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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To examine the postliver transplant recurrence of hepatitis C virus (HCV) infection in patients with pretransplant infection, as well as its acquisition in patients without prior infection, we used the polymerase chain reaction to amplify HCV RNA in serum and/or liver samples of 89 patients with alcoholic and cryptogenic cirrhosis undergoing liver transplantation. Results were correlated with histologic findings from posttransplant liver biopsies. Ninety-five percent of patients with pretransplant infection had posttransplant viremia. In contrast, 35% of patients without pretransplant infection acquired the virus (P less than 0.0001). Pretransplant HCV infection predisposed patients to hepatitis in the new graft. HCV RNA was present in serum of 96% of patients with posttransplant hepatitis. Fifty-six percent of patients with posttransplant HCV infection had no evidence of liver damage at least 1 year posttransplant. However, of those patients with histologic hepatitis, chronic active hepatitis was common. It is concluded that although HCV infection recurs posttransplant in almost all infected patients, acquisition of the HCV infection with transplant is common. Pretransplant HCV infection is an independent risk factor for the development of posttransplant hepatitis. HCV infection accounts for the majority of posttransplant hepatitis not due to cytomegalovirus, and although many patients with posttransplant viremia have little evidence of histologic hepatitis, significant hepatic damage may occur.
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PMID:Recurrent and acquired hepatitis C viral infection in liver transplant recipients. 137 43

Acute hepatitis can be caused by a number of viruses, especially A, B, C, E, delta, Epstein-Barr virus, and cytomegalovirus. Hepatitis A and B have been discussed previously in this series. The virus responsible for most cases of what commonly has been referred to as non-A non-B hepatitis has been tracked, and antibodies to certain proteins of this virus have been identified. This virus is now referred to as hepatitis C. The possible clinical outcomes after acute hepatitis C virus infection are similar to those for hepatitis B virus infection, except that hepatitis C is far more likely to become chronic. Clinical testing for hepatitis C virus infection is in its infancy and has certain limitations. Successful treatment of at least some cases of hepatitis C is possible. Hepatitis E has recently been described, primarily in third-world countries. It causes an acute hepatitis that may be particularly lethal for pregnant women. Herpesviruses may also cause hepatitis, particularly in the newborn or the immunocompromised. Exotic viruses causing acute hepatitis are enumerated.
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PMID:Viral hepatitis in the 1990s, Part III: Hepatitis C, hepatitis E, and other viruses. 138 12

50 pregnant women and 31 nonpregnant women (age 15-40 years) with viral hepatitis admitted to Wad Medani Teaching Hospital, Sudan, during the period January 1987-January 1990 were compared in a prospective case control study. The mean serum bilirubin level was higher in the control group and the difference was statistically significant (p = 0.0084). Significantly more case came from rural settings (76%) compared with control patients (48%) (p 0.01). The criteria for admission were the presence of symptoms and signs of hepatitis and bilirubin in the urine. Almost all patients admitted to the study had viral hepatitis caused by type A virus, type B virus, or non-A, non-B viruses, however, a very small number of diseases of patients could be attributed to rare viruses like EB or cytomegalovirus. No specific medication was given and patients were managed by bed rest and parenteral multivitamins (Parentrovit). All patients were kept in the hospital until they became asymptomatic and serum bilirubin dropped to less than 2 mg/100 ml. All cases and controls were followed up for 6 weeks. All the control patients were discharged after recovery and none of them died or developed recurrence of disease. Out of the 50 pregnant women, 7 died, giving a maternal mortality rate of 14%; the rest recovered and none of them developed recurrence of disease during the follow-up period. The difference between the 2 groups was statistically significant (p = 0.04). The estimated relative risk of death in viral hepatitis with pregnancy was 9.93. Among 5 deaths that occurred after delivery during the 3rd trimester 1 was at term and the baby was normal; 4 were preterm deliveries. Out of the 50 pregnant women, 1 died before delivery and 1 delivered at home. The outcome of pregnancy in the remaining 48 was: 2 abortions (4.2%), 10 preterm (20.8%), and 36 (75%) term deliveries. There were 2 stillbirths (4.2%) one at term and one at 34 weeks.
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PMID:Viral hepatitis in pregnancy. 139 11

Fibrin ring granuloma is characterized by a fibrinous ring surrounding a central fat vacuole. It has been found in the liver and bone marrow of patients with Q fever, and occasionally with visceral leishmaniasis, cytomegalovirus, Epstein-Barr virus, Staphylococcus epidermidis infections, Hodgkin's lymphoma, and hypersensitivity to allopurinol. We describe a case of serologically confirmed viral hepatitis A with this lesion in the liver biopsy. A false positive anti-hepatitis A virus IgM result has been excluded. This is, to our knowledge, the second reported case of type A hepatitis with hepatic fibrin ring granulomas. It confirms that hepatitis A should be included in the differential diagnosis of this lesion.
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PMID:Fibrin ring granulomas in hepatitis A. 147 40

The emergence of the acquired immunodeficiency syndrome (AIDS) has fueled concerns of both physicians and their patients about safety of blood transfusions. Although AIDS has generated the most fear, the risk today is extremely remote (1/60.000 units of blood). The risk of transmitting infectious disease by homologous transfusion is decreasing, as more donor screening and testing measures are implemented. The blood supply is safer that at any time, but small transfusion risks exist. The most common problems associated with transfusions are temporary: one in 100-300 recipients will experience fever or rash. The biggest problem is a mismatch of the well-known ABO blood groups and once in every 100-400.000 transfusions the hemolytic reaction is fatal. Viral hepatitis is another serious and important risk. At present hepatitis seems to strike between 1 and 3 percent of transfusion recipients. Most, if not all, of transfusion-associated hepatitis cases are caused by hepatitis C virus. Cytomegalovirus can cause primary infection, reactivation or reinfection by transfusion. Immunosuppressed patients are more likely to develop more severe disease. Epstein-Barr virus does not seem to cause significant post-transfusion disease. Bacterial or protozoal infections are an infrequently encountered adverse effect of transfusion. However, some clinical cases document the potential hazard of blood components as a vector for bacteria or protozoa. Homologous blood transfusion down-regulates some immune functions. Host defences against malignancy and infection may in some instances be severely compromised by transfusions of homologous blood.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Transfusion risks and alternatives to transfusion]. 149 80

In hepatic transplantation, the recipient and the graft must manage a difficult symbiosis. The causes that can unbalance the mutual adaptation are various, but the clinical-biochemical hepatic graft syndromes they produce are not specific. Morphological study of the graft shows a distinct pattern for each type of dysfunction etiopathogeny. Such study may find: (1) immune attack: acute rejection or chronic rejection; (2) technical complications in the biliary tract or in the blood perfusion of the graft; (3) nonspecific cholestasis secondary to graft cold ischemia or preceding development of chronic rejection; (4) recurrence of the previous illness: graft infected by hepatitis virus; (5) opportunistic viral infections (cytomegalovirus, Epstein-Barr virus, herpesvirus, adenovirus); (6) reactions to drugs and toxics; and (7) combinations of several etiologies. Morphological knowledge enables the pathologist to collaborate in hepatic transplantation programs: elaborating protocols, selecting patients, diagnosing hepatic graft dysfunction, and assessing program quality.
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PMID:The role of histopathology in hepatic transplantation. 152 58

Extrarenal sorbitol clearance was measured in liver transplant patients after a steady-state perfusion. Four measurements were performed in 3 patients with various liver diseases (beginning or patent acute rejection, cytomegalovirus hepatitis, hepatic metastasis). The mean (+/- SD) extrarenal sorbitol clearance was 14.8 +/- 0.1 ml/min.kg. In 5 patients with minimal or no liver abnormalities, the mean from 5 measurements of extrarenal sorbitol clearance was 18.9 +/- 5.0 ml/min.kg. Extrarenal sorbitol clearance values in this later group were higher than the values previously reported in healthy subjects.
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PMID:Extrarenal sorbitol clearance after liver transplantation. 152 94

Twelve patients with recently diagnosed acute viral hepatitis underwent serial 99mTc-galactosyl neoglycoalbumin scanning of the liver (for up to 8 mo). Injection of 99mTc-galactosyl neoglycoalbumin (150 mBq) at a rate of 3.5 mg (50 nmol; 1 ml) revealed that the liver is the exclusive site of tracer uptake. Simulation of 99mTc-galactosyl neoglycoalbumin kinetics allowed quantification of galactosyl neoglycoalbumin binding to human hepatic binding protein. Return of liver function test scores to normal values was associated in two patients with hepatitis A, in four patients with hepatitis B and in two patients with non-A, non-B hepatitis virus infection, with increases in hepatic binding protein concentration (up to three times the initial concentration), binding rate constant and hepatic blood flow. In the other four patients (three patients with hepatitis B and one patient with cytomegalovirus infection) a prolonged course of disease was monitored. In the mean, hepatic binding protein increased from 0.41 +/- 0.11 mumol/L after onset of acute hepatitis (n = 12) to 0.78 +/- 0.21 mumol/L after 6 mo of follow-up (n = 10) (p less than 0.001). During this period, binding rate constant (72.4 +/- 12.6 vs. 82 +/- 11.5 mumol/L/sec; p less than 0.05) and hepatic blood flow (0.027 +/- 0.0051 vs. 0.031 +/- 0.0083 L/sec; p less than 0.05) increased. Hepatic binding protein concentration correlated highly with actual laboratory test results for liver function (r = 0.98; p = 0.0001). We conclude that scintigraphic evaluation of functional liver cell mass using the new receptor-tracer 99mTc-galactosyl neoglycoalbumin could provide an in vivo diagnostic means of quantifying liver function and assessing liver morphology. In addition, our findings suggest that changes in hepatic binding protein-receptor concentration are likely to occur in vivo.
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PMID:Liver function in acute viral hepatitis as determined by a hepatocyte-specific ligand: 99mTc-galactosyl-neoglycoalbumin. 155 36

Among 530 consecutive patients hospitalized for acute hepatitis cytomegalovirus infection was diagnosed in 5 (0.9%). In 2 cases the infection was due to blood transfusion. The course of the disease was Got essentially different from hepatitis A, B, or non-A, non-B, however, clinical and biochemical manifestations of cholestasis were common. All biochemical abnormalities returned to normal within few weeks. In conclusion, it seems that cytomegalovirus is a rare cause of clinically overt hepatitis and its course is often cholestatic.
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PMID:[Cytomegalovirus hepatitis]. 164 69

The clinical pictures of 11 adults with cytomegalovirus-infection were analyzed. Characteristic symptom was fever of unknown origin lasting up to 50 days. Indications of an accompanying hepatitis were found in all patients and confirmed by increased serum levels of the transaminases which for al short time exceeded 5 mumols/s/l (AST) and 8 mumols/s/l (ALT) only in 2 patients. Mononucleosislike pictures, however, have not been seen. One patient developed neurological symptoms. The diagnosis was made by demonstrating IgM and IgG antibodies by way of the fluorescence antibody test. An antiviral therapy has not been introduced.
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PMID:[Clinical aspects of acute cytomegalovirus infection in adults without immune deficiency]. 164 71


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