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A child in whom a phenobarbital hypersensitivity drug reaction developed which consisted of fever, a prunitic desquamating erythrodermic rash, alopecia, icterus, protein-losing enteropathy, myositis, and nephritis, is described. Laboratory studies demonstrated eosinophilia, elevated serum IgE, and elevated T suppressor/cytotoxic cells in the peripheral blood. Findings from biopsy specimens of skin and jejunum suggested a cellmediated pathogenesis, and lymphoproliferative studies of the patient's mononuclear cells revealed a positive response to phenobarbital. The clinical findings and laboratory studies suggested an autoimmune cell-mediated hypersensitivity reaction triggered by phenobarbital.

The use of small amounts of a dilute solution of heparin (less than or equal to 100 IU) to keep indwelling intravenous needles or catheters patent for intermittent venous access either for intravenous therapy or timed blood sampling is a common clinical practice. It is considered safe since the amount of heparin required is much less than that required for heparinization. Herein, we describe a 13-yr-old patient with malabsorption who developed clinically significant bleeding shortly after a diagnostic test which required multiple small injections of heparin for intermittent venous access (total amount of heparin administered was 600 units over 5 hr). The coagulopathy was corrected by a single dose (10 mg) of parenteral vitamin K. As our patient had multiple risk factors for the development of vitamin K deficiency including malabsorption, decreased food intake, and antibiotic use, we postulate that the small amount of heparin precipitated the coagulopathy by increasing the antiprotease activity of antithrombin III on abnormal factors X and II formed in the vitamin K deficient state. We would therefore recommend administration of vitamin K to patients who are at risk of developing vitamin K deficiency before using even small amounts of heparin.