A 77-year-old patient is described who developed pemphigus vulgaris temporally with the administration of cefadroxil. The disease improved when the drug was discontinued but was exacerbated with the administration of ampicillin. This may be the first case of possible cefadroxil-induced and only the second case of ampicillin-induced pemphigus vulgaris reported. The pathophysiology, diagnosis, and treatment of pemphigus vulgaris is briefly described. Drug-induced pemphigus is reviewed. By far the most incriminated drug has been penicillamine. It is postulated that the sulfhydryl group of penicillamine alters the intercellular cement substance into an antigenic structure with subsequent antibody formation. The chemical similarity between penicillamine, the penicillins, and the cephalosporins is alluded to and the potential for cross-sensitivity between the penicillins and cephalosporins is emphasized. Although the pemphigus vulgaris could have occurred by chance, it seems probable that it was drug-induced.
A 47-year-old black male treated with phenytoin for generalized seizures developed a generalized maculopapular rash approximately three weeks after starting therapy. In addition, fever, jaundice, diffuse lymphadenopathy, and elevated liver function enzymes resulted. A liver biopsy revealed hepatic necrosis. Treatment with oral prednisone 60 mg/d led to a resolution of the patient's clinical symptomatology and a normalization of his liver function enzymes in approximately two weeks. An updated review of the literature involving phenytoin-induced hepatic dysfunction is discussed, as well as both the postulated mechanisms causing the reaction, and therapeutic modalities of treatment.
An 84-year-old black male with hypertensive cardiovascular disease and arthritis suffered deterioration in renal function when placed on indomethacin for an acute monoarticular arthritis. Renal function improved after discontinuing the indomethacin. The patient received indomethacin again, and there was a rapid increase in both the serum creatinine and blood urea nitrogen, which declined a second time when the drug was stopped. The plasma renin activity after indomethacin treatment was found to be markedly elevated. The counterbalancing effect of prostaglandins and plasma renin activity in preserving renal function in patients with underlying disease states is stressed. A review of the literature is provided and some rationalizations made as to what type of patient would be most susceptible to renal failure with indomethacin therapy.
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