Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: UMLS:C0023890 (cirrhosis)
42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We investigated the clinical and laboratory findings of hypogonadism and feminization in male patients with viral or alcoholic cirrhosis to determine whether chronic liver disease plays a primary role in the development of sexual dysfunction and hormonal changes. Two groups of male patients with liver cirrhosis (23 alcoholic, 33 viral) age- and Child's grade-matched, and 20 age-matched healthy men, as a control group, were included in this study. Clinical signs of hypogonadism and feminization were examined in the cirrhotic patients. Follicle-stimulating hormone, luteinizing hormone, prolactin, testosterone, free testosterone, estradiol, androstenedione, dehydroepiandrosterone sulfate, and sex hormone-binding globulin were estimated in all groups. Seminal fluid was also analyzed in 7 alcoholic and 15 viral cirrhotics. Serum levels of estradiol, androstenedione, and sex hormone-binding globulin were significantly higher, and free testosterone and dehydroepiandrosterone sulfate levels were significantly lower in both groups of cirrhotics compared with the control group. Child's C patients in both groups of cirrhotics were found to have higher estradiol and lower free testosterone levels than child's A and B patients. Alcoholic and viral cirrhotics had markedly reduced sperm motility and density. The differences between alcoholic and viral cirrhotic patients in the clinical signs of hypogonadism, serum levels of sex steroids, and the results of seminal fluid analysis were not statistically significant. These findings suggest that liver cirrhosis per se, independent of etiology, causes hypogonadism and feminization, and that the degree of hypogonadism and feminization correlates well with the severity of liver failure.
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PMID:Hypogonadism is not related to the etiology of liver cirrhosis. 896 92

Hepatocyte growth factor (HGF), identified in ultrafiltered ascites and plasma from patients with cirrhosis, enhances the DNA synthesis in adult rat hepatocytes cultured at low cell density. This study was carried out to investigate the effect of ascites and plasma from patients with cirrhosis on liver-specific functions such as albumin synthesis in adult rat hepatocytes cultured at confluent-cell density. Ultrafiltered ascites from patients with cirrhosis and its ascitic protein, partially purified by fractionation with ammonium sulfate and gel filtration on Sephadex G-200, stimulated albumin synthesis in a dose-dependent manner in the presence of 10(-8), M dexamethasone. This effect was greater than that of 10(-7) M insulin and similar to that of 10(-7) M dexamethasone, but was additive with that of insulin plus dexamethasone. The molecular weight of the ascitic factor was estimated as 100,000 to 150,000, corresponding to that of HGF purified from cirrhotic ascites. Moreover, the partially purified ascitic factor markedly stimulated DNA and protein synthesis in hepatocytes. These findings suggest that the ascitic factor may act as HGF by stimulating hepatocyte DNA and albumin synthesis in a cell density-dependent manner.
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PMID:Stimulation of albumin synthesis in rat hepatocytes by ascites from patients with cirrhosis. 910 Apr 64

Endoscopic sclerotherapy has emerged as an effective and safe mode of treatment for long-term management of esophageal varices due to cirrhosis of liver and extrahepatic portal venous obstruction. There are few studies that have evaluated the role of sclerotherapy in the management of esophageal varices in patients with noncirrhotic portal fibrosis (NCPF). We report our results of long-term sclerotherapy in patients with NCPF. Seventy-two consecutive patients (men 29, women 43; age 32.9 +/- 11.8 years) with recurrent variceal bleeding due to NCPF were entered into the sclerotherapy program. Forty-eight patients received intravariceal absolute alcohol and 24 patients received intravariceal sodium tetradecyl sulfate (STD). Variceal obliteration was achieved in 65 (90.3%) patients with a mean of 5.7 +/- 3.0 (range 1-14) sessions. These patients were followed-up for a mean of 21.4 +/- 20.4 (range 1-96) months. Thirteen (17.3%) patients had episodes of upper gastrointestinal bleeding during sclerotherapy. Rebleed after obliteration was seen in 6 (9.2%) patients. Sclerotherapy was associated with a significant reduction in bleeding rate (bleeds per month per patient) during sclerotherapy and after obliteration of varices as compared to presclerotherapy period (P < 0.000001 for both). Recurrence of esophageal varices after obliteration was seen in 9 (13.9%) patients with reobliteration of varices in five patients in whom sclerotherapy was attempted. Complications including esophageal ulcer and stricture formation were seen in 18 (25%) and 4 (5.6%) patients respectively; strictures were restricted to patients who received absolute alcohol. Two (2.77%) patients died of massive upper gastrointestinal bleed during follow-up. We conclude that sclerotherapy is an effective and safe modality in the prevention of variceal bleeds in patients with NCPF.
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PMID:Sclerotherapy in noncirrhotic portal fibrosis. 924 45

Plasma collagen-binding vitronectin was assayed in 62 patients with chronic liver disease and 14 healthy control subjects. It was measured by an enzyme immunoassay using type I collagen and monoclonal antibody to vitronectin before and after treatment with heparin or dextran sulfate in vitro. The pretreatment level of plasma collagen-binding vitronectin (mean +/- S.E.M.) was 5.5 +/- 0.5 micrograms/ml in the controls, 8.2 +/- 0.3 micrograms/ml in chronic persistent hepatitis, 8.3 +/- 0.7 micrograms/ml in chronic active hepatitis, 7.9 +/- 0.7 micrograms/ml in liver cirrhosis, and 8.2 +/- 0.5 micrograms/ml in hepatocellular carcinoma with cirrhosis. After treatment with heparin, the percent collagen-binding vitronectin to total vitronectin was 20.6 +/- 2.0% in the controls, 24.7 +/- 4.1% in chronic persistent hepatitis, 28.6 +/- 2.5% in chronic active hepatitis, 42.6 +/- 4.5% in liver cirrhosis, and 31.8 +/- 2.3% in hepatocellular carcinoma. All percents were significantly increased compared to the pretreatment percent. The same pattern was also found after dextran sulfate treatment. Compared to that in the pretreatment state, the collagen-binding vitronectin after these treatments was more closely correlated with the serum levels of 7S collagen and hyaluronic acid. These results suggest that the collagen-binding activity of vitronectin may play an important role in the progression of liver disease and/or fibrosis through its activation with some glycosaminoglycans.
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PMID:Plasma collagen-binding vitronectin activated by heparin and dextran sulfate in chronic liver disease. 938 91

The results of experimental and clinical studies support the hypothesis that gut-derived endotoxins might be of relevance for the development and course of alcoholic liver disease. The aim of this study was to test the effect of a nonabsorbable, broad-spectrum antibiotic on endotoxemia in patients with alcoholic liver disease. Fifty patients with alcoholic liver disease (27 with cirrhosis, 23 without cirrhosis) were randomly assigned to receive either paromomycin sulfate (3 x 1 g/day) or placebo in a double-blind fashion for at least 3 weeks, and if possible 4 weeks. Endotoxin concentration, liver function tests, and other laboratory parameters were determined in weekly intervals. Endotoxin concentration was also determined in 15 healthy controls. Groups receiving paromomycin or placebo were similar for clinical and biological items collected initially. Mean initial endotoxin concentrations were significantly elevated in both groups (mean +/- SEM; paromomycin, 16.7 +/- 5.3 pg/ml; placebo, 17.5 +/- 6.9 pg/ml; healthy controls, 2.3 +/- 0.4 pg/ml). Although the mean endotoxin concentration was lower in the verum group after 1 week (paromomycin, 8.0 +/- 1.9 pg/ml; placebo, 14.6 +/- 3.5 pg/ml; p > 0.05), paromomycin treatment had no significant effect on endotoxin concentration or liver function tests during the 4-week period. The beneficial effect of paromomycin treatment on endotoxemia in cirrhotics reported in earlier studies could not be reproduced under the conditions of this trial in patients with alcoholic liver disease.
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PMID:Effect of treatment with paromomycin on endotoxemia in patients with alcoholic liver disease--a double-blind, placebo-controlled trial. 939 6

Zinc absorption in alcoholism was studied by a combination of zinc tolerance tests in 382 male patients with alcoholism (more than 140 g/day of ethanol) who had alcohol-induced disease of the liver or pancreas. In study 1, the serum zinc level was measured in all patients, and serum zinc and fecal chymotrypsin levels were compared in various disease groups. In study 2, 14 patients with liver cirrhosis (LC), 15 with chronic pancreatitis (CP), 7 with LC + CP, and 7 controls underwent oral zinc tolerance and zinc dipicolinate tolerance tests, zinc absorption and disorders of pancreatic exocrine functions were examined. In study 1, the serum zinc concentration was significantly lower in the CP and LC groups than in the control group, and the fecal chymotrypsin activity was significantly lower in the CP than in the control groups. In study 2, during the oral zinc tolerance test, the serum zinc concentration 3 hours after administration was significantly lower in the LC, CP and LC + CP groups than in the control group. In these groups, the serum zinc concentration was significantly lower in the abnormal fecal chymotrypsin group than in the control group at 2 and 3 hours after administration of zinc sulfate. In the oral zinc dipicolinate tolerance test, the serum zinc levels 2 and 3 hours after administration were significantly elevated in the control and all disease groups; there were no significant differences between the control and each disease group. These results suggest that reduction of pancreatic exocrine functions by alcohol and chronic reduction of synthesis of ligands such as picolinic acid in the liver are involved in the reduction of serum zinc in alcoholism.
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PMID:Evaluation of pancreatic exocrine function and zinc absorption in alcoholism. 965 43

A circulating anticoagulant was isolated from the plasma of a 42-year-old man with cirrhosis and hepatocellular carcinoma who had an unusual coagulation test profile. The patient developed a fatal coagulopathy, unresponsive to protamine therapy or plasma exchange following liver biopsy. However, at presentation, routine hemostasis assays were normal. The patient had mucocutaneous bleeding but the sole laboratory abnormality was a prolonged thrombin time (TT = 99 s, normal 25-35 s). Protamine titration indicated activity equivalent to a heparin concentration of 6-7 U/ml. Antithrombin III (AT III) antigen and activity were markedly elevated. The anticoagulant activity, purified from plasma by DEAE chromatography, was identified as a glycosaminoglycan (GAG). GAG anti-thrombin activity was completely abolished by heparin lyase III. Based on the degree of sulfation and HPLC pattern, the GAG was classified as heparan sulfate. Low levels (4 microM) of purified GAG markedly prolonged the TT (>120 s) but not the activated partial thromboplastin time (PTT) (31.4 s). In a Factor Xa assay, the GAG exhibited a potency equivalent to 0.06 U of low molecular weight heparin per nmol of uronic acid. Patients with endogenous circulating glycosaminoglycans can present with unusual laboratory coagulation test profiles. These reflect complex dysfunction of hemostasis, leading to difficulty in providing diagnosis and effective care.
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PMID:Structural characterization and functional effects of a circulating heparan sulfate in a patient with hepatocellular carcinoma. 969 91

We describe a metabolic defect in bile acid synthesis involving a deficiency in 7alpha-hydroxylation due to a mutation in the gene for the microsomal oxysterol 7alpha-hydroxylase enzyme, active in the acidic pathway for bile acid synthesis. The defect, identified in a 10-wk-old boy presenting with severe cholestasis, cirrhosis, and liver synthetic failure, was established by fast atom bombardment ionization-mass spectrometry, which revealed elevated urinary bile acid excretion, a mass spectrum with intense ions at m/z 453 and m/z 510 corresponding to sulfate and glycosulfate conjugates of unsaturated monohydroxy-cholenoic acids, and an absence of primary bile acids. Gas chromatography-mass spectrometric analysis confirmed the major products of hepatic synthesis to be 3beta-hydroxy-5-cholenoic and 3beta-hydroxy-5-cholestenoic acids, which accounted for 96% of the total serum bile acids. Levels of 27-hydroxycholesterol were > 4,500 times normal. The biochemical findings were consistent with a deficiency in 7alpha-hydroxylation, leading to the accumulation of hepatotoxic unsaturated monohydroxy bile acids. Hepatic microsomal oxysterol 7alpha-hydroxylase activity was undetectable in the patient. Gene analysis revealed a cytosine to thymidine transition mutation in exon 5 that converts an arginine codon at position 388 to a stop codon. The truncated protein was inactive when expressed in 293 cells. These findings indicate the quantitative importance of the acidic pathway in early life in humans and define a further inborn error in bile acid synthesis as a metabolic cause of severe cholestatic liver disease.
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PMID:Identification of a new inborn error in bile acid synthesis: mutation of the oxysterol 7alpha-hydroxylase gene causes severe neonatal liver disease. 980 83

Diacerein is a drug for the treatment of patients with osteoarthritis. This drug is administered orally as 50 mg twice daily. Diacerein is entirely converted into rhein before reaching the systemic circulation. Rhein itself is either eliminated by the renal route (20%) or conjugated in the liver to rhein glucuronide (60%) and rhein sulfate (20%); these metabolites are mainly eliminated by the kidney. The pharmacokinetics characteristics of diacerein are about the same in young healthy volunteers and elderly people with normal renal function, both after a single dose (50 mg) or repeated doses (25 to 75 mg twice daily). Rhein kinetics after single oral doses of diacerein are linear in the range 50 to 200 mg. However, rhein kinetics are time-dependent, since the nonrenal clearance decreases with repeated doses. This results in a moderate increase in maximum plasma concentration, area under the plasma concentration-time curve and elimination half-life. Nevertheless, the steady-state is reached by the third administration and the mean elimination half-life is then around 7 to 8 hours. Taking diacerein with a standard meal delays systemic absorption, but is associated with a 25% increase in the amount absorbed. Mild-to-severe (Child Pugh's grade B to C) liver cirrhosis does not change the kinetics of diacerein, whereas mild-to-severe renal insufficiency (creatinine clearance < 2.4 L/h) is followed by accumulation of rhein which justifies a 50% reduction of the standard daily dosage. Rhein is highly bound to plasma proteins (about 99%), but this binding is not saturable so that no drug interactions are likely to occur, in contrast to those widely reported with nonsteroidal anti-inflammatory drugs. Except for moderate and transient digestive disturbances (soft stools, diarrhoea), diacerein is well tolerated and seems neither responsible for gastrointestinal bleeding nor for renal, liver or haematological toxicity.
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PMID:Clinical pharmacokinetics of diacerein. 983 88

An 82-year-old male patient was admitted for liver dysfunction. Laboratory test showed the following data; aspartate aminotransferase (AST) 79 IU/l, alanine aminotransferase (ALT) 28 IU/l, total bilirubin (T. Bil) 0.9 U, zinc sulfate turbidity test (ZTT) 48.9 U, gamma-globulin 4.9 g/dl, immunoglobulin G (IgG) 5,046 mg/dl, anti-nuclear antibodies x 320, anti-mitochondrial antibodies (-), hepatitis B virus surface antigen (HBsAg) (-), HBcAb (-), anti-hepatitis C virus (anti-HCV) (-), hepatitis C virus (HCV-RNA) (-), anti-hepatitis G virus (anti-HGV) (-), alpha-fetoprotein 306.8 ng/ml, carcinoembryonic antigen (CEA) 2.3 ng/ml, carbohydrate antigen (CA) 19-9 77.2 U/ml. Abdominal ultrasonography and computed tomography showed a large mass occupying most of the right lobe and portal thrombosis in the liver. Liver biopsy revealed cirrhosis with inactive hepatitis in the nontumorous lesion and well-differentiated hepatocellular carcinoma in the tumorous lesion. We report a rare case of an aged male patient with autoimmune hepatitis complicated by hepatocellular carcinoma.
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PMID:An aged male patient with autoimmune hepatitis complicated by hepatocellular carcinoma. 1039 80


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