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Disseminated cytomegalovirus infection.

Address for correspondence: Dr R F Miller, Department of Medicine, UCMSM, First Floor Cross Piece, Middlesex Hospital, London, WIN 8AA, UK Accepted for publication 14 February 1992 Case presentation (DrA Grant) A 42 year old male Caucasian homosexual was found to be HIV antibody positive in May 1986. In June 1986 he was recruited to the MRC/ANRS Concorde Study. This is a double-blind placebo controlled study of zidovudine in asymptomatic HIV infected individuals, to assess its effect on the progression of HIV disease and survival.' He remained well until January 1990, when because of evidence of progression of his HIV disease (he had developed ARC symptoms with weight loss and night sweats and his CD4 count had fallen to 60/mm3 on two occasions), trial capsules were stopped and "open" zidovudine was used at a dose of 250 mg four times daily. Primary prophylaxis for Pneumocystis carinii pneumonia was started with monthly inhaled pentamidine. In April 1991 he was notified to CDSC as having AIDS on the basis of chronic perianal ilceration due to Herpes simplex infection, but otherwise remained well on zidovudine and experienced no haematological or biochemical adverse reactions to this drug. He was also taking acyclovir 200 mg as prophylaxis for H simplex. In June 1991 he was admitted to hospital with a six week history of watery diarrhoea, passing up to six stools per day. He also complained of increasing right upper quadrant abdominal pain, constant in nature, made worse by ingestion of food and numbness of the feet. Examination revealed a thin man who had a low grade fever (37.4°C). The liver edge was just palpable. Fundoscopy showed evidence of cotton wool spots but no haemorrhages or other evidence of cytomegalovirus retinitis (fig 1). Investigations at this time revealed a haemoglobin of 9.7 g/dl and a white blood count of 2 1 x 1 09/dl (neutrophils = 1 *68 x 1 09/dl). Urea and electrolytes were normal. Liver function tests showed an alkaline phosphatase of 678 (normal < 282) iu/l, AST was at the upper limit of normal at 55 iu/1, serum albumin and bilirubin levels were normal. Ultrasonography of the upper abdomen showed that the common bile duct was dilated at 7 mm; no stones were evident within the biliary tree and the pancreas was normal. A technetium IODIDA scan was performed. This is a nuclear medicine imaging technique. In normal patients following intravenous injection of the radiotracer it is taken up by the liver within five to ten minutes and is then rapidly excreted into the biliary tree, appearing in the duodenum within 20 minutes. In this patient the scan showed rapid uptake of radiotracer into the liver parenchyma but there was delay of excretion into the duodenum and retention within the intraand extrahepatic ducts.2 These appearances were highly suggestive of sclerosing cholangitis. Stool culture revealed Salmonella enteritidis. Nerve conduction studies showed evidence of a mild peripheral sensory axonal type neuropathy. The patient was treated with oral ciprofloxacin 500 mg bd given for ten days for the salmonella infection. Endoscopic retrograde cholangiopancreatography (ERCP) was performed. At ERCP the ampulla appeared inflamed and this was biopsied. A sphincterotomy was performed as the bile duct orifice appeared stenosed. A cholangiogram showed a dilated common bile duct and also dilated intraand extrahepatic ducts. There was little pain relief following sphincterotomy but the alkaline phosphatase enzyme levels which had risen peaking at 1208 iu/1 just prior to ERCP and the AST which had risen to 98 iu/l both rapidly fell to normal levels. Histological examination of biopsy tissue revealed intranuclear and intracytoplasmic inclusions of cytomegalovirus infection (fig 2). Culture of biopsies from the ampulla later grew cytomegalovirus. Treatment with ganciclovir at a dose of 5 mg/kg twice daily was given for 21 days. He later developed a Staphylococcus aureus chest infection which was treated with erythromycin. A follow up stool