Norwegian scabies in the immunocompromised patient.

Norwegian, or crusted, scabies can be defined as a generalized severe scabies (Sarcoptes scabiei var. hominis) infestation usually affecting the immunocompromised patient that is most commonly seen with the leukemia-lymphoma group of neoplasms. The diagnosis is commonly missed, which can lead to mismanagement. We describe a patient with Norwegian scabies involving the lower extremities. The patient circumstances and treatment, as well as a review of the literature, are presented. The diagnosis of scabies should always be considered in patients with advanced malignancies and associated pruritus.

Disseminated candidiasis in a patient with acute myelogenous leukemia.

Disseminated candidiasis is a frequently fatal condition that is rising steadily in immunocompromised patients. We present the case of a 62-year-old African American woman with acute myelogenous leukemia who developed characteristic cutaneous signs of systemic candidiasis. Early cultures and biopsies resulted in early diagnosis, which prompted proper antifungal therapy and a positive outcome.

Possible mechanisms of hypopigmentation in lichen sclerosus.

Lichen sclerosus (LS) shares with vitiligo a milky-white appearance. By biopsy, pathognomonic dermal sclerosis readily distinguishes LS from vitiligo and other causes of leukoderma. To determine what the mechanism of hypopigmentation is in LS, we examined samples from LS cases for alterations in melanin content (Fontana-Masson stain) and melanocyte number (HMB-45 [PMEL-17/gp100], Mel-5 [TRP-1], Mart-1 [Melan A]) and compared these findings with those in controls of normal skin, acute scars, vitiligo, and lichen planus (LP; a common inflammatory cause of hyperpigmentation). The degree and extent of melanization found in LS overlapped with that in acute scars showing predominantly hypomelanized keratinocytes, with that in LP containing regions with numerous melanophages, and with that in vitiligo exhibiting focal regions of keratinocytes devoid of melanin pigment. By hematoxylin-eosin staining and immunocytochemistry for Mel-5 and Mart-1, LS had a lower mean count of melanocytes than acute scars, LP, and normal skin per 200 basal keratinocytes. In addition, a few LS cases had a significant loss of melanocytes comparable to that of vitiligo. Surprisingly, Mart-1 identified rare melanocytes in 67% of vitiligo cases and a significantly larger pool of melanocytes in LS and controls other than those labeled by Mel-5. Furthermore, LP and evolving lesions of LS contained the highest Mart-1 counts. HMB-45-immunoreactive melanocytes were found in the majority of acute scars and in LP and late-stage LS lesions at significantly lower levels than Mel-5- and Mart-1- labeled melanocytes, but they were not found in vitiligo or normal skin. We propose that several mechanisms may play a role in the production of leucoderma in LS: 1) decreased melanin production; 2) block in transfer of melanosomes to keratinocytes; and 3) melanocyte loss. The latter finding may be the pathogenic connection (lichenoid dermatitis of LS triggering an autoimmune reaction to melanocytes) that underlies the documented association of LS with vitiligo.