Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Twelve patients developed herpes simplex (HSV) hepatitis a median of 18 days after solid organ transplantation. This is earlier than cytomegalovirus hepatitis, which usually occurs 30-40 days after transplantation. Eight recipients (67%) died, and in seven, the diagnosis was made at autopsy or less than 48 h before death. Clinical manifestations associated with mortality were hypotension, disseminated intravascular coagulation (DIC), metabolic acidosis, gastrointestinal bleeding, and bacteremia. Laboratory abnormalities at diagnosis associated with mortality were high creatinine, low platelet counts, prolonged partial thromboplastin time, and a high percentage of band forms on the blood smear. Disseminated HSV disease was noted in four of six patients who had an autopsy and included involvement of lungs in three and the gastrointestinal tract in three. Five recipients developed DIC and all died. Pathologically, HSV hepatitis has two forms, focal and diffuse. All three patients with diffuse liver pathology died. However, three of seven with focal liver pathology survived with antiviral therapy, which suggests that early diagnosis and treatment may be lifesaving. None of these patients had received prophylactic acyclovir. It is possible that acyclovir prophylaxis may be able to prevent this disease.
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PMID:Herpes simplex virus hepatitis after solid organ transplantation in adults. 185 Apr 39

In 230 patients (90 females, 140 males aged between 20 and 73 years, average age 47.8 years) with and without exception histologically and/or laparoscopically ascertained chronic liver diseases (degenerative damages of liver parenchyma in 45, fatty liver stage I in 28, fatty liver stage II in 36, cholangiohepatitis in 4, chronic persisting hepatitis in 31, chronic active hepatitis in 57 and liver cirrhosis in 59 cases) the incorporation of the aminophenazon breathing test in the so-called laboratory chemical liver spectrum was controlled. The restriction of the microsomal biotransformation established by means of the aminophenazon breathing test behaved parallel to the degree of severity of the disease. The aminophenazon breathing test was performed in the modification after Haustein and Schenker (1985). The largest delays in the decomposition were found in the complete cirrhotic transformation of the liver. The unequivocally pathologic result of the aminophenazon breathing test in severe irreversible damages of the liver parenchyma was confirmed by the formation of correlations with parameters of the conventional laboratory spectrum of the liver. Thus the restriction of the performance of the synthesis of the liver for coagulation factors and albumins was parallel to the loss of function of the mixed functional oxidases. In all patients with chronic liver diseases a connection between the value of the thromboplastin time (Quick's test) and result of the breathing test was found. Positive linear correlation between serum albumin and results of the breathing test could also be proved particularly in the group of the severe chronic inflammatory liver diseases. In chronic fibrosing liver diseases there were positive inverse correlations between gamma-globulin concentration in the serum and thymol turbidity test on the one hand as well as the aminophenazon breathing test on the other. There were no correlations between liver enzyme and aminophenazon breathing test. The results of the own investigations incorporate the aminophenazon breathing test as indicator of a severe liver cell damage which at the same time is established by the pathological result of the so-called synthesis parameters of the liver.
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PMID:[The diagnostic value of the aminophenazone breath test in chronic liver diseases]. 196 92

A 2-month-old boy was admitted to our hospital because of poor sucking and jaundice. There were no abnormalities during the whole period of pregnancy and at birth. His mother was a HBeAb positive HBsAg carrier, but prophylactic maneuver such as anti-HB immunoglobulin and HB vaccine was not performed on him at birth. Physical examination on admission revealed mild disturbance of consciousness. The laboratory findings showed marked increments of serum bilirubin, GOT, GPT, and NH3, and prolongation of prothrombin time, activated partial thromboplastin time and hepaplastin test. Thus, he was diagnosed as fulminant hepatitis and treated with exchange transfusion once or twice a day. Biochemical data improved gradually, but hypocoagulable states remained unchanged. At that time we decided to use Factor VII concentrate, because we found that, among several coagulation factors, factor VII activity decreased most rapidly after exchange transfusion. The alternate therapy of exchange transfusion and Factor VII concentrate improved his coagulation abnormality without any side effects. Our experience suggests that the combination therapy of exchange transfusion and Factor VII concentrate may be useful for management of fulminant hepatitis, particularly for uncontrollable coagulopathy.
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PMID:[Successful treatment of an infant with fulminant hepatitis by factor VII concentrate]. 260 16

The effect of PG on patients with fulminant and subfulminant viral hepatitis (FHF) was studied. 17 patients presented with FHF secondary to hepatitis A (n = 3), hepatitis B (n = 6), and non-A, non-B (NANB) hepatitis (n = 8). 14 of the 17 patients had stage III or IV hepatic encephalopathy (HE). At presentation the mean aspartate transaminase (AST) was 1,844 +/- 1,246 U/liter, bilirubin 232 +/- 135 mumol/liter, prothrombin time (PT) 34 +/- 18, partial thromboplastin time (PTT) 73 +/- 26 s, and coagulation Factors V and VII 8 +/- 4 and 9 +/- 5%, respectively. Intravenous PGE1 was initiated 24-48 h later after a rise in AST (2,195 +/- 1,810), bilirubin (341 +/- 148), PT (36 +/- 15), and PTT (75 +/- 18). 12 of 17 responded rapidly with a decrease in AST from 1,540 +/- 833 to 188 +/- 324 U/liter. Improvement in hepatic synthetic function was indicated by a decrease in PT from 27 +/- 7 to 12 +/- 1 s and PTT from 61 +/- 10 to 31 +/- 2 s, and an increase in Factor V from 9 +/- 4 to 69 +/- 18% and Factor VII from 11 +/- 5 to 71 +/- 20%. Five responders with NANB hepatitis relapsed upon discontinuation of therapy, with recurrence of HE and increases in AST and PT, and improvement was observed upon retreatment. After 4 wk of intravenous therapy oral PGE2 was substituted. Two patients with NANB hepatitis recovered completely and remained in remission 6 and 12 mo after cessation of therapy. Two additional patients continued in remission after 2 and 6 mo of PGE2. No relapses were seen in the patients with hepatitis A virus and hepatitis B virus infection. Liver biopsies in all 12 surviving patients returned to normal. In the five nonresponders an improvement in hepatic function was indicated by a fall in AST (3,767 +/- 2,611 to 2,142 +/- 2,040 U/liter), PT (52 +/- 25 to 33 +/- 18 s), and PTT (103 +/- 29 to 77 +/- 44 s), but all deteriorated and died of cerebral edema (n = 3) or underwent liver transplantation (n = 2). These results suggest efficacy of PGE for FHF, and further investigation is warranted.
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PMID:Biochemical and clinical response of fulminant viral hepatitis to administration of prostaglandin E. A preliminary report. 279 44

Liver biopsy was performed in 38 patients with fulminant hepatitis and coma and repeated in 22. Stereological estimation of hepatocyte volume was correlated with levels of clotting factors. Early liver biopsy allowed prognosis in 55% of the cases. All patients with a hepatocyte volume of <35% and thromboplastin time </=10% died; all patients but two with hepatocyte volume >/=35% and thromboplastin time >10% recovered consciousness (n = 9) or at least showed evidence of marked liver regeneration (n = 2). On serial liver biopsy a significant increase in hepatocyte volume and clotting factors was only observed in patients who recovered consciousness. The estimated liver cell mass after regeneration in patients who recovered consciousness was >/=45% and <45% in the patients who did not.
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PMID:Liver biopsy and prognosis in acute liver failure. 478 82

Four groups of 6 pigs each were given 5 x 10(5) to 3 x 10(6) sporocysts of a Georgia isolate of Sarcocystis suicanis. Only the 6 pigs given 3 x 10(6) sporocysts became acutely ill at postinoculation days (PID) 12 to 15, and 3 of the 6 diet at PIG 14 or 15. Clinical signs included purpura of the skin of the ear, snout, and buttocks and dyspnea, muscle tremors, and severe locomotor difficulties. Clinical abnormalities were accompanied by laboratory findings of pyrexia, severe anemia, leukopenia, thrombocytopenia, megathrombocytosis, prolonged prothrombin time and activated partial thromboplastin time, and hypofibrinogenemia. Seemingly, excessive intravascular coagulation may be involved in the pathogenesis of this disease in swine. Pigs given 5 x 10(5) to 1 x 10(6) sporocysts did not exhibit clinical signs; however, leukopenia and thrombocytopenia were demonstrated in the pigs at all dosage levels. Growth rates were impaired in surviving pigs. Second-generation schizonts containing merozoites were found in vascular endothelium of pigs dying on PID 14 or 15. Nonsuppurative myocarditis and hepatitis were present. Numerous developing cysts were in the musculature of pigs enthanatized on PIG 35 to 52. Cyst dissolution and resorption occurred concomitantly, indicating that swine may be able to clear the infection.
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PMID:Experimental Sarcocystis suicanis infections: disease in growing pigs. 680 76

Vascular access thrombosis (VAT) is frequent in some hemodialysis patients. Antiphospholipid antibodies (APL) have been involved in thrombosis, and have been reported to be present in a high proportion of patients with chronic renal failure. We studied the relationship between APL and thrombosis in 97 hemodialysis patients (HD). Lupus anticoagulant (LA) was assessed by activated partial thromboplastin time (APTT) and by tissue thromboplastin inhibition assay (TTI). IgG-anticardiolipin (ACA) was measured by a solid phase ELISA. The prevalence of APL was 31%; LA was found in 16.5% and was detected in all cases by TTI. Only one patient was positive for APTT. ACA was found in 15.5%. Only one patient was positive for LA and ACA. We found no relation between APL and age, length of time on dialysis, sex, type of dialysis membrane, drugs, and chronic B and C hepatitis. A high prevalence of APL was found in patients with undetermined nephropathy. When histories of thrombosis were examined, VAT was found to be significantly more frequent in patients with LA than in patients without LA (62% vs. 26%; P = 0.01). This relation was not present with ACA. Since VAT is one of the most frequent causes of morbidity for HD, diagnostic evaluation of VAT in HD should now include assay for LA.
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PMID:Antiphospholipids in hemodialysis patients: relationship between lupus anticoagulant and thrombosis. 747 66

Previously, we demonstrated induction of a unique macrophage prothrombinase during infection of BALB/cJ mice by mouse hepatitis virus strain 3 (MHV-3). By immunologic screening, a clone representing this prothrombinase was isolated from a cDNA library and sequenced. The sequence identified this clone as representing part of a gene, musfiblp, that encodes a fibrinogen-like protein. Six additional clones were isolated, and one clone, p11-3-1, encompassed the entire coding region of musfiblp. Murine macrophages did not constitutively express musfiblp but, when infected with MHV-3, synthesized musfiblp-specific mRNA. musfiblp mRNA induction was earlier and significantly greater in BALB/cJ than A/J macrophages. Prothrombinase activity was demonstrated when musfiblp was expressed from p11-3-1 in RAW 264.7 cells. These data suggest that musfiblp encodes the MHV-induced prothrombinase.
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PMID:Association of mouse fibrinogen-like protein with murine hepatitis virus-induced prothrombinase activity. 760 73

An enzyme-linked immunosorbent assay (ELISA) was developed for the detection of anti-HCV antibody. We assayed for antibodies against either oligopeptide (S29-1) deduced from the nucleocapsid gene or the product of nonstructural region (NS3) synthesized in a recombinant Escherichia coli (S4). To reduce false-positive results induced by non-specific binding of antibodies with a carrier protein and to increase the sensitivity of an immunoassay, non-fused S4 peptide was prepared by the recombinant DNA technique and site-specific proteolysis (by factor Xa). In 71 non-A, non-B hepatitis patients with chronic liver disease, 70 (98.5%) were positive by S29-1/S4 ELISA as well as by a second-generation test (Abbott II). On the other hand, of 40 serum samples from blood donors, in which anti-N14 (core) and C100-3 antibodies were not detected but hepatitis C virus (HCV) RNA was detectable by polymerase chain reaction (PCR), 24 (60%) were positive by S29-1/S4 ELISA, whereas only 18 (45%) were diagnosed by Abbott II. In addition, based on results in a small group of 92 blood donors, detection of anti-S29-1/S4 antibody correlated well with HCV viremia as confirmed by PCR. These results indicated that the preparation of nonfused protein (S4) by recombinant DNA technique and a combination of S29-1 and S4 as immobilized antigens in an ELISA provide a sensitive and specific diagnosis for HCV infection with good correlation with the presence of viral RNA as confirmed by PCR.
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PMID:A sensitive serodiagnosis of hepatitis C virus (HCV) infection with two non-fused peptides: comparison of antibody responses detected with a newly developed assay and a commercial second-generation test. 768 47

A 52-year-old female was hospitalized with malaise, pruritus, jaundice, abdominal discomfort and vomiting. For 20 weeks she had been taking enalapril (Reniten) for hypertension. Serum aminotransferases and bilirubin were highly elevated with prolonged thromboplastin time. There was no evidence for extrahepatic cholestasis in ultrasonography. Serological investigations for a viral etiology of the liver failure were negative and the patient had no risk factors for viral hepatitis or exposure to hepatotoxic substances. Liver puncture revealed hepatitis of the fulminant viral hepatitis type, a picture that can be seen in a drug-induced hepatitis. The complete recovery of liver function after cessation of enalapril administration suggests acute toxic hepatitis due to enalapril. A metabolically mediated idiosyncratic reaction is the most plausible. Potential mechanisms of enalapril-induced hepatotoxicity are discussed and the current literature is surveyed.
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PMID:[Enalapril (Reniten)-associated toxic hepatitis]. 806 14


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