Am Fam Physician. 2003 Nov 1;68(9):1835-1836.
A 25-year-old man presented to the dermatology clinic with a one-week history of intensely pruritic lesions on the hands and penis. The lesions appeared about the same time in both areas (see accompanying figure). The patient had one sexual partner who denied having any skin lesions or pruritus. The patient's nephew, with whom he played frequently, had similar pruritic lesions on the hands, wrist, and trunk. The patient denied any penile discharge. His lesions consisted of firm papules about 1 to 4 mm in diameter. Some papules were present in the finger webs.
Based on the patient's history and physical examination, which one of the following is the most likely diagnosis?
A. Bullous pemphigoid.
B. Pemphigus vulgaris.
C. Genital herpes.
The answer is D: scabies. The history of intensely pruritic papules on the hands and penis is characteristic of scabies. The social history revealed similar signs and symptoms in the nephew, who had lesions on the wrists, hands, and trunk. On close examination, what appeared to be linear burrows were noticed.
Sexual transmission of scabies is common but, as in this case, the transmission also may occur from other close contact. It is important to treat all household members and to wash clothes and linens in hot water.
Scabies occurs in both sexes and in any age group. When several members of the same household experience pruritic eruptions, scabies should be considered. Norwegian scabies (crusted scabies) is a variant of scabies in which the entire skin becomes psoriasis-like, with severe scaling and crust. Crusted scabies most often occurs in patients with acquired immunodeficiency syndrome or other immunocompromised states, physically debilitated patienst, or elderly residents of nursing facilities.1
Topical treatment overnight with permethrin, lindane, or precipitated sulfur in ointment usually treats the infestation. Repeat treatment is often suggested about one week after the first treatment, but is likely unnecessary, because scabies eggs and mature mites are killed by the insecticides. Pruritus often persists for weeks after successful treatment because of antigenic stimulation by the decaying mites. In severe cases of scabies, oral ivermectin has been shown to be effective.2
Bullous pemphigoid is a blistering disease that is not pruritic. Bullae arise because of an autoimmune attack involving the basement membrane at the dermal-epidermal junction. The disease usually manifests in patients older than 60 years. Men are more commonly affected than women. Blisters initially appear on the extremities and later the trunk. Intact blisters outnumber erosions because these bullae are not easily unroofed.
Pemphigus vulgaris is another blistering disease, but it is characterized by more superficial bullae than are seen in pemphigoid. The site of skin disruption is in the epidermis. Vesicles are more fragile, and easily unroof, leading to ulcerated lesions. Nikolsky's sign is positive (pressure at the edge of a blister causes extension of the bulla into adjacent normal skin) in pemphigus, while in pemphigoid, the Nikolsky's sign is negative.3
Genital herpes is a sexually transmitted disease that is characterized by a prodrome of pain, itching, or other dysesthesia before the eruption of vesicles. Lesions are usually clustered in one area, not widely dispersed as with scabies.
Syphilis is the great mimicker. In this case, syphilis is a less likely diagnosis because of the intense pruritus and lack of an ulcer.4 The physician should always include syphilis in the differential diagnosis when treating a patient with lesions on the genitalia.
1. Fitzpatrick TB, Freedberg IM. Fitzpatrick's dermatology in general medicine. 6th ed New York: McGraw-Hill, 2003.
2. Victoria J, Trujillo R. Topical ivermectin: a new successful treatment for scabies. Pediatr Dermatol. 2001;18:63–5.
3. Cotell S, Robinson ND, Chan LS. Autoimmune blistering skin diseases. Am J Emerg Med. 2000;18:288–99.
4. Brown TJ, Yen-Moore A, Tyring SK. An overview of sexually transmitted diseases. Part I. J Am Acad Dermatol. 1999;41:511–32.
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