Article

The Diagnosis: Erythrodermic Allergic Contact Dermatitis

The worsening symptoms in our patient prompted intervention rather than observation and reassurance. Contact allergy to lanolin was suspected given the worsening presentation after the addition of Minerin, which was immediately discontinued. The patient’s family applied betamethasone cream 0.1% twice daily to severe plaques, pimecrolimus cream 1% to the face, and triamcinolone cream 0.1% to the rest of the body. At follow-up 1 week later, he experienced complete resolution of symptoms, which supported the diagnosis of erythrodermic allergic contact dermatitis (ACD).

The prevalence of ACD caused by lanolin varies among the general population from 1.2% to 6.9%.¹ Lanolin recently was named Allergen of the Year in 2023 by the American Contact Dermatitis Society.² It can be found in various commercial products, including creams, soaps, and ointments. Atopic dermatitis (AD) is a common pediatric inflammatory skin disorder that typically is treated with these products.³ In a study analyzing 533 products, up to 6% of skin care products for babies and children contained lanolin.⁴ Therefore, exposure to lanolin-containing products may be fairly common in the pediatric population.

Lanolin is a fatlike substance derived from sheep sebaceous gland secretions and extracted from sheep’s wool. Its composition varies by sheep breed, location, and extraction and purification methods. The most common allergens involve the alcoholic fraction produced by hydrolysis of lanolin.⁴ In 1996, Wolf⁵ described the “lanolin paradox,” which argued the difficulty with identifying lanolin as an allergen (similar to Fisher’s “paraben paradox”) based on 4 principles: (1) lanolin-containing topical medicaments tend to be more sensitizing than lanolin-containing cosmetics; (2) patients with ACD after applying lanolin-containing topical medicaments to damaged or ulcerated skin often can apply lanolin-containing cosmetics to normal or unaffected skin without a reaction; (3) false-negative patch test results often occur in lanolin-sensitive patients; and (4) patch testing with a single lanolin-containing agent (lanolin alcohol [30% in petrolatum]) is an unreliable and inadequate method of detecting lanolin allergy.^6,7 This theory elucidates the challenge of diagnosing contact allergies, particularly lanolin contact allergies.

Clinical features of acute ACD vary by skin type. Lighter skin types may have well-demarcated, pruritic, eczematous patches and plaques affecting the flexor surfaces. Asian patients may present with psoriasiform plaques with more well-demarcated borders and increased scaling and lichenification. In patients with darker skin types, dermatitis may manifest as papulation, lichenification, and color changes (violet, gray, or darker brown) along extensor surfaces.8 Chronic dermatitis manifests as lichenified scaly plaques. Given the diversity in dermatitis manifestation and the challenges of identifying erythema, especially in skin of color, clinicians may misidentify disease severity. These features aid in diagnosing and treating patients presenting with diffuse erythroderma and worsening eczematous patches and plaques despite use of typical topical treatments.

The differential diagnosis includes irritant contact dermatitis, AD, seborrheic dermatitis, and chronic plaque psoriasis. Negative patch testing suggests contact dermatitis based on exposure to a product. A thorough medication and personal history helps distinguish ACD from AD. Atopic dermatitis classically appears on the flexural areas, face, eyelids, and hands of patients with a personal or family history of atopy. Greasy scaly plaques on the central part of the face, eyelids, and scalp commonly are found in seborrheic dermatitis. In chronic plaque psoriasis, lesions typically are described as welldemarcated, inflamed plaques with notable scale located primarily in the scalp and diaper area in newborns and children until the age of 2 years. Our patient presented with scaly plaques throughout most of the body. The history of Minerin use over the course of 3 to 5 months and worsening skin eruptions involving a majority of the skin surface suggested continued exposure.

Patch testing assists in the diagnosis of ACD, with varying results due to manufacturing and processing inconsistencies in the composition of various substances used in the standard test sets, often making it difficult to diagnose lanolin as an allergen. According to Lee and Warshaw,6 the lack of uniformity within testing of lanolin-containing products may cause false-positive results, poor patch-test reproducibility, and loss of allergic contact response. A 2019 study utilized a combination of Amerchol L101 and lanolin alcohol to improve the diagnosis of lanolin allergy, as standard testing may not identify patients with lanolin sensitivities.1 A study with the North American Contact Dermatitis Group from 2005 to 2012 demonstrated that positive patch testing among children was the most consistent method for diagnosing ACD, and results were clinically relevant.⁹ However, the different lanolin-containing products are not standardized in patch testing, which often causes mixed reactions and does not definitely demonstrate classic positive results, even with the use of repeated open application tests.² Although there has been an emphasis on refining the standardization of the lanolin used for patch testing, lanolin contact allergy remains a predominantly clinical diagnosis.

Both AD and ACD are common pediatric skin findings, and mixed positive and neutral associations between AD and allergy to lanolin have been described in a few studies.^1,3,9,10 A history of atopy is more notable in a pediatric patient vs an adult, as sensitivities tend to subside into adulthood.⁹ Further studies and more precise testing are needed to investigate the relationship between AD and ACD.

The Diagnosis: Erythrodermic Allergic Contact Dermatitis

The worsening symptoms in our patient prompted intervention rather than observation and reassurance. Contact allergy to lanolin was suspected given the worsening presentation after the addition of Minerin, which was immediately discontinued. The patient’s family applied betamethasone cream 0.1% twice daily to severe plaques, pimecrolimus cream 1% to the face, and triamcinolone cream 0.1% to the rest of the body. At follow-up 1 week later, he experienced complete resolution of symptoms, which supported the diagnosis of erythrodermic allergic contact dermatitis (ACD).

The prevalence of ACD caused by lanolin varies among the general population from 1.2% to 6.9%.¹ Lanolin recently was named Allergen of the Year in 2023 by the American Contact Dermatitis Society.² It can be found in various commercial products, including creams, soaps, and ointments. Atopic dermatitis (AD) is a common pediatric inflammatory skin disorder that typically is treated with these products.³ In a study analyzing 533 products, up to 6% of skin care products for babies and children contained lanolin.⁴ Therefore, exposure to lanolin-containing products may be fairly common in the pediatric population.

Lanolin is a fatlike substance derived from sheep sebaceous gland secretions and extracted from sheep’s wool. Its composition varies by sheep breed, location, and extraction and purification methods. The most common allergens involve the alcoholic fraction produced by hydrolysis of lanolin.⁴ In 1996, Wolf⁵ described the “lanolin paradox,” which argued the difficulty with identifying lanolin as an allergen (similar to Fisher’s “paraben paradox”) based on 4 principles: (1) lanolin-containing topical medicaments tend to be more sensitizing than lanolin-containing cosmetics; (2) patients with ACD after applying lanolin-containing topical medicaments to damaged or ulcerated skin often can apply lanolin-containing cosmetics to normal or unaffected skin without a reaction; (3) false-negative patch test results often occur in lanolin-sensitive patients; and (4) patch testing with a single lanolin-containing agent (lanolin alcohol [30% in petrolatum]) is an unreliable and inadequate method of detecting lanolin allergy.^6,7 This theory elucidates the challenge of diagnosing contact allergies, particularly lanolin contact allergies.

Clinical features of acute ACD vary by skin type. Lighter skin types may have well-demarcated, pruritic, eczematous patches and plaques affecting the flexor surfaces. Asian patients may present with psoriasiform plaques with more well-demarcated borders and increased scaling and lichenification. In patients with darker skin types, dermatitis may manifest as papulation, lichenification, and color changes (violet, gray, or darker brown) along extensor surfaces.8 Chronic dermatitis manifests as lichenified scaly plaques. Given the diversity in dermatitis manifestation and the challenges of identifying erythema, especially in skin of color, clinicians may misidentify disease severity. These features aid in diagnosing and treating patients presenting with diffuse erythroderma and worsening eczematous patches and plaques despite use of typical topical treatments.

The differential diagnosis includes irritant contact dermatitis, AD, seborrheic dermatitis, and chronic plaque psoriasis. Negative patch testing suggests contact dermatitis based on exposure to a product. A thorough medication and personal history helps distinguish ACD from AD. Atopic dermatitis classically appears on the flexural areas, face, eyelids, and hands of patients with a personal or family history of atopy. Greasy scaly plaques on the central part of the face, eyelids, and scalp commonly are found in seborrheic dermatitis. In chronic plaque psoriasis, lesions typically are described as welldemarcated, inflamed plaques with notable scale located primarily in the scalp and diaper area in newborns and children until the age of 2 years. Our patient presented with scaly plaques throughout most of the body. The history of Minerin use over the course of 3 to 5 months and worsening skin eruptions involving a majority of the skin surface suggested continued exposure.

Patch testing assists in the diagnosis of ACD, with varying results due to manufacturing and processing inconsistencies in the composition of various substances used in the standard test sets, often making it difficult to diagnose lanolin as an allergen. According to Lee and Warshaw,6 the lack of uniformity within testing of lanolin-containing products may cause false-positive results, poor patch-test reproducibility, and loss of allergic contact response. A 2019 study utilized a combination of Amerchol L101 and lanolin alcohol to improve the diagnosis of lanolin allergy, as standard testing may not identify patients with lanolin sensitivities.1 A study with the North American Contact Dermatitis Group from 2005 to 2012 demonstrated that positive patch testing among children was the most consistent method for diagnosing ACD, and results were clinically relevant.⁹ However, the different lanolin-containing products are not standardized in patch testing, which often causes mixed reactions and does not definitely demonstrate classic positive results, even with the use of repeated open application tests.² Although there has been an emphasis on refining the standardization of the lanolin used for patch testing, lanolin contact allergy remains a predominantly clinical diagnosis.

Both AD and ACD are common pediatric skin findings, and mixed positive and neutral associations between AD and allergy to lanolin have been described in a few studies.^1,3,9,10 A history of atopy is more notable in a pediatric patient vs an adult, as sensitivities tend to subside into adulthood.⁹ Further studies and more precise testing are needed to investigate the relationship between AD and ACD.

The Diagnosis: Erythrodermic Allergic Contact Dermatitis

The worsening symptoms in our patient prompted intervention rather than observation and reassurance. Contact allergy to lanolin was suspected given the worsening presentation after the addition of Minerin, which was immediately discontinued. The patient’s family applied betamethasone cream 0.1% twice daily to severe plaques, pimecrolimus cream 1% to the face, and triamcinolone cream 0.1% to the rest of the body. At follow-up 1 week later, he experienced complete resolution of symptoms, which supported the diagnosis of erythrodermic allergic contact dermatitis (ACD).

The prevalence of ACD caused by lanolin varies among the general population from 1.2% to 6.9%.¹ Lanolin recently was named Allergen of the Year in 2023 by the American Contact Dermatitis Society.² It can be found in various commercial products, including creams, soaps, and ointments. Atopic dermatitis (AD) is a common pediatric inflammatory skin disorder that typically is treated with these products.³ In a study analyzing 533 products, up to 6% of skin care products for babies and children contained lanolin.⁴ Therefore, exposure to lanolin-containing products may be fairly common in the pediatric population.

Lanolin is a fatlike substance derived from sheep sebaceous gland secretions and extracted from sheep’s wool. Its composition varies by sheep breed, location, and extraction and purification methods. The most common allergens involve the alcoholic fraction produced by hydrolysis of lanolin.⁴ In 1996, Wolf⁵ described the “lanolin paradox,” which argued the difficulty with identifying lanolin as an allergen (similar to Fisher’s “paraben paradox”) based on 4 principles: (1) lanolin-containing topical medicaments tend to be more sensitizing than lanolin-containing cosmetics; (2) patients with ACD after applying lanolin-containing topical medicaments to damaged or ulcerated skin often can apply lanolin-containing cosmetics to normal or unaffected skin without a reaction; (3) false-negative patch test results often occur in lanolin-sensitive patients; and (4) patch testing with a single lanolin-containing agent (lanolin alcohol [30% in petrolatum]) is an unreliable and inadequate method of detecting lanolin allergy.^6,7 This theory elucidates the challenge of diagnosing contact allergies, particularly lanolin contact allergies.

Clinical features of acute ACD vary by skin type. Lighter skin types may have well-demarcated, pruritic, eczematous patches and plaques affecting the flexor surfaces. Asian patients may present with psoriasiform plaques with more well-demarcated borders and increased scaling and lichenification. In patients with darker skin types, dermatitis may manifest as papulation, lichenification, and color changes (violet, gray, or darker brown) along extensor surfaces.8 Chronic dermatitis manifests as lichenified scaly plaques. Given the diversity in dermatitis manifestation and the challenges of identifying erythema, especially in skin of color, clinicians may misidentify disease severity. These features aid in diagnosing and treating patients presenting with diffuse erythroderma and worsening eczematous patches and plaques despite use of typical topical treatments.

The differential diagnosis includes irritant contact dermatitis, AD, seborrheic dermatitis, and chronic plaque psoriasis. Negative patch testing suggests contact dermatitis based on exposure to a product. A thorough medication and personal history helps distinguish ACD from AD. Atopic dermatitis classically appears on the flexural areas, face, eyelids, and hands of patients with a personal or family history of atopy. Greasy scaly plaques on the central part of the face, eyelids, and scalp commonly are found in seborrheic dermatitis. In chronic plaque psoriasis, lesions typically are described as welldemarcated, inflamed plaques with notable scale located primarily in the scalp and diaper area in newborns and children until the age of 2 years. Our patient presented with scaly plaques throughout most of the body. The history of Minerin use over the course of 3 to 5 months and worsening skin eruptions involving a majority of the skin surface suggested continued exposure.

Patch testing assists in the diagnosis of ACD, with varying results due to manufacturing and processing inconsistencies in the composition of various substances used in the standard test sets, often making it difficult to diagnose lanolin as an allergen. According to Lee and Warshaw,6 the lack of uniformity within testing of lanolin-containing products may cause false-positive results, poor patch-test reproducibility, and loss of allergic contact response. A 2019 study utilized a combination of Amerchol L101 and lanolin alcohol to improve the diagnosis of lanolin allergy, as standard testing may not identify patients with lanolin sensitivities.1 A study with the North American Contact Dermatitis Group from 2005 to 2012 demonstrated that positive patch testing among children was the most consistent method for diagnosing ACD, and results were clinically relevant.⁹ However, the different lanolin-containing products are not standardized in patch testing, which often causes mixed reactions and does not definitely demonstrate classic positive results, even with the use of repeated open application tests.² Although there has been an emphasis on refining the standardization of the lanolin used for patch testing, lanolin contact allergy remains a predominantly clinical diagnosis.

Both AD and ACD are common pediatric skin findings, and mixed positive and neutral associations between AD and allergy to lanolin have been described in a few studies.^1,3,9,10 A history of atopy is more notable in a pediatric patient vs an adult, as sensitivities tend to subside into adulthood.⁹ Further studies and more precise testing are needed to investigate the relationship between AD and ACD.

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Migraine attacks are classified as chronic or episodic. Chronic migraines occur at least 15 days a month, and often prove functionally debilitating. In 2018, therapies that target the calcitonin gene-related peptide (CGRP) were first introduced to help manage migraine attacks.

Dr Stephanie Nahas from Thomas Jefferson University in Philadelphia, Pennsylvania, discusses optimal approaches for incorporating these therapies, which include small molecule agents called gepants, and monoclonal antibodies. In both cases, these therapies prevent CGRP from binding to its receptor, which helps to reduce migraine symptomatology, both acutely and over time

According to Dr Nahas, the choice of therapy for an individual patient depends primarily on patient preferences. Most gepants are administered orally, and monoclonal antibodies are injected.

Dr Nahas  recommends that these therapies should be considered when a previous treatment proves insufficient to reduce disease burden to the degree that allows improved functioning and quality of life for the patient.

--

Stephanie J. Nahas-Geiger, MD, MSEd, Associate Professor, Department of Neurology, Division of Headache Medicine, Thomas Jefferson University; Assistant Director, Headache Medicine Fellowship Program, Jefferson Headache Center, Philadelphia, Pennsylvania

Stephanie J. Nahas-Geiger, MD, MSEd, has disclosed the following relevant financial relationships:
Serve(d) as a consultant for: AbbVie; Eli Lilly; Lundbeck; Pfizer; Theranica; Tonix (no relationships are active)

Migraine attacks are classified as chronic or episodic. Chronic migraines occur at least 15 days a month, and often prove functionally debilitating. In 2018, therapies that target the calcitonin gene-related peptide (CGRP) were first introduced to help manage migraine attacks.

Dr Stephanie Nahas from Thomas Jefferson University in Philadelphia, Pennsylvania, discusses optimal approaches for incorporating these therapies, which include small molecule agents called gepants, and monoclonal antibodies. In both cases, these therapies prevent CGRP from binding to its receptor, which helps to reduce migraine symptomatology, both acutely and over time

According to Dr Nahas, the choice of therapy for an individual patient depends primarily on patient preferences. Most gepants are administered orally, and monoclonal antibodies are injected.

Dr Nahas  recommends that these therapies should be considered when a previous treatment proves insufficient to reduce disease burden to the degree that allows improved functioning and quality of life for the patient.

--

Stephanie J. Nahas-Geiger, MD, MSEd, Associate Professor, Department of Neurology, Division of Headache Medicine, Thomas Jefferson University; Assistant Director, Headache Medicine Fellowship Program, Jefferson Headache Center, Philadelphia, Pennsylvania

Stephanie J. Nahas-Geiger, MD, MSEd, has disclosed the following relevant financial relationships:
Serve(d) as a consultant for: AbbVie; Eli Lilly; Lundbeck; Pfizer; Theranica; Tonix (no relationships are active)

Migraine attacks are classified as chronic or episodic. Chronic migraines occur at least 15 days a month, and often prove functionally debilitating. In 2018, therapies that target the calcitonin gene-related peptide (CGRP) were first introduced to help manage migraine attacks.

Dr Stephanie Nahas from Thomas Jefferson University in Philadelphia, Pennsylvania, discusses optimal approaches for incorporating these therapies, which include small molecule agents called gepants, and monoclonal antibodies. In both cases, these therapies prevent CGRP from binding to its receptor, which helps to reduce migraine symptomatology, both acutely and over time

According to Dr Nahas, the choice of therapy for an individual patient depends primarily on patient preferences. Most gepants are administered orally, and monoclonal antibodies are injected.

Dr Nahas  recommends that these therapies should be considered when a previous treatment proves insufficient to reduce disease burden to the degree that allows improved functioning and quality of life for the patient.

--

Stephanie J. Nahas-Geiger, MD, MSEd, Associate Professor, Department of Neurology, Division of Headache Medicine, Thomas Jefferson University; Assistant Director, Headache Medicine Fellowship Program, Jefferson Headache Center, Philadelphia, Pennsylvania

Stephanie J. Nahas-Geiger, MD, MSEd, has disclosed the following relevant financial relationships:
Serve(d) as a consultant for: AbbVie; Eli Lilly; Lundbeck; Pfizer; Theranica; Tonix (no relationships are active)

Episodic migraine occurs fewer than 15 days per month but can become chronic if poorly controlled. It is estimated that preventive therapy is indicated in over one third of patients with episodic migraine. Dr Barbara Nye from Wake Forest University in Winston-Salem, North Carolina, discusses optimal approaches for managing episodic migraine. According to Dr Nye, several factors, including patient preference, clinical evidence, and insurance coverage, will help inform which treatments can be offered.

She mentions that currently approved treatments include nonspecific therapeutics such as antiseizure, antidepressant, and blood pressure medications. Newer therapies known as gepants and injectable monoclonal antibodies are also available to manage and prevent episodic migraine.

Dr Nye concludes that the appropriate therapeutic goal is a reduction in headache frequency, reduction in headache severity, and improved response to medications, as well as decreasing the level of disability that patients are experiencing.

--

Barbara L. Nye, MD, Associate Professor of Neurology, Wake Forest University; Director, Headache Fellowship, Department of Neurology, Atrium Health Wake Forest Baptist, Winston-Salem, North Carolina

Barbara L. Nye, MD, has disclosed no relevant financial relationships.

Episodic migraine occurs fewer than 15 days per month but can become chronic if poorly controlled. It is estimated that preventive therapy is indicated in over one third of patients with episodic migraine. Dr Barbara Nye from Wake Forest University in Winston-Salem, North Carolina, discusses optimal approaches for managing episodic migraine. According to Dr Nye, several factors, including patient preference, clinical evidence, and insurance coverage, will help inform which treatments can be offered.

She mentions that currently approved treatments include nonspecific therapeutics such as antiseizure, antidepressant, and blood pressure medications. Newer therapies known as gepants and injectable monoclonal antibodies are also available to manage and prevent episodic migraine.

Dr Nye concludes that the appropriate therapeutic goal is a reduction in headache frequency, reduction in headache severity, and improved response to medications, as well as decreasing the level of disability that patients are experiencing.

--

Barbara L. Nye, MD, Associate Professor of Neurology, Wake Forest University; Director, Headache Fellowship, Department of Neurology, Atrium Health Wake Forest Baptist, Winston-Salem, North Carolina

Barbara L. Nye, MD, has disclosed no relevant financial relationships.

Episodic migraine occurs fewer than 15 days per month but can become chronic if poorly controlled. It is estimated that preventive therapy is indicated in over one third of patients with episodic migraine. Dr Barbara Nye from Wake Forest University in Winston-Salem, North Carolina, discusses optimal approaches for managing episodic migraine. According to Dr Nye, several factors, including patient preference, clinical evidence, and insurance coverage, will help inform which treatments can be offered.

She mentions that currently approved treatments include nonspecific therapeutics such as antiseizure, antidepressant, and blood pressure medications. Newer therapies known as gepants and injectable monoclonal antibodies are also available to manage and prevent episodic migraine.

Dr Nye concludes that the appropriate therapeutic goal is a reduction in headache frequency, reduction in headache severity, and improved response to medications, as well as decreasing the level of disability that patients are experiencing.

--

Barbara L. Nye, MD, Associate Professor of Neurology, Wake Forest University; Director, Headache Fellowship, Department of Neurology, Atrium Health Wake Forest Baptist, Winston-Salem, North Carolina

Barbara L. Nye, MD, has disclosed no relevant financial relationships.

Migraine can be divided into two broad categories: episodic, in which attacks occur between two and four times a month; and chronic, in which individuals suffer from headaches for at least half the month and experience at least eight attacks.

Acute treatment is fundamental to reducing the immediate disability of migraine attack in both types, and several effective migraine-specific therapies have been approved.

Dr Jessica Ailani, director of the Headache Center at Medstar Georgetown University Hospital, Washington, DC, discusses the benefits, potential side effects, and optimal use of migraine-specific therapies available for acute migraine, including how they can be used to build an effective treatment plan for an individual patient.

These include triptans (5-HT1B/1D receptor agonists), ergotamines (dihydroergotamine), neuromodulation devices, ditans (5-HT1F agonists), and gepants (CGRP antagonists).

--

Jessica Ailani, MD, Professor of Clinical Neurology, Director, Headache Center, Medstar Georgetown University Hospital, Washington, DC

Jessica Ailani, MD, has disclosed the following relevant financial relationships:

Serve(d) as a director, officer, partner, employee, advisor, consultant, or trustee for: AbbVie; Aeon; electroCore; Dr. Reddy; Eli-Lilly; GlaxoSmithKline (2023); Lundbeck; Linpharma; Ipsen; Merz; Miravo; Pfizer; Neurolief; Gore; Satsuma; Scilex; Theranica; Tonix

Received research grant from: Parema; Ipsen; Lundbeck

Migraine can be divided into two broad categories: episodic, in which attacks occur between two and four times a month; and chronic, in which individuals suffer from headaches for at least half the month and experience at least eight attacks.

Acute treatment is fundamental to reducing the immediate disability of migraine attack in both types, and several effective migraine-specific therapies have been approved.

Dr Jessica Ailani, director of the Headache Center at Medstar Georgetown University Hospital, Washington, DC, discusses the benefits, potential side effects, and optimal use of migraine-specific therapies available for acute migraine, including how they can be used to build an effective treatment plan for an individual patient.

These include triptans (5-HT1B/1D receptor agonists), ergotamines (dihydroergotamine), neuromodulation devices, ditans (5-HT1F agonists), and gepants (CGRP antagonists).

--

Jessica Ailani, MD, Professor of Clinical Neurology, Director, Headache Center, Medstar Georgetown University Hospital, Washington, DC

Jessica Ailani, MD, has disclosed the following relevant financial relationships:

Serve(d) as a director, officer, partner, employee, advisor, consultant, or trustee for: AbbVie; Aeon; electroCore; Dr. Reddy; Eli-Lilly; GlaxoSmithKline (2023); Lundbeck; Linpharma; Ipsen; Merz; Miravo; Pfizer; Neurolief; Gore; Satsuma; Scilex; Theranica; Tonix

Received research grant from: Parema; Ipsen; Lundbeck

Migraine can be divided into two broad categories: episodic, in which attacks occur between two and four times a month; and chronic, in which individuals suffer from headaches for at least half the month and experience at least eight attacks.

Acute treatment is fundamental to reducing the immediate disability of migraine attack in both types, and several effective migraine-specific therapies have been approved.

Dr Jessica Ailani, director of the Headache Center at Medstar Georgetown University Hospital, Washington, DC, discusses the benefits, potential side effects, and optimal use of migraine-specific therapies available for acute migraine, including how they can be used to build an effective treatment plan for an individual patient.

These include triptans (5-HT1B/1D receptor agonists), ergotamines (dihydroergotamine), neuromodulation devices, ditans (5-HT1F agonists), and gepants (CGRP antagonists).

--

Jessica Ailani, MD, Professor of Clinical Neurology, Director, Headache Center, Medstar Georgetown University Hospital, Washington, DC

Jessica Ailani, MD, has disclosed the following relevant financial relationships:

Serve(d) as a director, officer, partner, employee, advisor, consultant, or trustee for: AbbVie; Aeon; electroCore; Dr. Reddy; Eli-Lilly; GlaxoSmithKline (2023); Lundbeck; Linpharma; Ipsen; Merz; Miravo; Pfizer; Neurolief; Gore; Satsuma; Scilex; Theranica; Tonix

Received research grant from: Parema; Ipsen; Lundbeck

Migraine can be divided into two broad categories: episodic, in which attacks occur between two and four times a month; and chronic, in which individuals suffer from headaches for at least half the month and experience at least eight attacks.

Acute treatment is fundamental to reducing the immediate disability of migraine attack in both types, and several effective migraine-specific therapies have been approved.

Dr Jessica Ailani, director of the Headache Center at Medstar Georgetown University Hospital, Washington, DC, discusses the benefits, potential side effects, and optimal use of migraine-specific therapies available for acute migraine, including how they can be used to build an effective treatment plan for an individual patient.

These include triptans (5-HT1B/1D receptor agonists), ergotamines (dihydroergotamine), neuromodulation devices, ditans (5-HT1F agonists), and gepants (CGRP antagonists).

--

Jessica Ailani, MD, Professor of Clinical Neurology, Director, Headache Center, Medstar Georgetown University Hospital, Washington, DC

Jessica Ailani, MD, has disclosed the following relevant financial relationships:

Serve(d) as a director, officer, partner, employee, advisor, consultant, or trustee for: AbbVie; Aeon; electroCore; Dr. Reddy; Eli-Lilly; GlaxoSmithKline (2023); Lundbeck; Linpharma; Ipsen; Merz; Miravo; Pfizer; Neurolief; Gore; Satsuma; Scilex; Theranica; Tonix

Received research grant from: Parema; Ipsen; Lundbeck

Migraine can be divided into two broad categories: episodic, in which attacks occur between two and four times a month; and chronic, in which individuals suffer from headaches for at least half the month and experience at least eight attacks.

Acute treatment is fundamental to reducing the immediate disability of migraine attack in both types, and several effective migraine-specific therapies have been approved.

Dr Jessica Ailani, director of the Headache Center at Medstar Georgetown University Hospital, Washington, DC, discusses the benefits, potential side effects, and optimal use of migraine-specific therapies available for acute migraine, including how they can be used to build an effective treatment plan for an individual patient.

These include triptans (5-HT1B/1D receptor agonists), ergotamines (dihydroergotamine), neuromodulation devices, ditans (5-HT1F agonists), and gepants (CGRP antagonists).

--

Jessica Ailani, MD, Professor of Clinical Neurology, Director, Headache Center, Medstar Georgetown University Hospital, Washington, DC

Jessica Ailani, MD, has disclosed the following relevant financial relationships:

Serve(d) as a director, officer, partner, employee, advisor, consultant, or trustee for: AbbVie; Aeon; electroCore; Dr. Reddy; Eli-Lilly; GlaxoSmithKline (2023); Lundbeck; Linpharma; Ipsen; Merz; Miravo; Pfizer; Neurolief; Gore; Satsuma; Scilex; Theranica; Tonix

Received research grant from: Parema; Ipsen; Lundbeck

Migraine can be divided into two broad categories: episodic, in which attacks occur between two and four times a month; and chronic, in which individuals suffer from headaches for at least half the month and experience at least eight attacks.

Acute treatment is fundamental to reducing the immediate disability of migraine attack in both types, and several effective migraine-specific therapies have been approved.

Dr Jessica Ailani, director of the Headache Center at Medstar Georgetown University Hospital, Washington, DC, discusses the benefits, potential side effects, and optimal use of migraine-specific therapies available for acute migraine, including how they can be used to build an effective treatment plan for an individual patient.

These include triptans (5-HT1B/1D receptor agonists), ergotamines (dihydroergotamine), neuromodulation devices, ditans (5-HT1F agonists), and gepants (CGRP antagonists).

--

Jessica Ailani, MD, Professor of Clinical Neurology, Director, Headache Center, Medstar Georgetown University Hospital, Washington, DC

Jessica Ailani, MD, has disclosed the following relevant financial relationships:

Serve(d) as a director, officer, partner, employee, advisor, consultant, or trustee for: AbbVie; Aeon; electroCore; Dr. Reddy; Eli-Lilly; GlaxoSmithKline (2023); Lundbeck; Linpharma; Ipsen; Merz; Miravo; Pfizer; Neurolief; Gore; Satsuma; Scilex; Theranica; Tonix

Received research grant from: Parema; Ipsen; Lundbeck

The Diagnosis: Hypertrophic Lichen Planus

Two biopsies from the left lateral foot revealed hyperkeratosis, wedge-shaped hypergranulosis, irregular acanthosis, and a bandlike lymphocytic infiltrate in the superficial dermis with a classic sawtooth pattern of the rete ridges (Figure 1). Based on the clinical findings and histopathology, the patient was diagnosed with hypertrophic lichen planus (LP) and was treated with clobetasol ointment 0.05%, which resulted in progression of the symptoms. She experienced notable improvement 3 months after adding methotrexate 12.5 mg weekly (Figure 2).

Lichen planus is an idiopathic chronic inflammatory condition of the skin and mucous membranes that classically manifests as pruritic violaceous papules and plaques, which commonly are found on the wrists, lower back, and ankles.¹ The most common variants of LP are hypertrophic, linear, mucosal, actinic, follicular, pigmented, annular, atrophic, and guttate.² The clinical presentation and biopsy results in our patient were consistent with the hypertrophic variant of LP, which is a chronic condition that most often manifests on the lower legs, especially around the ankles, as hyperkeratotic papules, plaques, and nodules.^2,3 The exact pathophysiology of hypertrophic LP is unknown, but there is evidence that the immune system plays a role in its development and that the Koebner phenomenon may contribute to its exacerbation.⁴ There is a well-known association between LP and hepatitis. Patients with chronic LP may develop squamous cell carcinoma.⁴ The variants of LP can overlap and do not exist independent of one another. Recognizing the overlap in these variants allows for earlier diagnosis and therapeutic intervention of the disease process to limit disease progression and patient clinic visits and to improve patient quality of life.

The differential diagnosis for hyperkeratotic plaques of the feet and ankles can be broad and may include keratosis lichenoides chronica, palmoplantar keratoderma, palmoplantar psoriasis, or lichen amyloidosis. These conditions are classified based on various criteria that include extent of disease manifestations, morphology of palmoplantar skin involvement, inheritance patterns, and molecular pathogenesis.⁵ Keratosis lichenoides chronica is a rare dermatosis that presents as a distinctive seborrheic dermatitis–like facial eruption. The facial eruption is accompanied by violaceous papular and nodular lesions that appear on the extremities and trunk, typically arranged in a linear or reticular pattern.⁶ Palmoplantar keratoderma represents a group of acquired and hereditary conditions that are characterized by excessive thickening of the palms and soles.⁵ Palmoplantar psoriasis is a variant of psoriasis that affects the palms and soles and can manifest as hyperkeratosis, pustular, or mixed morphology.⁷ Lichen amyloidosis is a subtype of primary localized cutaneous amyloidosis that manifests as multiple pruritic, firm, hyperpigmented, hyperkeratotic papules on the shins that later coalesce in a rippled pattern.^8,9

The first-line treatment for hypertrophic LP is topical corticosteroids. Alternative therapies include mycophenolate mofetil, acitretin, and intralesional corticosteroid injections.⁴ Treatment is similar for all of the LP variants.

The Diagnosis: Hypertrophic Lichen Planus

Two biopsies from the left lateral foot revealed hyperkeratosis, wedge-shaped hypergranulosis, irregular acanthosis, and a bandlike lymphocytic infiltrate in the superficial dermis with a classic sawtooth pattern of the rete ridges (Figure 1). Based on the clinical findings and histopathology, the patient was diagnosed with hypertrophic lichen planus (LP) and was treated with clobetasol ointment 0.05%, which resulted in progression of the symptoms. She experienced notable improvement 3 months after adding methotrexate 12.5 mg weekly (Figure 2).

Lichen planus is an idiopathic chronic inflammatory condition of the skin and mucous membranes that classically manifests as pruritic violaceous papules and plaques, which commonly are found on the wrists, lower back, and ankles.¹ The most common variants of LP are hypertrophic, linear, mucosal, actinic, follicular, pigmented, annular, atrophic, and guttate.² The clinical presentation and biopsy results in our patient were consistent with the hypertrophic variant of LP, which is a chronic condition that most often manifests on the lower legs, especially around the ankles, as hyperkeratotic papules, plaques, and nodules.^2,3 The exact pathophysiology of hypertrophic LP is unknown, but there is evidence that the immune system plays a role in its development and that the Koebner phenomenon may contribute to its exacerbation.⁴ There is a well-known association between LP and hepatitis. Patients with chronic LP may develop squamous cell carcinoma.⁴ The variants of LP can overlap and do not exist independent of one another. Recognizing the overlap in these variants allows for earlier diagnosis and therapeutic intervention of the disease process to limit disease progression and patient clinic visits and to improve patient quality of life.

The differential diagnosis for hyperkeratotic plaques of the feet and ankles can be broad and may include keratosis lichenoides chronica, palmoplantar keratoderma, palmoplantar psoriasis, or lichen amyloidosis. These conditions are classified based on various criteria that include extent of disease manifestations, morphology of palmoplantar skin involvement, inheritance patterns, and molecular pathogenesis.⁵ Keratosis lichenoides chronica is a rare dermatosis that presents as a distinctive seborrheic dermatitis–like facial eruption. The facial eruption is accompanied by violaceous papular and nodular lesions that appear on the extremities and trunk, typically arranged in a linear or reticular pattern.⁶ Palmoplantar keratoderma represents a group of acquired and hereditary conditions that are characterized by excessive thickening of the palms and soles.⁵ Palmoplantar psoriasis is a variant of psoriasis that affects the palms and soles and can manifest as hyperkeratosis, pustular, or mixed morphology.⁷ Lichen amyloidosis is a subtype of primary localized cutaneous amyloidosis that manifests as multiple pruritic, firm, hyperpigmented, hyperkeratotic papules on the shins that later coalesce in a rippled pattern.^8,9

The first-line treatment for hypertrophic LP is topical corticosteroids. Alternative therapies include mycophenolate mofetil, acitretin, and intralesional corticosteroid injections.⁴ Treatment is similar for all of the LP variants.

The Diagnosis: Hypertrophic Lichen Planus

Two biopsies from the left lateral foot revealed hyperkeratosis, wedge-shaped hypergranulosis, irregular acanthosis, and a bandlike lymphocytic infiltrate in the superficial dermis with a classic sawtooth pattern of the rete ridges (Figure 1). Based on the clinical findings and histopathology, the patient was diagnosed with hypertrophic lichen planus (LP) and was treated with clobetasol ointment 0.05%, which resulted in progression of the symptoms. She experienced notable improvement 3 months after adding methotrexate 12.5 mg weekly (Figure 2).

Lichen planus is an idiopathic chronic inflammatory condition of the skin and mucous membranes that classically manifests as pruritic violaceous papules and plaques, which commonly are found on the wrists, lower back, and ankles.¹ The most common variants of LP are hypertrophic, linear, mucosal, actinic, follicular, pigmented, annular, atrophic, and guttate.² The clinical presentation and biopsy results in our patient were consistent with the hypertrophic variant of LP, which is a chronic condition that most often manifests on the lower legs, especially around the ankles, as hyperkeratotic papules, plaques, and nodules.^2,3 The exact pathophysiology of hypertrophic LP is unknown, but there is evidence that the immune system plays a role in its development and that the Koebner phenomenon may contribute to its exacerbation.⁴ There is a well-known association between LP and hepatitis. Patients with chronic LP may develop squamous cell carcinoma.⁴ The variants of LP can overlap and do not exist independent of one another. Recognizing the overlap in these variants allows for earlier diagnosis and therapeutic intervention of the disease process to limit disease progression and patient clinic visits and to improve patient quality of life.

The differential diagnosis for hyperkeratotic plaques of the feet and ankles can be broad and may include keratosis lichenoides chronica, palmoplantar keratoderma, palmoplantar psoriasis, or lichen amyloidosis. These conditions are classified based on various criteria that include extent of disease manifestations, morphology of palmoplantar skin involvement, inheritance patterns, and molecular pathogenesis.⁵ Keratosis lichenoides chronica is a rare dermatosis that presents as a distinctive seborrheic dermatitis–like facial eruption. The facial eruption is accompanied by violaceous papular and nodular lesions that appear on the extremities and trunk, typically arranged in a linear or reticular pattern.⁶ Palmoplantar keratoderma represents a group of acquired and hereditary conditions that are characterized by excessive thickening of the palms and soles.⁵ Palmoplantar psoriasis is a variant of psoriasis that affects the palms and soles and can manifest as hyperkeratosis, pustular, or mixed morphology.⁷ Lichen amyloidosis is a subtype of primary localized cutaneous amyloidosis that manifests as multiple pruritic, firm, hyperpigmented, hyperkeratotic papules on the shins that later coalesce in a rippled pattern.^8,9

The first-line treatment for hypertrophic LP is topical corticosteroids. Alternative therapies include mycophenolate mofetil, acitretin, and intralesional corticosteroid injections.⁴ Treatment is similar for all of the LP variants.

As seen in red on the radiogram, the patient's heart is grossly enlarged, indicating cardiomegaly. Cardiomegaly often is first diagnosed on chest imaging, with diagnosis based on a cardiothoracic ratio of < 0.5. It is not a disease but rather a manifestation of an underlying cause. Patients may have few or no cardiomegaly-related symptoms or have symptoms typical of cardiac dysfunction, like this patient's dyspnea and edema. Conditions that impair normal circulation and that are associated with cardiomegaly development include hypertension, obesity, heart valve disorders, thyroid dysfunction, and anemia. In this patient, cardiomegaly probably has been triggered by uncontrolled hypertension and ongoing obesity. This patient's bloodwork also indicates prediabetes and incipient type 2 diabetes (T2D) (the diagnostic criteria for which are A1c ≥ 6.5% and fasting plasma glucose ≥ 126 mg/dL).

As many as 42% of adults in the United States meet criteria for obesity and are at risk for obesity-related conditions, including cardiomegaly. Guidelines for management of patients with obesity have been published by The Obesity Society and the American Association of Clinical Endocrinologists, and management of obesity is a necessary part of comprehensive care of patients with T2D  as well. For most patients, a BMI ≥ 30 diagnoses obesity; this patient has class 1 obesity, based on a BMI of 30 to 34.9. The patient also has complications of obesity, including stage 2 hypertension and prediabetes. As such, lifestyle management plus medical therapy is the recommended approach to weight loss, with a goal of losing 5% to 10% or more of baseline body weight.

The Obesity Society states that all patients with obesity should be offered effective, evidence-based interventions. Medical management of obesity includes use of pharmacologic interventions with proven benefit in weight loss, such as glucagon-like peptide-1 receptor agonists (GLP-1 RAs; eg, semaglutide) or dual gastric inhibitory polypeptide (GIP)/GLP-1 RAs (eg, tirzepatide). Semaglutide and tirzepatide are likely to have cardiovascular benefits for patients with obesity as well. Other medications approved for management of obesity include liraglutide, orlistat, phentermine HCl (with or without topiramate), and naltrexone plus bupropion. The American Diabetes Association (ADA) recommendations for management of obesity in patients with T2D give preference to semaglutide 2.4 mg/wk and tirzepatide at weekly doses of 5, 10, or 15 mg, depending on patient factors. 

As important for this patient is to get control of hypertension. Studies have shown that lowering blood pressure improves left ventricular hypertrophy, a common source of cardiomegaly. Hypertension guidelines from the American College of Cardiology/American Heart Association recommend a blood pressure goal < 130/80 mm Hg for most adults, which is consistent with the current recommendation from the ADA. Management of hypertension should first incorporate a low-sodium, healthy diet (such as the Dietary Approaches to Stop Hypertension [DASH] diet), physical activity, and weight loss; however, many patients (especially with stage 2 hypertension) require pharmacologic therapy as well. Single-pill combination therapies of drugs from different classes (eg, angiotensin-converting enzyme inhibitor plus calcium channel blocker) are preferred for patients with stage 2 hypertension to improve efficacy and enhance adherence.

Romesh K. Khardori, MD, PhD, Professor, Department of Internal Medicine, Division of Diabetes, Endocrine, and Metabolic Disorders, Eastern Virginia Medical School; EVMS Medical Group, Norfolk, Virginia.

Romesh K. Khardori, MD, PhD, has disclosed no relevant financial relationships.

Image Quizzes are fictional or fictionalized clinical scenarios intended to provide evidence-based educational takeaways.

As seen in red on the radiogram, the patient's heart is grossly enlarged, indicating cardiomegaly. Cardiomegaly often is first diagnosed on chest imaging, with diagnosis based on a cardiothoracic ratio of < 0.5. It is not a disease but rather a manifestation of an underlying cause. Patients may have few or no cardiomegaly-related symptoms or have symptoms typical of cardiac dysfunction, like this patient's dyspnea and edema. Conditions that impair normal circulation and that are associated with cardiomegaly development include hypertension, obesity, heart valve disorders, thyroid dysfunction, and anemia. In this patient, cardiomegaly probably has been triggered by uncontrolled hypertension and ongoing obesity. This patient's bloodwork also indicates prediabetes and incipient type 2 diabetes (T2D) (the diagnostic criteria for which are A1c ≥ 6.5% and fasting plasma glucose ≥ 126 mg/dL).

As many as 42% of adults in the United States meet criteria for obesity and are at risk for obesity-related conditions, including cardiomegaly. Guidelines for management of patients with obesity have been published by The Obesity Society and the American Association of Clinical Endocrinologists, and management of obesity is a necessary part of comprehensive care of patients with T2D  as well. For most patients, a BMI ≥ 30 diagnoses obesity; this patient has class 1 obesity, based on a BMI of 30 to 34.9. The patient also has complications of obesity, including stage 2 hypertension and prediabetes. As such, lifestyle management plus medical therapy is the recommended approach to weight loss, with a goal of losing 5% to 10% or more of baseline body weight.

The Obesity Society states that all patients with obesity should be offered effective, evidence-based interventions. Medical management of obesity includes use of pharmacologic interventions with proven benefit in weight loss, such as glucagon-like peptide-1 receptor agonists (GLP-1 RAs; eg, semaglutide) or dual gastric inhibitory polypeptide (GIP)/GLP-1 RAs (eg, tirzepatide). Semaglutide and tirzepatide are likely to have cardiovascular benefits for patients with obesity as well. Other medications approved for management of obesity include liraglutide, orlistat, phentermine HCl (with or without topiramate), and naltrexone plus bupropion. The American Diabetes Association (ADA) recommendations for management of obesity in patients with T2D give preference to semaglutide 2.4 mg/wk and tirzepatide at weekly doses of 5, 10, or 15 mg, depending on patient factors. 

As important for this patient is to get control of hypertension. Studies have shown that lowering blood pressure improves left ventricular hypertrophy, a common source of cardiomegaly. Hypertension guidelines from the American College of Cardiology/American Heart Association recommend a blood pressure goal < 130/80 mm Hg for most adults, which is consistent with the current recommendation from the ADA. Management of hypertension should first incorporate a low-sodium, healthy diet (such as the Dietary Approaches to Stop Hypertension [DASH] diet), physical activity, and weight loss; however, many patients (especially with stage 2 hypertension) require pharmacologic therapy as well. Single-pill combination therapies of drugs from different classes (eg, angiotensin-converting enzyme inhibitor plus calcium channel blocker) are preferred for patients with stage 2 hypertension to improve efficacy and enhance adherence.

Romesh K. Khardori, MD, PhD, Professor, Department of Internal Medicine, Division of Diabetes, Endocrine, and Metabolic Disorders, Eastern Virginia Medical School; EVMS Medical Group, Norfolk, Virginia.

Romesh K. Khardori, MD, PhD, has disclosed no relevant financial relationships.

Image Quizzes are fictional or fictionalized clinical scenarios intended to provide evidence-based educational takeaways.

As seen in red on the radiogram, the patient's heart is grossly enlarged, indicating cardiomegaly. Cardiomegaly often is first diagnosed on chest imaging, with diagnosis based on a cardiothoracic ratio of < 0.5. It is not a disease but rather a manifestation of an underlying cause. Patients may have few or no cardiomegaly-related symptoms or have symptoms typical of cardiac dysfunction, like this patient's dyspnea and edema. Conditions that impair normal circulation and that are associated with cardiomegaly development include hypertension, obesity, heart valve disorders, thyroid dysfunction, and anemia. In this patient, cardiomegaly probably has been triggered by uncontrolled hypertension and ongoing obesity. This patient's bloodwork also indicates prediabetes and incipient type 2 diabetes (T2D) (the diagnostic criteria for which are A1c ≥ 6.5% and fasting plasma glucose ≥ 126 mg/dL).

As many as 42% of adults in the United States meet criteria for obesity and are at risk for obesity-related conditions, including cardiomegaly. Guidelines for management of patients with obesity have been published by The Obesity Society and the American Association of Clinical Endocrinologists, and management of obesity is a necessary part of comprehensive care of patients with T2D  as well. For most patients, a BMI ≥ 30 diagnoses obesity; this patient has class 1 obesity, based on a BMI of 30 to 34.9. The patient also has complications of obesity, including stage 2 hypertension and prediabetes. As such, lifestyle management plus medical therapy is the recommended approach to weight loss, with a goal of losing 5% to 10% or more of baseline body weight.

The Obesity Society states that all patients with obesity should be offered effective, evidence-based interventions. Medical management of obesity includes use of pharmacologic interventions with proven benefit in weight loss, such as glucagon-like peptide-1 receptor agonists (GLP-1 RAs; eg, semaglutide) or dual gastric inhibitory polypeptide (GIP)/GLP-1 RAs (eg, tirzepatide). Semaglutide and tirzepatide are likely to have cardiovascular benefits for patients with obesity as well. Other medications approved for management of obesity include liraglutide, orlistat, phentermine HCl (with or without topiramate), and naltrexone plus bupropion. The American Diabetes Association (ADA) recommendations for management of obesity in patients with T2D give preference to semaglutide 2.4 mg/wk and tirzepatide at weekly doses of 5, 10, or 15 mg, depending on patient factors. 

As important for this patient is to get control of hypertension. Studies have shown that lowering blood pressure improves left ventricular hypertrophy, a common source of cardiomegaly. Hypertension guidelines from the American College of Cardiology/American Heart Association recommend a blood pressure goal < 130/80 mm Hg for most adults, which is consistent with the current recommendation from the ADA. Management of hypertension should first incorporate a low-sodium, healthy diet (such as the Dietary Approaches to Stop Hypertension [DASH] diet), physical activity, and weight loss; however, many patients (especially with stage 2 hypertension) require pharmacologic therapy as well. Single-pill combination therapies of drugs from different classes (eg, angiotensin-converting enzyme inhibitor plus calcium channel blocker) are preferred for patients with stage 2 hypertension to improve efficacy and enhance adherence.

Romesh K. Khardori, MD, PhD, Professor, Department of Internal Medicine, Division of Diabetes, Endocrine, and Metabolic Disorders, Eastern Virginia Medical School; EVMS Medical Group, Norfolk, Virginia.

Romesh K. Khardori, MD, PhD, has disclosed no relevant financial relationships.

Image Quizzes are fictional or fictionalized clinical scenarios intended to provide evidence-based educational takeaways.