This study will review the clinical features of dysplastic melanocytic nevi (DMN) in Japanese cases, and then show the fine structure of melanosomes/melanogenesis in the dysplastic melanocytes and the immunohistochemical property of DMN as identified by monoclonal antibodies against human melanosome specific antigen (HMSA). The incidence of DMN is quite low in the Japanese. It is indicated that this fact may partly explain the low incidence of malignant melanoma in Japanese; in particular, low incidence in sun-exposed areas. The patients with DMN were largely males. They were different from ordinary Japanese in that they usually burn and tan poorly after sun exposure. In addition, the synthesis of melanosomes in the dysplastic melanocytes was found to be abnormal and characterized by a significant alteration in the fine structure of the melanosomal matrix and the pattern of melanization. These abnormal melanosomes reacted positively with MoAb HMSA-1 and HMSA-2, which identify the structural matrix protein of melanosomes unique to neoplastic melanocytes. Importantly, HMSA was present in both dysplastic melanocytes and melanoma cells, but not in epidermal melanocytes (nevus cells) of common melanocytic nevi.

We report a case of generalized familial benign chronic pemphigus (FBCP) whose generalized condition was induced by an infection by Pseudomonas aeruginosa. A 34‐year‐old male suffered erythemato‐macerative lesions over most of his body. Upon microbiological examination, Pseudomonas aeruginosa was cultured from the pus of the lesions. Histologically, a specimen from the abdominal lesion revealed typical features of familial benign chronic pemphigus. It is well known that FBCP is exacerbated by topical infection. We supposed that, in this case, the infection by Pseudomonas aeruginosa was induced by inappropriate therapy with cortiosteroid. Topical application of silversulfadiazin cream was effective in improving the generalized lesions of this condition.

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A 58‐year‐old Japanese man visited our clinic in December 2000 with a complaint of an erythematous plaque with reddish papules and pigmentation on the penis shaft and glans. He noticed the lesion 1 month before his visit. He denied any previous homosexual activity. His wife denied any genital skin lesion or gynecologic abnormality. No history of human immunodeficiency virus infection could be obtained. Physical examination of the skin lesion revealed an asymptomatic, flat‐topped, approximately 10‐mm‐sized, reddish‐brown keratotic plaque on the penis shaft. It showed an irregular surface, irregular border, and color variegation. Multiple, small, reddish‐brown papules and plaques were distributed on the surrounding penis shaft and glans (Fig. 1). The patient had no symptomatic signs. No lymphadenopathy was noted in the inguinal area. Figure 1  Clinical features of BP lesions on the penis. A keratotic plaque shows an irregular surface, irregular border, and color variegation, and is surrounded by small, reddish‐brown papules A biopsy specimen revealed parakeratosis and an irregularly acanthotic epidermis composed of abnormal keratinocytes exhibiting cellular atypia and mitotic figures. The tumor cells had large, hyperchromatic, and pleomorphic nuclei (Fig. 2). These lesions were diagnosed as bowenoid papulosis (BP). For treatment, an operative excision with a 3 mm margin was performed. 2 Histologic features of the BP lesion. A parakeratotic and irregularly acanthotic epidermis is composed of abnormal keratinocytes exhibiting cellular atypia and mitotic figures. The tumor cells have large, hyperchromatic, and pleomorphic nuclei DNA was extracted from blocks of BP and non‐BP, normal‐looking skin tissue. Polymerase chain reaction (PCR) was performed utilizing L1 consensus primer set MY09 and MY11 (Bernard HU, Chan SY, Manos MM, et al. Identification and assessment of known and novel human papillomaviruses by polymerase chain reaction amplification, restriction fragment length polymorphisms, nucleotide sequence, and phylogenetic algorithms. J Infect Dis 1994; 170: 1077–1085). MY09/11 consensus PCR generated an approximately 450‐base‐pair fragment from all of the samples (Fig. 3). Nucleotide sequencing revealed that the amplified L1 sequences were identical to that of human papillomavirus (HPV) type 16 (nucleotide positions 6582–7018). All of the L1 sequences from the BP lesion and the normal regions were identical. Our case contained the prototype sequence reported by Dürst et al. (Dürst M, Gissmann L, Ikenberg H, zur Hausen H. A papillomavirus DNA from a cervical carcinoma and its prevalence in cancer biopsy samples from different geographic regions. Proc Natl Acad Sci USA 1983; 80: 3812–3815). 3 Amplification of the L1 sequence from a BP lesion and surrounding tissues. The polymerase chain reaction was carried out using MY09 and MY11 consensus primers. Lanes from left to right: M, 1‐kilobase ladder marker; N, negative control (H2O); P, positive control (HPV16 DNA); 1, DNA from BP lesion; 2 and 3, D...

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