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)

The effect of prostaglandins (PG) in patients with fulminant and subfulminant viral hepatitis was studied. Seventeen patients presented with FHF secondary to hepatitis A (N = 3), hepatitis B (N = 6) and non-A, non-B (NANB) hepatitis (N = 8). Fourteen of the 17 patients had stage III or IV hepatic encephalopathy (HE). At presentation, the mean AST was 1844 +/- 1246 units/liter, bilirubin 232 +/- 135 mumol/liter, PT 34 +/- 18 and PTT 73 +/- 26 sec, and coagulation factors V and VII were 8 +/- 4 and 9 +/- 51%, respectively. Twelve of 17 patients responded to PGE1 rapidly, with a decrease in AST from 1540 +/- 833 to 188 +/- 324 units/liter, a decrease in prothrombin time from 27 +/- 7 sec to 12 +/- 1 sec, PTT from 61 +/- 10 sec to 31 +/- 2 sec, 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 but improvement was observed upon retreatment. After four weeks of intravenous therapy, oral PGE2 was substituted. Two patients have recovered completely and remain in remission six and 12 months following cessation of therapy. Two additional patients continue in remission after two and six months of PGE2. No relapses have been seen in patients with hepatitis A virus (HAV) or hepatitis B virus (HBV) infection. Liver biopsies in the 12 surviving patients have returned to normal. These results suggest efficacy of PGE for FHF. Further investigation is warranted.
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PMID:Treatment of fulminant viral hepatic failure with prostaglandin E. A preliminary report. 190 42

Prostaglandin E1 (PGE1) was used to prevent veno-occlusive disease (VOD) of the liver after allogeneic bone marrow transplantation (BMT) for leukaemia. It was given in continuous i.v. infusion from day--8 to day 30 after BMT at a dose of 0.3 micrograms/kg/h. The patients were studied according to the risk factors for VOD: diagnosis, intensification of the conditioning and previous liver abnormalities. The diagnosis of VOD was made on at least two of the following factors: weight gain, hepatomegaly, jaundice, ascitis, pain of the right upper quadrant, increased platelet consumption. 109 patients were studied, 50 were treated by PGE1 and 59 did not receive it. The actuarial incidence of VOD was 12.2% in the PGE1 group and 25.5% in the non PGE1 group (P = 0.05). In acute leukaemia, the incidence was 39.1% in the non-treated group and 12.8% in the PGE1 treated group (P = 0.02). Patients with previous hepatitis had an incidence of 62.5% in the non treated group and 15.5% in the treated group (P = 0.05). A positive cytomegalovirus (CMV) serology seemed to increase the risk of VOD: the incidence of VOD was 31.4% in non-treated patients and 22% in PGE1 treated patients. The multivariate analysis of the risk factors for VOD shows that unfavourable factors were: recipient positive CMV serology (P = 0.06), hepatic disease prior to transplant (P = 0.02) and the absence of PGE1 treatment (P = 0.02). This study suggests that prophylactic PGE1 treatment may decrease the incidence of VOD in patients treated for leukaemia by allogeneic bone marrow transplantation.
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PMID:Use of prostaglandin E1 for prevention of liver veno-occlusive disease in leukaemic patients treated by allogeneic bone marrow transplantation. 204 74

Prostaglandin E1 was used to prevent veno-occlusive disease of the liver after allogeneic bone marrow transplantation for leukemia. It was given in continuous IV infusion from day -8 to day 30 after BMT at the dose of 0.3 microgram/kg/h. The patients were studied according to the risk factors of VOD: diagnosis, intensification of the conditioning and previous liver abnormalities. The diagnosis of VOD was made on at least two of the following factors: weight gain, hepatomegaly, jaundice, ascitis, pain of the right upper quadrant, increased platelet consumption. One hundred and nine patients were studied, 50 were treated by PGE1 and 59 did not receive it. Univariate analysis shows that the actuarial incidence of VOD was 12.2% in the PGE1 group and 25.5% in the non PGE1 group (P = 0.05). In acute leukemia, it was 39.1% in the non treated group and 12.8% in the PGE1 treated group (P = 0.02). Patients with previous hepatitis had an incidence of 62.5% in the non treated group and 15.5% in the treated group (P = 0.05). A positive CMV serology seemed to increase the risk of VOD: the incidence of VOD was 31.4% in non treated patients and 22% in PGE1 treated patients. The multivariate analysis of the risk factors of VOD show that unfavorable factors were: recipient positive CMV serology (P = 0.06), hepatic disease prior to transplant (P = 0.02) and the absence of PGE1 treatment (P = 0.02). This study suggests that prophylactic PGE1 treatment may decrease the incidence of VOD in patients at risk treated for leukemia by allogeneic bone marrow transplantation.
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PMID:Role of PGE1 to prevent veno-occlusive disease of the liver after bone marrow transplantation. 234 75

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

The effects of prostaglandin E1 on cell-mediated cytotoxicity against hepatocytes were investigated using an in vitro cytotoxic assay system. Isolated liver cells from normal C57BL/6 mice were used as the target cells, and effector cells were obtained from spleens of C57BL/6 mice in which experimental hepatitis had been induced by immunization with syngeneic liver antigens. In this assay system, spleen T cells adhering to nylon wool demonstrated a high cytotoxic activity against target liver cells. The cytotoxicity was markedly reduced by prostaglandin E1 at concentrations greater than 10(-7) M. Maximum suppressive activity was obtained when prostaglandin E1 was continuously present during the assay period. By contrast, indomethacin, a specific inhibitor of prostaglandin synthesis, enhanced the cytotoxic activity of effector cells. These data seem to indicate that exogenously added prostaglandin E1 has an inhibitory effect on cell-mediated cytotoxicity of effector spleen cells against target hepatocytes.
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PMID:Inhibitory effects of prostaglandin E1 on T-cell mediated cytotoxicity against isolated mouse liver cells. 325 31

The interaction between mouse hepatitis virus 3 (MHV3) and cells was studied in order to investigate whether or not early events occurring after infection could be involved in the difference in virus replication seen between mouse strains with different genetic sensitivities to MHV3 infection. Kinetic data showed that MHV3 uptake by both macrophages and L cells was time- and temperature-dependent. In addition, treatment of cells with cytochalasin B or prostaglandin E1, prior to virus infection, resulted in a strong inhibition of sheep red blood cell phagocytosis without any effect on MHV3 uptake. Similar uptake of radiolabelled MHV3 was shown by whole spleen cells, purified T lymphocytes and thymocytes. Furthermore, no difference in 3H-labelled MHV3 uptake was seen between macrophages originating from resistant A/J mice, semi-susceptible (C57Bl/6 x A/J)F1 and susceptible animals. These results indicate, therefore, that genetically related in vivo sensitivity toward MHV3 infection is not related to differential uptake of virus by cells.
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PMID:Early interaction between mouse hepatitis virus 3 and cells. 627 22

The effects of PGE1.CD on dimethylnitrosamine (DMN)-induced acute liver damage with intravascular coagulation in rats were biochemically and histopathologically investigated. PGE1.CD was administered i.v. from 30 min before to 24 hr after DMN-intoxication (pretreatment) and from 30 min after or from 4 hr after to 24 hr after DMN-intoxication (post-treatment). Pretreatment with PGE1.CD (0.2-2 micrograms/kg/min) dose-dependently suppressed the decrease of platelet counts and the elevation of blood biochemical parameters (PT, HPT, GOT, GPT, LDH, LAP, T-Bil) caused by DMN-intoxication. PGE1.CD (0.5 microgram/kg/min and over) significantly suppressed the DMN-induced histopathological changes (occurrence of hemorrhage and necrosis). Post-treatment with PGE1.CD (2 micrograms/kg/min) also suppressed the liver damage. Furthermore, pretreatment with PGE1.CD (2 micrograms/kg/min) not only suppressed the disruption of hepatocytes, but also prevented the damages of sinusoidal endothelial cells and lysosomal membrane, and it reduced the increase of lipid peroxidation. PGE1.CD (1 microgram/kg/min and over) significantly suppressed the decrease of hepatic tissue blood flow caused by DMN-intoxication. These results demonstrate that PGE1.CD has therapeutically efficacy against DMN-induced acute liver damage in rats; Therefore, it will be clinically useful for the treatment of severe hepatitis such as fulminant hepatitis with intravascular coagulation in the sinusoid.
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PMID:[Inhibitory effects of prostaglandin E1.alpha-cyclodextrin (PGE1.CD) on dimethylnitrosamine-induced acute liver damage in rats]. 777 59

Although prostaglandin E1 (PGE1) and prostacyclin (PGI2) exhibit pharmacological activities in free form, it has been hypothesized and experimentally verified that carrier preparations can target them more effectively at lower doses, thus causing fewer side effects. Lipid microspheres (LM) with a diameter of 0.2 micron are drug carriers prepared from soybean oil and lecithin, and the drug is incorporated within the LM. Lipo-PGE1 and lipo-PGI2 are LM preparations of PGE1 and a PGI2 derivative that are designed to accumulate at the vascular lesions. The authors have achieved remarkable clinical effects against neuropathy and ulcers, severe hepatitis, congenital heart diseases, and acute cerebral thrombosis using these preparations. In this review, clinical observations, some basic studies including targeting delivery of lipo-PGE1 to the liver, and future indications for these preparations are introduced. Development of a new lipo-PGE1 (lipo-AS013) that overcomes the disadvantages of the preparation currently available is also discussed. Lipo-AS013, a prodrug of PGE1, is considered superior to free PGE1 in terms of its chemical stability in LM and the retention ratio of the drug in LM in the body.
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PMID:Review: recent advances in lipid microsphere technology for targeting prostaglandin delivery. 806 57

The efficacy of prostaglandin E1 was demonstrated in the treatment of 4 patients with subfulminant hepatitis caused by a virus B. Three patients suffered from hepatic enchepalopathy of the first degree, and the remaining one of the second degree. In three patients the clinical and biochemical improvement came relatively quickly, followed by recovery. In one patient, due to drug intolerance, the treatment was discontinued on the third day. The recurrence of illness was noted with the moderate increase of serum aminotransferases activities without clinical deterioration, necessitating no further use of prostaglandin E1. Prostaglandin E1, applied in the treatment of patients with subfulminant form of hepatitis, has favorable effect on the course of illness.
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PMID:[Treatment of patients with subfulminant forms of viral hepatitis B using prostaglandin E1]. 854 89

A further series of 41 adult patients with late-onset hepatic failure was investigates with respect to aetiological factors, particularly hepatitis C and E, which have been identified since our earlier report of this condition. The increased use of transplantation and its impact on survival overall is assessed. Comparison is made with 64 patients admitted over the same period with fulminant hepatic failure of non-A, non-B aetiology. Screening for the hepatitis viruses revealed three cases of hepatitis A and one case of Epstein Barr virus hepatitis. There were no cases of hepatitis C or hepatitis E virus detected by enzyme immunoassay and reverse transcriptase/polymerase chain reaction techniques, although three patients had positivity for IgG anti-hepatitis E virus, demonstrating previous exposure. Serum autoantibodies in a titre greater than or equal to 1:40 were present in 29% of samples tested and in three cases, titres of SMA or ANF were greater than 1:320. In a further five cases, a potentially hepatotoxic agent had been given within 3 months of the onset of symptoms, leaving the majority of patients (29) with no identifiable cause for their disease. The frequency of symptoms, however, including nausea, abdominal discomfort with the subsequent development of ascites, encephalopathy and renal impairment suggest a similar disease process in these patients. Analysis of liver biopsy material showed similar patterns on all cases of map-like necrosis with nodular regeneration and without other additional features of aetiological significance. Differences in clinical and histological changes for the non-A, non-B fulminant hepatic failure comparison group reflect the tempo of disease process rather than the nature and cause of the liver damage. The introduction of transplantation has led to a marked improvement in survival (39% overall in the earlier series). In the 21 patients in whom transplantation was carried out, the 1-year actuarial survival is currently 55%. Treatment of late-onset hepatic failure with corticosteroids and the use of Prostaglandin E1 and interferon in individual cases has been disappointing, and the emphasis in management should be placed on teh early referral of such patients to a centre offering transplantation.
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PMID:Late-onset hepatic failure: clinical features, serology and outcome following transplantation. 865 52


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