MDedge Dermatology

PARIS – France is boosting its vaccination campaign in response to the increase in cases of monkeypox. After a sluggish start, newly appointed French health minister François Braun has announced the release of 42,000 vaccine doses. At the same time, medical students will be able to lend a helping hand at vaccination sites. However, some experts have criticized the measures taken as being too lax to combat what the World Health Organization has designated a global health emergency.

For Benjamin Davido, MD, MSc, PhD, an infectious disease specialist at the Raymond-Poincaré Hospital (Paris Public Hospital Trust, AP-HP, Garches region), the risks of this disease have been minimized and the measures taken are not adequate, despite the ready availability of the tools needed to manage the epidemic. We must remain alert to the risks posed by this monkeypox epidemic, which seems different from the sporadic outbreaks that usually crop up in Central and West Africa, he said. Dr. Davido recently shared his opinions in an interview.

Question: What do you think about the monkeypox vaccination campaign currently underway in France?

Dr. Davido: It doesn’t go far enough, and I am surprised by the lack of a concrete and specific objective. The effects of the disease are being minimized, and we seem to be in limbo. It seems we have to wait until the fire is out of control before we can call the fire department. We should have been more reactive and taken a more drastic approach from the get-go. In France, as in other countries affected by this epidemic, we are still, unfortunately, in a phase of observation, reassuring ourselves that this will surely not become another pandemic, as that would be really bad luck.

Yet we find ourselves in an unprecedented situation: We have known about the disease in question for a long time, the target population has been identified, and we have a vaccine immediately available. So, we have all the tools and knowledge acquired from the COVID-19 pandemic at our disposal, yet we are choosing to wait and see. We have clearly underestimated the risks of failing after a stalled start to the vaccination campaign.

Question: What exactly are the risks, in your opinion?  Should we already be worried about how the epidemic is progressing?

Dr. Davido: The situation is definitely worrying. I personally am convinced that this disease will be the syphilis of the 21st century. Although the risk is low, it is not beyond the bounds of possibility that this could be the start of a new pandemic. For the time being, its spread is limited to at-risk populations, mainly men who have sex with other men and who have multiple partners, which accounts for around 300,000 people in France. However, the risk for heterosexuals must not be minimized; we must not forget that this disease can also be transmitted through contact with an infected person and by respiratory droplets from people living in the same household. There have been recent cases of women and children infected with monkeypox. If monkeypox starts to spread in the community, rather than being a sexually transmitted infection, the epidemic could spread to the rest of the population. With the rise in cases, scientists are also concerned about transmission to animals. Monkeypox could become endemic like it is in Africa, where rodents are the main reservoir of the virus.

Question: What do we know about the dynamics of this epidemic?  What can be done to effectively improve the situation?

Dr. Davido: Experience gained from African countries affected by monkeypox, as well as from the spate of cases that occurred in the United States in 2003, has shown us that the epidemic can be controlled once the cases have been contained. It is hoped that further waves of the epidemic can be avoided, providing the monkeypox vaccine achieves its objectives.

But we need to give ourselves the means to do so. The expansion of the vaccination program to the most at-risk populations in early July was the right decision. We have seen that ring vaccination targeting close-contact cases does not work with monkeypox. The current problem is that this vaccine is nearly exclusively restricted to hospital settings. We are making the same mistakes as [we did] at the start of the COVID-19 epidemic. We don’t have the right infrastructure in place for this vaccination program. We need to get doctors, paramedics, pharmacists, etc., involved. And cut back on the red tape. After embracing digital procedures during COVID-19, we find ourselves having to complete paper copies of documents for every single person attending a vaccination site. It just doesn’t make sense!

Question: You highlighted the lack of a clear objective with this vaccination campaign. What should we be aiming for?

Dr. Davido: During the COVID-19 vaccination campaign, there was a set number of people to be vaccinated within a given time frame. The approach demanded a fast pace and a desired outcome. Yes, it was an ambitious target from the get-go, but it was one that we stuck to. Currently, no figure, no target, has been set for the monkeypox vaccination program. Ideally, we would have completed the vaccination campaign before the start of the new school year to limit new infections.

As it stands now, only 10% of the target population has received the vaccine. There is talk of the summer period not being favorable. Yet I remember that last year, the COVID-19 vaccination program was strengthened in the middle of August. If the monkeypox vaccination campaign is not given a boost by the end of the summer, we run the risk of encouraging transmission of the virus between close contacts when different groups mix after being on holiday at the start of the new school year. I think that, first and foremost, we must make general practitioners aware of the disease and train them in how to diagnose it so that patients can be isolated and vaccinated as quickly as possible.

Question: There has also been talk of increasing the set 28-day period between the two doses, or even getting rid of it entirely. Would this perhaps lead to better vaccine uptake?

Dr. Davido: The United Kingdom has chosen to give a single dose and recommends a second dose after exposure. I am not sure that this is the best strategy. Although the efficacy data are still limited, the results are not as good after a single dose. According to initial data from the French National Agency for the Safety of Medicines and Health Products (the ANSM), the rate of seroconversion after one dose rises from 10% to 56% on D28 in healthy volunteers, but is between 77% and 89% 2 weeks after the second dose administered on D28.

So, the second dose is needed, especially as immunological memory seems to drop 2 years after the first injection. The U.S. Centers for Disease Control and Prevention proposes leaving 35 days between the two doses. I think this is a reasonable time frame. So, delaying the second dose makes administration of the first dose even easier because the second often fell in the middle of the holiday period and so we also save precious doses. If the time between doses is longer, we risk vaccinated individuals becoming lax and possibly being tempted to skip the “optional” booster or simply forgetting about it.

Question: Are people who have already had the smallpox vaccine better protected against monkeypox?

Dr. Davido: The efficacy of this vaccine against monkeypox is not perfect on a very long-term basis and, to be honest, we don’t really know the level of protection afforded by first-generation vaccines after 20 years. We must not forget that 20% of people infected with monkeypox were vaccinated against smallpox before mandatory vaccination for this disease was abolished [Editor’s note: The requirement of an initial dose of smallpox vaccine was lifted in 1979, once smallpox had been eradicated].

It is hoped that, as a minimum, this vaccine protects against serious illness. Yet in my department, we regularly see severe cases of monkeypox with widespread lesions in the over 45s, who are said to be vaccinated against smallpox.

Question: By comparison, is it likely that a third-generation vaccine would afford better protection against severe illness?

Dr. Davido: We still don’t have enough data or hindsight to assess the real-world impact of third-generation vaccines. This vaccine has a better tolerance profile than its predecessors, but we currently don’t know if it protects against severe forms of monkeypox. We also need to learn more about the disease causing the current epidemic, since it seems different from the sporadic outbreaks that usually crop up in Central and West Africa. The lesions seen are notably milder. The WHO has given this vaccine an efficacy level of 85% against infection by the monkeypox virus, but we must remain cautious: This figure is based on data from Africa. The epidemic in which we find ourselves is not the same. Overall, we must be wary of overly optimistic rhetoric around this new epidemic.

A version of this article appeared on Medscape.com. The article was translated from the Medscape French edition.

PARIS – France is boosting its vaccination campaign in response to the increase in cases of monkeypox. After a sluggish start, newly appointed French health minister François Braun has announced the release of 42,000 vaccine doses. At the same time, medical students will be able to lend a helping hand at vaccination sites. However, some experts have criticized the measures taken as being too lax to combat what the World Health Organization has designated a global health emergency.

For Benjamin Davido, MD, MSc, PhD, an infectious disease specialist at the Raymond-Poincaré Hospital (Paris Public Hospital Trust, AP-HP, Garches region), the risks of this disease have been minimized and the measures taken are not adequate, despite the ready availability of the tools needed to manage the epidemic. We must remain alert to the risks posed by this monkeypox epidemic, which seems different from the sporadic outbreaks that usually crop up in Central and West Africa, he said. Dr. Davido recently shared his opinions in an interview.

Question: What do you think about the monkeypox vaccination campaign currently underway in France?

Dr. Davido: It doesn’t go far enough, and I am surprised by the lack of a concrete and specific objective. The effects of the disease are being minimized, and we seem to be in limbo. It seems we have to wait until the fire is out of control before we can call the fire department. We should have been more reactive and taken a more drastic approach from the get-go. In France, as in other countries affected by this epidemic, we are still, unfortunately, in a phase of observation, reassuring ourselves that this will surely not become another pandemic, as that would be really bad luck.

Yet we find ourselves in an unprecedented situation: We have known about the disease in question for a long time, the target population has been identified, and we have a vaccine immediately available. So, we have all the tools and knowledge acquired from the COVID-19 pandemic at our disposal, yet we are choosing to wait and see. We have clearly underestimated the risks of failing after a stalled start to the vaccination campaign.

Question: What exactly are the risks, in your opinion?  Should we already be worried about how the epidemic is progressing?

Dr. Davido: The situation is definitely worrying. I personally am convinced that this disease will be the syphilis of the 21st century. Although the risk is low, it is not beyond the bounds of possibility that this could be the start of a new pandemic. For the time being, its spread is limited to at-risk populations, mainly men who have sex with other men and who have multiple partners, which accounts for around 300,000 people in France. However, the risk for heterosexuals must not be minimized; we must not forget that this disease can also be transmitted through contact with an infected person and by respiratory droplets from people living in the same household. There have been recent cases of women and children infected with monkeypox. If monkeypox starts to spread in the community, rather than being a sexually transmitted infection, the epidemic could spread to the rest of the population. With the rise in cases, scientists are also concerned about transmission to animals. Monkeypox could become endemic like it is in Africa, where rodents are the main reservoir of the virus.

Question: What do we know about the dynamics of this epidemic?  What can be done to effectively improve the situation?

Dr. Davido: Experience gained from African countries affected by monkeypox, as well as from the spate of cases that occurred in the United States in 2003, has shown us that the epidemic can be controlled once the cases have been contained. It is hoped that further waves of the epidemic can be avoided, providing the monkeypox vaccine achieves its objectives.

But we need to give ourselves the means to do so. The expansion of the vaccination program to the most at-risk populations in early July was the right decision. We have seen that ring vaccination targeting close-contact cases does not work with monkeypox. The current problem is that this vaccine is nearly exclusively restricted to hospital settings. We are making the same mistakes as [we did] at the start of the COVID-19 epidemic. We don’t have the right infrastructure in place for this vaccination program. We need to get doctors, paramedics, pharmacists, etc., involved. And cut back on the red tape. After embracing digital procedures during COVID-19, we find ourselves having to complete paper copies of documents for every single person attending a vaccination site. It just doesn’t make sense!

Question: You highlighted the lack of a clear objective with this vaccination campaign. What should we be aiming for?

Dr. Davido: During the COVID-19 vaccination campaign, there was a set number of people to be vaccinated within a given time frame. The approach demanded a fast pace and a desired outcome. Yes, it was an ambitious target from the get-go, but it was one that we stuck to. Currently, no figure, no target, has been set for the monkeypox vaccination program. Ideally, we would have completed the vaccination campaign before the start of the new school year to limit new infections.

As it stands now, only 10% of the target population has received the vaccine. There is talk of the summer period not being favorable. Yet I remember that last year, the COVID-19 vaccination program was strengthened in the middle of August. If the monkeypox vaccination campaign is not given a boost by the end of the summer, we run the risk of encouraging transmission of the virus between close contacts when different groups mix after being on holiday at the start of the new school year. I think that, first and foremost, we must make general practitioners aware of the disease and train them in how to diagnose it so that patients can be isolated and vaccinated as quickly as possible.

Question: There has also been talk of increasing the set 28-day period between the two doses, or even getting rid of it entirely. Would this perhaps lead to better vaccine uptake?

Dr. Davido: The United Kingdom has chosen to give a single dose and recommends a second dose after exposure. I am not sure that this is the best strategy. Although the efficacy data are still limited, the results are not as good after a single dose. According to initial data from the French National Agency for the Safety of Medicines and Health Products (the ANSM), the rate of seroconversion after one dose rises from 10% to 56% on D28 in healthy volunteers, but is between 77% and 89% 2 weeks after the second dose administered on D28.

So, the second dose is needed, especially as immunological memory seems to drop 2 years after the first injection. The U.S. Centers for Disease Control and Prevention proposes leaving 35 days between the two doses. I think this is a reasonable time frame. So, delaying the second dose makes administration of the first dose even easier because the second often fell in the middle of the holiday period and so we also save precious doses. If the time between doses is longer, we risk vaccinated individuals becoming lax and possibly being tempted to skip the “optional” booster or simply forgetting about it.

Question: Are people who have already had the smallpox vaccine better protected against monkeypox?

Dr. Davido: The efficacy of this vaccine against monkeypox is not perfect on a very long-term basis and, to be honest, we don’t really know the level of protection afforded by first-generation vaccines after 20 years. We must not forget that 20% of people infected with monkeypox were vaccinated against smallpox before mandatory vaccination for this disease was abolished [Editor’s note: The requirement of an initial dose of smallpox vaccine was lifted in 1979, once smallpox had been eradicated].

It is hoped that, as a minimum, this vaccine protects against serious illness. Yet in my department, we regularly see severe cases of monkeypox with widespread lesions in the over 45s, who are said to be vaccinated against smallpox.

Question: By comparison, is it likely that a third-generation vaccine would afford better protection against severe illness?

Dr. Davido: We still don’t have enough data or hindsight to assess the real-world impact of third-generation vaccines. This vaccine has a better tolerance profile than its predecessors, but we currently don’t know if it protects against severe forms of monkeypox. We also need to learn more about the disease causing the current epidemic, since it seems different from the sporadic outbreaks that usually crop up in Central and West Africa. The lesions seen are notably milder. The WHO has given this vaccine an efficacy level of 85% against infection by the monkeypox virus, but we must remain cautious: This figure is based on data from Africa. The epidemic in which we find ourselves is not the same. Overall, we must be wary of overly optimistic rhetoric around this new epidemic.

A version of this article appeared on Medscape.com. The article was translated from the Medscape French edition.

PARIS – France is boosting its vaccination campaign in response to the increase in cases of monkeypox. After a sluggish start, newly appointed French health minister François Braun has announced the release of 42,000 vaccine doses. At the same time, medical students will be able to lend a helping hand at vaccination sites. However, some experts have criticized the measures taken as being too lax to combat what the World Health Organization has designated a global health emergency.

For Benjamin Davido, MD, MSc, PhD, an infectious disease specialist at the Raymond-Poincaré Hospital (Paris Public Hospital Trust, AP-HP, Garches region), the risks of this disease have been minimized and the measures taken are not adequate, despite the ready availability of the tools needed to manage the epidemic. We must remain alert to the risks posed by this monkeypox epidemic, which seems different from the sporadic outbreaks that usually crop up in Central and West Africa, he said. Dr. Davido recently shared his opinions in an interview.

Question: What do you think about the monkeypox vaccination campaign currently underway in France?

Dr. Davido: It doesn’t go far enough, and I am surprised by the lack of a concrete and specific objective. The effects of the disease are being minimized, and we seem to be in limbo. It seems we have to wait until the fire is out of control before we can call the fire department. We should have been more reactive and taken a more drastic approach from the get-go. In France, as in other countries affected by this epidemic, we are still, unfortunately, in a phase of observation, reassuring ourselves that this will surely not become another pandemic, as that would be really bad luck.

Yet we find ourselves in an unprecedented situation: We have known about the disease in question for a long time, the target population has been identified, and we have a vaccine immediately available. So, we have all the tools and knowledge acquired from the COVID-19 pandemic at our disposal, yet we are choosing to wait and see. We have clearly underestimated the risks of failing after a stalled start to the vaccination campaign.

Question: What exactly are the risks, in your opinion?  Should we already be worried about how the epidemic is progressing?

Dr. Davido: The situation is definitely worrying. I personally am convinced that this disease will be the syphilis of the 21st century. Although the risk is low, it is not beyond the bounds of possibility that this could be the start of a new pandemic. For the time being, its spread is limited to at-risk populations, mainly men who have sex with other men and who have multiple partners, which accounts for around 300,000 people in France. However, the risk for heterosexuals must not be minimized; we must not forget that this disease can also be transmitted through contact with an infected person and by respiratory droplets from people living in the same household. There have been recent cases of women and children infected with monkeypox. If monkeypox starts to spread in the community, rather than being a sexually transmitted infection, the epidemic could spread to the rest of the population. With the rise in cases, scientists are also concerned about transmission to animals. Monkeypox could become endemic like it is in Africa, where rodents are the main reservoir of the virus.

Question: What do we know about the dynamics of this epidemic?  What can be done to effectively improve the situation?

Dr. Davido: Experience gained from African countries affected by monkeypox, as well as from the spate of cases that occurred in the United States in 2003, has shown us that the epidemic can be controlled once the cases have been contained. It is hoped that further waves of the epidemic can be avoided, providing the monkeypox vaccine achieves its objectives.

But we need to give ourselves the means to do so. The expansion of the vaccination program to the most at-risk populations in early July was the right decision. We have seen that ring vaccination targeting close-contact cases does not work with monkeypox. The current problem is that this vaccine is nearly exclusively restricted to hospital settings. We are making the same mistakes as [we did] at the start of the COVID-19 epidemic. We don’t have the right infrastructure in place for this vaccination program. We need to get doctors, paramedics, pharmacists, etc., involved. And cut back on the red tape. After embracing digital procedures during COVID-19, we find ourselves having to complete paper copies of documents for every single person attending a vaccination site. It just doesn’t make sense!

Question: You highlighted the lack of a clear objective with this vaccination campaign. What should we be aiming for?

Dr. Davido: During the COVID-19 vaccination campaign, there was a set number of people to be vaccinated within a given time frame. The approach demanded a fast pace and a desired outcome. Yes, it was an ambitious target from the get-go, but it was one that we stuck to. Currently, no figure, no target, has been set for the monkeypox vaccination program. Ideally, we would have completed the vaccination campaign before the start of the new school year to limit new infections.

As it stands now, only 10% of the target population has received the vaccine. There is talk of the summer period not being favorable. Yet I remember that last year, the COVID-19 vaccination program was strengthened in the middle of August. If the monkeypox vaccination campaign is not given a boost by the end of the summer, we run the risk of encouraging transmission of the virus between close contacts when different groups mix after being on holiday at the start of the new school year. I think that, first and foremost, we must make general practitioners aware of the disease and train them in how to diagnose it so that patients can be isolated and vaccinated as quickly as possible.

Question: There has also been talk of increasing the set 28-day period between the two doses, or even getting rid of it entirely. Would this perhaps lead to better vaccine uptake?

Dr. Davido: The United Kingdom has chosen to give a single dose and recommends a second dose after exposure. I am not sure that this is the best strategy. Although the efficacy data are still limited, the results are not as good after a single dose. According to initial data from the French National Agency for the Safety of Medicines and Health Products (the ANSM), the rate of seroconversion after one dose rises from 10% to 56% on D28 in healthy volunteers, but is between 77% and 89% 2 weeks after the second dose administered on D28.

So, the second dose is needed, especially as immunological memory seems to drop 2 years after the first injection. The U.S. Centers for Disease Control and Prevention proposes leaving 35 days between the two doses. I think this is a reasonable time frame. So, delaying the second dose makes administration of the first dose even easier because the second often fell in the middle of the holiday period and so we also save precious doses. If the time between doses is longer, we risk vaccinated individuals becoming lax and possibly being tempted to skip the “optional” booster or simply forgetting about it.

Question: Are people who have already had the smallpox vaccine better protected against monkeypox?

Dr. Davido: The efficacy of this vaccine against monkeypox is not perfect on a very long-term basis and, to be honest, we don’t really know the level of protection afforded by first-generation vaccines after 20 years. We must not forget that 20% of people infected with monkeypox were vaccinated against smallpox before mandatory vaccination for this disease was abolished [Editor’s note: The requirement of an initial dose of smallpox vaccine was lifted in 1979, once smallpox had been eradicated].

It is hoped that, as a minimum, this vaccine protects against serious illness. Yet in my department, we regularly see severe cases of monkeypox with widespread lesions in the over 45s, who are said to be vaccinated against smallpox.

Question: By comparison, is it likely that a third-generation vaccine would afford better protection against severe illness?

Dr. Davido: We still don’t have enough data or hindsight to assess the real-world impact of third-generation vaccines. This vaccine has a better tolerance profile than its predecessors, but we currently don’t know if it protects against severe forms of monkeypox. We also need to learn more about the disease causing the current epidemic, since it seems different from the sporadic outbreaks that usually crop up in Central and West Africa. The lesions seen are notably milder. The WHO has given this vaccine an efficacy level of 85% against infection by the monkeypox virus, but we must remain cautious: This figure is based on data from Africa. The epidemic in which we find ourselves is not the same. Overall, we must be wary of overly optimistic rhetoric around this new epidemic.

A version of this article appeared on Medscape.com. The article was translated from the Medscape French edition.

PORTLAND, ORE. – When patients present to Brandon L. Adler, MD, with dermatitis on the eyelid, face, or neck, he routinely asks them if they apply essential oils on their skin, or if they have an essential oil diffuser or nebulizer in their home.

“The answer is frequently ‘yes,’ ” Dr. Adler, clinical assistant professor of dermatology at the University of Southern California, Los Angeles, said at the annual meeting of the Pacific Dermatologic Association. “Essential oils are widely used throughout the wellness industry. They are contained in personal care products, beauty products, natural cleaning products, and they’re being diffused by our patients into the air. More than 75 essential oils are reported to cause allergic contact dermatitis.”

yangna/iStock/Getty Images

Natural chemical components contained in essential oils can cause skin reactions, especially linalool and limonene. “Linalool is most classically associated with lavender, while limonene is associated with citrus, but they’re found in many different plants,” said Dr. Adler, who directs USC’s contact dermatitis clinic. “On their own, linalool and limonene are not particularly allergenic; they’re not a big deal in the patch test clinic. The problem comes when we add air to the mix, because they oxidize to hydroperoxides of linalool and limonene. These are quite potent allergens.”

According to the most recent North American Contact Dermatitis Group data, 8.9% of patients undergoing patch testing tested positive to linalool hydroperoxides and 2.6% were positive to limonene hydroperoxides.

Dr. Adler discussed the case of a female massage therapist who presented with refractory hand dermatitis and was on methotrexate and dupilumab at the time of consultation but was still symptomatic. She patch-tested positive to limonene and linalool hydroperoxides as well as multiple essential oils that she had been using with her clients, ranging from sacred frankincense oil to basil oil, and she was advised to massage using only coconut or vegetable oils.

Essential oil allergy may also be related to cannabis allergy. According to Dr. Adler, allergic contact dermatitis to cannabis has been rarely reported, but in an analysis of 103 commercial topical cannabinoid preparations that he published with Vincent DeLeo, MD, also with USC, 84% contained a NACDG allergen, frequently essential oils.

More recently, Dr. Adler and colleagues reported the case of a 40-year-old woman who was referred for patch testing for nummular dermatitis that wasn’t responding to treatment. The patient was found to be using topical cannabis and also grew cannabis at home. “She asked to be patch-tested to her homegrown cannabis and had a strong positive patch test to the cannabis, linalool and limonene hydroperoxides, and other essential oils,” Dr. Adler recalled. “We sent her cannabis sample for analysis at a commercial lab and found that it contained limonene and other allergenic terpene chemicals.

“We’re just starting to unravel what this means in terms of our patients and how to manage them, but many are using topical cannabis and topical CBD. I suspect this is a lot less rare than we realize.”

Another recent case from Europe reported allergic contact dermatitis to Cannabis sativa (hemp) seed oil following topical application, with positive patch testing.

Dr. Adler disclosed that he has received research grants from the American Contact Dermatitis Society. He is also an investigator for AbbVie and a consultant for the Skin Research Institute.

PORTLAND, ORE. – When patients present to Brandon L. Adler, MD, with dermatitis on the eyelid, face, or neck, he routinely asks them if they apply essential oils on their skin, or if they have an essential oil diffuser or nebulizer in their home.

“The answer is frequently ‘yes,’ ” Dr. Adler, clinical assistant professor of dermatology at the University of Southern California, Los Angeles, said at the annual meeting of the Pacific Dermatologic Association. “Essential oils are widely used throughout the wellness industry. They are contained in personal care products, beauty products, natural cleaning products, and they’re being diffused by our patients into the air. More than 75 essential oils are reported to cause allergic contact dermatitis.”

yangna/iStock/Getty Images

Natural chemical components contained in essential oils can cause skin reactions, especially linalool and limonene. “Linalool is most classically associated with lavender, while limonene is associated with citrus, but they’re found in many different plants,” said Dr. Adler, who directs USC’s contact dermatitis clinic. “On their own, linalool and limonene are not particularly allergenic; they’re not a big deal in the patch test clinic. The problem comes when we add air to the mix, because they oxidize to hydroperoxides of linalool and limonene. These are quite potent allergens.”

According to the most recent North American Contact Dermatitis Group data, 8.9% of patients undergoing patch testing tested positive to linalool hydroperoxides and 2.6% were positive to limonene hydroperoxides.

Dr. Adler discussed the case of a female massage therapist who presented with refractory hand dermatitis and was on methotrexate and dupilumab at the time of consultation but was still symptomatic. She patch-tested positive to limonene and linalool hydroperoxides as well as multiple essential oils that she had been using with her clients, ranging from sacred frankincense oil to basil oil, and she was advised to massage using only coconut or vegetable oils.

Essential oil allergy may also be related to cannabis allergy. According to Dr. Adler, allergic contact dermatitis to cannabis has been rarely reported, but in an analysis of 103 commercial topical cannabinoid preparations that he published with Vincent DeLeo, MD, also with USC, 84% contained a NACDG allergen, frequently essential oils.

More recently, Dr. Adler and colleagues reported the case of a 40-year-old woman who was referred for patch testing for nummular dermatitis that wasn’t responding to treatment. The patient was found to be using topical cannabis and also grew cannabis at home. “She asked to be patch-tested to her homegrown cannabis and had a strong positive patch test to the cannabis, linalool and limonene hydroperoxides, and other essential oils,” Dr. Adler recalled. “We sent her cannabis sample for analysis at a commercial lab and found that it contained limonene and other allergenic terpene chemicals.

“We’re just starting to unravel what this means in terms of our patients and how to manage them, but many are using topical cannabis and topical CBD. I suspect this is a lot less rare than we realize.”

Another recent case from Europe reported allergic contact dermatitis to Cannabis sativa (hemp) seed oil following topical application, with positive patch testing.

Dr. Adler disclosed that he has received research grants from the American Contact Dermatitis Society. He is also an investigator for AbbVie and a consultant for the Skin Research Institute.

PORTLAND, ORE. – When patients present to Brandon L. Adler, MD, with dermatitis on the eyelid, face, or neck, he routinely asks them if they apply essential oils on their skin, or if they have an essential oil diffuser or nebulizer in their home.

“The answer is frequently ‘yes,’ ” Dr. Adler, clinical assistant professor of dermatology at the University of Southern California, Los Angeles, said at the annual meeting of the Pacific Dermatologic Association. “Essential oils are widely used throughout the wellness industry. They are contained in personal care products, beauty products, natural cleaning products, and they’re being diffused by our patients into the air. More than 75 essential oils are reported to cause allergic contact dermatitis.”

yangna/iStock/Getty Images

Natural chemical components contained in essential oils can cause skin reactions, especially linalool and limonene. “Linalool is most classically associated with lavender, while limonene is associated with citrus, but they’re found in many different plants,” said Dr. Adler, who directs USC’s contact dermatitis clinic. “On their own, linalool and limonene are not particularly allergenic; they’re not a big deal in the patch test clinic. The problem comes when we add air to the mix, because they oxidize to hydroperoxides of linalool and limonene. These are quite potent allergens.”

According to the most recent North American Contact Dermatitis Group data, 8.9% of patients undergoing patch testing tested positive to linalool hydroperoxides and 2.6% were positive to limonene hydroperoxides.

Dr. Adler discussed the case of a female massage therapist who presented with refractory hand dermatitis and was on methotrexate and dupilumab at the time of consultation but was still symptomatic. She patch-tested positive to limonene and linalool hydroperoxides as well as multiple essential oils that she had been using with her clients, ranging from sacred frankincense oil to basil oil, and she was advised to massage using only coconut or vegetable oils.

Essential oil allergy may also be related to cannabis allergy. According to Dr. Adler, allergic contact dermatitis to cannabis has been rarely reported, but in an analysis of 103 commercial topical cannabinoid preparations that he published with Vincent DeLeo, MD, also with USC, 84% contained a NACDG allergen, frequently essential oils.

More recently, Dr. Adler and colleagues reported the case of a 40-year-old woman who was referred for patch testing for nummular dermatitis that wasn’t responding to treatment. The patient was found to be using topical cannabis and also grew cannabis at home. “She asked to be patch-tested to her homegrown cannabis and had a strong positive patch test to the cannabis, linalool and limonene hydroperoxides, and other essential oils,” Dr. Adler recalled. “We sent her cannabis sample for analysis at a commercial lab and found that it contained limonene and other allergenic terpene chemicals.

“We’re just starting to unravel what this means in terms of our patients and how to manage them, but many are using topical cannabis and topical CBD. I suspect this is a lot less rare than we realize.”

Another recent case from Europe reported allergic contact dermatitis to Cannabis sativa (hemp) seed oil following topical application, with positive patch testing.

Dr. Adler disclosed that he has received research grants from the American Contact Dermatitis Society. He is also an investigator for AbbVie and a consultant for the Skin Research Institute.

PORTLAND, ORE. – For those who hesitate to prescribe Janus kinase inhibitors for patients with moderate to severe atopic dermatitis (AD) because of the boxed warnings on currently approved agents, it’s time to reconsider, according to Andrew Blauvelt, MD, MBA.

“In dermatology, you need to know about JAK inhibitors, and you need to know how to use them,” Dr. Blauvelt, president of Oregon Medical Research Center, Portland, said at the annual meeting of the Pacific Dermatologic Association. “Making the choice, ‘I’m not going to use those drugs because of safety concerns,’ may be okay in 2022, but we are going to be getting a lot more indications for these drugs. So instead of avoiding JAK inhibitors, I would say try to learn [about] them, understand them, and get your messaging out on safety.”

It’s difficult to imagine a clinician-researcher who has more experience with the use of biologics and JAK inhibitors in AD than Dr. Blauvelt, who has been the international investigator on several important trials of treatments that include dupilumab, tralokinumab, abrocitinib, and upadacitinib for AD such as CHRONOS, ECZTEND, JADE REGIMEN, and HEADS UP. At the meeting, he discussed his clinical approach to selecting systemic agents for AD and shared prescribing tips. He began by noting that the approval of dupilumab for moderate to severe AD in 2017 ushered in a new era of treating the disease systemically.

“When it was approved, experts went right to dupilumab if they could, and avoided the use of cyclosporine or methotrexate,” said Dr. Blauvelt, who is also an elected member of the American Society for Clinical Investigation and the International Eczema Council. “I still think that dupilumab is a great agent to start with. We’ve had a bit of difficulty improving upon it.”

Following dupilumab’s approval, three other systemic options became available for patients with moderate to severe AD: the human IgG4 monoclonal antibody tralokinumab that binds to interleukin-13, which is administered subcutaneously; and, more recently, the oral JAK inhibitors abrocitinib and upadacitinib, approved in January for moderate to severe AD.

“I’m a big fan of JAK inhibitors because I think they offer things that biologic and topical therapies can’t offer,” Dr. Blauvelt said. “Patients like the pills versus shots. They also like the speed; JAK inhibitors work faster than dupilumab and tralokinumab. So, if you have a patient with bad AD who wants to get better quickly, that would be a reason to choose a JAK inhibitor over a biologic if you can.”

When Dr. Blauvelt has asked AD clinical trial participants if they’d rather be treated with a biologic agent or with a JAK inhibitor, about half choose one over the other.

“Patients who shy away from the safety issues would choose the biologic trial while the ones who wanted the fast relief would choose the JAK trial,” he said. “But if you present both options and the patients prefer a pill, I think the JAK inhibitors do better with a rapid control of inflammation as well as pruritus – the latter within 2 days of taking the pills.”

When counseling patients initiating a JAK inhibitor, Dr. Blauvelt mentioned three advantages, compared with biologics: the pill formulation, the rapidity of response in pruritus control, and better efficacy. “The downside is the safety,” he said. “Safety is the elephant in the room for the JAK inhibitors.”

The risks listed in the boxed warning in the labeling for JAK inhibitors include: an increased risk of serious bacterial, fungal, and opportunistic infections such as TB; a higher rate of all-cause mortality, including cardiovascular death; a higher rate of MACE (major adverse cardiovascular events, defined as cardiovascular death, MI, and stroke); the potential for malignancy, including lymphoma; and the potential for thrombosis, including an increased incidence of pulmonary embolism (PE).

“Risk of thrombosis seems to be a class effect for all JAK inhibitors,” Dr. Blauvelt said. “As far as I know, it’s idiosyncratic. For nearly all the DVT [deep vein thrombosis] cases that have been reported, patients had baseline risk factors for DVT and PE, which are obesity, smoking, and use of oral contraceptives.”

Dr. Blauvelt pointed out that the boxed warning related to mortality, malignancies, and MACE stemmed from a long-term trial of the JAK inhibitor tofacitinib in RA patients. “Those patients had to be at least 50 years old, 75% of them were on concomitant methotrexate and/or prednisone, and they had to have at least one cardiac risk factor to get into the trial,” he said.

“I’m not saying those things can’t happen in dermatology patients, but if you look at the safety data of JAK inhibitors in the AD studies and in the alopecia areata studies, we are seeing a few cases of these things here and there, but not major signals,” he said. To date, “they look safer in dermatologic diseases compared to tofacitinib in RA data in older populations.”

He emphasized the importance of discussing each of the risks in the boxed warning with patients who are candidates for JAK inhibitor therapy.

Dr. Blauvelt likened the lab monitoring required for JAK inhibitors to that required for methotrexate. This means ordering at baseline, a CBC with differential, a chem-20, a lipid panel, and a QuantiFERON-TB Gold test. The JAK inhibitor labels do not include information on the frequency of monitoring, “but I have a distinct opinion on this because of my blood test monitoring experience in the trials for many years,” he said.

“I think it’s good to do follow-up testing at 1 month, then every 3 months in the first year. In my experience, the people who drop blood cell counts or increase their lipids tend to do it in the first year.”

After 1 year of treatment, he continued, follow-up testing once every 6 months is reasonable. “If CPK [creatine phosphokinase] goes up, I don’t worry about it; it’s not clinically relevant. There is no recommendation for CPK monitoring, so if you’re getting that on your chem-20, I’d say don’t worry about it.”

Dr. Blauvelt reported that he is an investigator and a scientific adviser for several pharmaceutical companies developing treatments for AD, including companies that are evaluating or marketing JAK inhibitors for AD, including AbbVie, Incyte, and Pfizer, as well as dupilumab’s joint developers Sanofi and Regeneron.

PORTLAND, ORE. – For those who hesitate to prescribe Janus kinase inhibitors for patients with moderate to severe atopic dermatitis (AD) because of the boxed warnings on currently approved agents, it’s time to reconsider, according to Andrew Blauvelt, MD, MBA.

“In dermatology, you need to know about JAK inhibitors, and you need to know how to use them,” Dr. Blauvelt, president of Oregon Medical Research Center, Portland, said at the annual meeting of the Pacific Dermatologic Association. “Making the choice, ‘I’m not going to use those drugs because of safety concerns,’ may be okay in 2022, but we are going to be getting a lot more indications for these drugs. So instead of avoiding JAK inhibitors, I would say try to learn [about] them, understand them, and get your messaging out on safety.”

It’s difficult to imagine a clinician-researcher who has more experience with the use of biologics and JAK inhibitors in AD than Dr. Blauvelt, who has been the international investigator on several important trials of treatments that include dupilumab, tralokinumab, abrocitinib, and upadacitinib for AD such as CHRONOS, ECZTEND, JADE REGIMEN, and HEADS UP. At the meeting, he discussed his clinical approach to selecting systemic agents for AD and shared prescribing tips. He began by noting that the approval of dupilumab for moderate to severe AD in 2017 ushered in a new era of treating the disease systemically.

“When it was approved, experts went right to dupilumab if they could, and avoided the use of cyclosporine or methotrexate,” said Dr. Blauvelt, who is also an elected member of the American Society for Clinical Investigation and the International Eczema Council. “I still think that dupilumab is a great agent to start with. We’ve had a bit of difficulty improving upon it.”

Following dupilumab’s approval, three other systemic options became available for patients with moderate to severe AD: the human IgG4 monoclonal antibody tralokinumab that binds to interleukin-13, which is administered subcutaneously; and, more recently, the oral JAK inhibitors abrocitinib and upadacitinib, approved in January for moderate to severe AD.

“I’m a big fan of JAK inhibitors because I think they offer things that biologic and topical therapies can’t offer,” Dr. Blauvelt said. “Patients like the pills versus shots. They also like the speed; JAK inhibitors work faster than dupilumab and tralokinumab. So, if you have a patient with bad AD who wants to get better quickly, that would be a reason to choose a JAK inhibitor over a biologic if you can.”

When Dr. Blauvelt has asked AD clinical trial participants if they’d rather be treated with a biologic agent or with a JAK inhibitor, about half choose one over the other.

“Patients who shy away from the safety issues would choose the biologic trial while the ones who wanted the fast relief would choose the JAK trial,” he said. “But if you present both options and the patients prefer a pill, I think the JAK inhibitors do better with a rapid control of inflammation as well as pruritus – the latter within 2 days of taking the pills.”

When counseling patients initiating a JAK inhibitor, Dr. Blauvelt mentioned three advantages, compared with biologics: the pill formulation, the rapidity of response in pruritus control, and better efficacy. “The downside is the safety,” he said. “Safety is the elephant in the room for the JAK inhibitors.”

The risks listed in the boxed warning in the labeling for JAK inhibitors include: an increased risk of serious bacterial, fungal, and opportunistic infections such as TB; a higher rate of all-cause mortality, including cardiovascular death; a higher rate of MACE (major adverse cardiovascular events, defined as cardiovascular death, MI, and stroke); the potential for malignancy, including lymphoma; and the potential for thrombosis, including an increased incidence of pulmonary embolism (PE).

“Risk of thrombosis seems to be a class effect for all JAK inhibitors,” Dr. Blauvelt said. “As far as I know, it’s idiosyncratic. For nearly all the DVT [deep vein thrombosis] cases that have been reported, patients had baseline risk factors for DVT and PE, which are obesity, smoking, and use of oral contraceptives.”

Dr. Blauvelt pointed out that the boxed warning related to mortality, malignancies, and MACE stemmed from a long-term trial of the JAK inhibitor tofacitinib in RA patients. “Those patients had to be at least 50 years old, 75% of them were on concomitant methotrexate and/or prednisone, and they had to have at least one cardiac risk factor to get into the trial,” he said.

“I’m not saying those things can’t happen in dermatology patients, but if you look at the safety data of JAK inhibitors in the AD studies and in the alopecia areata studies, we are seeing a few cases of these things here and there, but not major signals,” he said. To date, “they look safer in dermatologic diseases compared to tofacitinib in RA data in older populations.”

He emphasized the importance of discussing each of the risks in the boxed warning with patients who are candidates for JAK inhibitor therapy.

Dr. Blauvelt likened the lab monitoring required for JAK inhibitors to that required for methotrexate. This means ordering at baseline, a CBC with differential, a chem-20, a lipid panel, and a QuantiFERON-TB Gold test. The JAK inhibitor labels do not include information on the frequency of monitoring, “but I have a distinct opinion on this because of my blood test monitoring experience in the trials for many years,” he said.

“I think it’s good to do follow-up testing at 1 month, then every 3 months in the first year. In my experience, the people who drop blood cell counts or increase their lipids tend to do it in the first year.”

After 1 year of treatment, he continued, follow-up testing once every 6 months is reasonable. “If CPK [creatine phosphokinase] goes up, I don’t worry about it; it’s not clinically relevant. There is no recommendation for CPK monitoring, so if you’re getting that on your chem-20, I’d say don’t worry about it.”

Dr. Blauvelt reported that he is an investigator and a scientific adviser for several pharmaceutical companies developing treatments for AD, including companies that are evaluating or marketing JAK inhibitors for AD, including AbbVie, Incyte, and Pfizer, as well as dupilumab’s joint developers Sanofi and Regeneron.

PORTLAND, ORE. – For those who hesitate to prescribe Janus kinase inhibitors for patients with moderate to severe atopic dermatitis (AD) because of the boxed warnings on currently approved agents, it’s time to reconsider, according to Andrew Blauvelt, MD, MBA.

“In dermatology, you need to know about JAK inhibitors, and you need to know how to use them,” Dr. Blauvelt, president of Oregon Medical Research Center, Portland, said at the annual meeting of the Pacific Dermatologic Association. “Making the choice, ‘I’m not going to use those drugs because of safety concerns,’ may be okay in 2022, but we are going to be getting a lot more indications for these drugs. So instead of avoiding JAK inhibitors, I would say try to learn [about] them, understand them, and get your messaging out on safety.”

It’s difficult to imagine a clinician-researcher who has more experience with the use of biologics and JAK inhibitors in AD than Dr. Blauvelt, who has been the international investigator on several important trials of treatments that include dupilumab, tralokinumab, abrocitinib, and upadacitinib for AD such as CHRONOS, ECZTEND, JADE REGIMEN, and HEADS UP. At the meeting, he discussed his clinical approach to selecting systemic agents for AD and shared prescribing tips. He began by noting that the approval of dupilumab for moderate to severe AD in 2017 ushered in a new era of treating the disease systemically.

“When it was approved, experts went right to dupilumab if they could, and avoided the use of cyclosporine or methotrexate,” said Dr. Blauvelt, who is also an elected member of the American Society for Clinical Investigation and the International Eczema Council. “I still think that dupilumab is a great agent to start with. We’ve had a bit of difficulty improving upon it.”

Following dupilumab’s approval, three other systemic options became available for patients with moderate to severe AD: the human IgG4 monoclonal antibody tralokinumab that binds to interleukin-13, which is administered subcutaneously; and, more recently, the oral JAK inhibitors abrocitinib and upadacitinib, approved in January for moderate to severe AD.

“I’m a big fan of JAK inhibitors because I think they offer things that biologic and topical therapies can’t offer,” Dr. Blauvelt said. “Patients like the pills versus shots. They also like the speed; JAK inhibitors work faster than dupilumab and tralokinumab. So, if you have a patient with bad AD who wants to get better quickly, that would be a reason to choose a JAK inhibitor over a biologic if you can.”

When Dr. Blauvelt has asked AD clinical trial participants if they’d rather be treated with a biologic agent or with a JAK inhibitor, about half choose one over the other.

“Patients who shy away from the safety issues would choose the biologic trial while the ones who wanted the fast relief would choose the JAK trial,” he said. “But if you present both options and the patients prefer a pill, I think the JAK inhibitors do better with a rapid control of inflammation as well as pruritus – the latter within 2 days of taking the pills.”

When counseling patients initiating a JAK inhibitor, Dr. Blauvelt mentioned three advantages, compared with biologics: the pill formulation, the rapidity of response in pruritus control, and better efficacy. “The downside is the safety,” he said. “Safety is the elephant in the room for the JAK inhibitors.”

The risks listed in the boxed warning in the labeling for JAK inhibitors include: an increased risk of serious bacterial, fungal, and opportunistic infections such as TB; a higher rate of all-cause mortality, including cardiovascular death; a higher rate of MACE (major adverse cardiovascular events, defined as cardiovascular death, MI, and stroke); the potential for malignancy, including lymphoma; and the potential for thrombosis, including an increased incidence of pulmonary embolism (PE).

“Risk of thrombosis seems to be a class effect for all JAK inhibitors,” Dr. Blauvelt said. “As far as I know, it’s idiosyncratic. For nearly all the DVT [deep vein thrombosis] cases that have been reported, patients had baseline risk factors for DVT and PE, which are obesity, smoking, and use of oral contraceptives.”

Dr. Blauvelt pointed out that the boxed warning related to mortality, malignancies, and MACE stemmed from a long-term trial of the JAK inhibitor tofacitinib in RA patients. “Those patients had to be at least 50 years old, 75% of them were on concomitant methotrexate and/or prednisone, and they had to have at least one cardiac risk factor to get into the trial,” he said.

“I’m not saying those things can’t happen in dermatology patients, but if you look at the safety data of JAK inhibitors in the AD studies and in the alopecia areata studies, we are seeing a few cases of these things here and there, but not major signals,” he said. To date, “they look safer in dermatologic diseases compared to tofacitinib in RA data in older populations.”

He emphasized the importance of discussing each of the risks in the boxed warning with patients who are candidates for JAK inhibitor therapy.

Dr. Blauvelt likened the lab monitoring required for JAK inhibitors to that required for methotrexate. This means ordering at baseline, a CBC with differential, a chem-20, a lipid panel, and a QuantiFERON-TB Gold test. The JAK inhibitor labels do not include information on the frequency of monitoring, “but I have a distinct opinion on this because of my blood test monitoring experience in the trials for many years,” he said.

“I think it’s good to do follow-up testing at 1 month, then every 3 months in the first year. In my experience, the people who drop blood cell counts or increase their lipids tend to do it in the first year.”

After 1 year of treatment, he continued, follow-up testing once every 6 months is reasonable. “If CPK [creatine phosphokinase] goes up, I don’t worry about it; it’s not clinically relevant. There is no recommendation for CPK monitoring, so if you’re getting that on your chem-20, I’d say don’t worry about it.”

Dr. Blauvelt reported that he is an investigator and a scientific adviser for several pharmaceutical companies developing treatments for AD, including companies that are evaluating or marketing JAK inhibitors for AD, including AbbVie, Incyte, and Pfizer, as well as dupilumab’s joint developers Sanofi and Regeneron.

There’s little doubt long COVID is real. The federal government recognizes long COVID as a condition and said in two reports issued in August that one in five adult COVID-19 survivors have a health condition related to their illness.

COVID-19 can damage multiple organs in the body. Sometimes this damage leads to long COVID; sometimes other reasons are at play. Doctors are beginning to sort it out.

There’s a difference between long COVID and an acute infection with lasting effects, doctors say.

“COVID itself can actually cause prolonged illness, and we don’t really call that long COVID,” said Nisha Viswanathan, MD, a doctor at UCLA Health in Los Angeles. But if symptoms extend beyond 12 weeks, that puts patients in the realm of long COVID.

Symptoms can range from mild to severe and can keep people from resuming their normal lives and jobs. Sometimes they last for months, according to the U.S. Department of Health & Human Services.
 

Multiorgan damage

Lung scarring and other lung problems are common after COVID, said Leora Horwitz, MD, an internal medicine specialist at New York University. Even after a mild case, people can have breathing issues for months, a team at Johns Hopkins Medicine, Baltimore, said in an online briefing. One study published in the journal Radiology found damage in people a full year after a COVID-19 diagnosis.

Some people have persistent heart, kidney, liver, and nervous system problems after COVID-19. A study published in 2020 in JAMA Cardiology found 60% of people who had COVID-19 had ongoing signs of heart inflammation. Nearly a third of people hospitalized for COVID-19 get kidney damage that can become chronic, and some end up needing dialysis or a transplant, said C. John Sperati, MD, a kidney specialist at Johns Hopkins Medicine.

This might be, in part, because SARS-CoV-2, the virus that causes COVID-19, directly infects the cells in many organs.

Nicole Bhave, MD, a cardiologist at University of Michigan Health, Ann Arbor is concerned that COVID-19 appears to increase the risk of heart problems in some people.

“Some of the uptick may just be recognition bias, in that people with symptoms are seeking care,” she said. “But there’s definitely a biological basis by which COVID could tip people over into a new diagnosis of heart failure.”
 

Inflammation

Inflammation is probably a key part of the long-term effects of COVID-19.

Some people have a serious immune reaction to COVID-19 called a cytokine storm, said Nitra Aggarwal Gilotra, MD, a cardiologist at Johns Hopkins Medicine. This release of inflammation-causing molecules called cytokines is meant to attack the invading virus. But it can be so severe that it wreaks havoc on healthy tissues and organs and causes lasting damage – if patients even survive it.

In some people, inflammation can affect the heart, causing myocarditis. Myocarditis symptoms include chest pain, breathlessness, and heart palpitations. Though rare, it can be serious and can raise the risk of other heart problems, including heart failure, down the line.

Long COVID may also trigger an autoimmune condition, said Eline Luning Prak, MD, PhD, a pathologist at the Hospital of the University of Pennsylvania, Philadelphia. Long COVID can share many hallmark symptoms with autoimmune diseases, including fatigue, widespread pain, memory problems, and mood disorders.
 

Blood clots

Studies have shown the overcharged inflammatory response to COVID-19 can cause blood clots. This sometimes overwhelming clotting was an early hallmark of COVID-19 infection, and when clots restrict blood flow in the brain, lungs, kidneys, or limbs, they can cause long-term damage. Some can be deadly. Researchers in Sweden found patients were at risk of deep vein thrombosis – a blood clot usually in the leg – up to 3 months after infection and at higher risk of a blood clot in the lung, called pulmonary embolism, for as long as 3 months.

Viral reservoirs

The virus itself may also linger in a patient’s body, causing continued symptoms and, potentially, new flare-ups. Zoe Swank, PhD, of Harvard Medical School, Boston, and colleagues reported in a preprint study that they found pieces of the SARS-CoV-2 virus in the blood of most patients with long COVID symptoms they tested – some as long as a year after infection. The study has not yet been peer reviewed.

Another team found evidence of the virus in stool up to 7 months later, which suggests the virus hides out in the gut. Other early studies have found bits of viral RNA in the appendix, breast tissue, heart, eyes, and brain.
 

Diabetes

Diabetes is a risk factor for getting severe COVID-19, and multiple studies have shown people can get diabetes both while battling infection and afterward. One study of veterans, published in The Lancet Diabetes and Endocrinology, found COVID-19 survivors were about 40% more likely to get diabetes over the next year.

There are a few ways this might happen. Insulin-producing cells in the pancreas have SARS-CoV-2 receptors – a type of molecular doorway the coronavirus can attach to. Damage to these cells could make the body less able to produce insulin, which in turn can lead to diabetes. The virus could also disrupt the balance in the body or cause inflammation that leads to insulin resistance, which can develop into diabetes, Ziad Al-Aly, MD, of the Veterans Affairs St. Louis Health Care System, and colleagues wrote.
 

Nervous system issues

People who get COVID-19 are also more vulnerable to postural orthostatic tachycardia syndrome (POTS). This affects what’s known as the autonomic nervous system, which regulates blood circulation, and includes those things that happen in your body without your having to think about them, like breathing, heartbeat, and digestion. POTS can cause common long COVID neurologic symptoms, including headaches, fatigue, brain fog, insomnia, and problems thinking and concentrating. “This was a known condition prior to COVID, but it was incredibly rare,” said Dr. Viswanathan. “After COVID, I’ve seen it with increasing frequency.”

Long-term outlook

Lasting issues after COVID-19 are much more likely after a moderate or severe infection. Still, plenty of people are battling them even after a mild illness. “As for why, that’s the billion-dollar question,” said Dr. Horwitz. “It’s well known that viral infections can cause long-term dysregulation. Why that is, we really just don’t know.”

Whether it’s virus hiding out in the body, long-term organ damage, or an autoimmune reaction likely differs from person to person. “I’m believing, increasingly, that it’s a combination of all of these, just based on how different patients are responding to different medications,” said Dr. Viswanathan. “One patient will respond to something beautifully, and another patient won’t at all.”

But it’s clear a significant number of people are facing long-term health struggles because of COVID-19, which has infected at least 580 million people globally and 92 million – likely many more – in the United States, according to Johns Hopkins University.

Even a small increased risk of conditions like heart disease or diabetes translates to a huge number of people, Dr. Horwitz said. “If even 1% of people getting COVID have long-term symptoms, that’s a major public health crisis, because that’s 1% of pretty much everybody in the country.”

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

There’s little doubt long COVID is real. The federal government recognizes long COVID as a condition and said in two reports issued in August that one in five adult COVID-19 survivors have a health condition related to their illness.

COVID-19 can damage multiple organs in the body. Sometimes this damage leads to long COVID; sometimes other reasons are at play. Doctors are beginning to sort it out.

There’s a difference between long COVID and an acute infection with lasting effects, doctors say.

“COVID itself can actually cause prolonged illness, and we don’t really call that long COVID,” said Nisha Viswanathan, MD, a doctor at UCLA Health in Los Angeles. But if symptoms extend beyond 12 weeks, that puts patients in the realm of long COVID.

Symptoms can range from mild to severe and can keep people from resuming their normal lives and jobs. Sometimes they last for months, according to the U.S. Department of Health & Human Services.
 

Multiorgan damage

Lung scarring and other lung problems are common after COVID, said Leora Horwitz, MD, an internal medicine specialist at New York University. Even after a mild case, people can have breathing issues for months, a team at Johns Hopkins Medicine, Baltimore, said in an online briefing. One study published in the journal Radiology found damage in people a full year after a COVID-19 diagnosis.

Some people have persistent heart, kidney, liver, and nervous system problems after COVID-19. A study published in 2020 in JAMA Cardiology found 60% of people who had COVID-19 had ongoing signs of heart inflammation. Nearly a third of people hospitalized for COVID-19 get kidney damage that can become chronic, and some end up needing dialysis or a transplant, said C. John Sperati, MD, a kidney specialist at Johns Hopkins Medicine.

This might be, in part, because SARS-CoV-2, the virus that causes COVID-19, directly infects the cells in many organs.

Nicole Bhave, MD, a cardiologist at University of Michigan Health, Ann Arbor is concerned that COVID-19 appears to increase the risk of heart problems in some people.

“Some of the uptick may just be recognition bias, in that people with symptoms are seeking care,” she said. “But there’s definitely a biological basis by which COVID could tip people over into a new diagnosis of heart failure.”
 

Inflammation

Inflammation is probably a key part of the long-term effects of COVID-19.

Some people have a serious immune reaction to COVID-19 called a cytokine storm, said Nitra Aggarwal Gilotra, MD, a cardiologist at Johns Hopkins Medicine. This release of inflammation-causing molecules called cytokines is meant to attack the invading virus. But it can be so severe that it wreaks havoc on healthy tissues and organs and causes lasting damage – if patients even survive it.

In some people, inflammation can affect the heart, causing myocarditis. Myocarditis symptoms include chest pain, breathlessness, and heart palpitations. Though rare, it can be serious and can raise the risk of other heart problems, including heart failure, down the line.

Long COVID may also trigger an autoimmune condition, said Eline Luning Prak, MD, PhD, a pathologist at the Hospital of the University of Pennsylvania, Philadelphia. Long COVID can share many hallmark symptoms with autoimmune diseases, including fatigue, widespread pain, memory problems, and mood disorders.
 

Blood clots

Studies have shown the overcharged inflammatory response to COVID-19 can cause blood clots. This sometimes overwhelming clotting was an early hallmark of COVID-19 infection, and when clots restrict blood flow in the brain, lungs, kidneys, or limbs, they can cause long-term damage. Some can be deadly. Researchers in Sweden found patients were at risk of deep vein thrombosis – a blood clot usually in the leg – up to 3 months after infection and at higher risk of a blood clot in the lung, called pulmonary embolism, for as long as 3 months.

Viral reservoirs

The virus itself may also linger in a patient’s body, causing continued symptoms and, potentially, new flare-ups. Zoe Swank, PhD, of Harvard Medical School, Boston, and colleagues reported in a preprint study that they found pieces of the SARS-CoV-2 virus in the blood of most patients with long COVID symptoms they tested – some as long as a year after infection. The study has not yet been peer reviewed.

Another team found evidence of the virus in stool up to 7 months later, which suggests the virus hides out in the gut. Other early studies have found bits of viral RNA in the appendix, breast tissue, heart, eyes, and brain.
 

Diabetes

Diabetes is a risk factor for getting severe COVID-19, and multiple studies have shown people can get diabetes both while battling infection and afterward. One study of veterans, published in The Lancet Diabetes and Endocrinology, found COVID-19 survivors were about 40% more likely to get diabetes over the next year.

There are a few ways this might happen. Insulin-producing cells in the pancreas have SARS-CoV-2 receptors – a type of molecular doorway the coronavirus can attach to. Damage to these cells could make the body less able to produce insulin, which in turn can lead to diabetes. The virus could also disrupt the balance in the body or cause inflammation that leads to insulin resistance, which can develop into diabetes, Ziad Al-Aly, MD, of the Veterans Affairs St. Louis Health Care System, and colleagues wrote.
 

Nervous system issues

People who get COVID-19 are also more vulnerable to postural orthostatic tachycardia syndrome (POTS). This affects what’s known as the autonomic nervous system, which regulates blood circulation, and includes those things that happen in your body without your having to think about them, like breathing, heartbeat, and digestion. POTS can cause common long COVID neurologic symptoms, including headaches, fatigue, brain fog, insomnia, and problems thinking and concentrating. “This was a known condition prior to COVID, but it was incredibly rare,” said Dr. Viswanathan. “After COVID, I’ve seen it with increasing frequency.”

Long-term outlook

Lasting issues after COVID-19 are much more likely after a moderate or severe infection. Still, plenty of people are battling them even after a mild illness. “As for why, that’s the billion-dollar question,” said Dr. Horwitz. “It’s well known that viral infections can cause long-term dysregulation. Why that is, we really just don’t know.”

Whether it’s virus hiding out in the body, long-term organ damage, or an autoimmune reaction likely differs from person to person. “I’m believing, increasingly, that it’s a combination of all of these, just based on how different patients are responding to different medications,” said Dr. Viswanathan. “One patient will respond to something beautifully, and another patient won’t at all.”

But it’s clear a significant number of people are facing long-term health struggles because of COVID-19, which has infected at least 580 million people globally and 92 million – likely many more – in the United States, according to Johns Hopkins University.

Even a small increased risk of conditions like heart disease or diabetes translates to a huge number of people, Dr. Horwitz said. “If even 1% of people getting COVID have long-term symptoms, that’s a major public health crisis, because that’s 1% of pretty much everybody in the country.”

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

There’s little doubt long COVID is real. The federal government recognizes long COVID as a condition and said in two reports issued in August that one in five adult COVID-19 survivors have a health condition related to their illness.

COVID-19 can damage multiple organs in the body. Sometimes this damage leads to long COVID; sometimes other reasons are at play. Doctors are beginning to sort it out.

There’s a difference between long COVID and an acute infection with lasting effects, doctors say.

“COVID itself can actually cause prolonged illness, and we don’t really call that long COVID,” said Nisha Viswanathan, MD, a doctor at UCLA Health in Los Angeles. But if symptoms extend beyond 12 weeks, that puts patients in the realm of long COVID.

Symptoms can range from mild to severe and can keep people from resuming their normal lives and jobs. Sometimes they last for months, according to the U.S. Department of Health & Human Services.
 

Multiorgan damage

Lung scarring and other lung problems are common after COVID, said Leora Horwitz, MD, an internal medicine specialist at New York University. Even after a mild case, people can have breathing issues for months, a team at Johns Hopkins Medicine, Baltimore, said in an online briefing. One study published in the journal Radiology found damage in people a full year after a COVID-19 diagnosis.

Some people have persistent heart, kidney, liver, and nervous system problems after COVID-19. A study published in 2020 in JAMA Cardiology found 60% of people who had COVID-19 had ongoing signs of heart inflammation. Nearly a third of people hospitalized for COVID-19 get kidney damage that can become chronic, and some end up needing dialysis or a transplant, said C. John Sperati, MD, a kidney specialist at Johns Hopkins Medicine.

This might be, in part, because SARS-CoV-2, the virus that causes COVID-19, directly infects the cells in many organs.

Nicole Bhave, MD, a cardiologist at University of Michigan Health, Ann Arbor is concerned that COVID-19 appears to increase the risk of heart problems in some people.

“Some of the uptick may just be recognition bias, in that people with symptoms are seeking care,” she said. “But there’s definitely a biological basis by which COVID could tip people over into a new diagnosis of heart failure.”
 

Inflammation

Inflammation is probably a key part of the long-term effects of COVID-19.

Some people have a serious immune reaction to COVID-19 called a cytokine storm, said Nitra Aggarwal Gilotra, MD, a cardiologist at Johns Hopkins Medicine. This release of inflammation-causing molecules called cytokines is meant to attack the invading virus. But it can be so severe that it wreaks havoc on healthy tissues and organs and causes lasting damage – if patients even survive it.

In some people, inflammation can affect the heart, causing myocarditis. Myocarditis symptoms include chest pain, breathlessness, and heart palpitations. Though rare, it can be serious and can raise the risk of other heart problems, including heart failure, down the line.

Long COVID may also trigger an autoimmune condition, said Eline Luning Prak, MD, PhD, a pathologist at the Hospital of the University of Pennsylvania, Philadelphia. Long COVID can share many hallmark symptoms with autoimmune diseases, including fatigue, widespread pain, memory problems, and mood disorders.
 

Blood clots

Studies have shown the overcharged inflammatory response to COVID-19 can cause blood clots. This sometimes overwhelming clotting was an early hallmark of COVID-19 infection, and when clots restrict blood flow in the brain, lungs, kidneys, or limbs, they can cause long-term damage. Some can be deadly. Researchers in Sweden found patients were at risk of deep vein thrombosis – a blood clot usually in the leg – up to 3 months after infection and at higher risk of a blood clot in the lung, called pulmonary embolism, for as long as 3 months.

Viral reservoirs

The virus itself may also linger in a patient’s body, causing continued symptoms and, potentially, new flare-ups. Zoe Swank, PhD, of Harvard Medical School, Boston, and colleagues reported in a preprint study that they found pieces of the SARS-CoV-2 virus in the blood of most patients with long COVID symptoms they tested – some as long as a year after infection. The study has not yet been peer reviewed.

Another team found evidence of the virus in stool up to 7 months later, which suggests the virus hides out in the gut. Other early studies have found bits of viral RNA in the appendix, breast tissue, heart, eyes, and brain.
 

Diabetes

Diabetes is a risk factor for getting severe COVID-19, and multiple studies have shown people can get diabetes both while battling infection and afterward. One study of veterans, published in The Lancet Diabetes and Endocrinology, found COVID-19 survivors were about 40% more likely to get diabetes over the next year.

There are a few ways this might happen. Insulin-producing cells in the pancreas have SARS-CoV-2 receptors – a type of molecular doorway the coronavirus can attach to. Damage to these cells could make the body less able to produce insulin, which in turn can lead to diabetes. The virus could also disrupt the balance in the body or cause inflammation that leads to insulin resistance, which can develop into diabetes, Ziad Al-Aly, MD, of the Veterans Affairs St. Louis Health Care System, and colleagues wrote.
 

Nervous system issues

People who get COVID-19 are also more vulnerable to postural orthostatic tachycardia syndrome (POTS). This affects what’s known as the autonomic nervous system, which regulates blood circulation, and includes those things that happen in your body without your having to think about them, like breathing, heartbeat, and digestion. POTS can cause common long COVID neurologic symptoms, including headaches, fatigue, brain fog, insomnia, and problems thinking and concentrating. “This was a known condition prior to COVID, but it was incredibly rare,” said Dr. Viswanathan. “After COVID, I’ve seen it with increasing frequency.”

Long-term outlook

Lasting issues after COVID-19 are much more likely after a moderate or severe infection. Still, plenty of people are battling them even after a mild illness. “As for why, that’s the billion-dollar question,” said Dr. Horwitz. “It’s well known that viral infections can cause long-term dysregulation. Why that is, we really just don’t know.”

Whether it’s virus hiding out in the body, long-term organ damage, or an autoimmune reaction likely differs from person to person. “I’m believing, increasingly, that it’s a combination of all of these, just based on how different patients are responding to different medications,” said Dr. Viswanathan. “One patient will respond to something beautifully, and another patient won’t at all.”

But it’s clear a significant number of people are facing long-term health struggles because of COVID-19, which has infected at least 580 million people globally and 92 million – likely many more – in the United States, according to Johns Hopkins University.

Even a small increased risk of conditions like heart disease or diabetes translates to a huge number of people, Dr. Horwitz said. “If even 1% of people getting COVID have long-term symptoms, that’s a major public health crisis, because that’s 1% of pretty much everybody in the country.”

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

Most people with Omicron likely don’t know it.

That’s according to a study in JAMA Network Open, which says 56% of people who have the Omicron variant of the coronavirus are unaware of their infection.

And it has an upside and a downside, depending on how you look at it, according to Time magazine.

“It’s good news, in some ways, since it underscores the fact that Omicron tends to cause relatively mild symptoms (or no symptoms at all) in vaccinated people,” Time says. “The downside is that many people are likely spreading the virus unintentionally.”

The study looked at 210 hospital patients and employees in the Los Angeles area. More than half who tested positive didn’t know it – because they had no symptoms, or they assumed they merely had a cold or allergies.

“The findings support early data from around the world suggesting that throughout the pandemic, anywhere from 25% to 40% of SARS-CoV-2 infections have been asymptomatic, which presents challenges for public health officials trying to control the spread of the virus,” Time reports.

The study found that awareness of infection rose after at-home tests became available this year. About three-quarters of people in January and February didn’t know their status, for example.

“Findings of this study suggest that low rates of Omicron variant infection awareness may be a key contributor to rapid transmission of the virus within communities,” the authors wrote. “Given that unawareness of active infection precludes self-initiated interventions, such as testing and self-isolation, even modest levels of undiagnosed infection can contribute to substantial population-level transmission.”

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

Most people with Omicron likely don’t know it.

That’s according to a study in JAMA Network Open, which says 56% of people who have the Omicron variant of the coronavirus are unaware of their infection.

And it has an upside and a downside, depending on how you look at it, according to Time magazine.

“It’s good news, in some ways, since it underscores the fact that Omicron tends to cause relatively mild symptoms (or no symptoms at all) in vaccinated people,” Time says. “The downside is that many people are likely spreading the virus unintentionally.”

The study looked at 210 hospital patients and employees in the Los Angeles area. More than half who tested positive didn’t know it – because they had no symptoms, or they assumed they merely had a cold or allergies.

“The findings support early data from around the world suggesting that throughout the pandemic, anywhere from 25% to 40% of SARS-CoV-2 infections have been asymptomatic, which presents challenges for public health officials trying to control the spread of the virus,” Time reports.

The study found that awareness of infection rose after at-home tests became available this year. About three-quarters of people in January and February didn’t know their status, for example.

“Findings of this study suggest that low rates of Omicron variant infection awareness may be a key contributor to rapid transmission of the virus within communities,” the authors wrote. “Given that unawareness of active infection precludes self-initiated interventions, such as testing and self-isolation, even modest levels of undiagnosed infection can contribute to substantial population-level transmission.”

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

Most people with Omicron likely don’t know it.

That’s according to a study in JAMA Network Open, which says 56% of people who have the Omicron variant of the coronavirus are unaware of their infection.

And it has an upside and a downside, depending on how you look at it, according to Time magazine.

“It’s good news, in some ways, since it underscores the fact that Omicron tends to cause relatively mild symptoms (or no symptoms at all) in vaccinated people,” Time says. “The downside is that many people are likely spreading the virus unintentionally.”

The study looked at 210 hospital patients and employees in the Los Angeles area. More than half who tested positive didn’t know it – because they had no symptoms, or they assumed they merely had a cold or allergies.

“The findings support early data from around the world suggesting that throughout the pandemic, anywhere from 25% to 40% of SARS-CoV-2 infections have been asymptomatic, which presents challenges for public health officials trying to control the spread of the virus,” Time reports.

The study found that awareness of infection rose after at-home tests became available this year. About three-quarters of people in January and February didn’t know their status, for example.

“Findings of this study suggest that low rates of Omicron variant infection awareness may be a key contributor to rapid transmission of the virus within communities,” the authors wrote. “Given that unawareness of active infection precludes self-initiated interventions, such as testing and self-isolation, even modest levels of undiagnosed infection can contribute to substantial population-level transmission.”

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

Key clinical point: Childhood maltreatment (CM) is associated with poor physical and mental health outcomes in adults; however, it was not found to be a risk factor for the development of adult atopic dermatitis (AD).

Major finding: Similar proportion of adults with and without AD (20.6% and 21.6%, respectively; P  =  .80) reported experiencing ≥1 type of moderate-to-severe CM, such as emotional, physical, and sexual abuse and emotional and physical neglect. Neither type of CM was associated with the development of AD in adults.

Study details: Findings are from an analysis of a cross-sectional population-based study including 2973 adults, of which 131 were diagnosed with AD.

Disclosures: This study was funded by the Federal Ministry of Education and Research and other sources. Some authors declared receiving honoraria, research funding, consulting fees, or support for attending meetings or travel from several sources.

Source: Piontek K et al. J Childhood maltreatment is not associated with atopic dermatitis in adults: Results from a cross-sectional population-based cohort study. Eur Acad Dermatol Venereol. 2022 (Aug 3). Doi: 10.1111/jdv.18480

Key clinical point: Childhood maltreatment (CM) is associated with poor physical and mental health outcomes in adults; however, it was not found to be a risk factor for the development of adult atopic dermatitis (AD).

Major finding: Similar proportion of adults with and without AD (20.6% and 21.6%, respectively; P  =  .80) reported experiencing ≥1 type of moderate-to-severe CM, such as emotional, physical, and sexual abuse and emotional and physical neglect. Neither type of CM was associated with the development of AD in adults.

Study details: Findings are from an analysis of a cross-sectional population-based study including 2973 adults, of which 131 were diagnosed with AD.

Disclosures: This study was funded by the Federal Ministry of Education and Research and other sources. Some authors declared receiving honoraria, research funding, consulting fees, or support for attending meetings or travel from several sources.

Source: Piontek K et al. J Childhood maltreatment is not associated with atopic dermatitis in adults: Results from a cross-sectional population-based cohort study. Eur Acad Dermatol Venereol. 2022 (Aug 3). Doi: 10.1111/jdv.18480

Key clinical point: Childhood maltreatment (CM) is associated with poor physical and mental health outcomes in adults; however, it was not found to be a risk factor for the development of adult atopic dermatitis (AD).

Major finding: Similar proportion of adults with and without AD (20.6% and 21.6%, respectively; P  =  .80) reported experiencing ≥1 type of moderate-to-severe CM, such as emotional, physical, and sexual abuse and emotional and physical neglect. Neither type of CM was associated with the development of AD in adults.

Study details: Findings are from an analysis of a cross-sectional population-based study including 2973 adults, of which 131 were diagnosed with AD.

Disclosures: This study was funded by the Federal Ministry of Education and Research and other sources. Some authors declared receiving honoraria, research funding, consulting fees, or support for attending meetings or travel from several sources.

Source: Piontek K et al. J Childhood maltreatment is not associated with atopic dermatitis in adults: Results from a cross-sectional population-based cohort study. Eur Acad Dermatol Venereol. 2022 (Aug 3). Doi: 10.1111/jdv.18480

Key clinical point: Maternal exposure to nickel was associated with increased serum interleukin (IL)-2 levels but decreased serum eotaxin-1 levels and was negatively associated with the development of atopic dermatitis (AD) in children aged 3 years.

Major finding: Maternal nickel exposure was associated with increased serum levels of IL-2 (β 16.820; P < .001) but decreased serum levels of eotaxin-1 (β −5.065; P < .01) and was negatively associated with the development of AD (P  =  .024) in children aged 3 years.

Study details: Findings are from the analysis of an ongoing birth cohort study including 140 mother-child pairs.

Disclosures: This work was supported by grants from the Ministry of Science and Technology, Taiwan, and National Health Research Institutes. The authors declared no conflicts of interest.

Source: Ho JC et al. Prenatal exposure to nickel and atopic dermatitis at age 3 years: A birth cohort study with cytokine profiles. J Eur Acad Dermatol Venereol. 2022 (Jul 16). Doi: 10.1111/jdv.18425

Key clinical point: Maternal exposure to nickel was associated with increased serum interleukin (IL)-2 levels but decreased serum eotaxin-1 levels and was negatively associated with the development of atopic dermatitis (AD) in children aged 3 years.

Major finding: Maternal nickel exposure was associated with increased serum levels of IL-2 (β 16.820; P < .001) but decreased serum levels of eotaxin-1 (β −5.065; P < .01) and was negatively associated with the development of AD (P  =  .024) in children aged 3 years.

Study details: Findings are from the analysis of an ongoing birth cohort study including 140 mother-child pairs.

Disclosures: This work was supported by grants from the Ministry of Science and Technology, Taiwan, and National Health Research Institutes. The authors declared no conflicts of interest.

Source: Ho JC et al. Prenatal exposure to nickel and atopic dermatitis at age 3 years: A birth cohort study with cytokine profiles. J Eur Acad Dermatol Venereol. 2022 (Jul 16). Doi: 10.1111/jdv.18425

Key clinical point: Maternal exposure to nickel was associated with increased serum interleukin (IL)-2 levels but decreased serum eotaxin-1 levels and was negatively associated with the development of atopic dermatitis (AD) in children aged 3 years.

Major finding: Maternal nickel exposure was associated with increased serum levels of IL-2 (β 16.820; P < .001) but decreased serum levels of eotaxin-1 (β −5.065; P < .01) and was negatively associated with the development of AD (P  =  .024) in children aged 3 years.

Study details: Findings are from the analysis of an ongoing birth cohort study including 140 mother-child pairs.

Disclosures: This work was supported by grants from the Ministry of Science and Technology, Taiwan, and National Health Research Institutes. The authors declared no conflicts of interest.

Source: Ho JC et al. Prenatal exposure to nickel and atopic dermatitis at age 3 years: A birth cohort study with cytokine profiles. J Eur Acad Dermatol Venereol. 2022 (Jul 16). Doi: 10.1111/jdv.18425

Key clinical point: Interleukin (IL)-13 inhibitors, such as lebrikizumab and tralokinumab, rapidly reduced disease severity and were well tolerated in patients with moderate-to-severe atopic dermatitis (AD).

Major finding: A significantly higher proportion of patients receiving lebrikizumab or tralokinumab vs placebo achieved ≥75% improvement in the Eczema Area and Severity Index as early as week 4 (risk ratio [RR] 2.09; P  =  .006) and ≥4-point improvement in the Pruritus Numerical Rating Scale score (RR 1.59; 95% CI 1.23-2.05). Lebrikizumab/tralokinumab was associated with a higher risk for conjunctivitis than placebo (RR 2.318; P < .001).

Study details: Findings are from a meta-analysis of 7 randomized controlled trials including 2946 adults with moderate-to-severe AD who were randomly assigned to receive lebrikizumab, tralokinumab, or placebo for 12-16 weeks.

Disclosures: This study was supported by the Natural Science Foundation of China and other sources. The authors declared no conflicts of interest.

Source: Zhang Y et al. The efficacy and safety of IL-13 inhibitors in atopic dermatitis: A systematic review and meta-analysis. Front Immunol. 2022;13:923362 (Jul 27). Doi: 10.3389/fimmu.2022.923362

Key clinical point: Interleukin (IL)-13 inhibitors, such as lebrikizumab and tralokinumab, rapidly reduced disease severity and were well tolerated in patients with moderate-to-severe atopic dermatitis (AD).

Major finding: A significantly higher proportion of patients receiving lebrikizumab or tralokinumab vs placebo achieved ≥75% improvement in the Eczema Area and Severity Index as early as week 4 (risk ratio [RR] 2.09; P  =  .006) and ≥4-point improvement in the Pruritus Numerical Rating Scale score (RR 1.59; 95% CI 1.23-2.05). Lebrikizumab/tralokinumab was associated with a higher risk for conjunctivitis than placebo (RR 2.318; P < .001).

Study details: Findings are from a meta-analysis of 7 randomized controlled trials including 2946 adults with moderate-to-severe AD who were randomly assigned to receive lebrikizumab, tralokinumab, or placebo for 12-16 weeks.

Disclosures: This study was supported by the Natural Science Foundation of China and other sources. The authors declared no conflicts of interest.

Source: Zhang Y et al. The efficacy and safety of IL-13 inhibitors in atopic dermatitis: A systematic review and meta-analysis. Front Immunol. 2022;13:923362 (Jul 27). Doi: 10.3389/fimmu.2022.923362

Key clinical point: Interleukin (IL)-13 inhibitors, such as lebrikizumab and tralokinumab, rapidly reduced disease severity and were well tolerated in patients with moderate-to-severe atopic dermatitis (AD).

Major finding: A significantly higher proportion of patients receiving lebrikizumab or tralokinumab vs placebo achieved ≥75% improvement in the Eczema Area and Severity Index as early as week 4 (risk ratio [RR] 2.09; P  =  .006) and ≥4-point improvement in the Pruritus Numerical Rating Scale score (RR 1.59; 95% CI 1.23-2.05). Lebrikizumab/tralokinumab was associated with a higher risk for conjunctivitis than placebo (RR 2.318; P < .001).

Study details: Findings are from a meta-analysis of 7 randomized controlled trials including 2946 adults with moderate-to-severe AD who were randomly assigned to receive lebrikizumab, tralokinumab, or placebo for 12-16 weeks.

Disclosures: This study was supported by the Natural Science Foundation of China and other sources. The authors declared no conflicts of interest.

Source: Zhang Y et al. The efficacy and safety of IL-13 inhibitors in atopic dermatitis: A systematic review and meta-analysis. Front Immunol. 2022;13:923362 (Jul 27). Doi: 10.3389/fimmu.2022.923362

Key clinical point: A 2-week treatment with a test cream (TC) containing a steroid and pseudoceramide rapidly improved skin barrier function compared with a control cream (CC) containing only steroids in patients with mild-to-moderate atopic dermatitis (AD).

Major finding: In the TC group, the mean skin hydration value (48.0; P < .01) and transepidermal water loss (−2.1; P < .05) improved significantly as early as at 1 week after application, with similar improvements observed at 2 weeks; however, no significant improvements were observed in the CC group.

Study details: Findings are from a parallel, double-blind study including 36 patients with mild-to-moderate AD skin symptoms on the inner forearm who were randomly assigned to receive a TC containing 0.15% prednisolone valerate acetate (PVA)+3% synthetic pseudoceramide or a CC containing 0.15% PVA for 2 weeks.

Disclosures: This study was fully funded by Kao Corporation, Japan. The authors declared no conflicts of interest.

Source: Okoshi K et al. Efficacy of pseudo-ceramide-containing steroid lamellar cream in patients with mild to moderate atopic dermatitis: A randomized, double-blind study. Dermatol Ther (Heidelb). 2022;12:1823–1834 (Jul 19). Doi: 10.1007/s13555-022-00766-2

Key clinical point: A 2-week treatment with a test cream (TC) containing a steroid and pseudoceramide rapidly improved skin barrier function compared with a control cream (CC) containing only steroids in patients with mild-to-moderate atopic dermatitis (AD).

Major finding: In the TC group, the mean skin hydration value (48.0; P < .01) and transepidermal water loss (−2.1; P < .05) improved significantly as early as at 1 week after application, with similar improvements observed at 2 weeks; however, no significant improvements were observed in the CC group.

Study details: Findings are from a parallel, double-blind study including 36 patients with mild-to-moderate AD skin symptoms on the inner forearm who were randomly assigned to receive a TC containing 0.15% prednisolone valerate acetate (PVA)+3% synthetic pseudoceramide or a CC containing 0.15% PVA for 2 weeks.

Disclosures: This study was fully funded by Kao Corporation, Japan. The authors declared no conflicts of interest.

Source: Okoshi K et al. Efficacy of pseudo-ceramide-containing steroid lamellar cream in patients with mild to moderate atopic dermatitis: A randomized, double-blind study. Dermatol Ther (Heidelb). 2022;12:1823–1834 (Jul 19). Doi: 10.1007/s13555-022-00766-2

Key clinical point: A 2-week treatment with a test cream (TC) containing a steroid and pseudoceramide rapidly improved skin barrier function compared with a control cream (CC) containing only steroids in patients with mild-to-moderate atopic dermatitis (AD).

Major finding: In the TC group, the mean skin hydration value (48.0; P < .01) and transepidermal water loss (−2.1; P < .05) improved significantly as early as at 1 week after application, with similar improvements observed at 2 weeks; however, no significant improvements were observed in the CC group.

Study details: Findings are from a parallel, double-blind study including 36 patients with mild-to-moderate AD skin symptoms on the inner forearm who were randomly assigned to receive a TC containing 0.15% prednisolone valerate acetate (PVA)+3% synthetic pseudoceramide or a CC containing 0.15% PVA for 2 weeks.

Disclosures: This study was fully funded by Kao Corporation, Japan. The authors declared no conflicts of interest.

Source: Okoshi K et al. Efficacy of pseudo-ceramide-containing steroid lamellar cream in patients with mild to moderate atopic dermatitis: A randomized, double-blind study. Dermatol Ther (Heidelb). 2022;12:1823–1834 (Jul 19). Doi: 10.1007/s13555-022-00766-2

Key clinical point: Dupilumab demonstrated comparable long-term efficacy and safety in patients with moderate-to-severe atopic dermatitis (AD) and other major comorbidities (special population) as well as patients with only AD.

Major finding: Patients with AD and concomitant comorbidities achieved significant improvements in the Eczema Area and Severity Index at weeks 4, 16, and 52 (all P < .0001), with comparable outcomes observed in patients with only AD. Patients with vs without concomitant comorbidities reported injection site reactions (12.0% vs 17.22%) and conjunctivitis (8.0% vs 11.34%) as the main adverse events.

Study details: Findings are from a 52-week retrospective study including 263 adults with moderate-to-severe AD who received dupilumab for 16 weeks, including 25 patients with severe kidney failure, hepatitis B/C, neurological diseases, AIDS, or a history of cancer or organ transplantation who were classified as the special population.

Disclosures: This study did not receive any funding. Some authors declared serving as investigators, speakers, consultants, or advisory board members for several sources.

Source: Patruno C et al. Dupilumab for the treatment of adult atopic dermatitis in special populations. J Dermatolog Treat. 2022 (Jul 19). Doi: 10.1080/09546634.2022.2102121

Key clinical point: Dupilumab demonstrated comparable long-term efficacy and safety in patients with moderate-to-severe atopic dermatitis (AD) and other major comorbidities (special population) as well as patients with only AD.

Major finding: Patients with AD and concomitant comorbidities achieved significant improvements in the Eczema Area and Severity Index at weeks 4, 16, and 52 (all P < .0001), with comparable outcomes observed in patients with only AD. Patients with vs without concomitant comorbidities reported injection site reactions (12.0% vs 17.22%) and conjunctivitis (8.0% vs 11.34%) as the main adverse events.

Study details: Findings are from a 52-week retrospective study including 263 adults with moderate-to-severe AD who received dupilumab for 16 weeks, including 25 patients with severe kidney failure, hepatitis B/C, neurological diseases, AIDS, or a history of cancer or organ transplantation who were classified as the special population.

Disclosures: This study did not receive any funding. Some authors declared serving as investigators, speakers, consultants, or advisory board members for several sources.

Source: Patruno C et al. Dupilumab for the treatment of adult atopic dermatitis in special populations. J Dermatolog Treat. 2022 (Jul 19). Doi: 10.1080/09546634.2022.2102121

Key clinical point: Dupilumab demonstrated comparable long-term efficacy and safety in patients with moderate-to-severe atopic dermatitis (AD) and other major comorbidities (special population) as well as patients with only AD.

Major finding: Patients with AD and concomitant comorbidities achieved significant improvements in the Eczema Area and Severity Index at weeks 4, 16, and 52 (all P < .0001), with comparable outcomes observed in patients with only AD. Patients with vs without concomitant comorbidities reported injection site reactions (12.0% vs 17.22%) and conjunctivitis (8.0% vs 11.34%) as the main adverse events.

Study details: Findings are from a 52-week retrospective study including 263 adults with moderate-to-severe AD who received dupilumab for 16 weeks, including 25 patients with severe kidney failure, hepatitis B/C, neurological diseases, AIDS, or a history of cancer or organ transplantation who were classified as the special population.

Disclosures: This study did not receive any funding. Some authors declared serving as investigators, speakers, consultants, or advisory board members for several sources.

Source: Patruno C et al. Dupilumab for the treatment of adult atopic dermatitis in special populations. J Dermatolog Treat. 2022 (Jul 19). Doi: 10.1080/09546634.2022.2102121