A 19-year-old white woman w i t h urticaria, arthrdgias, a n d hepatitis B-associated antigen i n her serum developed a progressive encephalopathy despite only mild hepatic dysfunction. The patient's serum at 4°C produced a cryoprecipitate containing the hepatitis B-associated antigen and its antibody. Serum complement levels were borderline low. A t autopsy, gross and histological examination of t h e brain revealed only mild residual cerebral edema. Indirect immunofluorescent studies of t h e cerebral cortex and choroid plexus showed no evidence of immune complex deposition. T h e patient's progressive encephalopathy may have been related to t h e presence of cryoprecipitable hepatitis B antigen, a relationship not previously reported. ical basis, the hepatitis-associated antigen and t h e development of a n acute encephalopathy.
Case ReportA 19-year-old white woman who was comatose and bilaterally decerebrate was seen in the emergency room of Parkland Memorial Hospital. Her history, obtained from the patient's sister, indicated that she had lived with a jaundiced heroin addict until two months before admission and had developed arthralgias and urticaria six weeks previously. An assay for the hepatitis B surface antigen (HBsAg) obtained at that time was positive [4] (Table). Four weeks later the patient developed anorexia, nausea and vomiting, a mild headache, and some neck sriffness. She was irritable, slept most of the day, and continued to have joint pains that required salicylates for relief. O n the morning of admission the patient was found comatose on the floor. Physical examination in the emergency room revealed a pulse of 140 per minute, temperature of 4 V C , and Cheyne-Stokes respirations. She had mild scleral icterus and a normal-sized liver. Rectal examination revealed guaiacpositive stools. O n neurological examination her disc margins were found to be blurred bilaterally, indicating increased intracranial pressure. She had downbeat nystagmus and alternated between decorticate and decerebrate poscuring. The hemoglobin concentration was 1 I .7 gm/dl with a leukocyte count of 6,800 cells/mm3 and a placelet count of 470,000/mm3. H e r serum chemistry, arterial blood gas, and clotting studies were normal except for a direct1indirect bilirubin concentrarion of 7.215 .0 mgidl, serum glutamic oxaloacetic acid transaminase reading above 500 units, and alkaline phosphatase of 160 and 244 units (normal, < 80).The prothrombin time was normal. Arterial and cerebrospinal fluid (CSF) ammonia levels were only minimally elevated. H e r HBsAg in serum remained positive. The patient's serum was also positive for anti-HAA antibody by radioimmunoassay [4-6] (see the Table). The results of serological tests for collagen vascular disease (antinuclear antibody titer, lupus erythematosus cell preparations, serum protein electrophoresis) were negarive. A screen for toxic substances and a salicylate level were both normal. Urinalysis revealed trace proteinuria.Changes observed in a four-vessel intracranial arteriogram were...
