Cases reported "Prurigo"

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1/5. A case of severe actinic prurigo successfully treated with thalidomide.

    Actinic prurigo is an uncommon and usually persistent idiopathic photodermatosis with typical human leukocyte antigen (HLA) associations (HLA-DR4, particularly subtypes DRB1*0407 and DRB1*0401). Although its mechanism of action is not clearly understood, thalidomide has been shown to be particularly efficacious in treating actinic prurigo, among other conditions. A 31-year-old Australian woman who had suffered actinic prurigo for most of her life was treated with two courses of thalidomide (50-100 mg nocte) over consecutive summers. Remission was observed after cessation of the second course of thalidomide and had continued 4 years later. Abnormalities in the cutaneous response to ultraviolet radiation at the time of diagnosis, detected by monochromator phototesting, reverted to normal following treatment.
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2/5. Long-term thalidomide for actinic prurigo.

    A 35-year-old man presented at the age of 8 years with recurrent pruritic papulovesicular lesions on his face and body appearing within minutes of light exposure. A recent positive finding of human leukocyte antigen (HLA) DR4 with the rare DRB1*0407 subtype confirmed a diagnosis of actinic prurigo. thalidomide (100 mg/day) was commenced at the age of 11 years after an unsuccessful trial of other treatments and his lesions resolved within 2 months. Attempts to withdraw thalidomide have resulted in recurrence of photosensitivity and the patient has remained on a virtually continuous maintenance dose of thalidomide (50 mg/ day) for 23 years. His cumulative dose is estimated to be over 400 g. To date, he has not experienced any adverse effects and investigations have shown no evidence of neuropathy. This case illustrates the safe long-term use of thalidomide.
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3/5. Primary cutaneous B-cell lymphoma associated with actinic prurigo.

    We describe two patients with a diagnosis of actinic prurigo who subsequently developed cutaneous B-cell lymphoma. This is the first report, to our knowledge, of this association. We propose that chronic antigenic stimulation by ultraviolet radiation, in the context of actinic prurigo, may have been causal in the development of these unusual lymphomas.
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4/5. prurigo pigmentosa: role of ICAM-1 in the localization of the eruption.

    Immunohistochemical studies were carried out on the skin lesions of two cases of prurigo pigmentosa. There was a predominance of CD4 cells in the dermal infiltrate, whereas those lymphocytes in the epidermis were mainly CD8 cells. The majority of dermal and epidermotropic lymphocytes showed an intense expression of lymphocyte function-associated antigen 1 (LFA-1). The number of CD1 cells was increased in the epidermis. There was intense expression of ICAM-1 by keratinocytes in the erythematous papules. Focal expression of ICAM-1 was still observed in the residual pigmented areas and could explain the recurrence of the lesions at these sites.
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5/5. Mycobacteria in prurigo nodularis: the cause or a consequence?

    BACKGROUND: prurigo nodularis (PN) is a chronic skin disorder; its cause remains unknown. OBJECTIVE: We evaluated mycobacteria as a possible cause of PN. methods: Forty-three patients with PN were examined. skin biopsy specimens were obtained for microbiologic and histopathologic studies. The patients were tested for intracutaneous reactivity to 12 mycobacterial antigens with the Mantoux technique. RESULTS: Six specimens (14%) grew mycobacteria in culture: M. avium-intracellulare (3), M. malmoense (1), and mycobacterium sp. (2). Histopathologically, 12 samples (28%) were positive for acid-fast bacilli, and granulomatous changes were present in one sample. patients whose cultures were positive for mycobacteria had significantly larger skin reactions to mycobacterial antigens. Two patients underwent 2 years of antituberculous chemotherapy; one had an excellent response and the other a partial response. CONCLUSION: Detection of mycobacteria by culture or staining, combined with elevated skin reactivity to mycobacteria in a high proportion of patients with PN, suggests a mycobacterial cause.
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