Tsunemi Numata

THE ROLE OF MITE, HOUSE DUST AND CANDIDA ALLERGENS IN CHRONIC URTICARIA

Intradermal skin tests and in vitro antigen‐induced histamine release from leucocytes were carried out using mite, house dust and candida allergens in 49 patients with chronic urticaria in whom the cause was not identifiable from the history. None of them had other atopic diseases. Among the 49 cases, the number of patients who gave positive skin reactions to different allergens was as follows: mite, 24; house dust, 18; candida, 17. Significant histamine release from leucocytes by mite antigen was observed in 8 out of 12 patients who had 2+ or 3+ skin reactions. The present results suggest that mite, house dust and candida allergens may play a role in chronic urticaria, and especially that the mite may be one of the possible allergens in chronic urticaria.

Antigen-induced histamine release by penetration of egg albumin antigen through excised guinea pig skin

Urticarial reaction is evoked by numerous different stimuli, both immunologic and non-immunologic. In previous studies, we demonstrated the possibility that type 1 reaction may be involved in chronic urticaria and that mite may be one of the allergens [1,2]. This is because a good correlation was observed between skin sensitivity to mite allergen and mite-antigen-induced histamine release from leukocytes in some of the chronic urticarial patients [1]. It is not clear, however, how the mite allergen reaches the mast cells in the skin. Allergen may be absorbed through the respiratory or gastrointestinal tracts. An additional possibility is that the allergen may be capable of penetrating the skin in quantities sufficient to induce urticarial reactions. We, therefore, investigated this possibility in diffusion cells using excised guinea pig skin. Male albino guinea pigs of Hartley strain weighing 250300 g were sensitized using a 0.2 % solution of egg albumin (grade V, Sigma) in saline. Each hind limb was injected with 0.25 ml s.c. The animals were used after 2 weeks. The experiments were concluded by the 5th week. The penetration of egg albumin antigen through the sensitized guinea pig skin was determined in diffusion cells (diameter = 2.7 cm). Carefully shaved abdominal and dorsal skin of the sensitized guinea pig was excised and s.c.tissue was removed by surgical scissors. Several circular skin pieces for diffusion cells were obtained from the excised skin and washed three times in Tyrode solution. One milliliter of antigen solution (egg albumin, 10 gg/ml in Tyrode solution) was placed on the epidermal side of the skin in the upper compartment of the chamber and Tyrode solution in the lower compartment, these reactants being separated by the circular skin piece obtained from the sensitized guinea pig (Fig. 1). The chamber was incubated at 37 ~ C and histamine content in

Monosaccharide in high fructose syrup as an etiological factor of urticaria.

A 30 year‐old man developed urticaria by taking a refreshing drink. Two of its ingredients, invert sugar and high fructose syrup (GF sugar), induced urticarial attacks. GF sugar was analyzed by thin layer chromatography. A by‐product monosaccharide, psicose, was suspected as the responsible factor. Psicose‐rich sugar of Lobry de Bruyn transformation was prepared and skin‐tested. It and its psicose containing fraction of thin layer chromatography induced positive skin reactions. Furthermore, GF sugar released histamine from leukocytes presensitized with the patients serum. It is therefore concluded that the urticarial reaction observed in this patient was mediated by Type I hypersensitivity against psicose.

Release of neutrophil and eosinophil chemotactic factor from sensitized skin in vitro cutaneous anaphylactic reactions.

NCF ECF Chemotactic factor HPLC LTB4 Skin, anaphylactic reaction Tsunemi Numata, MD, Department of Dermatology, Hiroshima University School of Medicine, Kasumi 1-2-3, Minamiku, Hiroshima 734 (Japan) Histamine is considered to play a critical role in anaphylaxis and produce wheal and flare reactions in skin. On the other hand, it is known that inflammatory cells such as neutrophils and eosinophils migrate into the site of anaphylactic reactions in skin. The cellular infiltrations might produce a prolonged inflammatory reaction after immediate wheal and flare reactions in the cutaneous anaphylaxis. In order to analyze the mechanisms of the neutrophil and eosinophil migration into the site of anaphylactic reactions in skin, in vitro antigen-evoked release of neutrophil chemotactic factor (NCF) and eosinophil chemotactic factor (ECF) from skin was investigated. The abdominal skin of guinea pig sensitized with egg albumin was cleaned of subcutaneous tissue and cut into 0.5-mm-thick slices. The slices were incubated with 50 μg/ml egg albumin at 37 °C for 20 min, and NCF and ECF activity in the supernatant were measured with a modification of Boyden technique [1]. using guinea pig neutrophils and eosinophils as indicator cells, respectively. The antigen-evoked NCF and ECF activities were detected in the supernatant. The results of Sephadex G-10 or G-25 gel filtration of the supernatant indicated that the molecular weight of the NCF and ECF were between 300 and 1,300. The release of the NCF and ECF was abolished in the absence of calcium in the reaction mixture. Furthermore, the release of NCF and ECF was suppressed by preincu-bating the slices with nordihydroguaiaretic acid (50 μM), a 5-lipoxygenase inhibitor, and enhanced with indo-methacin (8.5 μM), a cyclooxygenase inhibitor. The NCF and ECF partially purified by Sep-Pak C18 cartridge had the same retention time as leukotriene B4 (LTB4) on reverse-phase HPLC. The significant release of LTB4 by antigen from sensitized guinea pig skin was ascertained by radioimmunoassay.

A light and electron microscopic study of a case of radiation induced malignant giant cell tumor of the soft tissue.

A case of malignant giant cell tumor of the soft tissue in a 59‐year‐old female is presented. Total hysterectomy was performed for uterine carcinoma (histologically squamous cell carcinoma) in 1963, followed by radiation treatment for 6 months. Chronic radiodermatitis developed thereafter on the skin of the hip joint region, buttocks and lower abdominal region. A tumor developed in the lesion of chronic radiodermatitis of the left hip joint region in August 1976 and this was excised on February 23, 1977. Two recurrent tumors and a metastatic lesion in the inguinal lymph node developed, which were surgically removed. The main tumor, measuring 7.5 cm in maximum diameter, was found chiefly in the subcutaneous adipose tissue. Histologically, it was composed of a mixture of fibroblastic spindle‐shaped cells, histiocytic mononuclear cells, bizarre giant cells and osteoclast‐like multinucleated giant cells. Occasionally osteoid tissues were seen. Electron microscopically, undifferentiated cells, fibroblastic cells, monohistiocytic cells, osteoclast like multinucleated giant cells and macrophages were observed, and these cells were considered to be divided into three cell lines, that is an undifferentiated cell line, fibroblastic cell line and histiocytic cell line.