A case of Sweet’s syndrome associated with acute myelogenous leukemia was reported. This patient was 52-year-old man who had fever and tender, vesicular, erythematous plaques on the elbow area, hand, back and buttocks. Histologically, the skin biopsy showed a dense dermal infiltrate of polymorphonuclear leukocytes. Forty-eight days after the onset of the dermatosis, hematological examinations showed findings of acute myelogenous leukemia. From a study of 27 published reported cases of Sweet’s syndrome associated with malignant neoplasm plus our case, we conclude that Sweet’s syndrome may be one of the non-specific cutaneous lesions of acute myelogenous leukemia.

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We treated two patients with reticulohistiocytic granuloma (RG) which showed typical histopathological findings. Clinical and histopathological differences between RG and solitary xanthogranuloma (adult type) (adult XG) were discussed. Although it was difficult to detect clinical differences between the two diseases, RG could be differentiated from adult XG by the presence of multiform histiocytes and peculiar giant cells.

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We report localized neurofibroma on the left chest and upper arm in a 67-year-old woman. Her family history was unremarkable. X-ray examination showed slight thoracic scoliosis, but which was considered to be a coincidental complication. There were no other cutaneous or systemic abnormalities associated with von Recklinghausen’s disease.

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A 58-year-old woman was given an injection of paraffin into her breasts in 1958. Twenty-four years later, an ulcer appeared in the right breast. Light and electron microscopic observations were performed. Histologically, numerous large and small ovoid or round cavities that appeared like Swiss cheese were seen. The spaces between the cavities were taken up in part by hyalinoid stroma and in part by a cellular infiltrate of macrophages and lymphoid cells. The ultrastructural study showed evidence of paraffin located below. 1) Paraffin solitarily located in collagen fibers. 2) Paraffin surrounded by fibroblasts. 3) Macrophages containing paraffin. 4) Deposition of paraffin in the lymph nodes.

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Transplantable skin cancer in C3H mice was used for hyperthermia, which was done by hot sheets (Hisamitsu Pharmaceutical Co. Ltd.) for one hour at 43°C on the inside of the tumor and at 45°C on the surface of the tumor. Ultrastructural changes of experimental skin cancer after topical hyperthermia were as follow: Initial changes were noted in the nuclei and the cytoplasm of the tumor cells; intercellular spaces were widened. Changes in the nuclei included pyknosis, condensation of the nucleoplasm, vacuolization, separation of the nuclear membrane from the nucleoplasm, and rupture of the nuclear membrane, while those in the cytoplasm were vacuolar and vesicular formation, disappearance of mitochondrial cristae, lysosomal formation, nucleolar changes. Twenty-four hours after hyperthermia, deformed tumor cells as well as regenerated ones were observed in the tumor cell group. It is considered that hyperthermia can serve as an effective treatment for skin cancer.

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Biopsies were taken before and at 30min., 3 and 5 days after dry ice press therapy from the skin of patients with nevus Ota. Dry ice was pressed for 7 seconds and this procedure was repeated. At 30 minutes after the procedure, many free melanosomes were scattered in the dermis and the cell membrane of the dermal melanocytes was obscure. At 3 days after the treatment, all melanin-laden cells were vacuolated, some has a single vacuole and some multiple ones in which there were many melanosomes of stage IV. The basal lamina-like structure was not discernible under electron microscopy, and a this time, the basal lamina in the epidermal dermal junction, was clearly observed. At 5 days after the treatment, the dermal melanin-laden cells have melanosomes, in a package form in the cytoplasm. These results suggest that the degeneration of the dermal melanocytes first occurs by direct effects of freezing with dry ice and melanosomes become scattered in the dermis. These free melanosomes were partly taken up by monocytes and carried to the regional lymphnode and some melanosomes go to the outside in the crust, when the tissue damage was relatively severe. The amount of the dermal melanin decreases after dry ice therapy.

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The following results were obtained by staining normal human skin tissue with modified Sternberger PAP stain for S100 protein, with or without supplemental Giemsa staining.
1) Nerves: The peripheral areas of the sections of nerve fibers (Fig. 1) were positive for S100 protein, while their central areas were negative (Fig. 2). Namely, S100 protein was located in Schwann cell cytoplasm but not in the axon. This protein was demonstrated not only in the fascicle of nerve fibers, but also in isolated nerve fibers adjacent to blood vessels (Fig. 8), sweat ducts (Fig. 5) and hair follicles (Fig. 7). Isolated S100 protein positive nerve fibers were also found in the arrector muscles (Fig. 6). Meissner corpuscles (Fig. 3) and inner bulbs of Vater-Pacini corpuscles (Fig. 4).
2) Epidermis: Langerhans cells (Fig. 9) were positive for S100 protein. The staining of melanocytes (Fig. 10) was variable and weak, if any.
3) Dermis: S100 protein positive histiocytes (dermal Langerhans cells or T-zone histiocytes) (Fig. 11) were found in perivascular areas and were clearly evident in Schwann cells of isolated nerve fibers, as they had a dendritic shape.
4) Fat cells and chondrocytes: S100 protein was located in the cytoplasm of subcutaneous fat cells (Fig. 12). The chondrocytes (Fig. 13) in the cartilage of the external ear were also S100 protein positive.
5) Skin appendages: Some of eccrine secretory cells (Fig. 5) were S100 protein positive, while others were negative. None of the apocrine secretory cells were stained. The myoepithelial cells (Fig. 14) of both eccrine and apocrine glands were S100 protein positive. The staining S100 protein of secreted substance (Fig. 5) in both ductal and secretory lumina of eccrine gland and also cuticula (Fig. 5) of eccrine glands were slightly positive or negative. The apocrine lumina and cuticula were negative for S100 protein.
The description given by previous authors was confirmed by our findings of (1) to (4). Detailed comparisons of findings in eccrine and apocrine secretory cells have been reported herein, for the first time. The findings described by previous authors merely of “sweat gland excretory cells” concerns eccrine and not apocrine glands.

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Nevus cells are known to be possess a high amount of S100 protein. The sensitivity and specificity of PAP and ABC immunoperoxidase methods were monitored using three kinds of anti-S100 protein antibody. The titer of each antibody was checked using the Ouchterlony technique. PAP staining method revealed that optimal dilution of the primary antiserum was 800× (our antiserum) and 400× (DAKO). The ABC staining method revealed the optimal dilution to be 1,600× (ours) and 400× (DAKO). Anti S 100 protein antibody made by IBL showed no precipitation line (Ouchterlony technique) and no specificity. Background staining was diminished by adding 1% bovine serum albumin to the primary antibody. The ABC method proved to be twice as sensitive as the PAP method for staining of S100 protein in nevus cells.

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[in Japanese]

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A survey was made on 20 cases of metastatic skin cancer seen at the Department of Dermatology, Asahikawa Medical College from November, 1976 to December, 1982. 1) The most commonly occurring cutaneous metastases were from patient with breast carcinoma. 2) The chest wall was a frequent site for metastases. 3) The most frequent lesion was a nodule. 4) Most frequently, an adenocarcinoma detected pathologically. 5) The survival rate was an average of 9.4 months.

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A statistical survey was made of cases of dermatomycoses seen at the Dermatology Clinic of Nippon Medical School from 1975 to 1982. The proportion of dermatomycoses to the out-patients was 14.8% Dermatomycoses were classified to tinea (81.0%), candidiasis (14.9%), pityriasis versicolor (3.9%), sporotrichosis (0.2%) and chromomycosis (0.1%). Causative organisms of the tinea were identified to be Trichophyton rubrum (68.8%), T. mentagrophytes (27.7%), Epidermophyton floccosum (1.9%), Microsporum canis (1.0%), M. gypseum (0.6%) and T. violaceum (0.1%).

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[in Japanese]

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[in Japanese]

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[in Japanese]

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[in Japanese]

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[in Japanese]

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