Skin test reactions were evaluated in 242 patients who appeared to develop delayed type drug eruptions from the clinical course. The patch testing was positive in 62 (31.5%) of 197 patients tested and the intradermal testing in 105 (89.7%) of 117 patients. The positive ratios of intradermal testing were higher in maculopapular (MP), erythema multiforme (EM), and erythrodermic (ED) types than in eczematous (Ecz) type drug eruptions, while those of patch testing were comparatively high in ED, Ecz type, and anticonvulsant-induced drug eruptions. It is considered that the combination of patch testing and intradermal testing is useful for determination of causative drugs in delayed type drug eruptions.

Sulfhydryl drug-induced skin eruptions were studied clinically and histologically in 23 patients. In this study, tiopronin, D-penicillamine, captopril and gold sodium thiomalate were considered to be sulfhydryl drugs, because they have a thiol group or release sulfhydryl compounds. The clinical features included skin eruptions that were maculopapular, erythema multiforme-like, eczematous, psoriasis-like, seborrheic dermatitis-like, Gibert-like, lichen planus-like, and pemphigus-like. These clinical findings were reminiscent of the wide variety of eruptions seen in cutaneous graft-versus-host reactions (GVHR). Histologically, areas of vacuolation and eosinophilic necrosis with a satellite infiltrate of lymphoid cells were seen in the epidermis, and perivascular infiltrates were noted in the dermis. These findings were similar to the histological picture of cutaneous GVHR. In skin tests with sulfhydryl compounds, 19 out of 20 subjects showed positive reactions, and autoantibodies were found in 8 out of 12 subjects tested. Sulfhydryl drugs seem likely to induce immunologic changes in the host and to produce a distinctive reaction similar to that of cutaneous GVHR.

We have recently seen two cases of hyperpigmentation in children, which was reticulate and distributed in a zosteriform fashion. As another two cases of hyperpigmentation of this kind in children have been reported previously, described as reticulate hyperpigmentation distributed in a zosteriform fashion, this gives a total of four cases of hyperpigmentation of this kind reported recently from Japan. These four cases differed from progressive cribriform and zosteriform hyperpigmentation, the condition which these cases resembled most closely, with respect to the age of onset of the hyperpigmentation, which in the four Japanese cases was not confined to a dermatome. Like a variant of incontinentia pigmenti (IP), all four cases showed eosinophilia. But they differed from IP in that there was no inflammatory stage, no pigmentary incontinence detectable on histology, and no evidence that the condition was hereditary. These four cases do not conform completely to any described entities and we suggest that they represent a new clinical entity.

A 65‐year‐old man was seen at the Ushioda Hospital in Au‐gust 1989, because of a 1‐month history of a tumor on the scalp. The tumor was excised and the diagnosis was malig‐nant lymphoma. The patient was then referred to our de‐partment in September 1989. Several nut‐sized lymph nodes wvepa‐b and m‐fepa for 2 months. Since then, the patient has been free of disease up to the time of writing, July 1992, a period of 2.5 years. Biopsy samples taken from the tumor on the scalp showed a monomorphous infiltrate of large lymphoid cells throughout the entire dermis and subcutis, with a definite clear zone (Fig.1). A high‐power view showed diffuse large lymphoid cell infiltration. Numerous mitotic figures were also seen. The lymphoid cells had multilobated nuclei and distinct nucleoli (Fig. 2). Monoclonal antibodies such as Leui (CD5), Leu2a (CD8), Leu3a (CD4), Leu4 (CD3), MT‐1 (CD43), Leu14 (CD22), LN1 (CDw75), and Leu26 (CD20), and polyclonal antibodies such as anti‐kappa, anti‐lambda, anti‐IgG, anti‐lgA, anti‐IgM, and anti‐lgD were purchased from commercial sources. Optimal dilutions of the monoclonal antibodies and heteroantisera were assessed beforehand by titration on suitable tissue samples. The antigens recognized by the monoclonal anti‐bodies and heteroantisera were investigated by either the avidin‐biotin peroxidase complex (ABC) method on cryostat sections or the peroxidase‐antiperoxidase complex (PAP) method on paraffin sections, as described elsewhere.1 The immunologic properties of the infiltrating cells were determined using skin biopsied in August 1989, and October 1989. Large lymphoid cells, which formed the major popu‐lation of infiltrating cells, were positive for CD20, CD22, and HLA‐DR and negative for CD3, CD4, CD43, and CD45RO. From these findings the patient was diagnosed as hav‐ing primary cutaneous B‐cell lymphoma, diffuse large non‐cleaved cell type, as classified by the Working Formulation.2

This report describes a case of Mycobacterium marinum skin infection. A granulomatous plaque on the dorsum of the left hand of a 71‐year‐old man who kept a tank of tropical fish was followed by erythema and induration on the left forearm of the lymphocutaneous type. The lesion was successfully treated with 6 weeks of administration of amikacin (28 intramuscular injections) a total of 3500 mg. The isolated M. marinum strain was sensitive in vitro to amikacin at 0.78 μg/ml. Furthermore, another 15 clinical strains of M. marinum showed high sensitivity in vitro to this drug (93% of the 16 strains were sensitive to between 0.78 and 1.56 μg/ml).