The histopathological features of allergic contact dermatitis were compared with those of irritant contact dermatitis in a group of 17 subjects. Each patient received simultaneous patch tests of a known allergen and a standardized irritant (benzalkonium chloride). The cellular changes occurring between 3 h and 7 days after patch test application were studied by light and electron microscopy and immunocytochemistry. No differences were observed between the induced allergic contact dermatitis (ACD) and the irritant contact dermatitis (ICD), either in the responding cell types or the sequence of cellular events. Both reactions showed a predominantly T lymphocyte infiltrate with no polymorphonuclear leukocyte involvement. Apposition of Langerhans cells to lymphocytes in the epidermis was seen in both types of response. Considerable variability in the intensity of reaction to irritant and allergen occurred within individuals. There was no statistically significant difference between the intensity of the reactions to the irritant and the allergen.

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The hybrid-hybrid monoclonal antibody 28-19-8 has specificity for the tumour-associated antigen carcinoembryonic antigen and the vinca alkaloids. This bifunctional antibody has been used to target unmodified vinblastine sulphate to well-established MAWI human tumour xenografts implanted in nude mice. The highly significant suppression of tumour growth achieved throughout treatment has also been sustained for over 2 months after the withdrawal of treatment. Histological examination of excised tumours from treated animals has shown profound changes in their morphology when compared with tumours from control animals. Cells in tumours that had started to grow again after withdrawal of therapy were shown still to express carcinoembryonic antigen, the target antigen recognised by the bispecific antibody.

Thrombocytopenia is defined as a decrease in the platelet count to less than 100 x 10(9)/L and it is the most commonly reported drug-induced blood dyscrasia. Heparin is the most commonly reported cause of drug-induced thrombocytopenia with a reported incidence between one and ten percent. Thrombocytopenia induced by cephalosporins has been reported but is relatively rare. This report does not completely document that two third-generation cephalosporins caused platelet counts to fall less than 100 x 10(9)/L in the patient described but there was no other explanation available. Platelet counts began to fall with the institution of third-generation cephalosporins and began to rise when these agents were stopped. In order to document that thrombocytopenia was induced by the third-generation cephalosporins a rechallenge would have been necessary; this was not considered to be safe in this patient. A review of the literature is presented describing similar cases of cephalosporin-induced thrombocytopenia.