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Itchy, scaly lesions with sweating

Scaly lesions

The patient’s history of a rash that worsened with sweating and clinical findings of erythematous papulosquamous lesions was consistent with Grover disease, also known as transient acantholytic dermatosis. Typically, this is a short-lived condition; however, when symptoms have manifested for years, it is deemed persistent acantholytic dermatosis. The gold standard for diagnostic confirmation is a skin biopsy, although it can also be diagnosed clinically. Since the patient had previously received this diagnosis from another clinician, and his clinical presentation was consistent, a confirmatory biopsy was not performed.

The specific pathophysiology of acantholytic dermatosis is unclear. A study to assess for an autoimmune component found that all participants had autoantibodies that are reactive to proteins involved in cell development, activation, growth, death, adhesion, and motility. Another hypothesis involves occlusion of eccrine sweat glands.

Typical triggers are sweating, heat, sunlight, and mechanical irritation, although it can also be triggered by end-stage renal disease and solid organ transplantation. It has also been linked to certain drugs (eg, ribavirin, anastrozole), other skin diseases (eg, atopic dermatitis, xerosis cutis), bacterial/viral infections, and malignancies.

As heat and perspiration are common triggers, avoidance of activities that expose patients to these conditions is recommended. Otherwise, topical corticosteroids and emollients are the recommended first-line therapy, along with antihistamines to control itching. Other therapies include systemic corticosteroids, topical vitamin D analogs (eg, calcipotriene), systemic retinoids (acitretin or isotretinoin), phototherapy and photochemotherapy (PUVA), red-light 5-aminolevulinic acid photodynamic therapy (ALA-PDT), and etanercept.

Although the patient could not remember the name of the previously prescribed medication, his description suggested that a systemic retinoid had already been tried, with no improvement. Treatment with emollients and oral antihistamines was also unsuccessful, as was topical antiperspirants to control perspiration on his affected skin. The patient agreed to try topical calcipotriene twice daily. He also agreed to switch to a topical emollient containing ceramides.

Image courtesy of Esther Walker, MD, and text courtesy of Esther Walker, MD, Department of Internal Medicine, and Daniel Stulberg, MD, FAAFP, Department of Family and Community Medicine, University of New Mexico School of Medicine, Albuquerque.

References

Phillips C, Kalantari-Dehaghi M, Marchenko S, et al. Is Grover's disease an autoimmune dermatosis? Exp Dermatol. 2013;22:781-784.

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The Journal of Family Practice - 69(10)
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Scaly lesions

The patient’s history of a rash that worsened with sweating and clinical findings of erythematous papulosquamous lesions was consistent with Grover disease, also known as transient acantholytic dermatosis. Typically, this is a short-lived condition; however, when symptoms have manifested for years, it is deemed persistent acantholytic dermatosis. The gold standard for diagnostic confirmation is a skin biopsy, although it can also be diagnosed clinically. Since the patient had previously received this diagnosis from another clinician, and his clinical presentation was consistent, a confirmatory biopsy was not performed.

The specific pathophysiology of acantholytic dermatosis is unclear. A study to assess for an autoimmune component found that all participants had autoantibodies that are reactive to proteins involved in cell development, activation, growth, death, adhesion, and motility. Another hypothesis involves occlusion of eccrine sweat glands.

Typical triggers are sweating, heat, sunlight, and mechanical irritation, although it can also be triggered by end-stage renal disease and solid organ transplantation. It has also been linked to certain drugs (eg, ribavirin, anastrozole), other skin diseases (eg, atopic dermatitis, xerosis cutis), bacterial/viral infections, and malignancies.

As heat and perspiration are common triggers, avoidance of activities that expose patients to these conditions is recommended. Otherwise, topical corticosteroids and emollients are the recommended first-line therapy, along with antihistamines to control itching. Other therapies include systemic corticosteroids, topical vitamin D analogs (eg, calcipotriene), systemic retinoids (acitretin or isotretinoin), phototherapy and photochemotherapy (PUVA), red-light 5-aminolevulinic acid photodynamic therapy (ALA-PDT), and etanercept.

Although the patient could not remember the name of the previously prescribed medication, his description suggested that a systemic retinoid had already been tried, with no improvement. Treatment with emollients and oral antihistamines was also unsuccessful, as was topical antiperspirants to control perspiration on his affected skin. The patient agreed to try topical calcipotriene twice daily. He also agreed to switch to a topical emollient containing ceramides.

Image courtesy of Esther Walker, MD, and text courtesy of Esther Walker, MD, Department of Internal Medicine, and Daniel Stulberg, MD, FAAFP, Department of Family and Community Medicine, University of New Mexico School of Medicine, Albuquerque.

Scaly lesions

The patient’s history of a rash that worsened with sweating and clinical findings of erythematous papulosquamous lesions was consistent with Grover disease, also known as transient acantholytic dermatosis. Typically, this is a short-lived condition; however, when symptoms have manifested for years, it is deemed persistent acantholytic dermatosis. The gold standard for diagnostic confirmation is a skin biopsy, although it can also be diagnosed clinically. Since the patient had previously received this diagnosis from another clinician, and his clinical presentation was consistent, a confirmatory biopsy was not performed.

The specific pathophysiology of acantholytic dermatosis is unclear. A study to assess for an autoimmune component found that all participants had autoantibodies that are reactive to proteins involved in cell development, activation, growth, death, adhesion, and motility. Another hypothesis involves occlusion of eccrine sweat glands.

Typical triggers are sweating, heat, sunlight, and mechanical irritation, although it can also be triggered by end-stage renal disease and solid organ transplantation. It has also been linked to certain drugs (eg, ribavirin, anastrozole), other skin diseases (eg, atopic dermatitis, xerosis cutis), bacterial/viral infections, and malignancies.

As heat and perspiration are common triggers, avoidance of activities that expose patients to these conditions is recommended. Otherwise, topical corticosteroids and emollients are the recommended first-line therapy, along with antihistamines to control itching. Other therapies include systemic corticosteroids, topical vitamin D analogs (eg, calcipotriene), systemic retinoids (acitretin or isotretinoin), phototherapy and photochemotherapy (PUVA), red-light 5-aminolevulinic acid photodynamic therapy (ALA-PDT), and etanercept.

Although the patient could not remember the name of the previously prescribed medication, his description suggested that a systemic retinoid had already been tried, with no improvement. Treatment with emollients and oral antihistamines was also unsuccessful, as was topical antiperspirants to control perspiration on his affected skin. The patient agreed to try topical calcipotriene twice daily. He also agreed to switch to a topical emollient containing ceramides.

Image courtesy of Esther Walker, MD, and text courtesy of Esther Walker, MD, Department of Internal Medicine, and Daniel Stulberg, MD, FAAFP, Department of Family and Community Medicine, University of New Mexico School of Medicine, Albuquerque.

References

Phillips C, Kalantari-Dehaghi M, Marchenko S, et al. Is Grover's disease an autoimmune dermatosis? Exp Dermatol. 2013;22:781-784.

References

Phillips C, Kalantari-Dehaghi M, Marchenko S, et al. Is Grover's disease an autoimmune dermatosis? Exp Dermatol. 2013;22:781-784.

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