Nihon Hifuka Gakkai zasshi. The Japanese journal of dermatology最新文献

Using a computer stereographic analysis, the normal human forehead skin from 16 males of ages ranging from 7 to 77 years were investigated to known the morphological changes of the sebaceous glands with aging. The volume of sebaceous glands increased abruptly in teens, reaching maximum in the 20s; it was maintained at high levels even at middle ages and then began to decrease gradually in the 60s. The volume of sebaceous glands positively correlated with the number of the sebaceous cells but not with their sizes. Ultrastructually, in the large sebaceous glands, and peripheral cells were cuboidal, whereas they were flat in the small sebaceous glands. It is concluded that the sebaceous glands in males show no morphological change in relation to age between the 20s and 50s.

The present article describes 94 patients (34 male and 60 female) with delusions of parasitosis, admitted to our dermatology clinic between 1978 and 1989. The female to male ratio was to one under the age of 45, and 1:2.1 over 45. The mean age of onset in males was 46.4 years, and in females, 52.8. In nine patients (6 male and 3 female), the delusions began shortly after their retirement, while in seven (1 male and 6 female) after separation from their families. The ratio of the number of patients living alone to that of patients living with their families was one to two, three times higher than that of the general population (1:6). About half of the patients had no skin lesions, while half the rest had excoriations. Three had eczematous lesions caused by the application of insecticides. In 58 patients, the creatures of delusion were mites. Most patients complained of some kind of cutaneous sensations of the skin, such as itching, tickling and prickling, while only two complained of auditory sensations. The color of creatures of delusion was black or white. Folie á deux was observed in 23 groups and affected both sexes.

A 30-year-old SLE patient developed a xanthoma on her alopecia lesion. Histological examination showed typical lupus changes including immunofluorescence stainings. In addition, there were numerous xanthoma cells existed through the dermis, interlobular spaces of subcutaneous fat tissue, perivascular areas of small blood vessels, and subendothelial spaces and inside of intraluminal thrombosis of subcutaneous small arteries. These xanthoma cells contained granular materials in their cytoplasm. Histochemically, these materials are diastase resistant P.A.S. (+), immunoglobulin (+), Sudan BB (+), Sudan III (+), Nile blue (pinkish red), and yellowish orange autofluorescence suggesting that they are lipofuscin or lipid peroxidation products. Further histological findings showed destruction of sebaceus glands and peri-glandular++ infiltration of lymphocytes and histiocytes. These histiocytes contained phagocytic neutral lipid droplets in their cytoplasm. Very small lipid peroxides were also seen on surface and/or cytoplasm of infiltrating lymphocytes existing not only peri-lobular area but also intraluminal area of blood vessels. The marker profile of these infiltrating lymphocytes are B-cell predominant admixed with some CD8(+) T-cells. These data suggest that the mechanism of developing xanthoma is initiated by immune-complex deposition on basal lamina of sebaceus glands, followed by destruction of sebaceus glands by lympho-histiocytic cells infiltration with some antigen presenting and/or effector cells, and finally xanthoma cells were developed by phagocytosis of lipid peroxides caused by macrophage-derived oxygen radicals. Interestingly, our data suggest that the lipid peroxides, which may act as photosensitizer, may leave the skin and may enter the small vessels carried by lymphocytes. Furthermore the xanthoma cells may also enter the circulation through the small arteries.

This previously healthy 43-year-old man was admitted to our hospital with a history of rash, dysphagia and severe myalgia for two months. Physical examination showed prominent edema and erythema over the face and the chest, scattered ulcerations on the trunk, and muscle atrophy most prominent proximally. Serum levels of muscle enzymes were remarkably increased. Two weeks of oral prednisolone therapy (40 mg/day) was not effective, and betamethasone intravenous pulse therapy (3 x 1000 mg) was followed by slight clinical improvement. However, 12 days after pulse therapy, he complained abdominal pain on the right lower quadrant. The surgical findings included peritonitis due to single perforation of the cecum. After operation, cyclosporine therapy was added and over the next 14 month a considerable clinical improvement was noted. Prednisolone was reduced from 80 mg to 10 mg daily. Biopsy specimens from ulcerated+ skin and perforated cecum showed prominent vascular abnormalities: arterial and venous intimal hyperplasia, occlusion of vessels by fibrin thrombi, and lymphocytic infiltration which affected veins of all sizes. The evidence strongly suggests that both skin ulcers and cecum perforation were caused by vasculitis and occlusion of vessels, which often seen in childhood dermatomyositis.

Two cases of transient acantholytic dermatosis were reported. The first case was a 78-year-old male and showed pruritic papulovesicular lesions on the face, head, neck and back. Darier-like pattern was observed histologically. Oral administration of etretinate (40 mg/day) was effective. The second case was a 57-year-old male showed asymptomatic, herpetiform confluent vesiculo-papules on the right forearm. Darier-like pattern was dominantly observed with a focal spongiotic acantholysis histologically. Also 20 cases (10 males and 10 females) reported in Japan were collected and analyzed.

Localization of HTLV-I-associated antigens was studied in adult T cell leukemia (ATL) cells and HTLV-I-infected cell line cells using monoclonal and human polyclonal antibodies against the viral-related antigens. Two monoclonal antibodies that we obtained by hybridoma technique reacted with HTLV-I-virus core antigens, P19 and P24, respectively. Human anti-HTLV-I-antibodies, which were purified from sera from ATL patients reacted with not only HTLV-I virus particles but also their precursors located in the cytoplasm. In tumor cells freshly isolated from ATL patients, no expression of the virus antigens was observed. When the cells were cultured for several days, the virus antigens were defined in about 3-5% of the cultured cells by the monoclonal antibodies, and in 5-10% by the purified human anti-HTLV-I antibodies. Addition of 5-iodo-2'-deoxyuridine to the culture inhibited cell growth, and at the same time, increased the percentage of the virus antigen-positive cells. Established HTLV-I-infected cell lines showed different cytological profiles from the original ATL cells in the viral replication and morphology.

In attempt to prove the hypothesis that corneocyte surface area in diabetics is larger than that in age-matched non-diabetics, we collected corneocytes from 50 diabetics and 43 non-diabetics in different decades of life. We measured surface areas of 27 +/- 3 corneocytes in each subject, utilizing an image analyser (Kontron MOP-10), then we counted mean number of corneocytes collected in 7 diabetics and 7 non-diabetics. There was a significant correlation between corneocyte surface area and chronological age in non-diabetics, whereas there was no significant correlation in diabetics. Corneocyte surface area of diabetics was larger than that of non-diabetics in every decades of life. The differences were statistically significant in 4th, 7th and 8th decades of life. Mean number of corneocytes collected in non-diabetics was 2.21 +/- 0.47 (X 10(5)), whereas that in diabetics was 2.49 +/- 0.55 (X 10(5)). The present study suggested that turnover time of corneal layer of the skin might be delayed in diabetics.

Blood Group related antigens Lewis A, Lewis B, CA 19-9, and sialyl SSEA-1 were examined in normal human skin and oral mucosa, using monoclonal antibodies to the respective antigen immunohistochemically. These antigens were not expressed on normal keratinocytes but Lewis A and Lewis B were expressed on oral mucous epithelium. Lewis A, Lewis B, and CA 19-9 were expressed clearly on intraepidermal and dermal eccrine duct, but sialyl SSEA-1 was poorly expressed in some cases. In secreting portion of eccrine gland, Lewis A was expressed in 20%, Lewis B was expressed in 70%, and CA 19-9 was expressed in 10%, and sialyl SSEA-1 was expressed weakly in 20% of cases. It's noteworthy that sialyl SSEA-1 was expressed on dendritic cell in epidermis and some infiltrated small round cell in dermis. There is no correlation between patient's peripheral blood type (Lewis) and expression of Lewis antigen in normal skin.

To investigate alterations in the basement membrane (BM) components around tumor nests, Bowen's disease (BD), actinic keratosis (AK), basal cell epithelioma (BCE), squamous cell carcinoma (SCC) were studied by double immunofluorescent staining with antibodies to laminin (LN), type IV collagen (CIV), heparan sulfate proteoglycan (HSPG), and chondroitin 6-sulfate glycosaminoglycan (C6S). In BD, all BM components were continuous on the dermo-epidermal junction. In AK, C6S was partially disrupted, but the other components were continuous. In BCE, LN and CIV were continuous around the tumor nests, but HSPG and C6S were varied. SCCs were divided into two groups by the patterns of LN, CIV, and HSPG; SCC with continuous BM components or disrupted ones. The former SCC had a tendency to show the more infiltrative growth. C6S was detected partially on the BMs of SCCs which have cytological characteristics of BD, while it was absent on those of other SCCs. The difference in the patterns of the BM components suggests variation of tumor invasion.

The anticentromere antibody is considered to be a useful serologic marker for the CREST syndrome. But this antibody also appears in other related conditions less frequently. We classified 29 patients with anticentromere antibodies into 3 groups: (1) 16 patients with systemic sclerosis or Raynaud's phenomenon alone; (2) 7 patients with other connective tissue diseases; (3) 6 patients with other conditions. Ig class reactivities and complement-fixing abilities of anticentromere antibody were measured by the indirect immunofluorescence test. The whole Ig titers were high (1025 or more) in all patients belonging to group 1. However, the properdin-fixing anticentromere antibody titers of these patients were relatively low (256 or less). In contrast, the patients in group 2 and 3 were shown to have higher C3- and properdin-activating abilities which were determined by the ratios of the titers of C3- and properdin-fixing anticentromere antibody to the IgG titers although the whole Ig titers of these patients were widely distributed. These data suggest that the patients who have low whole Ig titers and/or high properdin-fixing titers do not belong to the scleroderma spectrum and that the patients without clinical features of scleroderma have high C3- and properdin-activating abilities.