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Exacerbation of diazepam-induced phlebitis by oral penicillamine Penicillamine, a heavy metal antagonist, is used in the treatment of Wilson's disease, cystinuria, rheumatoid arthritis, and various other conditions. Adverse reactions to the drug are many and frequent and range in severity from gastrointestinal distress, stomatitis, unpleasant skin odours, and rashes to proteinuria, leucopenia, and thrombocytopenia.1 Up to one-third of patients given the drug for rheumatoid arthritis have to discontinue treatment because of toxicity.' Intravenous diazepam is widely used as a sedative, muscle relaxant, and anticonvulsant. Local complications with this drug, including pain at injection site, phlebitis, and thrombophlebitis, have likewise been reported frequently.2We describe a patient who developed phlebitis from intravenous diazepam. The phlebitis resolved with local heat but recurred on two separate occasions after oral penicillamine. Case reportA 33-ycar-old white man underwent endoseopic retrograde eholepanereatography for investigation of persistent raised activity of alkaline phosphatase and 5'-nucleotidase. He had had ulcerative colitis 10 years earlier which had been effectively treated with sulphasalazine. Five years later an asymptomatic rise of alkaline phosphatase and 5'-nucleotidase activities and findings on oral cholecystogram consistent with cholecystitis prompted a cholecystectomy. This showed acalculus cholecystitis. Minimal biliary duct inflammation was found on liver biopsy. Although the patient had remained asymptomatic the alkaline phosphatase activity remained raised at 70 to 225 IU/l (normal 13-40) as did the 5 '-nucleotidase activity at more than 17 Bodansky units (normal 0 3-3-2). Results of tests for antimitochondrial and antismooth muscle antibodies were negative and serum bile acid concentrations were normal. An endoscopic retrograde

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SUMMARY Plasma immunoreactive thyrotrophin (TSH) responses to synthetic thyrotrophin releasing hormone (TRH) have been measured in forty‐five patients with pituitary or hypothalamic disease (largely non‐functioning and functioning pituitary tumours) tested before and/or after ablative treatment. Subnormal TSH responses usually indicated impaired pituitary function but were less sensitive indices than those of human growth hormone (HGH) after hypoglycaemia. High basal TSH values with exaggerated rises after TRH were occasionally found with hypothyroidism and impaired HGH and cortisol secretion. Delayed TSH responses were indicative of hypothalamic disease in some cases, but in others were associated with pituitary tumours without overt hypothalamic disease. Normal TRH tests were found with hypothyroidism, while five abnormal tests (four delayed) were found in euthyroid patients. Patterns of TSH response to TRH in hypothalamic‐pituitary disease are complex and their significance is not always clear.