MDedge Dermatology

To the Editor:

A 52-year-old man who was otherwise healthy and a long-distance runner presented with the sudden onset of diminished sweating on the left side of the body of 6 weeks’ duration. While training for a marathon, he reported that he perspired only on the right side of the body during runs of 12 to 15 miles; he observed a lack of sweating on the left side of the face, left side of the trunk, left arm, and left leg. This absence of sweating was accompanied by intense flushing on the right side of the face and trunk.

The patient did not take any medications. He reported no history of trauma and exhibited no neurologic deficits. A chest radiograph was negative. Thyroid function testing and a comprehensive metabolic panel were normal. Contrast-enhanced computed tomography of the chest and abdomen revealed a 4.3-cm soft-tissue mass in the left superior mediastinum that was superior to the aortic arch, posterior to the left subclavian artery in proximity to the sympathetic chain, and lateral to the trachea. The patient was diagnosed with Harlequin syndrome (HS).

Open thoracotomy was performed to remove the lesion. Analysis of the mass showed cystic areas, areas of hemorrhage (Figure 1A), and alternating zones of compact Antoni A spindle cells admixed with areas of less orderly Antoni B spindle cells within a hypocellular stroma (Figure 1B). Individual cells were characterized by eosinophilic cytoplasm and tapered nuclei. The mass appeared to be completely encapsulated. No mitotic figures were seen on multiple slides. The cells stained diffusely positive for S-100 proteins. At 6-month follow-up, the patient reported that he did not notice any return of normal sweating on the left side. However, the right-sided flushing had resolved.

Harlequin syndrome (also called the Harlequin sign) is a rare disorder of the sympathetic nervous system and should not be confused with lethal harlequin-type ichthyosis, an autosomal-recessive congenital disorder in which the affected newborn’s skin is hard and thickened over most of the body.¹ Harlequin syndrome usually is characterized by unilateral flushing and sweating that can affect the face, trunk, and extremities.² Physical stimuli, such as exercising (as in our patient), high body temperature, and the consumption of spicy or pungent food, or an emotional response can unmask or exacerbate symptoms of HS. The syndrome also can present with cluster headache.³ Harlequin syndrome is more common in females (66% of cases).⁴ Originally, the side of the face marked by increased sweating and flushing was perceived to be the pathologic side; now it is recognized that the anhidrotic side is affected by the causative pathology. The side of the face characterized by flushing might gradually darken as it compensates for lack of thermal regulation on the other side.^2,5

Usually, HS is an idiopathic condition associated with localized failure of upper thoracic sympathetic chain ganglia.⁵ A theory is that HS is part of a spectrum of autoimmune autonomic ganglionopathy.⁶ Typically, the syndrome is asymptomatic at rest, but testing can reveal an underlying sympathetic lesion.⁷ Structural lesions have been reported as a cause of the syndrome,⁶ similar to our patient.

Disrupted thermoregulatory vasodilation in HS is caused by an ipsilateral lesion of the sympathetic vasodilator neurons that innervate the face. Hemifacial anhidrosis also occurs because sudomotor neurons travel within the same pathways as vasodilator neurons.⁴

Our patient had a posterior mediastinal ancient schwannoma to the left of the subclavian artery, lateral to the trachea, with ipsilateral anhidrosis of the forehead, cheek, chin, and torso. In the medical literature, the forehead, cheek, and chin are described as being affected in HS when the lesion is located under the bifurcation of the carotid artery.^3,5 Most of the sudomotor and vasomotor fibers that innervate the face leave the spinal cord through ventral roots T2-T3⁴ (symptomatic areas are described in Figure 2), which correlates with the hypothesis that HS results from a deficit originating in the third thoracic nerve that is caused by a peripheral lesion affecting sympathetic outflow through the third thoracic root.² The location of our patient’s lesion supports this claim.

Harlequin syndrome can present simultaneously with ipsilateral Horner, Adie, and Ross syndromes.⁸ There are varying clinical presentations of Horner syndrome. Some patients with HS show autonomic ocular signs, such as miosis and ptosis, exhibiting Horner syndrome as an additional feature.⁵ Adie syndrome is characterized by tonic pupils with hyporeflexia and is unilateral in most cases. Ross syndrome is similar to Adie syndrome—including tonic pupils with hyporeflexia—in addition to a finding of segmental anhidrosis; it is bilateral in most cases.⁴

In some cases, Horner syndrome and HS originate from unilateral pharmaceutical sympathetic denervation (ie, as a consequence of paravertebral spread of local anesthetic to ipsilateral stellate ganglion).⁹ Facial nonflushing areas in HS typically are identical with anhidrotic areas¹⁰; Horner syndrome often is ipsilateral to the affected sympathetic region.¹¹

Our patient exhibited secondary HS from a tumor effect; however, an underlying tumor or infarct is absent in many cases. In primary (idiopathic) cases of HS, treatment is not recommended because the syndrome is benign.^10,11

If symptoms of HS cause notable social embarrassment, contralateral sympathectomy can be considered.^5,12 Repeated stellate ganglion block with a local anesthetic could be a less invasive treatment option.¹³ When considered on a case-by-case-basis, botulinum toxin type A has been effective as a treatment of compensatory hyperhidrosis on the unaffected side.¹⁴

In cases of secondary HS, surgical removal of the lesion may alleviate symptoms, though thoracotomy in our patient to remove the schwannoma did not alleviate anhidrosis. The Table lists treatment options for primary and secondary HS.^4,5,11

To the Editor:

A 52-year-old man who was otherwise healthy and a long-distance runner presented with the sudden onset of diminished sweating on the left side of the body of 6 weeks’ duration. While training for a marathon, he reported that he perspired only on the right side of the body during runs of 12 to 15 miles; he observed a lack of sweating on the left side of the face, left side of the trunk, left arm, and left leg. This absence of sweating was accompanied by intense flushing on the right side of the face and trunk.

The patient did not take any medications. He reported no history of trauma and exhibited no neurologic deficits. A chest radiograph was negative. Thyroid function testing and a comprehensive metabolic panel were normal. Contrast-enhanced computed tomography of the chest and abdomen revealed a 4.3-cm soft-tissue mass in the left superior mediastinum that was superior to the aortic arch, posterior to the left subclavian artery in proximity to the sympathetic chain, and lateral to the trachea. The patient was diagnosed with Harlequin syndrome (HS).

Open thoracotomy was performed to remove the lesion. Analysis of the mass showed cystic areas, areas of hemorrhage (Figure 1A), and alternating zones of compact Antoni A spindle cells admixed with areas of less orderly Antoni B spindle cells within a hypocellular stroma (Figure 1B). Individual cells were characterized by eosinophilic cytoplasm and tapered nuclei. The mass appeared to be completely encapsulated. No mitotic figures were seen on multiple slides. The cells stained diffusely positive for S-100 proteins. At 6-month follow-up, the patient reported that he did not notice any return of normal sweating on the left side. However, the right-sided flushing had resolved.

Harlequin syndrome (also called the Harlequin sign) is a rare disorder of the sympathetic nervous system and should not be confused with lethal harlequin-type ichthyosis, an autosomal-recessive congenital disorder in which the affected newborn’s skin is hard and thickened over most of the body.¹ Harlequin syndrome usually is characterized by unilateral flushing and sweating that can affect the face, trunk, and extremities.² Physical stimuli, such as exercising (as in our patient), high body temperature, and the consumption of spicy or pungent food, or an emotional response can unmask or exacerbate symptoms of HS. The syndrome also can present with cluster headache.³ Harlequin syndrome is more common in females (66% of cases).⁴ Originally, the side of the face marked by increased sweating and flushing was perceived to be the pathologic side; now it is recognized that the anhidrotic side is affected by the causative pathology. The side of the face characterized by flushing might gradually darken as it compensates for lack of thermal regulation on the other side.^2,5

Usually, HS is an idiopathic condition associated with localized failure of upper thoracic sympathetic chain ganglia.⁵ A theory is that HS is part of a spectrum of autoimmune autonomic ganglionopathy.⁶ Typically, the syndrome is asymptomatic at rest, but testing can reveal an underlying sympathetic lesion.⁷ Structural lesions have been reported as a cause of the syndrome,⁶ similar to our patient.

Disrupted thermoregulatory vasodilation in HS is caused by an ipsilateral lesion of the sympathetic vasodilator neurons that innervate the face. Hemifacial anhidrosis also occurs because sudomotor neurons travel within the same pathways as vasodilator neurons.⁴

Our patient had a posterior mediastinal ancient schwannoma to the left of the subclavian artery, lateral to the trachea, with ipsilateral anhidrosis of the forehead, cheek, chin, and torso. In the medical literature, the forehead, cheek, and chin are described as being affected in HS when the lesion is located under the bifurcation of the carotid artery.^3,5 Most of the sudomotor and vasomotor fibers that innervate the face leave the spinal cord through ventral roots T2-T3⁴ (symptomatic areas are described in Figure 2), which correlates with the hypothesis that HS results from a deficit originating in the third thoracic nerve that is caused by a peripheral lesion affecting sympathetic outflow through the third thoracic root.² The location of our patient’s lesion supports this claim.

Harlequin syndrome can present simultaneously with ipsilateral Horner, Adie, and Ross syndromes.⁸ There are varying clinical presentations of Horner syndrome. Some patients with HS show autonomic ocular signs, such as miosis and ptosis, exhibiting Horner syndrome as an additional feature.⁵ Adie syndrome is characterized by tonic pupils with hyporeflexia and is unilateral in most cases. Ross syndrome is similar to Adie syndrome—including tonic pupils with hyporeflexia—in addition to a finding of segmental anhidrosis; it is bilateral in most cases.⁴

In some cases, Horner syndrome and HS originate from unilateral pharmaceutical sympathetic denervation (ie, as a consequence of paravertebral spread of local anesthetic to ipsilateral stellate ganglion).⁹ Facial nonflushing areas in HS typically are identical with anhidrotic areas¹⁰; Horner syndrome often is ipsilateral to the affected sympathetic region.¹¹

Our patient exhibited secondary HS from a tumor effect; however, an underlying tumor or infarct is absent in many cases. In primary (idiopathic) cases of HS, treatment is not recommended because the syndrome is benign.^10,11

If symptoms of HS cause notable social embarrassment, contralateral sympathectomy can be considered.^5,12 Repeated stellate ganglion block with a local anesthetic could be a less invasive treatment option.¹³ When considered on a case-by-case-basis, botulinum toxin type A has been effective as a treatment of compensatory hyperhidrosis on the unaffected side.¹⁴

In cases of secondary HS, surgical removal of the lesion may alleviate symptoms, though thoracotomy in our patient to remove the schwannoma did not alleviate anhidrosis. The Table lists treatment options for primary and secondary HS.^4,5,11

To the Editor:

A 52-year-old man who was otherwise healthy and a long-distance runner presented with the sudden onset of diminished sweating on the left side of the body of 6 weeks’ duration. While training for a marathon, he reported that he perspired only on the right side of the body during runs of 12 to 15 miles; he observed a lack of sweating on the left side of the face, left side of the trunk, left arm, and left leg. This absence of sweating was accompanied by intense flushing on the right side of the face and trunk.

The patient did not take any medications. He reported no history of trauma and exhibited no neurologic deficits. A chest radiograph was negative. Thyroid function testing and a comprehensive metabolic panel were normal. Contrast-enhanced computed tomography of the chest and abdomen revealed a 4.3-cm soft-tissue mass in the left superior mediastinum that was superior to the aortic arch, posterior to the left subclavian artery in proximity to the sympathetic chain, and lateral to the trachea. The patient was diagnosed with Harlequin syndrome (HS).

Open thoracotomy was performed to remove the lesion. Analysis of the mass showed cystic areas, areas of hemorrhage (Figure 1A), and alternating zones of compact Antoni A spindle cells admixed with areas of less orderly Antoni B spindle cells within a hypocellular stroma (Figure 1B). Individual cells were characterized by eosinophilic cytoplasm and tapered nuclei. The mass appeared to be completely encapsulated. No mitotic figures were seen on multiple slides. The cells stained diffusely positive for S-100 proteins. At 6-month follow-up, the patient reported that he did not notice any return of normal sweating on the left side. However, the right-sided flushing had resolved.

Harlequin syndrome (also called the Harlequin sign) is a rare disorder of the sympathetic nervous system and should not be confused with lethal harlequin-type ichthyosis, an autosomal-recessive congenital disorder in which the affected newborn’s skin is hard and thickened over most of the body.¹ Harlequin syndrome usually is characterized by unilateral flushing and sweating that can affect the face, trunk, and extremities.² Physical stimuli, such as exercising (as in our patient), high body temperature, and the consumption of spicy or pungent food, or an emotional response can unmask or exacerbate symptoms of HS. The syndrome also can present with cluster headache.³ Harlequin syndrome is more common in females (66% of cases).⁴ Originally, the side of the face marked by increased sweating and flushing was perceived to be the pathologic side; now it is recognized that the anhidrotic side is affected by the causative pathology. The side of the face characterized by flushing might gradually darken as it compensates for lack of thermal regulation on the other side.^2,5

Usually, HS is an idiopathic condition associated with localized failure of upper thoracic sympathetic chain ganglia.⁵ A theory is that HS is part of a spectrum of autoimmune autonomic ganglionopathy.⁶ Typically, the syndrome is asymptomatic at rest, but testing can reveal an underlying sympathetic lesion.⁷ Structural lesions have been reported as a cause of the syndrome,⁶ similar to our patient.

Disrupted thermoregulatory vasodilation in HS is caused by an ipsilateral lesion of the sympathetic vasodilator neurons that innervate the face. Hemifacial anhidrosis also occurs because sudomotor neurons travel within the same pathways as vasodilator neurons.⁴

Our patient had a posterior mediastinal ancient schwannoma to the left of the subclavian artery, lateral to the trachea, with ipsilateral anhidrosis of the forehead, cheek, chin, and torso. In the medical literature, the forehead, cheek, and chin are described as being affected in HS when the lesion is located under the bifurcation of the carotid artery.^3,5 Most of the sudomotor and vasomotor fibers that innervate the face leave the spinal cord through ventral roots T2-T3⁴ (symptomatic areas are described in Figure 2), which correlates with the hypothesis that HS results from a deficit originating in the third thoracic nerve that is caused by a peripheral lesion affecting sympathetic outflow through the third thoracic root.² The location of our patient’s lesion supports this claim.

Harlequin syndrome can present simultaneously with ipsilateral Horner, Adie, and Ross syndromes.⁸ There are varying clinical presentations of Horner syndrome. Some patients with HS show autonomic ocular signs, such as miosis and ptosis, exhibiting Horner syndrome as an additional feature.⁵ Adie syndrome is characterized by tonic pupils with hyporeflexia and is unilateral in most cases. Ross syndrome is similar to Adie syndrome—including tonic pupils with hyporeflexia—in addition to a finding of segmental anhidrosis; it is bilateral in most cases.⁴

In some cases, Horner syndrome and HS originate from unilateral pharmaceutical sympathetic denervation (ie, as a consequence of paravertebral spread of local anesthetic to ipsilateral stellate ganglion).⁹ Facial nonflushing areas in HS typically are identical with anhidrotic areas¹⁰; Horner syndrome often is ipsilateral to the affected sympathetic region.¹¹

Our patient exhibited secondary HS from a tumor effect; however, an underlying tumor or infarct is absent in many cases. In primary (idiopathic) cases of HS, treatment is not recommended because the syndrome is benign.^10,11

If symptoms of HS cause notable social embarrassment, contralateral sympathectomy can be considered.^5,12 Repeated stellate ganglion block with a local anesthetic could be a less invasive treatment option.¹³ When considered on a case-by-case-basis, botulinum toxin type A has been effective as a treatment of compensatory hyperhidrosis on the unaffected side.¹⁴

In cases of secondary HS, surgical removal of the lesion may alleviate symptoms, though thoracotomy in our patient to remove the schwannoma did not alleviate anhidrosis. The Table lists treatment options for primary and secondary HS.^4,5,11

One year after hospitalization for COVID-19 only a minority of people feel fully recovered, with being female, obesity, and having had mechanical ventilation in hospital risk factors for not feeling fully recovered.

In the new U.K. study of more than 2,000 patients, presented at this year’s European Congress of Clinical Microbiology & Infectious Diseases (ECCMID 2022), and published in The Lancet Respiratory Medicine, research showed that one in four patients feel fully well again 1 year after hospitalization for COVID-19.

For their study, researchers from the University of Leicester used data from the post-hospitalization COVID-19 (PHOSP-COVID) prospective, longitudinal cohort study, which assessed adults aged 18 years and over who had been hospitalized with COVID-19 across the United Kingdom and subsequently discharged. The researchers assessed the recovery of 2,320 participants discharged from 39 U.K. hospitals between March 7, 2020, and April 18, 2021, who were assessed via patient-reported outcome measures, physical performance, and organ function at 5 months and at 1 year after hospital discharge. Blood samples were taken at the 5-month visit to be analyzed for the presence of various inflammatory proteins.

All participants were assessed at 5 months after discharge and 807 participants (33%) completed both the 5-month and 1-year visits at the time of the analysis. The study is ongoing. The 807 patients were mean age of 59 years, 36% were women, and 28% received invasive mechanical ventilation. The proportion of patients reporting full recovery was similar between 5 months (26%) and 1 year (29%).
 

Female sex and obesity major risk factors for not recovering

Being female, obese, and having had mechanical ventilation in hospital makes someone 32%, 50%, and 58%, respectively, less likely to feel fully recovered 1 year after COVID-19 hospitalization, the authors said.

“We found female sex and obesity were major risk factors for not recovering at one year,” said the researchers, led by Rachael Evans, PhD, Louise V. Wain, and Christopher E. Brightling, PhD, National Institute for Health Research, Leicester Biomedical Research Centre, University of Leicester.

The authors said fatigue, muscle pain, physically slowing down, poor sleep, and breathlessness were most common ongoing long COVID symptoms. They noted how the total number and range of ongoing symptoms at 1 year was “striking,” positively associated with the severity of long COVID, and emphasizes the “multisystem nature of long COVID.”
 

Several inflammatory mediators increased

An earlier publication from this study identified four groups or “clusters” of symptom severity at 5 months, which were confirmed by this new study at 1 year, the authors said. They reported that 20% had very severe physical and mental health impairment, 30% had severe physical and mental health impairment, 11% had moderate physical health impairment with cognitive impairment, and 39% had mild mental and physical health impairment.

They added that having obesity, reduced exercise capacity, a greater number of symptoms, and increased levels of C-reactive protein were associated with the “more severe clusters.” In both the very severe and the moderate with cognitive impairment clusters, levels of interleukin-6 (IL-6) were higher when compared with the mild cluster.

“The limited recovery from 5 months to 1 year after hospitalisation in our study across symptoms, mental health, exercise capacity, organ impairment, and quality-of-life is striking,” the researchers noted.

“In our clusters, female sex and obesity were also associated with more severe ongoing health impairments including reduced exercise performance and health-related quality of life at one year,” and suggested that this potentially highlighted a group that “might need higher intensity interventions such as supervised rehabilitation,” they added.

There are no specific therapeutics for long COVID, the researchers said, noting that “effective interventions are urgently required.” The persistent systemic inflammation identified, particularly in those in the very severe and moderate with cognitive impairment clusters, suggested that these groups “might respond to anti-inflammatory strategies,” the authors wrote.

“We found that a minority of participants felt fully recovered 1 year after hospital discharge, with minimal improvement after a 5-month assessment,” they noted.

They added that the findings suggest the need for complex interventions that target both physical and mental health impairments to alleviate symptoms, and that specific therapeutic approaches to manage posttraumatic stress disorder might also be needed. The authors pointed out how “pharmacological and non-pharmacological interventions are urgently needed,” with a “precision-medicine approach with potential treatable traits of systemic inflammation and obesity.”

They said their study highlighted the “urgent need for health-care services to support the large and rapidly increasing patient population in whom a substantial burden of symptoms exist, including reduced exercise capacity and substantially decreased health-related quality of life one year after hospital discharge.”

They warned that without effective treatments, long COVID could become a “highly prevalent new long-term condition.”

A version of this article first appeared on Medscape UK.

One year after hospitalization for COVID-19 only a minority of people feel fully recovered, with being female, obesity, and having had mechanical ventilation in hospital risk factors for not feeling fully recovered.

In the new U.K. study of more than 2,000 patients, presented at this year’s European Congress of Clinical Microbiology & Infectious Diseases (ECCMID 2022), and published in The Lancet Respiratory Medicine, research showed that one in four patients feel fully well again 1 year after hospitalization for COVID-19.

For their study, researchers from the University of Leicester used data from the post-hospitalization COVID-19 (PHOSP-COVID) prospective, longitudinal cohort study, which assessed adults aged 18 years and over who had been hospitalized with COVID-19 across the United Kingdom and subsequently discharged. The researchers assessed the recovery of 2,320 participants discharged from 39 U.K. hospitals between March 7, 2020, and April 18, 2021, who were assessed via patient-reported outcome measures, physical performance, and organ function at 5 months and at 1 year after hospital discharge. Blood samples were taken at the 5-month visit to be analyzed for the presence of various inflammatory proteins.

All participants were assessed at 5 months after discharge and 807 participants (33%) completed both the 5-month and 1-year visits at the time of the analysis. The study is ongoing. The 807 patients were mean age of 59 years, 36% were women, and 28% received invasive mechanical ventilation. The proportion of patients reporting full recovery was similar between 5 months (26%) and 1 year (29%).
 

Female sex and obesity major risk factors for not recovering

Being female, obese, and having had mechanical ventilation in hospital makes someone 32%, 50%, and 58%, respectively, less likely to feel fully recovered 1 year after COVID-19 hospitalization, the authors said.

“We found female sex and obesity were major risk factors for not recovering at one year,” said the researchers, led by Rachael Evans, PhD, Louise V. Wain, and Christopher E. Brightling, PhD, National Institute for Health Research, Leicester Biomedical Research Centre, University of Leicester.

The authors said fatigue, muscle pain, physically slowing down, poor sleep, and breathlessness were most common ongoing long COVID symptoms. They noted how the total number and range of ongoing symptoms at 1 year was “striking,” positively associated with the severity of long COVID, and emphasizes the “multisystem nature of long COVID.”
 

Several inflammatory mediators increased

An earlier publication from this study identified four groups or “clusters” of symptom severity at 5 months, which were confirmed by this new study at 1 year, the authors said. They reported that 20% had very severe physical and mental health impairment, 30% had severe physical and mental health impairment, 11% had moderate physical health impairment with cognitive impairment, and 39% had mild mental and physical health impairment.

They added that having obesity, reduced exercise capacity, a greater number of symptoms, and increased levels of C-reactive protein were associated with the “more severe clusters.” In both the very severe and the moderate with cognitive impairment clusters, levels of interleukin-6 (IL-6) were higher when compared with the mild cluster.

“The limited recovery from 5 months to 1 year after hospitalisation in our study across symptoms, mental health, exercise capacity, organ impairment, and quality-of-life is striking,” the researchers noted.

“In our clusters, female sex and obesity were also associated with more severe ongoing health impairments including reduced exercise performance and health-related quality of life at one year,” and suggested that this potentially highlighted a group that “might need higher intensity interventions such as supervised rehabilitation,” they added.

There are no specific therapeutics for long COVID, the researchers said, noting that “effective interventions are urgently required.” The persistent systemic inflammation identified, particularly in those in the very severe and moderate with cognitive impairment clusters, suggested that these groups “might respond to anti-inflammatory strategies,” the authors wrote.

“We found that a minority of participants felt fully recovered 1 year after hospital discharge, with minimal improvement after a 5-month assessment,” they noted.

They added that the findings suggest the need for complex interventions that target both physical and mental health impairments to alleviate symptoms, and that specific therapeutic approaches to manage posttraumatic stress disorder might also be needed. The authors pointed out how “pharmacological and non-pharmacological interventions are urgently needed,” with a “precision-medicine approach with potential treatable traits of systemic inflammation and obesity.”

They said their study highlighted the “urgent need for health-care services to support the large and rapidly increasing patient population in whom a substantial burden of symptoms exist, including reduced exercise capacity and substantially decreased health-related quality of life one year after hospital discharge.”

They warned that without effective treatments, long COVID could become a “highly prevalent new long-term condition.”

A version of this article first appeared on Medscape UK.

One year after hospitalization for COVID-19 only a minority of people feel fully recovered, with being female, obesity, and having had mechanical ventilation in hospital risk factors for not feeling fully recovered.

In the new U.K. study of more than 2,000 patients, presented at this year’s European Congress of Clinical Microbiology & Infectious Diseases (ECCMID 2022), and published in The Lancet Respiratory Medicine, research showed that one in four patients feel fully well again 1 year after hospitalization for COVID-19.

For their study, researchers from the University of Leicester used data from the post-hospitalization COVID-19 (PHOSP-COVID) prospective, longitudinal cohort study, which assessed adults aged 18 years and over who had been hospitalized with COVID-19 across the United Kingdom and subsequently discharged. The researchers assessed the recovery of 2,320 participants discharged from 39 U.K. hospitals between March 7, 2020, and April 18, 2021, who were assessed via patient-reported outcome measures, physical performance, and organ function at 5 months and at 1 year after hospital discharge. Blood samples were taken at the 5-month visit to be analyzed for the presence of various inflammatory proteins.

All participants were assessed at 5 months after discharge and 807 participants (33%) completed both the 5-month and 1-year visits at the time of the analysis. The study is ongoing. The 807 patients were mean age of 59 years, 36% were women, and 28% received invasive mechanical ventilation. The proportion of patients reporting full recovery was similar between 5 months (26%) and 1 year (29%).
 

Female sex and obesity major risk factors for not recovering

Being female, obese, and having had mechanical ventilation in hospital makes someone 32%, 50%, and 58%, respectively, less likely to feel fully recovered 1 year after COVID-19 hospitalization, the authors said.

“We found female sex and obesity were major risk factors for not recovering at one year,” said the researchers, led by Rachael Evans, PhD, Louise V. Wain, and Christopher E. Brightling, PhD, National Institute for Health Research, Leicester Biomedical Research Centre, University of Leicester.

The authors said fatigue, muscle pain, physically slowing down, poor sleep, and breathlessness were most common ongoing long COVID symptoms. They noted how the total number and range of ongoing symptoms at 1 year was “striking,” positively associated with the severity of long COVID, and emphasizes the “multisystem nature of long COVID.”
 

Several inflammatory mediators increased

An earlier publication from this study identified four groups or “clusters” of symptom severity at 5 months, which were confirmed by this new study at 1 year, the authors said. They reported that 20% had very severe physical and mental health impairment, 30% had severe physical and mental health impairment, 11% had moderate physical health impairment with cognitive impairment, and 39% had mild mental and physical health impairment.

They added that having obesity, reduced exercise capacity, a greater number of symptoms, and increased levels of C-reactive protein were associated with the “more severe clusters.” In both the very severe and the moderate with cognitive impairment clusters, levels of interleukin-6 (IL-6) were higher when compared with the mild cluster.

“The limited recovery from 5 months to 1 year after hospitalisation in our study across symptoms, mental health, exercise capacity, organ impairment, and quality-of-life is striking,” the researchers noted.

“In our clusters, female sex and obesity were also associated with more severe ongoing health impairments including reduced exercise performance and health-related quality of life at one year,” and suggested that this potentially highlighted a group that “might need higher intensity interventions such as supervised rehabilitation,” they added.

There are no specific therapeutics for long COVID, the researchers said, noting that “effective interventions are urgently required.” The persistent systemic inflammation identified, particularly in those in the very severe and moderate with cognitive impairment clusters, suggested that these groups “might respond to anti-inflammatory strategies,” the authors wrote.

“We found that a minority of participants felt fully recovered 1 year after hospital discharge, with minimal improvement after a 5-month assessment,” they noted.

They added that the findings suggest the need for complex interventions that target both physical and mental health impairments to alleviate symptoms, and that specific therapeutic approaches to manage posttraumatic stress disorder might also be needed. The authors pointed out how “pharmacological and non-pharmacological interventions are urgently needed,” with a “precision-medicine approach with potential treatable traits of systemic inflammation and obesity.”

They said their study highlighted the “urgent need for health-care services to support the large and rapidly increasing patient population in whom a substantial burden of symptoms exist, including reduced exercise capacity and substantially decreased health-related quality of life one year after hospital discharge.”

They warned that without effective treatments, long COVID could become a “highly prevalent new long-term condition.”

A version of this article first appeared on Medscape UK.

BOSTON – When patients present with complaints of hair loss or changes in hair color or texture, make sure to ask if they are taking oral hair growth supplements.

This is an important question because patients consider supplements as “natural and healthy,” not as drugs or chemicals, Wilma F. Bergfeld, MD, said at the annual meeting of the American Academy of Dermatology.

Some of these products contain botanicals, which are not always safe, added Dr. Bergfeld, professor of dermatology and pathology at the Cleveland Clinic. “They have many activities, and they are being touted as having some activity in helping the hair or enhancing hair growth,” including having 5-alpha-reductase inhibitors as an ingredient. “Saw palmetto is probably the most common one, but there are a host of natural ingredients that are being put into these supplements, including those that promote androgen induction, as well as antioxidants and anti-inflammatories.”

In the opinion of Dr. Bergfeld, a nutrition-focused physical assessment should include an examination of the scalp and all hairy areas. “It’s also important to see the symmetry and shape of hair growth or hair loss areas, the distribution, hair color, the thickness and texture of the hair fibers,” she added.

Besides asking about what supplements patients are taking, other questions to ask during the visit include: Are you noticing more hair on your brush, pillow, and shoulders, or in the shower? Do you think your hair is thinning? What are your medical problems? Have you experienced rapid weight loss? Have you started any new medications? What medication(s) are you on? What foods do you eat? Do you have a family history of hair loss?

Possible causes of hair loss or changes include environmental factors, stress, hormonal changes, medications, and nutrition.

Common ingredients contained in healthy hair supplements include biotin, folic acid, L-cysteine, L-methionine, MSM (methylsulfonylmethane), vitamin B complex, and vitamins A, C, D, and E. “Vitamin D and A are associated on the hair follicle receptor sites, and they balance each other, so if one is down the other is usually down,” said Dr. Bergfeld, who directs Cleveland Clinic’s hair disorders clinic and its dermatopathology program. Other important ingredients include iron, zinc, manganese, amino acids including L-Lysine, and fatty acids.

Iron deficiency is a known cause of hair loss. “The absorption of iron relies on vitamin C and sometimes lysine,” she said. Red meat has a high iron content and since many patients are restricting red meat intake, “they do need to think about that.” Zinc deficiency is less common in Western countries, she continued, “but when you find it, it’s revolutionary because if they’re shedding hair and their hair character is changing, often some supplementation will do the trick. But remember: Zinc is not only an anti-inflammatory, it’s also an antiandrogen. It has 5-alpha-reductase inhibitor capabilities.”.

Dr. Bergfeld noted that biotin, also known as vitamin B₇ and found in many foods, is used in many vitamin supplements marketed for hair loss. The recommended daily allowance (RDA) is 30 mcg/day in adults but the amount in hair supplements can be up to 650% of RDA. “Biotin at high levels is believed to be safe, but can interfere with troponin and other lab testing,” she cautioned. “This can lead to dangerous false laboratory results.”

To date, insufficient data exist to recommend supplementation with zinc, riboflavin, folic acid, or vitamin B₁₂ for hair loss, “but they may help in cases of deficiency,” said Dr. Bergfeld, a past president of the American Hair Research Society. The use of vitamin E and biotin supplementation is not supported in the literature for treating androgenetic alopecia or telogen effluvium. Excessive vitamin A (not beta carotene) and selenium can contribute to hair loss and studies have shown a relationship between androgenetic alopecia and low vitamin D levels. “Vitamin D should be supplemented if serum levels are low, but more studies are needed to determine the effect of iron and zinc supplementation” in patients with androgenetic alopecia, she said.

While there are not enough data to support a recommendation for supplementation of folic or B₁₂ for alopecia, she said, “vitamin B₁₂ deficiency may occur in androgenetic alopecia patients, associated with pernicious anemia.”

She added that the use biotin supplementation for the treatment of androgenetic alopecia is not supported by available data, and “it is also unclear if selenium plays a role in this disease.”

Dr. Bergfeld reported having no disclosures related to her presentation.

BOSTON – When patients present with complaints of hair loss or changes in hair color or texture, make sure to ask if they are taking oral hair growth supplements.

This is an important question because patients consider supplements as “natural and healthy,” not as drugs or chemicals, Wilma F. Bergfeld, MD, said at the annual meeting of the American Academy of Dermatology.

Some of these products contain botanicals, which are not always safe, added Dr. Bergfeld, professor of dermatology and pathology at the Cleveland Clinic. “They have many activities, and they are being touted as having some activity in helping the hair or enhancing hair growth,” including having 5-alpha-reductase inhibitors as an ingredient. “Saw palmetto is probably the most common one, but there are a host of natural ingredients that are being put into these supplements, including those that promote androgen induction, as well as antioxidants and anti-inflammatories.”

In the opinion of Dr. Bergfeld, a nutrition-focused physical assessment should include an examination of the scalp and all hairy areas. “It’s also important to see the symmetry and shape of hair growth or hair loss areas, the distribution, hair color, the thickness and texture of the hair fibers,” she added.

Besides asking about what supplements patients are taking, other questions to ask during the visit include: Are you noticing more hair on your brush, pillow, and shoulders, or in the shower? Do you think your hair is thinning? What are your medical problems? Have you experienced rapid weight loss? Have you started any new medications? What medication(s) are you on? What foods do you eat? Do you have a family history of hair loss?

Possible causes of hair loss or changes include environmental factors, stress, hormonal changes, medications, and nutrition.

Common ingredients contained in healthy hair supplements include biotin, folic acid, L-cysteine, L-methionine, MSM (methylsulfonylmethane), vitamin B complex, and vitamins A, C, D, and E. “Vitamin D and A are associated on the hair follicle receptor sites, and they balance each other, so if one is down the other is usually down,” said Dr. Bergfeld, who directs Cleveland Clinic’s hair disorders clinic and its dermatopathology program. Other important ingredients include iron, zinc, manganese, amino acids including L-Lysine, and fatty acids.

Iron deficiency is a known cause of hair loss. “The absorption of iron relies on vitamin C and sometimes lysine,” she said. Red meat has a high iron content and since many patients are restricting red meat intake, “they do need to think about that.” Zinc deficiency is less common in Western countries, she continued, “but when you find it, it’s revolutionary because if they’re shedding hair and their hair character is changing, often some supplementation will do the trick. But remember: Zinc is not only an anti-inflammatory, it’s also an antiandrogen. It has 5-alpha-reductase inhibitor capabilities.”.

Dr. Bergfeld noted that biotin, also known as vitamin B₇ and found in many foods, is used in many vitamin supplements marketed for hair loss. The recommended daily allowance (RDA) is 30 mcg/day in adults but the amount in hair supplements can be up to 650% of RDA. “Biotin at high levels is believed to be safe, but can interfere with troponin and other lab testing,” she cautioned. “This can lead to dangerous false laboratory results.”

To date, insufficient data exist to recommend supplementation with zinc, riboflavin, folic acid, or vitamin B₁₂ for hair loss, “but they may help in cases of deficiency,” said Dr. Bergfeld, a past president of the American Hair Research Society. The use of vitamin E and biotin supplementation is not supported in the literature for treating androgenetic alopecia or telogen effluvium. Excessive vitamin A (not beta carotene) and selenium can contribute to hair loss and studies have shown a relationship between androgenetic alopecia and low vitamin D levels. “Vitamin D should be supplemented if serum levels are low, but more studies are needed to determine the effect of iron and zinc supplementation” in patients with androgenetic alopecia, she said.

While there are not enough data to support a recommendation for supplementation of folic or B₁₂ for alopecia, she said, “vitamin B₁₂ deficiency may occur in androgenetic alopecia patients, associated with pernicious anemia.”

She added that the use biotin supplementation for the treatment of androgenetic alopecia is not supported by available data, and “it is also unclear if selenium plays a role in this disease.”

Dr. Bergfeld reported having no disclosures related to her presentation.

BOSTON – When patients present with complaints of hair loss or changes in hair color or texture, make sure to ask if they are taking oral hair growth supplements.

This is an important question because patients consider supplements as “natural and healthy,” not as drugs or chemicals, Wilma F. Bergfeld, MD, said at the annual meeting of the American Academy of Dermatology.

Some of these products contain botanicals, which are not always safe, added Dr. Bergfeld, professor of dermatology and pathology at the Cleveland Clinic. “They have many activities, and they are being touted as having some activity in helping the hair or enhancing hair growth,” including having 5-alpha-reductase inhibitors as an ingredient. “Saw palmetto is probably the most common one, but there are a host of natural ingredients that are being put into these supplements, including those that promote androgen induction, as well as antioxidants and anti-inflammatories.”

In the opinion of Dr. Bergfeld, a nutrition-focused physical assessment should include an examination of the scalp and all hairy areas. “It’s also important to see the symmetry and shape of hair growth or hair loss areas, the distribution, hair color, the thickness and texture of the hair fibers,” she added.

Besides asking about what supplements patients are taking, other questions to ask during the visit include: Are you noticing more hair on your brush, pillow, and shoulders, or in the shower? Do you think your hair is thinning? What are your medical problems? Have you experienced rapid weight loss? Have you started any new medications? What medication(s) are you on? What foods do you eat? Do you have a family history of hair loss?

Possible causes of hair loss or changes include environmental factors, stress, hormonal changes, medications, and nutrition.

Common ingredients contained in healthy hair supplements include biotin, folic acid, L-cysteine, L-methionine, MSM (methylsulfonylmethane), vitamin B complex, and vitamins A, C, D, and E. “Vitamin D and A are associated on the hair follicle receptor sites, and they balance each other, so if one is down the other is usually down,” said Dr. Bergfeld, who directs Cleveland Clinic’s hair disorders clinic and its dermatopathology program. Other important ingredients include iron, zinc, manganese, amino acids including L-Lysine, and fatty acids.

Iron deficiency is a known cause of hair loss. “The absorption of iron relies on vitamin C and sometimes lysine,” she said. Red meat has a high iron content and since many patients are restricting red meat intake, “they do need to think about that.” Zinc deficiency is less common in Western countries, she continued, “but when you find it, it’s revolutionary because if they’re shedding hair and their hair character is changing, often some supplementation will do the trick. But remember: Zinc is not only an anti-inflammatory, it’s also an antiandrogen. It has 5-alpha-reductase inhibitor capabilities.”.

Dr. Bergfeld noted that biotin, also known as vitamin B₇ and found in many foods, is used in many vitamin supplements marketed for hair loss. The recommended daily allowance (RDA) is 30 mcg/day in adults but the amount in hair supplements can be up to 650% of RDA. “Biotin at high levels is believed to be safe, but can interfere with troponin and other lab testing,” she cautioned. “This can lead to dangerous false laboratory results.”

To date, insufficient data exist to recommend supplementation with zinc, riboflavin, folic acid, or vitamin B₁₂ for hair loss, “but they may help in cases of deficiency,” said Dr. Bergfeld, a past president of the American Hair Research Society. The use of vitamin E and biotin supplementation is not supported in the literature for treating androgenetic alopecia or telogen effluvium. Excessive vitamin A (not beta carotene) and selenium can contribute to hair loss and studies have shown a relationship between androgenetic alopecia and low vitamin D levels. “Vitamin D should be supplemented if serum levels are low, but more studies are needed to determine the effect of iron and zinc supplementation” in patients with androgenetic alopecia, she said.

While there are not enough data to support a recommendation for supplementation of folic or B₁₂ for alopecia, she said, “vitamin B₁₂ deficiency may occur in androgenetic alopecia patients, associated with pernicious anemia.”

She added that the use biotin supplementation for the treatment of androgenetic alopecia is not supported by available data, and “it is also unclear if selenium plays a role in this disease.”

Dr. Bergfeld reported having no disclosures related to her presentation.

To the Editor:

A 53-year-old Hispanic woman presented to our dermatology clinic for evaluation of an expanding plaque on the right cheek of 2 months’ duration. The patient stated the plaque began as a pimple, which she picked with subsequent spread laterally across the cheek. The area was intermittently tender, but she denied tingling, burning, or pruritus of the site. She had been treated with doxycycline and amoxicillin–clavulanic acid prior to presentation without improvement. She had a history of levamisole-induced vasculitis approximately 6 months prior. A review of systems was notable for diffuse joint pain. The patient denied tobacco, alcohol, or illicit drug use in the preceding 3 months and denied any changes in her medications or in health within the last year.

Physical examination revealed a well-appearing, alert, and afebrile patient with a pink, well-demarcated plaque on the right cheek (Figure 1). The borders of the plaque were indurated, and the lateral aspect of the plaque was eroded secondary to digital manipulation by the patient. She had no cervical lymphadenopathy. There were no other abnormal cutaneous findings.

There is a broad differential diagnosis for a pink expanding plaque on the face, which requires histopathologic correlation for correct diagnosis. Three broad categories in the differential are infectious (eg, bacterial, fungal), medication related (eg, fixed drug eruption), and granulomatous (eg, granuloma faciale [GF], sarcoidosis, tumid lupus, leprosy, granulomatous rosacea). A biopsy of the lesion revealed a mixed inflammatory cell dermal infiltrate with perivascular accentuation and intense vasculitis that was consistent with GF (Figure 2). Gomori methenamine-silver, periodic acid–Schiff, Fite-Faraco, acid-fast bacilli, and Gram staining were negative for organisms. Tissue cultures were negative for bacterial, mycobacterial, and fungal etiology. The patient was started on high-potency topical steroids with a 50% improvement in the appearance of the skin lesion at 1-month follow-up.

Granuloma faciale is a rare chronic inflammatory dermatosis with a predilection for the face that is difficult to diagnose and treat. The diagnosis is based on clinical and histologic findings, and it typically presents as single or multiple, well-demarcated, red-brown nodules, papules, or plaques that range from several millimeters to centimeters in diameter.^1,2 Extrafacial lesions may be seen.³ Granuloma faciale usually is asymptomatic but occasionally has associated pruritus and rarely ulceration. The prevalence and pathophysiology of GF is not well defined; however, GF more commonly is reported in middle-aged White males.¹

Histologic examination of GF reveals a mixed inflammatory cellular infiltrate in the upper dermis. A grenz zone, which is a narrow area of the papillary dermis uninvolved by the underlying pathology, may be seen.¹ Contrary to the name, granulomas are not found histologically. Rather, vascular changes or damage frequently are present and may indicate a small vessel vasculitis pathologic mechanism. Granuloma faciale also has been associated with follicular ostia accentuation and telangiectases.⁴

Many cases of GF have been misdiagnosed as sarcoidosis, lymphoma, lupus, and basal cell carcinoma.¹ In addition, GF shares many clinical and histologic features with erythema elevatum diutinum (EED). However, the defining features that suggest EED over GF is that EED has a predilection for the skin overlying the joints. Histopathologically, EED displays granulomas and fibrosis with few eosinophils.^5,6

The variable response of GF to treatments and lack of efficacy data have contributed to the complexity and uncertainty of managing GF. The current first-line therapies are topical tacrolimus,⁷ cryotherapy,⁸ or corticosteroid therapy.⁹

To the Editor:

A 53-year-old Hispanic woman presented to our dermatology clinic for evaluation of an expanding plaque on the right cheek of 2 months’ duration. The patient stated the plaque began as a pimple, which she picked with subsequent spread laterally across the cheek. The area was intermittently tender, but she denied tingling, burning, or pruritus of the site. She had been treated with doxycycline and amoxicillin–clavulanic acid prior to presentation without improvement. She had a history of levamisole-induced vasculitis approximately 6 months prior. A review of systems was notable for diffuse joint pain. The patient denied tobacco, alcohol, or illicit drug use in the preceding 3 months and denied any changes in her medications or in health within the last year.

Physical examination revealed a well-appearing, alert, and afebrile patient with a pink, well-demarcated plaque on the right cheek (Figure 1). The borders of the plaque were indurated, and the lateral aspect of the plaque was eroded secondary to digital manipulation by the patient. She had no cervical lymphadenopathy. There were no other abnormal cutaneous findings.

There is a broad differential diagnosis for a pink expanding plaque on the face, which requires histopathologic correlation for correct diagnosis. Three broad categories in the differential are infectious (eg, bacterial, fungal), medication related (eg, fixed drug eruption), and granulomatous (eg, granuloma faciale [GF], sarcoidosis, tumid lupus, leprosy, granulomatous rosacea). A biopsy of the lesion revealed a mixed inflammatory cell dermal infiltrate with perivascular accentuation and intense vasculitis that was consistent with GF (Figure 2). Gomori methenamine-silver, periodic acid–Schiff, Fite-Faraco, acid-fast bacilli, and Gram staining were negative for organisms. Tissue cultures were negative for bacterial, mycobacterial, and fungal etiology. The patient was started on high-potency topical steroids with a 50% improvement in the appearance of the skin lesion at 1-month follow-up.

Granuloma faciale is a rare chronic inflammatory dermatosis with a predilection for the face that is difficult to diagnose and treat. The diagnosis is based on clinical and histologic findings, and it typically presents as single or multiple, well-demarcated, red-brown nodules, papules, or plaques that range from several millimeters to centimeters in diameter.^1,2 Extrafacial lesions may be seen.³ Granuloma faciale usually is asymptomatic but occasionally has associated pruritus and rarely ulceration. The prevalence and pathophysiology of GF is not well defined; however, GF more commonly is reported in middle-aged White males.¹

Histologic examination of GF reveals a mixed inflammatory cellular infiltrate in the upper dermis. A grenz zone, which is a narrow area of the papillary dermis uninvolved by the underlying pathology, may be seen.¹ Contrary to the name, granulomas are not found histologically. Rather, vascular changes or damage frequently are present and may indicate a small vessel vasculitis pathologic mechanism. Granuloma faciale also has been associated with follicular ostia accentuation and telangiectases.⁴

Many cases of GF have been misdiagnosed as sarcoidosis, lymphoma, lupus, and basal cell carcinoma.¹ In addition, GF shares many clinical and histologic features with erythema elevatum diutinum (EED). However, the defining features that suggest EED over GF is that EED has a predilection for the skin overlying the joints. Histopathologically, EED displays granulomas and fibrosis with few eosinophils.^5,6

The variable response of GF to treatments and lack of efficacy data have contributed to the complexity and uncertainty of managing GF. The current first-line therapies are topical tacrolimus,⁷ cryotherapy,⁸ or corticosteroid therapy.⁹

To the Editor:

A 53-year-old Hispanic woman presented to our dermatology clinic for evaluation of an expanding plaque on the right cheek of 2 months’ duration. The patient stated the plaque began as a pimple, which she picked with subsequent spread laterally across the cheek. The area was intermittently tender, but she denied tingling, burning, or pruritus of the site. She had been treated with doxycycline and amoxicillin–clavulanic acid prior to presentation without improvement. She had a history of levamisole-induced vasculitis approximately 6 months prior. A review of systems was notable for diffuse joint pain. The patient denied tobacco, alcohol, or illicit drug use in the preceding 3 months and denied any changes in her medications or in health within the last year.

Physical examination revealed a well-appearing, alert, and afebrile patient with a pink, well-demarcated plaque on the right cheek (Figure 1). The borders of the plaque were indurated, and the lateral aspect of the plaque was eroded secondary to digital manipulation by the patient. She had no cervical lymphadenopathy. There were no other abnormal cutaneous findings.

There is a broad differential diagnosis for a pink expanding plaque on the face, which requires histopathologic correlation for correct diagnosis. Three broad categories in the differential are infectious (eg, bacterial, fungal), medication related (eg, fixed drug eruption), and granulomatous (eg, granuloma faciale [GF], sarcoidosis, tumid lupus, leprosy, granulomatous rosacea). A biopsy of the lesion revealed a mixed inflammatory cell dermal infiltrate with perivascular accentuation and intense vasculitis that was consistent with GF (Figure 2). Gomori methenamine-silver, periodic acid–Schiff, Fite-Faraco, acid-fast bacilli, and Gram staining were negative for organisms. Tissue cultures were negative for bacterial, mycobacterial, and fungal etiology. The patient was started on high-potency topical steroids with a 50% improvement in the appearance of the skin lesion at 1-month follow-up.

Granuloma faciale is a rare chronic inflammatory dermatosis with a predilection for the face that is difficult to diagnose and treat. The diagnosis is based on clinical and histologic findings, and it typically presents as single or multiple, well-demarcated, red-brown nodules, papules, or plaques that range from several millimeters to centimeters in diameter.^1,2 Extrafacial lesions may be seen.³ Granuloma faciale usually is asymptomatic but occasionally has associated pruritus and rarely ulceration. The prevalence and pathophysiology of GF is not well defined; however, GF more commonly is reported in middle-aged White males.¹

Histologic examination of GF reveals a mixed inflammatory cellular infiltrate in the upper dermis. A grenz zone, which is a narrow area of the papillary dermis uninvolved by the underlying pathology, may be seen.¹ Contrary to the name, granulomas are not found histologically. Rather, vascular changes or damage frequently are present and may indicate a small vessel vasculitis pathologic mechanism. Granuloma faciale also has been associated with follicular ostia accentuation and telangiectases.⁴

Many cases of GF have been misdiagnosed as sarcoidosis, lymphoma, lupus, and basal cell carcinoma.¹ In addition, GF shares many clinical and histologic features with erythema elevatum diutinum (EED). However, the defining features that suggest EED over GF is that EED has a predilection for the skin overlying the joints. Histopathologically, EED displays granulomas and fibrosis with few eosinophils.^5,6

The variable response of GF to treatments and lack of efficacy data have contributed to the complexity and uncertainty of managing GF. The current first-line therapies are topical tacrolimus,⁷ cryotherapy,⁸ or corticosteroid therapy.⁹

Mohs micrographic surgery (MMS) frequently is used in surgical removal of cancerous cutaneous lesions on cosmetically sensitive areas and anatomically challenging sites, including the ears. The vascular supply of the ear is complex and includes several watershed regions that are susceptible to injury during surgical resection or operative closure.

Case Reports

Patient 1—An 82-year-old woman with a 100-pack-year smoking history and no known history of diabetes mellitus or coronary artery disease presented with a superficial and micronodular basal cell carcinoma (BCC) of the left postauricular skin of approximately 18 months’ duration. Mohs micrographic surgery was performed for lesion removal. The BCC was noted to be deeply penetrating and by the second stage was to the depth of the deep subcutaneous tissue (Figure 1A [inset]). Frozen section histopathology revealed a micronodular and superficial BCC. A 2.1×2.0-cm postoperative defect including the posterior surface of the ear, postauricular sulcus, and postauricular scalp remained. To minimize the area left to heal via secondary intention, partial layered closure was performed by placing four 4-0 polyglactin sutures from the scalp side of the defect on the postauricular skin to the postauricular sulcus (Figure 1A).

The patient presented to the clinic on postoperative day (POD) 4, noting pain and redness since the evening of the surgery on the anterior surface of the ear, specifically the cavum concha. Physical examination revealed that the incision site appeared to be healing as expected, but the cavum concha demonstrated erosions and ecchymosis (Figure 1B). A fluid culture was collected, and the patient was started on doxycycline 100 mg twice daily for 10 days. The patient returned to the clinic at POD 10 with skin sloughing and a small border of dark purple discoloration, consistent with early necrosis.

At the 1-month postsurgery follow-up visit, the wound had persistent anterior sloughing and discoloration with adherent debris suggestive of vascular compromise. At the 5-month wound check, the left conchal bowl had a 1-cm through-and-through defect of the concha cavum (Figure 1B [inset]). The favored etiology was occlusion of the posterior auricular artery during the patient’s MMS and reconstruction. Once healed, options including reconstruction, prosthesis, and no treatment were discussed with the patient. The patient decided to pursue partial closure of the defect.

Patient 2—A 71-year-old man with coronary artery disease and no known smoking or diabetes mellitus history presented with a 0.7×0.6-cm cutaneous squamous cell carcinoma of the left helix (Figure 2A [inset]). Mohs micrographic surgery was completed, resulting in a 1.1×1.0-cm defect that extended to the perichondrium. Given the location and size, a linear closure was performed with a deep layer of 5-0 polyglactin sutures and a cutaneous layer of 6-0 polypropylene sutures. The final closure length was 2.1 cm (Figure 2A).

On POD 14, the patient presented for suture removal and reported the onset of brown discoloration of the ear on POD 3. Physical examination revealed the left ear appeared dusky around the mid helix with extension onto the antihelix (Figure 2B). Because one of the main concerns was necrosis, a thin layer of nitropaste ointment 2% was prescribed to be applied twice daily to the affected area, in addition to liberal application of petroleum jelly. On POD 21, the left mid helix demonstrated a well-defined area of necrosis on the helical rim extending to the antihelix, and conservative treatment was continued. Four weeks later, the left ear had a prominent eschar, which was debrided. On follow-up 6 weeks later, the area was well healed with an obvious notched defect of the helix and scaphoid fossa (Figure 2B [inset]). The favored etiology was occlusion of the middle helical arcade during the patient’s MMS and reconstruction. Reconstructive options were discussed with the patient; however, he declined any further reconstructive intervention.

Comment

Auricular Vasculature—In our patients, the auricular vascular supply was compromised during routine MMS followed by reconstruction, resulting in tissue necrosis. Given the relative frequency of these procedures and the risk for tissue necrosis, a review of the auricular vasculature with special attention to the conchal bowl and helical rim was warranted (Figure 3).

The auricle is supplied by 2 main arterial sources arising from the external carotid artery: the superficial temporal artery (STA) supplying the anterior auricle and the posterior auricular artery (PAA) supplying the posterior auricle and the concha.¹ Anastomoses between these 2 blood supplies occur through perforating arteries and vascular arcades.

As the STA courses cranially, it moves from a deep position—deep to the parotidomasseteric fascia—to the superficial temporal fascia approximately 1 cm anterior and superior to the tragus. In approximately 80% of patients, 3 perpendicular branches stem from the STA—the upper, middle, and lower anterior branches—which supply the ascending helix, tragus, and lower margin of the earlobe, respectively.² The upper anterior branch of the STA joins other branches to form 2 dominant arcades: the first with the nonperforating branches of the PAA forming the upper third of the helical arcade, and the second with the lower anterior branch of the STA forming the middle portion of the helical arcade.^3,4 In 75% of patients, the middle helical arcade was identified as a single connecting artery, whereas in the remaining 25% of patients, a robust capillary network was formed.² In patient 2, the middle helical arcade was likely disrupted during closure, resulting in the helical necrosis seen postoperatively.

The second main blood supply of the auricle is the PAA, which enters in a more superficial position after traversing superiorly from the meatal cartilage, between the mastoid process and the posterior surface of the concha. From this point, the PAA runs in the deep subcutaneous tissue in the groove formed by the conchal cartilage and the mastoid process. Near the midpoint of the postauricular groove, it passes inferior to the postauricular muscle. The PAA has multiple radial branches that anastomose with helical branches; it also sends perforating branches (there were 2–4 branches in a recent study²) through the cartilage to the anterior surface of the concha. The 2 primary perforating arteries most commonly are located at the level of the antihelix and the antitragus.⁵ These arteries transverse through a vascular foramen located approximately 11 mm from the tragus in the horizontal plane and supply blood to the conchal bowl.⁶ In patient 1, the PAA itself, or the perforating arteries that course anteriorly through the vascular foramen, was likely disrupted, resulting in the conchal defect.

Special Considerations Before Surgery—As evidenced by these cases, special attention is needed during operative planning to account for the external ear vascular arcades. Damage to the helical arcades (patient 2) or the perforating arteries within the conchal bowl (patient 1) can lead to unintended consequences such as postoperative tissue necrosis. Tissue manipulation in these areas should be approached cautiously and with the least invasive treatment and closure options available. In doing so, blood flow and tissue integrity can be maintained, resulting in improved postoperative outcomes. Further research is warranted to identify the best intervention in cases involving these watershed regions.

Mohs micrographic surgery (MMS) frequently is used in surgical removal of cancerous cutaneous lesions on cosmetically sensitive areas and anatomically challenging sites, including the ears. The vascular supply of the ear is complex and includes several watershed regions that are susceptible to injury during surgical resection or operative closure.

Case Reports

Patient 1—An 82-year-old woman with a 100-pack-year smoking history and no known history of diabetes mellitus or coronary artery disease presented with a superficial and micronodular basal cell carcinoma (BCC) of the left postauricular skin of approximately 18 months’ duration. Mohs micrographic surgery was performed for lesion removal. The BCC was noted to be deeply penetrating and by the second stage was to the depth of the deep subcutaneous tissue (Figure 1A [inset]). Frozen section histopathology revealed a micronodular and superficial BCC. A 2.1×2.0-cm postoperative defect including the posterior surface of the ear, postauricular sulcus, and postauricular scalp remained. To minimize the area left to heal via secondary intention, partial layered closure was performed by placing four 4-0 polyglactin sutures from the scalp side of the defect on the postauricular skin to the postauricular sulcus (Figure 1A).

The patient presented to the clinic on postoperative day (POD) 4, noting pain and redness since the evening of the surgery on the anterior surface of the ear, specifically the cavum concha. Physical examination revealed that the incision site appeared to be healing as expected, but the cavum concha demonstrated erosions and ecchymosis (Figure 1B). A fluid culture was collected, and the patient was started on doxycycline 100 mg twice daily for 10 days. The patient returned to the clinic at POD 10 with skin sloughing and a small border of dark purple discoloration, consistent with early necrosis.

At the 1-month postsurgery follow-up visit, the wound had persistent anterior sloughing and discoloration with adherent debris suggestive of vascular compromise. At the 5-month wound check, the left conchal bowl had a 1-cm through-and-through defect of the concha cavum (Figure 1B [inset]). The favored etiology was occlusion of the posterior auricular artery during the patient’s MMS and reconstruction. Once healed, options including reconstruction, prosthesis, and no treatment were discussed with the patient. The patient decided to pursue partial closure of the defect.

Patient 2—A 71-year-old man with coronary artery disease and no known smoking or diabetes mellitus history presented with a 0.7×0.6-cm cutaneous squamous cell carcinoma of the left helix (Figure 2A [inset]). Mohs micrographic surgery was completed, resulting in a 1.1×1.0-cm defect that extended to the perichondrium. Given the location and size, a linear closure was performed with a deep layer of 5-0 polyglactin sutures and a cutaneous layer of 6-0 polypropylene sutures. The final closure length was 2.1 cm (Figure 2A).

On POD 14, the patient presented for suture removal and reported the onset of brown discoloration of the ear on POD 3. Physical examination revealed the left ear appeared dusky around the mid helix with extension onto the antihelix (Figure 2B). Because one of the main concerns was necrosis, a thin layer of nitropaste ointment 2% was prescribed to be applied twice daily to the affected area, in addition to liberal application of petroleum jelly. On POD 21, the left mid helix demonstrated a well-defined area of necrosis on the helical rim extending to the antihelix, and conservative treatment was continued. Four weeks later, the left ear had a prominent eschar, which was debrided. On follow-up 6 weeks later, the area was well healed with an obvious notched defect of the helix and scaphoid fossa (Figure 2B [inset]). The favored etiology was occlusion of the middle helical arcade during the patient’s MMS and reconstruction. Reconstructive options were discussed with the patient; however, he declined any further reconstructive intervention.

Comment

Auricular Vasculature—In our patients, the auricular vascular supply was compromised during routine MMS followed by reconstruction, resulting in tissue necrosis. Given the relative frequency of these procedures and the risk for tissue necrosis, a review of the auricular vasculature with special attention to the conchal bowl and helical rim was warranted (Figure 3).

The auricle is supplied by 2 main arterial sources arising from the external carotid artery: the superficial temporal artery (STA) supplying the anterior auricle and the posterior auricular artery (PAA) supplying the posterior auricle and the concha.¹ Anastomoses between these 2 blood supplies occur through perforating arteries and vascular arcades.

As the STA courses cranially, it moves from a deep position—deep to the parotidomasseteric fascia—to the superficial temporal fascia approximately 1 cm anterior and superior to the tragus. In approximately 80% of patients, 3 perpendicular branches stem from the STA—the upper, middle, and lower anterior branches—which supply the ascending helix, tragus, and lower margin of the earlobe, respectively.² The upper anterior branch of the STA joins other branches to form 2 dominant arcades: the first with the nonperforating branches of the PAA forming the upper third of the helical arcade, and the second with the lower anterior branch of the STA forming the middle portion of the helical arcade.^3,4 In 75% of patients, the middle helical arcade was identified as a single connecting artery, whereas in the remaining 25% of patients, a robust capillary network was formed.² In patient 2, the middle helical arcade was likely disrupted during closure, resulting in the helical necrosis seen postoperatively.

The second main blood supply of the auricle is the PAA, which enters in a more superficial position after traversing superiorly from the meatal cartilage, between the mastoid process and the posterior surface of the concha. From this point, the PAA runs in the deep subcutaneous tissue in the groove formed by the conchal cartilage and the mastoid process. Near the midpoint of the postauricular groove, it passes inferior to the postauricular muscle. The PAA has multiple radial branches that anastomose with helical branches; it also sends perforating branches (there were 2–4 branches in a recent study²) through the cartilage to the anterior surface of the concha. The 2 primary perforating arteries most commonly are located at the level of the antihelix and the antitragus.⁵ These arteries transverse through a vascular foramen located approximately 11 mm from the tragus in the horizontal plane and supply blood to the conchal bowl.⁶ In patient 1, the PAA itself, or the perforating arteries that course anteriorly through the vascular foramen, was likely disrupted, resulting in the conchal defect.

Special Considerations Before Surgery—As evidenced by these cases, special attention is needed during operative planning to account for the external ear vascular arcades. Damage to the helical arcades (patient 2) or the perforating arteries within the conchal bowl (patient 1) can lead to unintended consequences such as postoperative tissue necrosis. Tissue manipulation in these areas should be approached cautiously and with the least invasive treatment and closure options available. In doing so, blood flow and tissue integrity can be maintained, resulting in improved postoperative outcomes. Further research is warranted to identify the best intervention in cases involving these watershed regions.

Mohs micrographic surgery (MMS) frequently is used in surgical removal of cancerous cutaneous lesions on cosmetically sensitive areas and anatomically challenging sites, including the ears. The vascular supply of the ear is complex and includes several watershed regions that are susceptible to injury during surgical resection or operative closure.

Case Reports

Patient 1—An 82-year-old woman with a 100-pack-year smoking history and no known history of diabetes mellitus or coronary artery disease presented with a superficial and micronodular basal cell carcinoma (BCC) of the left postauricular skin of approximately 18 months’ duration. Mohs micrographic surgery was performed for lesion removal. The BCC was noted to be deeply penetrating and by the second stage was to the depth of the deep subcutaneous tissue (Figure 1A [inset]). Frozen section histopathology revealed a micronodular and superficial BCC. A 2.1×2.0-cm postoperative defect including the posterior surface of the ear, postauricular sulcus, and postauricular scalp remained. To minimize the area left to heal via secondary intention, partial layered closure was performed by placing four 4-0 polyglactin sutures from the scalp side of the defect on the postauricular skin to the postauricular sulcus (Figure 1A).

The patient presented to the clinic on postoperative day (POD) 4, noting pain and redness since the evening of the surgery on the anterior surface of the ear, specifically the cavum concha. Physical examination revealed that the incision site appeared to be healing as expected, but the cavum concha demonstrated erosions and ecchymosis (Figure 1B). A fluid culture was collected, and the patient was started on doxycycline 100 mg twice daily for 10 days. The patient returned to the clinic at POD 10 with skin sloughing and a small border of dark purple discoloration, consistent with early necrosis.

At the 1-month postsurgery follow-up visit, the wound had persistent anterior sloughing and discoloration with adherent debris suggestive of vascular compromise. At the 5-month wound check, the left conchal bowl had a 1-cm through-and-through defect of the concha cavum (Figure 1B [inset]). The favored etiology was occlusion of the posterior auricular artery during the patient’s MMS and reconstruction. Once healed, options including reconstruction, prosthesis, and no treatment were discussed with the patient. The patient decided to pursue partial closure of the defect.

Patient 2—A 71-year-old man with coronary artery disease and no known smoking or diabetes mellitus history presented with a 0.7×0.6-cm cutaneous squamous cell carcinoma of the left helix (Figure 2A [inset]). Mohs micrographic surgery was completed, resulting in a 1.1×1.0-cm defect that extended to the perichondrium. Given the location and size, a linear closure was performed with a deep layer of 5-0 polyglactin sutures and a cutaneous layer of 6-0 polypropylene sutures. The final closure length was 2.1 cm (Figure 2A).

On POD 14, the patient presented for suture removal and reported the onset of brown discoloration of the ear on POD 3. Physical examination revealed the left ear appeared dusky around the mid helix with extension onto the antihelix (Figure 2B). Because one of the main concerns was necrosis, a thin layer of nitropaste ointment 2% was prescribed to be applied twice daily to the affected area, in addition to liberal application of petroleum jelly. On POD 21, the left mid helix demonstrated a well-defined area of necrosis on the helical rim extending to the antihelix, and conservative treatment was continued. Four weeks later, the left ear had a prominent eschar, which was debrided. On follow-up 6 weeks later, the area was well healed with an obvious notched defect of the helix and scaphoid fossa (Figure 2B [inset]). The favored etiology was occlusion of the middle helical arcade during the patient’s MMS and reconstruction. Reconstructive options were discussed with the patient; however, he declined any further reconstructive intervention.

Comment

Auricular Vasculature—In our patients, the auricular vascular supply was compromised during routine MMS followed by reconstruction, resulting in tissue necrosis. Given the relative frequency of these procedures and the risk for tissue necrosis, a review of the auricular vasculature with special attention to the conchal bowl and helical rim was warranted (Figure 3).

The auricle is supplied by 2 main arterial sources arising from the external carotid artery: the superficial temporal artery (STA) supplying the anterior auricle and the posterior auricular artery (PAA) supplying the posterior auricle and the concha.¹ Anastomoses between these 2 blood supplies occur through perforating arteries and vascular arcades.

As the STA courses cranially, it moves from a deep position—deep to the parotidomasseteric fascia—to the superficial temporal fascia approximately 1 cm anterior and superior to the tragus. In approximately 80% of patients, 3 perpendicular branches stem from the STA—the upper, middle, and lower anterior branches—which supply the ascending helix, tragus, and lower margin of the earlobe, respectively.² The upper anterior branch of the STA joins other branches to form 2 dominant arcades: the first with the nonperforating branches of the PAA forming the upper third of the helical arcade, and the second with the lower anterior branch of the STA forming the middle portion of the helical arcade.^3,4 In 75% of patients, the middle helical arcade was identified as a single connecting artery, whereas in the remaining 25% of patients, a robust capillary network was formed.² In patient 2, the middle helical arcade was likely disrupted during closure, resulting in the helical necrosis seen postoperatively.

The second main blood supply of the auricle is the PAA, which enters in a more superficial position after traversing superiorly from the meatal cartilage, between the mastoid process and the posterior surface of the concha. From this point, the PAA runs in the deep subcutaneous tissue in the groove formed by the conchal cartilage and the mastoid process. Near the midpoint of the postauricular groove, it passes inferior to the postauricular muscle. The PAA has multiple radial branches that anastomose with helical branches; it also sends perforating branches (there were 2–4 branches in a recent study²) through the cartilage to the anterior surface of the concha. The 2 primary perforating arteries most commonly are located at the level of the antihelix and the antitragus.⁵ These arteries transverse through a vascular foramen located approximately 11 mm from the tragus in the horizontal plane and supply blood to the conchal bowl.⁶ In patient 1, the PAA itself, or the perforating arteries that course anteriorly through the vascular foramen, was likely disrupted, resulting in the conchal defect.

Special Considerations Before Surgery—As evidenced by these cases, special attention is needed during operative planning to account for the external ear vascular arcades. Damage to the helical arcades (patient 2) or the perforating arteries within the conchal bowl (patient 1) can lead to unintended consequences such as postoperative tissue necrosis. Tissue manipulation in these areas should be approached cautiously and with the least invasive treatment and closure options available. In doing so, blood flow and tissue integrity can be maintained, resulting in improved postoperative outcomes. Further research is warranted to identify the best intervention in cases involving these watershed regions.

Key clinical point: Abrocitinib improved signs of atopic dermatitis (AD) rapidly and consistently in difficult-to-treat or cosmetically important anatomical regions, such as the head and neck area.

Major finding: Eczema Area and Severity Index (EASI) score of the head and neck region improved significantly as early as at 2 weeks with 200 mg abrocitinib (least square mean % change from baseline [Δ] 52.5%) and 100 mg abrocitinib (Δ 47.8%) vs. placebo (0.1%; both P < .0001) and improvements were sustained up to 16 weeks (both P ≤ .0002).

Study details: Findings are from a post hoc analysis of the phase 3 JADE COMPARE study including 837 patients with moderate-to-severe AD who were randomly assigned to receive 16 weeks of treatment with 200 mg abrocitinib, 100 mg abrocitinib, dupilumab, or placebo, all with background topical therapy.

Disclosures: This study was funded by Pfizer Inc. Five authors declared being current/former employees and shareholders of Pfizer and other authors reported ties with various sources, including Pfizer.

Source: Alexis A et al. Rapidity of improvement in signs/symptoms of moderate-to-severe atopic dermatitis by body region with abrocitinib in the phase 3 JADE COMPARE study. Dermatol Ther (Heidelb). 2022;12:771-785 (Mar 17). Doi: 10.1007/s13555-022-00694-1

Key clinical point: Abrocitinib improved signs of atopic dermatitis (AD) rapidly and consistently in difficult-to-treat or cosmetically important anatomical regions, such as the head and neck area.

Major finding: Eczema Area and Severity Index (EASI) score of the head and neck region improved significantly as early as at 2 weeks with 200 mg abrocitinib (least square mean % change from baseline [Δ] 52.5%) and 100 mg abrocitinib (Δ 47.8%) vs. placebo (0.1%; both P < .0001) and improvements were sustained up to 16 weeks (both P ≤ .0002).

Study details: Findings are from a post hoc analysis of the phase 3 JADE COMPARE study including 837 patients with moderate-to-severe AD who were randomly assigned to receive 16 weeks of treatment with 200 mg abrocitinib, 100 mg abrocitinib, dupilumab, or placebo, all with background topical therapy.

Disclosures: This study was funded by Pfizer Inc. Five authors declared being current/former employees and shareholders of Pfizer and other authors reported ties with various sources, including Pfizer.

Source: Alexis A et al. Rapidity of improvement in signs/symptoms of moderate-to-severe atopic dermatitis by body region with abrocitinib in the phase 3 JADE COMPARE study. Dermatol Ther (Heidelb). 2022;12:771-785 (Mar 17). Doi: 10.1007/s13555-022-00694-1

Key clinical point: Abrocitinib improved signs of atopic dermatitis (AD) rapidly and consistently in difficult-to-treat or cosmetically important anatomical regions, such as the head and neck area.

Major finding: Eczema Area and Severity Index (EASI) score of the head and neck region improved significantly as early as at 2 weeks with 200 mg abrocitinib (least square mean % change from baseline [Δ] 52.5%) and 100 mg abrocitinib (Δ 47.8%) vs. placebo (0.1%; both P < .0001) and improvements were sustained up to 16 weeks (both P ≤ .0002).

Study details: Findings are from a post hoc analysis of the phase 3 JADE COMPARE study including 837 patients with moderate-to-severe AD who were randomly assigned to receive 16 weeks of treatment with 200 mg abrocitinib, 100 mg abrocitinib, dupilumab, or placebo, all with background topical therapy.

Disclosures: This study was funded by Pfizer Inc. Five authors declared being current/former employees and shareholders of Pfizer and other authors reported ties with various sources, including Pfizer.

Source: Alexis A et al. Rapidity of improvement in signs/symptoms of moderate-to-severe atopic dermatitis by body region with abrocitinib in the phase 3 JADE COMPARE study. Dermatol Ther (Heidelb). 2022;12:771-785 (Mar 17). Doi: 10.1007/s13555-022-00694-1

Key clinical point: Long-term dupilumab treatment reduced the severity of hand eczema (HE) and enhanced the quality of life (QoL) in patients with moderate-to-severe atopic dermatitis (AD).

Major finding: At week 52, 87.1% patients achieved ≥75% improvement in Hand Eczema Severity Index score, 90.3% patients achieved “clear” or “almost clear” endpoint based on the photographic guide, and mean HE-specific Health-related QoL improved by 63.5% (95% CI −71.1% to −55.9%).

Study details: This was a prospective, observational study including 72 adults with moderate-to-severe AD and concomitant HE, of whom 62 patients completed the 52-week dupilumab treatment.

Disclosures: This study was supported by Sanofi and Regeneron Pharmaceuticals. MLA Schuttelaar and MS de Bruin-Welle declared serving as advisors, consultants, speakers, investigators, and advisory board members or receiving grants from several sources, including Regeneron and Sanofi Genzyme.

Source: Voorberg AN et al. The long-term effect of dupilumab on chronic hand eczema in patients with moderate to severe atopic dermatitis – 52 week results from the Dutch BioDay registry. Contact Dermatitis. 2022 (Mar 13). Doi: 10.1111/cod.14104

Key clinical point: Long-term dupilumab treatment reduced the severity of hand eczema (HE) and enhanced the quality of life (QoL) in patients with moderate-to-severe atopic dermatitis (AD).

Major finding: At week 52, 87.1% patients achieved ≥75% improvement in Hand Eczema Severity Index score, 90.3% patients achieved “clear” or “almost clear” endpoint based on the photographic guide, and mean HE-specific Health-related QoL improved by 63.5% (95% CI −71.1% to −55.9%).

Study details: This was a prospective, observational study including 72 adults with moderate-to-severe AD and concomitant HE, of whom 62 patients completed the 52-week dupilumab treatment.

Disclosures: This study was supported by Sanofi and Regeneron Pharmaceuticals. MLA Schuttelaar and MS de Bruin-Welle declared serving as advisors, consultants, speakers, investigators, and advisory board members or receiving grants from several sources, including Regeneron and Sanofi Genzyme.

Source: Voorberg AN et al. The long-term effect of dupilumab on chronic hand eczema in patients with moderate to severe atopic dermatitis – 52 week results from the Dutch BioDay registry. Contact Dermatitis. 2022 (Mar 13). Doi: 10.1111/cod.14104

Key clinical point: Long-term dupilumab treatment reduced the severity of hand eczema (HE) and enhanced the quality of life (QoL) in patients with moderate-to-severe atopic dermatitis (AD).

Major finding: At week 52, 87.1% patients achieved ≥75% improvement in Hand Eczema Severity Index score, 90.3% patients achieved “clear” or “almost clear” endpoint based on the photographic guide, and mean HE-specific Health-related QoL improved by 63.5% (95% CI −71.1% to −55.9%).

Study details: This was a prospective, observational study including 72 adults with moderate-to-severe AD and concomitant HE, of whom 62 patients completed the 52-week dupilumab treatment.

Disclosures: This study was supported by Sanofi and Regeneron Pharmaceuticals. MLA Schuttelaar and MS de Bruin-Welle declared serving as advisors, consultants, speakers, investigators, and advisory board members or receiving grants from several sources, including Regeneron and Sanofi Genzyme.

Source: Voorberg AN et al. The long-term effect of dupilumab on chronic hand eczema in patients with moderate to severe atopic dermatitis – 52 week results from the Dutch BioDay registry. Contact Dermatitis. 2022 (Mar 13). Doi: 10.1111/cod.14104

Key clinical point: Under maximum use conditions, ruxolitinib cream was well-tolerated and reduced the severity of atopic dermatitis (AD) in patients with ≥25% body surface area (BSA) involvement.

Major finding: Treatment-emergent adverse events (AE) of mostly mild and moderate intensity and treatment-related AE were reported by 31.7% and 9.8% of patients, respectively. At day 56, 94.6% of patients reported ≥75% improvement in the Eczema Area and Severity Index.

Study details: Findings are from the phase 1 maximum-use trial including 41 patients with AD who had ≥25% BSA involvement and were administered 1.5% ruxolitinib cream twice daily for 28 days. Of these, 37 patients did not experience any safety concerns and continued treatment for an additional 28 days.

Disclosures: This study was funded by Incyte Corporation. Three authors declared being employees and shareholders of Incyte Corporation and other authors reported ties with several sources.

Source: Bissonnette R et al. A maximum-use trial of ruxolitinib cream in adolescents and adults with atopic dermatitis. Am J Clin Dermatol. 2022 (Apr 4). Doi: 10.1007/s40257-022-00690-3

Key clinical point: Under maximum use conditions, ruxolitinib cream was well-tolerated and reduced the severity of atopic dermatitis (AD) in patients with ≥25% body surface area (BSA) involvement.

Major finding: Treatment-emergent adverse events (AE) of mostly mild and moderate intensity and treatment-related AE were reported by 31.7% and 9.8% of patients, respectively. At day 56, 94.6% of patients reported ≥75% improvement in the Eczema Area and Severity Index.

Study details: Findings are from the phase 1 maximum-use trial including 41 patients with AD who had ≥25% BSA involvement and were administered 1.5% ruxolitinib cream twice daily for 28 days. Of these, 37 patients did not experience any safety concerns and continued treatment for an additional 28 days.

Disclosures: This study was funded by Incyte Corporation. Three authors declared being employees and shareholders of Incyte Corporation and other authors reported ties with several sources.

Source: Bissonnette R et al. A maximum-use trial of ruxolitinib cream in adolescents and adults with atopic dermatitis. Am J Clin Dermatol. 2022 (Apr 4). Doi: 10.1007/s40257-022-00690-3

Key clinical point: Under maximum use conditions, ruxolitinib cream was well-tolerated and reduced the severity of atopic dermatitis (AD) in patients with ≥25% body surface area (BSA) involvement.

Major finding: Treatment-emergent adverse events (AE) of mostly mild and moderate intensity and treatment-related AE were reported by 31.7% and 9.8% of patients, respectively. At day 56, 94.6% of patients reported ≥75% improvement in the Eczema Area and Severity Index.

Study details: Findings are from the phase 1 maximum-use trial including 41 patients with AD who had ≥25% BSA involvement and were administered 1.5% ruxolitinib cream twice daily for 28 days. Of these, 37 patients did not experience any safety concerns and continued treatment for an additional 28 days.

Disclosures: This study was funded by Incyte Corporation. Three authors declared being employees and shareholders of Incyte Corporation and other authors reported ties with several sources.

Source: Bissonnette R et al. A maximum-use trial of ruxolitinib cream in adolescents and adults with atopic dermatitis. Am J Clin Dermatol. 2022 (Apr 4). Doi: 10.1007/s40257-022-00690-3

Key clinical point: In patients with moderate-to-severe atopic dermatitis (AD), baricitinib therapy resulted in rapid and sustained improvement in skin pain leading to an enhanced quality of life (QoL).

Major finding: Skin pain improved as early as by day 1 with 2 mg baricitinib (least square mean % change from baseline [Δ] −4.4%; P = .048) and by day 2 with 1 mg baricitinib (Δ −6.7%; P = .011) vs. placebo, with improvements maintained through week 16 for both baricitinib doses (P ≤ .05) and 70.9% vs. 10.4% of skin pain responders vs. nonresponders experiencing clinically meaningful improvement in QoL (P < .0001).

Study details: Findings are from a post hoc analysis of the phase 3 BREEZE-AD5 study including 440 adults with moderate-to-severe AD and inadequate response to topical therapy who were randomly assigned to receive once-daily 1 mg baricitinib, 2 mg baricitinib, or placebo for 16 weeks.

Disclosures: This study was sponsored by Eli Lilly and Company. Three authors declared being employees and shareholders of Eli Lilly and other authors reported ties with several sources, including Eli Lilly.

Source: Rosmarin D et al. Rapid improvement in skin pain severity and its impact on quality of life in adult patients with moderate-to-severe atopic dermatitis from a double-blind, placebo-controlled baricitinib phase 3 study. J Cutan Med Surg. 2022 (Mar 31). Doi: 10.1177/12034754221088542

Key clinical point: In patients with moderate-to-severe atopic dermatitis (AD), baricitinib therapy resulted in rapid and sustained improvement in skin pain leading to an enhanced quality of life (QoL).

Major finding: Skin pain improved as early as by day 1 with 2 mg baricitinib (least square mean % change from baseline [Δ] −4.4%; P = .048) and by day 2 with 1 mg baricitinib (Δ −6.7%; P = .011) vs. placebo, with improvements maintained through week 16 for both baricitinib doses (P ≤ .05) and 70.9% vs. 10.4% of skin pain responders vs. nonresponders experiencing clinically meaningful improvement in QoL (P < .0001).

Study details: Findings are from a post hoc analysis of the phase 3 BREEZE-AD5 study including 440 adults with moderate-to-severe AD and inadequate response to topical therapy who were randomly assigned to receive once-daily 1 mg baricitinib, 2 mg baricitinib, or placebo for 16 weeks.

Disclosures: This study was sponsored by Eli Lilly and Company. Three authors declared being employees and shareholders of Eli Lilly and other authors reported ties with several sources, including Eli Lilly.

Source: Rosmarin D et al. Rapid improvement in skin pain severity and its impact on quality of life in adult patients with moderate-to-severe atopic dermatitis from a double-blind, placebo-controlled baricitinib phase 3 study. J Cutan Med Surg. 2022 (Mar 31). Doi: 10.1177/12034754221088542

Key clinical point: In patients with moderate-to-severe atopic dermatitis (AD), baricitinib therapy resulted in rapid and sustained improvement in skin pain leading to an enhanced quality of life (QoL).

Major finding: Skin pain improved as early as by day 1 with 2 mg baricitinib (least square mean % change from baseline [Δ] −4.4%; P = .048) and by day 2 with 1 mg baricitinib (Δ −6.7%; P = .011) vs. placebo, with improvements maintained through week 16 for both baricitinib doses (P ≤ .05) and 70.9% vs. 10.4% of skin pain responders vs. nonresponders experiencing clinically meaningful improvement in QoL (P < .0001).

Study details: Findings are from a post hoc analysis of the phase 3 BREEZE-AD5 study including 440 adults with moderate-to-severe AD and inadequate response to topical therapy who were randomly assigned to receive once-daily 1 mg baricitinib, 2 mg baricitinib, or placebo for 16 weeks.

Disclosures: This study was sponsored by Eli Lilly and Company. Three authors declared being employees and shareholders of Eli Lilly and other authors reported ties with several sources, including Eli Lilly.

Source: Rosmarin D et al. Rapid improvement in skin pain severity and its impact on quality of life in adult patients with moderate-to-severe atopic dermatitis from a double-blind, placebo-controlled baricitinib phase 3 study. J Cutan Med Surg. 2022 (Mar 31). Doi: 10.1177/12034754221088542

Key clinical point: Children born to mothers who had a cumulative exposure to psychological distress in the prenatal and postnatal periods were at an increased risk of developing atopic dermatitis (AD) at 1-2 years of age.

Major finding: Maternal psychological distress vs. no psychological distress in both prenatal and postnatal periods (adjusted relative risk [RR] 1.34; 95% CI 1.20-1.47) and only in the postnatal period (adjusted RR 1.23; 95% CI 1.07-1.39) was significantly associated with an increased risk of developing AD in children at 1-2 years of age.

Study details: This study analyzed maternal psychological distress during early pregnancy and 1 year after delivery in 8377 mother-child pairs, wherein the child had not developed AD by the age of 1 year.

Disclosures: This study was supported by the Ministry of Education, Culture, Sports, Science, and Technology, Japan. K Murakami declared being an editorial board member of BMC Public Health.

Source: Kawaguchi C et al. Cumulative exposure to maternal psychological distress in the prenatal and postnatal periods and atopic dermatitis in children: Findings from the TMM BirThree Cohort Study. BMC Pregnancy Childbirth. 2022;22:242 (Mar 24). Doi: 10.1186/s12884-022-04556-8

Key clinical point: Children born to mothers who had a cumulative exposure to psychological distress in the prenatal and postnatal periods were at an increased risk of developing atopic dermatitis (AD) at 1-2 years of age.

Major finding: Maternal psychological distress vs. no psychological distress in both prenatal and postnatal periods (adjusted relative risk [RR] 1.34; 95% CI 1.20-1.47) and only in the postnatal period (adjusted RR 1.23; 95% CI 1.07-1.39) was significantly associated with an increased risk of developing AD in children at 1-2 years of age.

Study details: This study analyzed maternal psychological distress during early pregnancy and 1 year after delivery in 8377 mother-child pairs, wherein the child had not developed AD by the age of 1 year.

Disclosures: This study was supported by the Ministry of Education, Culture, Sports, Science, and Technology, Japan. K Murakami declared being an editorial board member of BMC Public Health.

Source: Kawaguchi C et al. Cumulative exposure to maternal psychological distress in the prenatal and postnatal periods and atopic dermatitis in children: Findings from the TMM BirThree Cohort Study. BMC Pregnancy Childbirth. 2022;22:242 (Mar 24). Doi: 10.1186/s12884-022-04556-8

Key clinical point: Children born to mothers who had a cumulative exposure to psychological distress in the prenatal and postnatal periods were at an increased risk of developing atopic dermatitis (AD) at 1-2 years of age.

Major finding: Maternal psychological distress vs. no psychological distress in both prenatal and postnatal periods (adjusted relative risk [RR] 1.34; 95% CI 1.20-1.47) and only in the postnatal period (adjusted RR 1.23; 95% CI 1.07-1.39) was significantly associated with an increased risk of developing AD in children at 1-2 years of age.

Study details: This study analyzed maternal psychological distress during early pregnancy and 1 year after delivery in 8377 mother-child pairs, wherein the child had not developed AD by the age of 1 year.

Disclosures: This study was supported by the Ministry of Education, Culture, Sports, Science, and Technology, Japan. K Murakami declared being an editorial board member of BMC Public Health.

Source: Kawaguchi C et al. Cumulative exposure to maternal psychological distress in the prenatal and postnatal periods and atopic dermatitis in children: Findings from the TMM BirThree Cohort Study. BMC Pregnancy Childbirth. 2022;22:242 (Mar 24). Doi: 10.1186/s12884-022-04556-8