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The lysosomal enzymes, acid-phosphatase and beta-glucuronidase, were released from rat liver lysosome when exposed to 400 nm irradiation in the presence of haematoporphyrin, and the release was prevented by adding vitamin E, diazabicyclo-octane, bovine serum albumin, superoxide dismutase or D-mannitol to the reaction mixture. Monochromatic irradiation with wavelengths from 380 to 410 nm caused no significant differences in the release of lysosomal enzymes, but 420 nm irradiation caused three-fifths of that of 400 nm irradiation. The malondialdehyde level in rat liver homogenate increased after 400 nm irradiation in the presence of haematoporphyrin. Reduction of nitroblue-tetrazolium was not observed when haematoporphyrin was excited by 400 nm; it was considered that superoxide anion radical (O2--) was not primarily generated. The following mechanism was assumed: that porphyrin which had been excited by 400 nm, converted ground-state molecular oxygen (3O2) to excited singlet oxygen (1O2), which formed lipid peroxides in lysosomal membrane resulting in destruction of the membrane; skin changes would occur from these released lysosomal enzymes.

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A 25-year-old man with solar urticaria is described. The action spectrum ranged from 400 to 500 nm. An inhibition spectrum was found to be in the visible light range above 660 nm. Simultaneous or alternate exposure to ‘blue-violet light’ and ‘red light’ mostly inhibited weal formation. The urticarial reaction was not blocked by local injection of antihistamines and not prevented by histamine depletion with polymyxin B sulfate. These data suggest that histamine may not play a major role in weal production in this case.

A 2.5-year-old boy presented with skin lesions consistent with Mucha-Habermann disease, which appeared about 5 days after an injection of freeze-dried live attenuated measles vaccine. He responded to both oral and topical corticosteroid therapy. To my knowledge, this represents the first such association of Mucha-Habermann disease with virus vaccination.

We quantitated numbers of mast cells in the sclerotic skin noted on the dorsa of the hands of 10 patients with porphyria cutanea tarda (PCT) and compared them with those of diffuse scleroderma and healthy controls. Mast cell counts in sclerodermoid skin of PCT patients were significantly greater than those in involved skin of 9 patients with diffuse scleroderma in its late stage and also greater than those in normal skin of 8 controls. When mast cell density was analyzed according to the depth of the dermis, an 84% increase was noted in the uppermost layer (0–0.2 mm in depth) and a 150% increase in the second uppermost layer (0.2–0.4 mm in depth) in the patients with PCT when compared with those in the corresponding sites of the controls. These results suggest a possible role of mast cells in the pathogenesis of sclerodermoid skin of PCT.

Tsutsugamushi disease, one of the rickettsiosis, is known to be occasionally accompanied by elevation of hepatic enzyme levels. However, there are only a few reports on histopathological findings of the liver. We presented a case of Tsutsugamushi disease with liver involvement. A 51-year-old man suffered from eruptions and a high fever with a mild transaminasemia. He was diagnosed as Tsutsugamushi disease by detection of IgM class antibody against Rickettsia tsutsugamushi. Laparoscopic examination showed a dark-brown liver with diffuse whitish markings. Microscopic findings were consistent with the features of non-specific reactive hepatitis: sinusoidal small lymphocyte infiltrations, mild disarray of hepatocytes and aggregation of T lymphocytes and macrophages in the lobule.