering,” according to Dr. Leiter. “It will typically be used as an add-on to statins, but will also be very useful in the statin-intolerant patient, especially when used in combination with ezetimib.”

The fixed-dose combination of bempedoic acid plus ezetimibe (Nexlizet; Esperion), was also approved in the United States in February, just days after bempedoic acid as a solo agent was cleared for marketing.

“Bempedoic acid would not be chosen in preference to a statin, ezetimibe, or PCSK9 inhibitor,” Dr. Guyton said. Rather, “its chief use will be in patients with statin intolerance and either FH or ASCVD when LDL-cholesterol is poorly controlled despite maximum tolerated lipid-lowering therapy.”

According to Dr. Guyton, “use of bempedoic acid should be undertaken only when provider-patient discussion acknowledges that it has not been shown to reduce cardiovascular events, although preliminary evidence from genetic analysis [Mendelian randomization study] suggests that it will,” as previously reported.

The CLEAR Outcomes cardiovascular outcomes trial of bempedoic acid completed enrollment in August 2019, involving 14,032 patients with hypercholesterolemia and high CVD risk according to a company statement.

The study was funded by Esperion. Dr. Leiter has reported being on advisory panels for Abbott, Amgen, AstraZeneca, Boehringer Ingelheim, Eli Lilly, HLS Therapeutics, Janssen, Merck, Novo Nordisk, Sanofi, and Servier, receiving research support from Amgen, AstraZeneca, Kowa Pharmaceuticals, and the Medicines Company, and being on speakers bureaus for Amgen, AstraZeneca, Boehringer Ingelheim, Eli Lilly, HLS Therapeutics, Janssen, Medscape, Merck, Novo Nordisk, Sanofi, and Servier. Disclosures for the other authors are listed with the abstract. Dr. Guyton has reported being a consultant for Amarin and receiving research support form Regeneron.

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

In an analysis of four phase 3 trials, the oral lipid-lowering drug bempedoic acid (Nexletol; Esperion) did not worsen glycemic control or increase the incidence of type 2 diabetes.

As previously reported, this first-in-class drug, which acts by inhibiting ATP-citrate lyase, was approved by the Food and Drug Administration in February 2020.

Lawrence A. Leiter MD, from the University of Toronto, delivered the findings of this latest analysis in an oral presentation at the virtual American Diabetes Association 80th Scientific Sessions.

“The current study is important as it shows overall consistent efficacy and safety regardless of glycemic status and no increase in new-onset diabetes,” Dr. Leiter said in an interview.

There is interest in how lipid-lowering drugs might affect glycemia because “meta-analyses have shown about a 10% increased risk of new-onset diabetes in statin users, although the absolute increased risk is 1 extra case per 255 treated patients [in whom one would expect 5.4 cardiovascular events to be prevented by the statin],” he noted.

In a comment, John R. Guyton, MD, from Duke University Medical Center, Durham, N.C., agreed that the new study demonstrates that “patients with diabetes and prediabetes respond to bempedoic acid with LDL cholesterol lowering that is similar to that in patients with normal glucose tolerance.”

Although “statins have a slight effect of worsening glucose tolerance and a modest effect of increasing cases of new-onset diabetes,” the current research shows that “bempedoic acid appears to be free of these effects,” said Dr. Guyton, who discussed this drug in another symposium at the meeting where he also discussed how the agent will “fit” into prescribing patterns.
 

How do patients with diabetes, prediabetes fare?

“Current guidelines support aggressive LDL cholesterol lowering in patients with diabetes, given the increased risk of cardiovascular morbidity and mortality,” said Dr. Leiter.

Bempedoic acid was approved as an adjunct to diet and maximally tolerated statin therapy to treat adults with atherosclerotic cardiovascular disease (ASCVD) and/or heterozygous familial hypercholesterolemia (HeFH) who require additional lowering of LDL cholesterol, although its effect on cardiovascular morbidity and mortality has not been determined, the prescribing information states.

However, it has been unknown how bempedoic acid affects LDL cholesterol or hemoglobin A1c levels in patients with diabetes, prediabetes, or normoglycemia.

To examine this, the researchers pooled data from four phase 3 trials in 3623 patients with ASCVD or HeFH who had been randomized 2:1 to bempedoic acid 180 mg/day or placebo for 12 or 24 weeks (if they were statin intolerant) or 52 weeks (if they were also on statins).

In the pooled sample, about half the patients had prediabetes (52%), and the rest had diabetes (31%) or normoglycemia (17%). Overall, 75%-84% of patients had a history of ASCVD.

Mean LDL cholesterol levels were higher in patients with normoglycemia (119 mg/dL) or prediabetes (115 mg/dL) than in patients with diabetes (110 mg/dL).

The primary outcome was percent change in LDL cholesterol from baseline to week 12.

In the two types of patients (all with ASCVD or HeFH) – those on statins and those with statin intolerance – LDL cholesterol at 12 weeks was significantly lower in patients who received bempedoic acid, compared with placebo, regardless of whether they had no diabetes, prediabetes, or diabetes (all P < .001).

Similarly, patients who received bempedoic acid also had significant reductions in total cholesterol, non–HDL cholesterol, apolipoprotein B, and high-sensitivity C-reactive protein (hsCRP) at 12 weeks, compared with patients who received placebo (all P < .01).

The safety profile of bempedoic acid was similar to placebo and did not vary by glycemic status.

“Of course, with any lipid-lowering therapy, there’s lots of interest in changes in glycemic parameters,” said Dr. Leiter. “A1c did not increase. In fact, it was significantly lower in patients with prediabetes and diabetes on bempedoic acid versus placebo.”

In addition, “statin trials have shown small increases in body weight. We did not observe this,” he reported.
 

Where does bempedoic acid ‘fit?’

“Bempedoic acid will be a useful add-on to any patient who requires additional LDL cholesterol lowering,” according to Dr. Leiter. “It will typically be used as an add-on to statins, but will also be very useful in the statin-intolerant patient, especially when used in combination with ezetimib.”

The fixed-dose combination of bempedoic acid plus ezetimibe (Nexlizet; Esperion), was also approved in the United States in February, just days after bempedoic acid as a solo agent was cleared for marketing.

“Bempedoic acid would not be chosen in preference to a statin, ezetimibe, or PCSK9 inhibitor,” Dr. Guyton said. Rather, “its chief use will be in patients with statin intolerance and either FH or ASCVD when LDL-cholesterol is poorly controlled despite maximum tolerated lipid-lowering therapy.”

According to Dr. Guyton, “use of bempedoic acid should be undertaken only when provider-patient discussion acknowledges that it has not been shown to reduce cardiovascular events, although preliminary evidence from genetic analysis [Mendelian randomization study] suggests that it will,” as previously reported.

The CLEAR Outcomes cardiovascular outcomes trial of bempedoic acid completed enrollment in August 2019, involving 14,032 patients with hypercholesterolemia and high CVD risk according to a company statement.

The study was funded by Esperion. Dr. Leiter has reported being on advisory panels for Abbott, Amgen, AstraZeneca, Boehringer Ingelheim, Eli Lilly, HLS Therapeutics, Janssen, Merck, Novo Nordisk, Sanofi, and Servier, receiving research support from Amgen, AstraZeneca, Kowa Pharmaceuticals, and the Medicines Company, and being on speakers bureaus for Amgen, AstraZeneca, Boehringer Ingelheim, Eli Lilly, HLS Therapeutics, Janssen, Medscape, Merck, Novo Nordisk, Sanofi, and Servier. Disclosures for the other authors are listed with the abstract. Dr. Guyton has reported being a consultant for Amarin and receiving research support form Regeneron.

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

In an analysis of four phase 3 trials, the oral lipid-lowering drug bempedoic acid (Nexletol; Esperion) did not worsen glycemic control or increase the incidence of type 2 diabetes.

As previously reported, this first-in-class drug, which acts by inhibiting ATP-citrate lyase, was approved by the Food and Drug Administration in February 2020.

Lawrence A. Leiter MD, from the University of Toronto, delivered the findings of this latest analysis in an oral presentation at the virtual American Diabetes Association 80th Scientific Sessions.

“The current study is important as it shows overall consistent efficacy and safety regardless of glycemic status and no increase in new-onset diabetes,” Dr. Leiter said in an interview.

There is interest in how lipid-lowering drugs might affect glycemia because “meta-analyses have shown about a 10% increased risk of new-onset diabetes in statin users, although the absolute increased risk is 1 extra case per 255 treated patients [in whom one would expect 5.4 cardiovascular events to be prevented by the statin],” he noted.

In a comment, John R. Guyton, MD, from Duke University Medical Center, Durham, N.C., agreed that the new study demonstrates that “patients with diabetes and prediabetes respond to bempedoic acid with LDL cholesterol lowering that is similar to that in patients with normal glucose tolerance.”

Although “statins have a slight effect of worsening glucose tolerance and a modest effect of increasing cases of new-onset diabetes,” the current research shows that “bempedoic acid appears to be free of these effects,” said Dr. Guyton, who discussed this drug in another symposium at the meeting where he also discussed how the agent will “fit” into prescribing patterns.
 

How do patients with diabetes, prediabetes fare?

“Current guidelines support aggressive LDL cholesterol lowering in patients with diabetes, given the increased risk of cardiovascular morbidity and mortality,” said Dr. Leiter.

Bempedoic acid was approved as an adjunct to diet and maximally tolerated statin therapy to treat adults with atherosclerotic cardiovascular disease (ASCVD) and/or heterozygous familial hypercholesterolemia (HeFH) who require additional lowering of LDL cholesterol, although its effect on cardiovascular morbidity and mortality has not been determined, the prescribing information states.

However, it has been unknown how bempedoic acid affects LDL cholesterol or hemoglobin A1c levels in patients with diabetes, prediabetes, or normoglycemia.

To examine this, the researchers pooled data from four phase 3 trials in 3623 patients with ASCVD or HeFH who had been randomized 2:1 to bempedoic acid 180 mg/day or placebo for 12 or 24 weeks (if they were statin intolerant) or 52 weeks (if they were also on statins).

In the pooled sample, about half the patients had prediabetes (52%), and the rest had diabetes (31%) or normoglycemia (17%). Overall, 75%-84% of patients had a history of ASCVD.

Mean LDL cholesterol levels were higher in patients with normoglycemia (119 mg/dL) or prediabetes (115 mg/dL) than in patients with diabetes (110 mg/dL).

The primary outcome was percent change in LDL cholesterol from baseline to week 12.

In the two types of patients (all with ASCVD or HeFH) – those on statins and those with statin intolerance – LDL cholesterol at 12 weeks was significantly lower in patients who received bempedoic acid, compared with placebo, regardless of whether they had no diabetes, prediabetes, or diabetes (all P < .001).

Similarly, patients who received bempedoic acid also had significant reductions in total cholesterol, non–HDL cholesterol, apolipoprotein B, and high-sensitivity C-reactive protein (hsCRP) at 12 weeks, compared with patients who received placebo (all P < .01).

The safety profile of bempedoic acid was similar to placebo and did not vary by glycemic status.

“Of course, with any lipid-lowering therapy, there’s lots of interest in changes in glycemic parameters,” said Dr. Leiter. “A1c did not increase. In fact, it was significantly lower in patients with prediabetes and diabetes on bempedoic acid versus placebo.”

In addition, “statin trials have shown small increases in body weight. We did not observe this,” he reported.
 

Where does bempedoic acid ‘fit?’

“Bempedoic acid will be a useful add-on to any patient who requires additional LDL cholesterol lowering,” according to Dr. Leiter. “It will typically be used as an add-on to statins, but will also be very useful in the statin-intolerant patient, especially when used in combination with ezetimib.”

The fixed-dose combination of bempedoic acid plus ezetimibe (Nexlizet; Esperion), was also approved in the United States in February, just days after bempedoic acid as a solo agent was cleared for marketing.

“Bempedoic acid would not be chosen in preference to a statin, ezetimibe, or PCSK9 inhibitor,” Dr. Guyton said. Rather, “its chief use will be in patients with statin intolerance and either FH or ASCVD when LDL-cholesterol is poorly controlled despite maximum tolerated lipid-lowering therapy.”

According to Dr. Guyton, “use of bempedoic acid should be undertaken only when provider-patient discussion acknowledges that it has not been shown to reduce cardiovascular events, although preliminary evidence from genetic analysis [Mendelian randomization study] suggests that it will,” as previously reported.

The CLEAR Outcomes cardiovascular outcomes trial of bempedoic acid completed enrollment in August 2019, involving 14,032 patients with hypercholesterolemia and high CVD risk according to a company statement.

The study was funded by Esperion. Dr. Leiter has reported being on advisory panels for Abbott, Amgen, AstraZeneca, Boehringer Ingelheim, Eli Lilly, HLS Therapeutics, Janssen, Merck, Novo Nordisk, Sanofi, and Servier, receiving research support from Amgen, AstraZeneca, Kowa Pharmaceuticals, and the Medicines Company, and being on speakers bureaus for Amgen, AstraZeneca, Boehringer Ingelheim, Eli Lilly, HLS Therapeutics, Janssen, Medscape, Merck, Novo Nordisk, Sanofi, and Servier. Disclosures for the other authors are listed with the abstract. Dr. Guyton has reported being a consultant for Amarin and receiving research support form Regeneron.

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

The US Food and Drug Administration has approved rapid-acting insulin lispro-aabc injection 100 and 200 units/mL (Lyumjev, Eli Lilly) for the treatment of adults with type 1 and type 2 diabetes.

The product is a novel formulation of insulin lispro developed to speed absorption of insulin into the bloodstream. It will be available in two strengths: U-100 (100 units/mL) and U-200 (200 units/mL). The Lyumjev U-200 prefilled pen contains twice as much insulin per 1 mL as standard (U-100) insulin.

Approval was based on data from two phase 3 randomized, active-controlled, treat-to-target studies comparing lispro-aabc with insulin lispro injection 100 units/mL (Humalog, Lilly) in people with type 1 diabetes (PRONTO-T1D) and type 2 diabetes (PRONTO-T2D).

In both studies, noninferiority in A1c reduction was demonstrated when the two insulins were dosed at mealtime, but lispro-aabc showed superior blood glucose reduction at 1-hour and 2-hours post-meal compared with lispro.

Lyumjev is approved only in the United States for use as part of a multiple daily injection regimen, not for use in insulin pumps. Lilly intends to submit for this latter indication later in 2020.

Lyumjev will compete with Novo Nordisk’s fast-acting insulin aspart injection 100 units/mL (Fiasp).

Fiasp had a big head start: It was approved for use in adults in the United States in September 2017, for use in insulin pumps in October 2019, and for use in children with diabetes in January 2020.

However, in a poster presented at the American Diabetes Association 79th Scientific Sessions in 2019, lispro-aabb demonstrated faster insulin absorption than lispro, insulin aspart (Novolog/Novorapid, Novo Nordisk), or Fiasp.

Early half-maximal drug concentration was reached at 13 minutes with lispro-aabb, compared with 19 minutes with faster aspart and 25-27 minutes with the two conventional insulins (P < .05 for lispro-aabb vs other insulins).  

Insulin lispro-aabc was approved in the European Union and Japan in March 2020.

Lilly is currently working to make Lyumjev available to adults with diabetes in the United States as quickly as possible and says it will be included in the Lilly Insulin Value Program, allowing anyone with commercial insurance and those without insurance to fill their monthly prescription of Lyumjev for $35.

The list price of Lyumjev will be the same as the list price for Humalog, it adds.
 

This article first appeared on Medscape.com.

The US Food and Drug Administration has approved rapid-acting insulin lispro-aabc injection 100 and 200 units/mL (Lyumjev, Eli Lilly) for the treatment of adults with type 1 and type 2 diabetes.

The product is a novel formulation of insulin lispro developed to speed absorption of insulin into the bloodstream. It will be available in two strengths: U-100 (100 units/mL) and U-200 (200 units/mL). The Lyumjev U-200 prefilled pen contains twice as much insulin per 1 mL as standard (U-100) insulin.

Approval was based on data from two phase 3 randomized, active-controlled, treat-to-target studies comparing lispro-aabc with insulin lispro injection 100 units/mL (Humalog, Lilly) in people with type 1 diabetes (PRONTO-T1D) and type 2 diabetes (PRONTO-T2D).

In both studies, noninferiority in A1c reduction was demonstrated when the two insulins were dosed at mealtime, but lispro-aabc showed superior blood glucose reduction at 1-hour and 2-hours post-meal compared with lispro.

Lyumjev is approved only in the United States for use as part of a multiple daily injection regimen, not for use in insulin pumps. Lilly intends to submit for this latter indication later in 2020.

Lyumjev will compete with Novo Nordisk’s fast-acting insulin aspart injection 100 units/mL (Fiasp).

Fiasp had a big head start: It was approved for use in adults in the United States in September 2017, for use in insulin pumps in October 2019, and for use in children with diabetes in January 2020.

However, in a poster presented at the American Diabetes Association 79th Scientific Sessions in 2019, lispro-aabb demonstrated faster insulin absorption than lispro, insulin aspart (Novolog/Novorapid, Novo Nordisk), or Fiasp.

Early half-maximal drug concentration was reached at 13 minutes with lispro-aabb, compared with 19 minutes with faster aspart and 25-27 minutes with the two conventional insulins (P < .05 for lispro-aabb vs other insulins).  

Insulin lispro-aabc was approved in the European Union and Japan in March 2020.

Lilly is currently working to make Lyumjev available to adults with diabetes in the United States as quickly as possible and says it will be included in the Lilly Insulin Value Program, allowing anyone with commercial insurance and those without insurance to fill their monthly prescription of Lyumjev for $35.

The list price of Lyumjev will be the same as the list price for Humalog, it adds.
 

This article first appeared on Medscape.com.

The US Food and Drug Administration has approved rapid-acting insulin lispro-aabc injection 100 and 200 units/mL (Lyumjev, Eli Lilly) for the treatment of adults with type 1 and type 2 diabetes.

The product is a novel formulation of insulin lispro developed to speed absorption of insulin into the bloodstream. It will be available in two strengths: U-100 (100 units/mL) and U-200 (200 units/mL). The Lyumjev U-200 prefilled pen contains twice as much insulin per 1 mL as standard (U-100) insulin.

Approval was based on data from two phase 3 randomized, active-controlled, treat-to-target studies comparing lispro-aabc with insulin lispro injection 100 units/mL (Humalog, Lilly) in people with type 1 diabetes (PRONTO-T1D) and type 2 diabetes (PRONTO-T2D).

In both studies, noninferiority in A1c reduction was demonstrated when the two insulins were dosed at mealtime, but lispro-aabc showed superior blood glucose reduction at 1-hour and 2-hours post-meal compared with lispro.

Lyumjev is approved only in the United States for use as part of a multiple daily injection regimen, not for use in insulin pumps. Lilly intends to submit for this latter indication later in 2020.

Lyumjev will compete with Novo Nordisk’s fast-acting insulin aspart injection 100 units/mL (Fiasp).

Fiasp had a big head start: It was approved for use in adults in the United States in September 2017, for use in insulin pumps in October 2019, and for use in children with diabetes in January 2020.

However, in a poster presented at the American Diabetes Association 79th Scientific Sessions in 2019, lispro-aabb demonstrated faster insulin absorption than lispro, insulin aspart (Novolog/Novorapid, Novo Nordisk), or Fiasp.

Early half-maximal drug concentration was reached at 13 minutes with lispro-aabb, compared with 19 minutes with faster aspart and 25-27 minutes with the two conventional insulins (P < .05 for lispro-aabb vs other insulins).  

Insulin lispro-aabc was approved in the European Union and Japan in March 2020.

Lilly is currently working to make Lyumjev available to adults with diabetes in the United States as quickly as possible and says it will be included in the Lilly Insulin Value Program, allowing anyone with commercial insurance and those without insurance to fill their monthly prescription of Lyumjev for $35.

The list price of Lyumjev will be the same as the list price for Humalog, it adds.
 

This article first appeared on Medscape.com.