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)

High levels of acute phase proteins (acute phase reactants, APR) suppress acute inflammatory reactions in the rat. As many APR have antiprotease properties, including an anticollagenase activity, the effect of APR on the development of CCl4-induced liver fibrosis was investigated in rats. APR were provoked by repeated injections of epinephrine, inducing a broad spectrum of APR. This reaction can be monitored measuring alpha 2-macroglobulin levels in the rat (alpha 2-macrofetoprotein, alpha M FP). This protein was found to inhibit both acute galactosamine hepatitis and acute CCl4-induced liver toxicity. The animals with high levels of APR at the start of CCl4 treatment developed a more severe degree of fibrosis and cirrhosis than the control group in which no acute phase reaction was induced. Epinephrine alone had no such effects. Additionally, the APR positive group showed an initially lower degree of hepatocellular damage when compared to control animals. This uncoupling of liver cell damage and subsequent fibrosis may demonstrate that higher levels of APR might be important as to the development of cirrhosis, possibly based on the anticollagenase activity of these proteins.
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PMID:Acute phase reactants enhance CCl4 induced liver cirrhosis in the rat. 369 34

Liver biopsies of 152 patients with post-cholecystectomy syndrome are studied. Liver alterations observed in these patients are subdivided into morphological syndromes (portal and periportal hepatitis, liver fibrosis and cirrhosis) and their evolution is investigated. Changes of intrahepatic bile ducts are studied and their adaptive-compensatory character is shown. Compensatory processes in the liver parenchyma are also investigated. Patho- and morphogenesis of alterations observed is discussed.
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PMID:[Morphologic characteristics of the liver in the postcholecystectomy syndrome]. 374 Nov 74

Seven males with liver cirrhosis associated with hepatitis and one with schistosomal liver fibrosis were studied for hypophyseal gonadal dysfunction and compared to six age matched controls. Cirrhotics as a group had higher serum 17 beta estradiol levels (22.1 +/- 6.3 vs 7.8 +/- 0.8 pg/ml, p less than 0.05) which did not rise after four days of human chorionic gonadotropin (hCG) stimulation. Conversely, there was an adequate rise in serum testosterone level after hCG stimulation (332.8 +/- 99.7 ng/dl baseline to 887.6 +/- 67.1 ng/dl, p less than 0.01). Compared to the controls, cirrhotics had lower baseline serum follicle stimulating hormone (FSH) (3.6 +/- 1.7 vs. 10.2 +/- 1.5 mIu/ml, p less than 0.02) and higher serum prolactin (13.5 +/- 2.5 vs. 6.8 +/- 1.0 ng/ml, p less than 0.05). Pituitary dynamic function testing in cirrhotics revealed blunted response of luteinizing hormone (LH) and FSH, to luteinizing hormone releasing hormone (LHRH) in four out of eight subjects tested. We conclude that the mechanism of hypogonadism in non-alcoholic cirrhosis is mostly hypogonadotropic in origin rather than primary gonadal injury which is common in alcoholic cirrhosis.
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PMID:Hypophyseal-gonadal dysfunction in men with non-alcoholic liver cirrhosis. 392 49

The aflatoxin B1 content of liver tissue was measured in patients who died from chronic liver disease [hepatocellular carcinoma (HCG) (5), schistosomal liver fibrosis (1), chronic aggressive hepatitis (1)] and compared with fifteen controls who died of motor traffic accidents (10), drowning (1), malnutrition (1), idiopathic cardiomegaly (1) and lung infection (2). Significant levels of aflatoxin B1 were found in hepatocellular carcinoma patients who were also hepatitis B surface antigen (HBsAg) negative. Histology showed HCC arising in macronodular cirrhosis.
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PMID:Aflatoxin B1 in hepatocellular carcinoma. 625 85

Microsomal UDP-glucuronosyltransferase activity toward the bile acids (chenodeoxycholic, deoxycholic, ursodeoxycholic, lithocholic, and glycolithocholic) has been detected in human specimens of liver, kidney, and intestinal mucosa. The characteristics of hepatic and extrahepatic UDP-glucuronosyltransferase activities toward these bile acids were compared with respect to kinetic parameters and other catalytic properties. Whereas no organ-specific differences in the affinities of individual bile acids to hepatic and extrahepatic UDP-glucuronosyltransferases were observed, the individual bile acids showed reaction rates in liver that were about twice the rates estimated in kidney and about twice to three times the rates observed in duodenal mucosa. In intestinal mucosa the rate of chenodeoxycholic acid glucuronidation exhibited a progressive decrease from duodenum to colon, where it was 30% of the duodenal level. Comparison of the glucuronidation rates that were estimated with different bile acids in hepatic or extrahepatic tissues showed that for each organ a bile acid structure-activity relationship existed, with highest activity observed for lithocholic and ursodeoxycholic acids, which was about twofold higher compared with chenodeoxycholic or deoxycholic acids. Lowest activity was estimated for glycolithocholic acid. UDP-glucuronosyltransferase activity toward chenodeoxycholic acid was studied in biopsy specimens of liver that were obtained from a large group of patients with the following liver diseases: liver cirrhosis, liver fibrosis, granulomatous hepatitis, fatty liver hepatitis, and fatty liver. A significant decrease in enzyme activity was observed in patients with liver cirrhosis and in patients with granulomatous hepatitis compared with patients without liver disease.
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PMID:Hepatic and extrahepatic glucuronidation of bile acids in man. Characterization of bile acid uridine 5'-diphosphate-glucuronosyltransferase in hepatic, renal, and intestinal microsomes. 643 Sep 60

To evaluate the diagnostic and prognostic significance of the N-terminal propeptide of collagen Type III (Col 1-3) in chronic liver disease, the peptide level was measured in the serum of 4 patients with primary biliary cirrhosis, 5 with chronic persistent hepatitis, 12 with chronic active hepatitis, and 1 with autoimmune hepatitis, for a period of 2 to 10 years and compared with liver function and histology. In primary biliary cirrhosis, Col 1-3 peptide levels were always elevated, regardless of medical therapy; however, after liver transplantation in one patient, the Col 1-3 peptide level decreased. In chronic persistent hepatitis, the peptide level fluctuated around the upper limit of normal. Among patients with chronic active hepatitis, the Col 1-3 peptide level normalized in 2 patients during remission, but was elevated in 7 patients who developed cirrhosis. Only in a patient with autoimmune hepatitis was the Col 1-3 peptide level normal, although the patient developed cirrhosis during prednisone therapy. When prednisone was withdrawn, the Col 1-3 peptide level increased. The data suggest that the serum Col 1-3 peptide may estimate the course of liver fibrosis in chronic liver disease and has prognostic value, particularly in chronic active hepatitis. Persistent elevation suggests ongoing fibrosis and development of cirrhosis; normalization suggests remission.
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PMID:Long-term follow-up of serum N-terminal propeptide of collagen type III levels in patients with chronic liver disease. 647 52

Specific antibodies to collagen type IV, laminin, and fibronectin were used to localise these proteins by indirect immunofluorescence in frozen sections of normal and fibrotic liver. In normal livers distinct staining was found in basement membranes of blood and lymph vessels, of bile ducts and ductules and around nerve axons. Positive reactions for type IV collagen and fibronectin were also observed in the perisinusoidal space, while hepatocytes and most of the interstitial matrix of portal fields remained unstained. Liver specimens obtained from patients with alcoholic liver disease (fatty liver, hepatitis or cirrhosis) and chronic active hepatitis showed a more intense reaction with the antibodies in the perisnusoidal space including now distinct staining for laminin. These patterns were particularly prominent at borders between fibrotic septa and remnants of parenchyma or pseudolobules. Strong reactions were also found for type IV collagen and fibronectin in the periportal interstitium and in large fibrotic areas. The findings support previous electron-microscopical and chemical evidence for increased basement membrane production in human liver fibrosis and demonstrate that this may involve different proteins and occur at different anatomical sites.
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PMID:Distribution of basement membrane proteins in normal and fibrotic human liver: collagen type IV, laminin, and fibronectin. 698 3

Hassab's operation for selected case of oesophageal varices is believed by many workers to be a very satisfactory procedure. Various complications following this procedure have been reported, but none has reported a case of Cup-and-Spill gastric deformity following this operation. We present such a complication following this procedure on a senior medical colleague with oesophageal varices resulting from a subclinical or previously undiagnosed hepatitis resulting in liver fibrosis. He responded fairly well to conservative treatment and small feed at frequent interval.
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PMID:Cup-and-spill gastric deformity following Hassab's procedure for oesophageal varices: case report. 749 33

Since the assay of HCV antibody has been developed, it became clear that HCV is involved not only in patients with non-A non-B hepatitis but also in some alcoholic patients. The aim of this study is to examine the prevalence of HCV in chronic alcoholics and to elucidate the influence of HCV and its subtypes on pathogenesis and clinical feature of alcoholic liver disease. To that effect, sera from 100 alcoholics were tested for antibody against C100 of HCV by ELISA and for HCV RNA by reverse transcriptation and the PCR method. The incidence of HCV Ab/RNA was 0%/17% in patients with non specific reactive hepatitis, 0%/0% in fatty liver, 17%/17% in alcoholic hepatitis, 50%/73% in chronic hepatitis, 15%/18% in liver fibrosis and 19%/31% in liver cirrhosis. HCV Ab and RNA were positive in 21% and 31% of alcoholics, respectively. Subtypes of HCV were identified by dot blot hybridization method. Type K1, K2a and K2b were detected in 68%, 25% and 7% of 28 patients with positive HCV RNA, respectively. Type PT was not detected. In addition, serum transaminase activities were evaluated after 4 weeks abstinence. The incidence of normalization of the enzyme activity was lower in patients with positive HCV RNA than that with negative HCV RNA. Furthermore, when it was estimated in relation to HCV subtypes, the incidence of normalization in patients with type K1 was lower than that with type K2. In conclusion, the prevalence of HCV infection in alcoholic patients was much greater than general population.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Influence of HCV infection and its subtypes on clinical course of alcoholic liver disease. 768 16

The aim of this study was to evaluate the effect of interferon-alpha on liver fibrosis with an established quantitative histochemical method for determining collagen as a marker. 59 patients (31 men, 28 women; 47 +/- 14 yr) with chronic non-A, non-B hepatitis (92% with hepatitis C virus antibody) received subcutaneous injections of 3 or 1 MU recombinant interferon-alpha 2b or placebo thrice weekly for 24 wk. Needle-biopsy sections taken before and after interferon treatment were examined for histological evaluation and collagen quantitation. Values were compared with results obtained by means of morphometrical analysis of liver collagen and Knodell scoring histological index. The index of periportal and/or bridging necrosis was the only component of Knodell's histological score significantly decreased (p < 0.05) in patients treated with 3 MU interferon compared with placebo-treated controls. The fibrosis score was not significantly changed. In contrast, liver total collagen variations measured colorimetrically and morphometrically were significantly decreased in patients treated with 3 MU and 1 MU compared with the increase observed in the placebo-treated controls (p < 0.05). From these results, we conclude that a 6-mo course of 3 MU or 1 MU interferon-alpha 2b causes slight but nonetheless significant regression of liver fibrosis as assessed on the basis of quantitative estimation of liver collagen, irrespective of other response criteria, whereas progression of liver fibrosis can be observed in the absence of treatment.
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PMID:Interferon-alpha 2b therapy reduces liver fibrosis in chronic non-A, non-B hepatitis: a quantitative histological evaluation. 824 59


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