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)

In cardiovascular diseases with potential atherosclerosis, the serum concentration of HDL cholesterol as determined by a precipitation method with dextran sulfate and Mg++ was lower while that of total cholesterol was normal or elevated. Treatment with a daily dose of 1,200 mg of Nicomol, a derivative of nicotinic acid, for 1 to 3 months increased the mean HDL cholesterol level by 3 to 5 mg/dl and reduced the total cholesterol level by 14 to 15 mg/dl and total/HDL cholesterol ratio by 0.8 (3 months) to 0.9 (1 month, p less than 0.05). Similar decreases in HDL cholesterol concentration were also found in parenchymal and obstructive liver diseases with normal total cholesterol values except in fulminant hepatitis and intrahepatic cholestasis.
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PMID:Effect of nicomol on HDL cholesterol level. 22 32

Total cholesterol (Ch-T), HDL cholesterol (Ch-HDL) and (VLDL + HDL) cholesterol (Ch-(VLDL + LDL) were evaluated in 78 cases of various hepatodigestive diseases (11 icterus, 14 hepatitis, 30 chronic alcoholisms, 8 Crohn's diseases and 15 haemorragic rectocolitis (RCH], and in 76 control subjects. High cholesterol levels were found in icterus, but its distribution between lipoproteic fractions remained unchanged. In the group of hepatitis, a deficit in Ch-(VLDL + LDL) was elicited by a significant decrease of Ch-(VLDL + LDL)/Ch-T ratio. The same was observed in chronic alcoholism. In Crohn's disease the levels of every cholesterol fraction were low, while in RCH they were not significantly different from those of the control group. But, in RCH, the Ch-HDL/Ch-T ratios showed significant low values with concommitant higher values of Ch-(VLDL + LDL)/Ch-HDL ratios, suggesting that, in RCH, the metabolism of cholesterol is unbalanced with a deficit of Ch-HDL. In conclusion, the evaluation of cholesterol in lipoproteic fractions by a simple assay may contribute to specify the diagnostic of these disorders.
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PMID:[Analysis of the distribution of HDL-cholesterol and (VLDL + LDL)-cholesterol in hepatic and intestinal disorders]. 236 Jul 49

HDL-cholesterol was estimated along with other biochemical parameters of hepatic function in infective hepatitis. Infective hepatitis was characterized by significantly decreased levels of HDL-cholesterol. Follow up studies indicated a good correlation of changes in HDL-cholesterol to severity of disease in all the cases whereas standard liver function tests showed equivocal changes in some cases. HDL-cholesterol may serve as a sensitive indicator of hepatic function in infective hepatitis.
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PMID:HDL-cholesterol--a sensitive parameter of hepatic function in infective hepatitis. 262 Nov 90

The study includes 108 patients with acute alcohol hepatitis, 45 patients with cholestasis and 124 healthy controls. In 14 patients (13%) cholestatic acute alcohol hepatitis was found. The patients with cholestatic acute alcohol hepatitis consumed considerably more alcohol than the other patients with acute alcohol hepatitis. The intensive jaundice led half of the patients with cholestatic acute alcohol hepatitis to the infectious diseases clinic and 32% of them to the surgical clinic. The course of the disease was heavy, with disturbed general condition, high temperature, pain in the right subcostal region but without itching. The patients showed higher levels of timol test, cholesterol, LDL-cholesterol, coefficient LDL/HDL-cholesterol, beta-lipoproteins, total lipids, gamma-GTP, ASAT and lower levels of leucocytes, bilirubin, SMC, alkaline phosphatase and LAP than the other patients with cholestasis. The patients with cholestatic acute alcohol hepatitis showed a higher level of total lipids and gamma-GTP than the other patients examined. The confirmation of the diagnosis implies the application of contemporary instrumental and invasive methods. The ultrasound examination is of special importance.
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PMID:[The clinico-laboratory characteristics of the cholestatic form of acute alcoholic hepatitis]. 263 77

The plasma lipid and apoprotein concentrations were monitored in a group of 12 patients with chronic alcohol abuse entering an abstinence program for 3 weeks. 6 of them had a normal liver function as expressed by the levels of liver enzymes gamma GT, GOT, GPT, while 6 had elevated plasma liver enzyme concentrations. None had evidence of either cirrhosis or alcohol hepatitis. Patients with abnormal liver enzymes had elevated HDL-cholesterol, apo AI and apo AII concentrations in plasma, with normal total cholesterol and apo 8 concentrations. In the group of patients with normal liver enzyme concentrations, the apoproteins and lipids did not significantly differ from the control group. In the course of the abstinence treatment a parallel decrease of apoproteins, HDL-cholesterol and liver enzyme concentrations was observed. The values normalized after 10-15 days. These data indicate that the effect of alcohol on the plasma apoprotein and lipids occurs mostly in the HDL fraction, that it correlates with the state of hepatic function and that it can be reversed by an abstinence treatment.
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PMID:Plasma apoproteins levels in chronic alcohol abuse. 710 48

The apoprotein and lipid composition and the morphology of lipoproteins was determined in rats with D-(+)-galactosamine (GalN) hepatitis. Single intraperitoneal injections of GalN at several dose levels and postinjection exsanguination times resulted in depressed levels of cholesteryl esters, an index of plasma lecithin:cholesterol acyltransferase (LCAT) activity, and increased levels of phospholipids, unesterified cholesterol, and triglycerides. Plasma withdrawn from rats 24 hr after injection of 1000 mg/kg GalN was most deficient in cholesteryl ester and was studied further by sequential isolation of VLDL, LDL, HDL1, HDL2, and HDL3. The increased plasma triglyceride (TG) after GalN treatment accumulated in TG-rich VLDL which contained two types of particles: a large (mean diameter 193.6 +/- 48.3 nm) and rough-edged particle, and a smooth one with a mean diameter (63.4 +/- 13.2 nm) similar to control VLDL (69.4 +/- 20.2 nm). The increased phospholiThe increased plasma triglyceride (TG) after GalN treatment accumulated in TG-rich VLDL which contained two types of particles: a large (mean diameter 193.6 +/- 48.3 nm) and rough-edged particle, and a smooth one with a mean diameter (63.4 +/- 13.2 nm) similar to control VLDL (69.4 +/- 20.2 nm). The increased phospholiThe increased plasma triglyceride (TG) after GalN treatment accumulated in TG-rich VLDL which contained two types of particles: a large (mean diameter 193.6 +/- 48.3 nm) and rough-edged particle, and a smooth one with a mean diameter (63.4 +/- 13.2 nm) similar to control VLDL (69.4 +/- 20.2 nm). The increased phospholipids and unesterified cholesterol were predominantly in LDL, HDL1, and HDL2 which were largely rouleaux of flattened vesicles. Density gradient ultracentrifugation of d greater than 1.006 g/ml lipoproteins confirmed these results. GalN hepatitis appeared to decrease the larger apoB335K subspecies and the apoC-III0 and apoC-III2 content of VLDL. However, total apoB concentration as GalN VLDL was increased 2.6-fold over control. LDL and HDL were markedly enriched in apoE. LDL apoB concentration was decreased by 41% while HDL was deficient in apoA-I, A-II and A-IV, and C. These results demonstrate association of increased plasma triglycerides with particles of grossly abnormal apoprotein composition, and the association of increased plasma phospholipids and unesterified cholesterol with apoE-rich lipoproteins during the LCAT defect produced by GalN hepatitis. These abnormal lipoproteins may represent an abnormal level of normal LCAT substrates important in the transport and esterification of plasma cholesterol.
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PMID:Alterations in lipoprotein composition associated with galactosamine-induced rat liver injury. 711 68

Total serum cholesterol (C) and triglyceride (TG) levels, C and TG-VLDL, C-LDL and C-HDL, total apoprotein B (apo B) and albumin (alb.) have been studied in three groups of patients with liver cirrhosis (CE), persistent hepatitis (EPS) and alcoholic chronic liver disease (EA) divided in two sub-groups of 4 EPS and 4 CE, and have been compared with controls values. In all cases the diagnosis was made on liver biopsy C, C-LDL and C-HDL levels were significantly lower in EPS, C and C-LDL in EA and CE; comparing the three groups each other, the only statistically significant difference was found for C-HDL values, more elevated in the 4 cases of EPS with alcoholism than in CE and EPS without alcoholism.
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PMID:[Serum lipoprotein fractions in chronic liver diseases with and without alcoholism]. 730 12

Out of 665 patients after liver biopsy performed during 14 years of the work of the Clinic, 35 cases of patients with non-alcoholic liver steatosis and hyperlipoproteinaemia were selected and analysed retrospectively. The cases of patients with the presence of HBV or HCV infection markers were excluded. The histological material was divided according to the intensity of steatosis expressed as the per cent of hepatocytes with the features of fatty degeneration and also according to the following classification: I--steatosis, II--steatosis with hepatitis, III--steatosis with portal fibrosis, IV--steatotic cirrhosis. In the patients in whom the per cent of hepatocytes with fatty degeneration in biopsy examination exceeded 60%, the mean serum triglyceride concentration was 5.53 mmol/l and was over twice higher than that in the group with steatosis not exceeding 30% of hepatocytes. Similarly, in the patients with steatosis and accompanying hepatitis (steatohepatitis), the mean triglyceride concentration was 5.28 mmol/l and was over twice higher than that in the patients with steatosis with accompanying portal fibrosis. The patients with steatohepatitis had significantly lower HDL concentrations than those with the remaining types of histological changes.
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PMID:[Fatty liver assessed by histologic examination in patients with hyperlipoproteinemia]. 748 18

Niacin has been used for many years to treat hyperlipidemia. It has been shown to reduce coronary death and non-fatal myocardial infarction and, in a separate analysis of long-term (15-year) follow-up, all cause mortality. It reduces total cholesterol, low density lipoprotein cholesterol (LDL-C) and triglycerides and increases high density lipoprotein cholesterol (HDL-C). Sustained-release niacin may be associated with more dramatic changes in LDL-C and triglyceride, whereas the short acting preparation causes greater increases in HDL-C. The increase of HDL-C occurs at a lower dose (1500 mg/day) than the reduction of LDL-C (> 1500 mg/day). Niacin also favorably influences other lipid parameters including lipoprotein(a) [Lp(a)], alimentary lipemia, familial defective apolipoprotein B-100 and small dense LDL. Combination of niacin with a bile acid sequestrant or a reductase inhibitor represents a powerful lipid-altering regimen. Whereas the reductase inhibitors and bile acid binding resins primarily affect LDL-C, the combined therapy has a synergistic effect to reduce LDL-C and, in addition, the niacin reduces triglycerides and increases HDL-C. The major drawback in the use of niacin is associated side effects (flushing and palpitations) and toxicity (worsening of diabetes control, exacerbation of peptic ulcer disease, gout, hepatitis). Niacin has a long history of use as a lipid lowering agent and has several attractive features. Unfortunately, the side effect profile of this agent warrants its use only in patients with marked dyslipidemia in whom side effects and potential toxicity are closely monitored.
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PMID:New developments in the use of niacin for treatment of hyperlipidemia: new considerations in the use of an old drug. 885 85

In order to investigate whether a difference might exist in blood cholesterol and its subtractions between patients with chronic hepatitis B virus (HBV) or hepatitis C virus (HCV) infection, serum cholesterol, HDL-cholesterol, triglycerides and common liver function tests were measured in 138 patients (92 male, 46 female) with biopsy-proven chronic viral hepatitis without cirrhosis. Twenty-four had hepatitis B and 114 hepatitis C. Mean serum cholesterol was lower in HCV-infected in comparison to HBV-infected patients (175 +/- 36 mg/dl vs. 189 +/- 28 mg/dl, p < 0.05). On multivariate analysis, etiology of hepatitis appeared to be associated with the value of serum cholesterol, independently of age, sex and liver synthetic function (improvement of chi-square 4.40, p < 0.05). In patients with HBV infection, circulating tumor necrosis factor-alpha demonstrated a correlation with serum triglycerides (p = 0.618) and an inverse correlation with serum HDL-cholesterol (p = -0.456); in the group of patients with HCV infection, interleukin-6 correlated with triglycerides (p = 0.370) and HDL-cholesterol (p = -0.355). Thus, differences in the mechanisms of liver damage and of viral clearance in hepatitis C in comparison to hepatitis B, reflected in these patients by the levels of circulating cytokines, may be mirrored by differences in their blood lipid composition.
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PMID:Blood lipids of patients with chronic hepatitis: differences related to viral etiology. 920 35


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