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

To establish the impact of transplantation on the course of chronic hepatitis B liver disease we performed a prospective study of the clinical and pathological sequelae of hepatitis B disease in all 22 patients who had renal allografts that functioned for more than 1 year and who were hepatitis B surface antigen (HBsAg)-positive following transplantation. No patient converted to HBsAg-negative. During a mean follow-up of 83 months serial liver biopsies were performed in 20 patients and 1 liver biopsy was available in the remaining 2 patients. Eleven patients died of liver disease, 5 of whom died of hepatic failure, 3 with hepatoma, 2 of gastrointestinal hemorrhage, and 1 of ascites with pleuroperitoneal fistula. Aggressive liver disease was observed in the vast majority of patients: 12 ultimately developed cirrhosis, (mean follow-up 81 months), 6 chronic active hepatitis (mean follow-up 93 months), 3 chronic persistent hepatitis (mean follow-up 89 months), and in 1 patient the presence of HB virus in hepatocytes was the sole morphologic alteration (follow-up 42 months). There was a marked tendency to progression in that 82% of patients with virus only, reactive hepatitis, or chronic persistent hepatitis on initial biopsy subsequently developed chronic active hepatitis or cirrhosis. For comparison, 10 HBsAg-positive patients whose renal failure had been treated by hemodialysis were also studied over a comparable period. Four patients converted to the negative state. Biochemical evidence of persistent liver dysfunction occurred in only 1 patient and no patient has died from complications of liver disease. We conclude that in the immunosuppressed renal transplant patient HB infection often results in the development of cirrhosis, leading to death from hepatoma and hepatic failure. This course is worse than that in dialysis patients. Renal transplantation of HBsAg-positive patients with end-stage renal failure may be inadvisable.
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PMID:The impact of renal transplantation on the course of hepatitis B liver disease. 389 Feb 90

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.
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PMID:Fulminant hepatitis: Mayo Clinic experience with 34 cases. 392 80

Combined hepatocellular injury and renal tubular necrosis developed in five alcoholic patients who were receiving acetaminophen therapeutically. Two patients were taking doses prescribed by a physician. The hepatitis was characterized by extremely high serum transaminase values that were maximal on admission. Two patients died, and autopsy disclosed hepatic centrizonal necrosis and acute renal tubular necrosis. The three who survived had clinical features typical of acute tubular necrosis. All five had measurable concentrations of acetaminophen in plasma, although measurements were requested on admission only in two patients. When an alcoholic presents with combined hepatic and renal insufficiency, acetaminophen should be considered as a possible inciting agent. This diagnosis should be considered when serum transaminase levels are markedly elevated and when renal failure is due to acute tubular necrosis.
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PMID:Combined hepatic and renal injury in alcoholics during therapeutic use of acetaminophen. 406 53

The clinical syndrome of "shock liver," also known as ischemic hepatitis, is characterized by sudden elevation (to more than 20 times the upper limit of normal) of SGOT and SGPT in response to cellular anoxia, followed by resolution to near normal levels within seven to ten days. In our experience with ten cases, systemic hypotension was documented in only four, but processes characterized by decreased cellular perfusion were identified in all and included cardiac failure or arrhythmia, sepsis, cerebrovascular accidents, renal failure, and chronic obstructive pulmonary disease. We were also able to document the transient rise in serum bilirubin and alkaline phosphatase levels and prolonged prothrombin time that followed the transaminase elevations by 24 to 48 hours in most cases, followed by rapid resolution. In neither of the two cases in which tissue was available by biopsy after resolution of the biochemical abnormalities did we find the classic histologic picture of necrosis in zone 3 ("centrilobular necrosis"). The clinical picture of shock liver is so characteristic and resolves so rapidly that there should be no confusion with other causes of marked elevations of transaminase levels.
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PMID:Shock liver. 407 Nov 67

A 34-year-old male presented with fulminant hepatitis A associated with acute renal failure. The patient was admitted four days after flu-like symptoms developed. Physical examination was unremarkable except for icteric sclerae. Laboratory studies showed SGOT 10719 U/l, SGPT 5780 U/l, prothrombin time 22%, BUN 25.5 mg/dl, and creatinine 2 mg/dl. Serum complements were within normal ranges, and circulating immune complexes were not detected. Anti-HAV IgM was positive. He developed hepatic coma on the fourth hospital day, and his renal function deteriorated progressively. He was treated with hemodialysis, but there was no improvement in consciousness. Although acute liver failure improved, he died on the 74th hospital day of subendocardial infarction. Autopsy examination showed acute renal tubular necrosis. The liver was enlarged and was in the residual stage of acute hepatitis without submassive necrosis. The development of fulminant hepatitis in hepatitis A has been rare, but in recent years acute renal failure in hepatitis A has been reported. Although the mechanisms responsible for renal failure in liver diseases are uncertain but could be multifactorial, immune complex-mediated nephritis and/or endotoxemia have been considered.
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PMID:Report of a case with fulminant hepatitis A associated with acute renal failure. 407 29

Using enzyme-linked immunosorbent assay technique (Boehring Institute Laboratory), eighty-one adult patients were studied for hepatitis Bs antigenaemia. Nine of the patients had asymptomatic persistent proteinuria, thirty-nine, nephrotic syndrome, and thirty-three had profuse proteinuria, azotoaemia and hypertension. The histopathology obtained in forty showed twenty-two with MCGN, four with focal glomerulosclerosis, three with proliferative glomerulonephritis, one with minimal change glomerulonephritis and ten with end-stage kidney disease. None of the patients had apparent clinical evidence of liver disease nor a past history of jaundice. One hundred and eighty apparently normal adults served as controls; 33.3% of the patients had positive hepatitis Bs antigenaemia, in contrast to 6% (P less than 0.001) in the normal controls. Hepatitis Bs antigenaemia was more prevalent in the groups with nephrotic syndrome and persistent asymptomatic proteinuria than in the group with advanced renal failure. Hepatitis Bs antigenaemia was detected in all histopathologic forms but was most prevalent in the MCGN (P less than 0.001) which is also the more commonly encountered lesion. The implications of these findings are discussed.
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PMID:Role of hepatitis Bs antigen in chronic glomerulonephritides in Nigerians. 608 37

21 patients with periarteritis nodosa (PN) were examined for evidence of viral hepatitis-B infection. Histologic evidence of PN was present in 11 patients, whereas in 10 patients the diagnosis of PN was based on the clinical presentation only. In the sera of 9 of the 21 patients (42%) HBsAg (4 patients) or anti-HBs (5 patients) was detected, while findings were present in 4-8% of blood donors. Hypertension, glomerulonephritis and renal failure developed more frequently in patients with hepatitis-B associated PN. The detection of immune complexes in the sera of hepatitis-B negative patients tends to suggest immune complex mediated mechanisms not related to hepatitis-B virus.
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PMID:[Significance of hepatitis B serology in periarteritis nodosa]. 613 34

A retrospective record study of six cases of meningitis caused by group A beta-hemolytic Streptococcus is presented. Associated findings included otitis media, pharyngitis, and erysipelas. All patients survived their infections despite major complications including seizures, shock, coma, renal failure, and hepatitis. Two patients had neurologic sequelae. Group A Streptococcus causes a severe form of bacterial meningitis in apparently healthy children.
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PMID:Group A streptococcal meningitis. 633 34

Amiodarone was administered to 80 patients with recurrent cardiac tachyarrhythmias previously resistant to drug treatment. Forty nine patients were treated for ventricular tachycardia or fibrillation and 31 for supra-ventricular arrhythmias. The mean (range six days to 51 months), permitting a total of 100 patient years of observation. Adverse reactions were observed in 69 patients. Severe side effects were encountered in 13: four patients developed interstitial pneumonitis, four patients developed incessant ventricular tachycardia, three patients taking amiodarone and digoxin sustained sinus node arrest with depression of escape foci, one patient developed hepatitis, and one patient developed hypercalcaemia with renal failure. Furthermore, a rise in the serum concentration of digoxin and potentiation of warfarin anticoagulation occurred in cases in which these agents were combined with amiodarone. Amiodarone was stopped in 14 patients because of side effects. Although amiodarone is effective in suppressing arrhythmias in most patients in whom extensive use of antiarrhythmic drugs has been unsuccessful, it is associated with diverse and serious toxicity. These observations suggest that at present the use of amiodarone should be reserved for patients with life threatening or seriously disabling arrhythmias in whom longer established drugs have been ineffective or are contraindicated.
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PMID:Adverse reactions during treatment with amiodarone hydrochloride. 640 40

Patients with renal failure have characteristic systemic and oral conditions that require special precautions during dental treatment. Drugs must be administered with caution and patients undergoing hemodialysis must receive special consideration. Both hemodialysis and transplant patients must be protected against infection. This is achieved by early, aggressive, and thorough dental treatment. Use of antibiotics during dental treatment is essential in transplant patients and is often necessary in hemodialysis patients to protect them against bacteremia. Bacterial endocarditis is a concern in patients with renal failure and with heart disease and, in these patients, antibiotic prophylaxis is essential. Hepatitis is often present in patients with renal failure, and precautions should be taken against its spread. Before dental treatment of patients with renal failure is begun, the dentist should consult the patient's physician regarding specific precautions. A treatment plan should be constructed which best restores the patient's dentition and protects from potentially severe infection of dental origin.
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PMID:Dental care for patients with renal failure and renal transplants. 646 52


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