Incidence of cytomegalovirus infection and its relationship to donor-recipient serologic status in liver transplantation.
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Biomedical subjects
Publications and source records attributed to J Rakela.
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A 22-yr-old woman presented with fulminant Wilson's disease. The diagnosis was suspected clinically and was later confirmed with chemical and pathologic studies. She presented with acute hepatic failure, hemolysis, and acute anuric renal failure. Postdilution hemofiltration and continuous arteriovenous hemofiltration with oral D-penicillamine allowed removal of a total of 95,700 micrograms of copper; 78,665 micrograms of the total were removed via postdilution hemofiltration alone. On the 57th day, the patient received successful liver and renal transplants. We found that the determination of serum copper was instrumental in the diagnosis of fulminant Wilson's disease, that postdilution hemofiltration allowed a rapid removal of copper in the presence of renal failure, and that, finally, orthotopic liver transplantation should be performed early in the clinical course of these patients. This patient is the longest survivor of this serious condition.
Of 560 hepatitis B surface antigen-positive patients who were tested for antibody to hepatitis delta-antigen by blocking radioimmunoassay, 29 (5%) were seropositive. Patients with chronic active hepatitis had a greater frequency of seropositivity than those with chronic persistent hepatitis (26% vs. 0%, p less than 0.05), and patients with symptomatic chronic disease harbored the antibody more commonly than asymptomatic counterparts (14% vs. 2%, p less than 0.01) or patients with acute hepatitis (14% vs. 1%, p less than 0.02). Of 8 patients with acute fulminant hepatitis, including 6 who died of liver failure, none were seropositive. Antibody was detected in drug users, dialysis patients, hemophiliacs, and transfusion recipients; in 17 patients, however, including 3 homosexuals, it occurred sporadically. Samples harvested in 1969 contained delta-antibody. Antibody was found in most ethnic groups, including Orientals, where it occurred only in relocated Vietnamese. We conclude that delta-antibody is detected infrequently in a diverse referral population within the United States. Seropositivity is associated with symptomatic chronic disease and histologic findings of chronic active hepatitis. Homosexuals and resettled Vietnamese are susceptible to sporadic delta-infection.
From 1974 through 1982, fulminant hepatitis was diagnosed in 34 patients at our institution. Of these patients, only two survived (survival rate, 6%). This syndrome was caused by viruses (B and non-B hepatitis and herpes simplex) in 23 patients, hepatotoxic drug in 6, Wilson's disease (hepatolenticular degeneration) in 3, and industrial poisons in 2. Most of the patients died within 10 days after the onset of encephalopathy. The poor prognosis in our group of patients was probably related to the preponderance of older patients and cases caused by non-B hepatitis virus. In our patients, the clinical course was complicated by renal failure, ascites, bleeding, sepsis, pancreatitis, and seizures. The major cause of death was hepatic failure.
Of 20 patients with alcoholic liver cirrhosis and a superimposed episode of acute viral hepatitis, 12 developed hepatic encephalopathy or ascites or both. Four died of hepatic failure. Seventeen patients had received blood transfusions within 6 months before the acute hepatitic episode. Two patients were HBsAg-positive; the other 18 were presumptively diagnosed as having non-A, non-B hepatitis. However, hepatitis A virus infection was excluded in only three of the 18 patients. Histologic examination performed in 13 cases disclosed necrotizing inflammatory activity, which is commonly observed in acute viral hepatitis. The distinctive histologic feature was a meager regenerating activity. We conclude that patients with alcoholic cirrhosis complicated by acute viral hepatitis frequently develop hepatic failure and have a high fatality rate (20% in our series).
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We have studied three patients with chronic HBV infection who had a superimposed bout of type A hepatitis. The patients recovered uneventfully without observing a change in their clinical course afterwards. In one patient we observed transient disappearance of DNA polymerase during type A hepatitis; we have postulated that this is probably related to hepatic necrosis.
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We have studied the effect of short-term high-dose prednisone therapy on aminotransferase levels and hepatitis B virus markers in 6 patients with chronic type B hepatitis. All showed a decrease in amino transferase levels during treatment. This was followed by a transient increase in aminotransferase levels after prednisone was discontinued. In 5 patients, there was a decrease in hepatitis B virus deoxyribonucleic acid polymerase activity at the time of postprednisone peak of aminotransferase levels. Three of them became transiently deoxyribonucleic acid polymerase negative. All the patients have remained hepatitis B e antigen-positive throughout the period of observation. We have also found transient deoxyribonucleic acid polymerase negativity unrelated to prednisone therapy in 2 patients with chronic type B hepatitis: in one during a superimposed episode of acute type A hepatitis, and in the other during a period of pronounced alanine aminotransferase elevation. We postulate that these periods of deoxyribonucleic acid polymerase negativity are due to a decreased number of hepatitis B virus-infected cells in the liver as a consequence of hepatic necrosis.
The occurrence of hepatitis A virus (HAV) infection in a small boarding school for mildly to moderately mentally retarded children in Umka, Yugoslavia, in the spring of 1979, six years after the last recognized occurrence, provided an opportunity to study the spread of the agent among 79 classroom and dormitory contacts. Only 51% of those who had entered subsequent to the prior outbreak had detectable antibody (anti-HAV) with immunoglobulin G predominance, and the proportion within the first six years of training did not vary. Both findings suggest a lack of endemicity during the interval. The outbreak ended spontaneously just before the summer vacation with an anti-HAV prevalence of 90%. The ratio of silent to overt cases was approximately 2:1. HAV was found in fecal samples from susceptible residents with inapparent infection as well as those with hepatitis. Among those with prior experience, there were no significant anti-HAV increases to suggest HAV reinfection in this group. Overall, 32% were seropositive for markers of past or chronic hepatitis B virus (HBV) infection, but this status did not correlate with sex, year of training, or HAV experience. Only one instance of HBV transmission was observed in the same interval as the 26 HAV infections.
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Eighty-three women with acute icteric hepatitis during pregnancy were followed for evidence of viral transmission to their infants. Six women had acute hepatitis A as diagnosed by appearance of anti-HAV during convalescence. Except for passively acquired antibodies which were present at birth, anti-HAV did not appear in these infants, and there was no clinical or biochemical evidence for hepatitis during follow-up. Sixty-five pregnant women had acute hepatitis B during pregnancy or in the immediate postpartum period. Transmission to infants often occurred when both maternal HBsAg and HBeAg were positive at delivery of postpartum. A majority of these infants never developed jaundice, have remained persistently HBsAg-positive, and have had periodic serum ALT elevations during follow-up. Twelve women had acute non-A, non-B hepatitis during pregnancy. Infants born to 6 of these women near term had transient elevations of serum ALT values at 4-8 wk of age, suggesting maternal transmissibility of the non-A, non-B viral agent.
We have analyzed the frequency of chronicity and its distribution according to epidemiologic background following acute non-A, non-B hepatitis. Eighteen of 45 cases (40%) developed chronic liver disease. The incidence of chronicity was significantly higher following transfusion and among drug addicts (54% and 58%) than among patients without obvious source of infection (20%). Chronic active hepatitis developed in 4 of 13 patients (31%) with posttransfusion hepatitis. This lesion was not observed among the addicts or the patients without obvious source for the acute hepatitis.
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Three patients with hepatitis B surface antigen (HBsAg)-positive polyarteritis nodosa (PAN) who are clinically well 4 1/2-5 1/2 years after their initial illnesses are described. In each case electron microscopic studies demonstrated the presence of aggregates of HBsAg in both acute and quiescent phase sera. One patient had a lower circulating HBsAg titer during the acute illness, while no change in serial HBsAg titers was observed in the other two patients. Two of the three patients showed lymphocyte transformation to purified HBsAg during the quiescent phase of the PAN. The role of immune complexes in the pathogenesis of HBsAg-positive PAN is discussed.