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)

Four markers for hepatic fibrosis--N-terminal peptide of Type III procollagen (PIIIP), Laminin P1 (laminin), Type IV collagen (Type IV-C), and 7S domain (7S)--were measured in the sera of 90 patients with various chronic liver diseases diagnosed by liver biopsy--fatty liver (FL), chronic inactive hepatitis (CIH), chronic active hepatitis (CAH), and liver cirrhosis (LC)--and in the sera of 20 healthy controls. The values of markers were compared with the grade of histologic findings of the liver. Four markers were significantly raised in the CAH group and the LC group, and they were considered to be indicators of hepatic fibrosis. PIIIP reflected necrosis and inflammation as well as fibrosis of the liver. Laminin, Type IV-C, and 7S reflected severe fibrosis. 7S was considered to be useful marker for liver cirrhosis.
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PMID:[Clinical significance of measurement of PIIIP, laminin P1, type IV-C and 7S in patients with chronic liver diseases--with special reference to histological findings]. 140 88

Eighteen immuno-compromised children (malignancies, hematological diseases, collagen diseases) with neutropenia and infections were treated with imipenem/cilastatin sodium (IPM/CS), and the efficacy and the safety of the drug were evaluated. 1. Responses to IPM/CS were excellent in 13 patients, good in 1, and fair in 4. None of the patients displayed a poor response to the treatment thus the efficacy rate was 77.8%. 2. Of 5 patients with sepsis, 4 had excellent or good responses. IPM/CS was effective against sepsis caused by Enterococcus faecalis and Pseudomonas aeruginosa. 3. In patients with severe neutropenia (WBC less than 100/mm3), the efficacy rate was 70%. 4. As for side effects, elevations of GOT and GPT were observed in 1 patient with liver cirrhosis. These results indicate that IPM/CS is safe and effective in immuno-compromised children with neutropenia and infections.
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PMID:[Clinical evaluation of imipenem/cilastatin sodium against infections in compromised children (malignancy, hematological disease, collagen disease)]. 143 90

Previous our studies showed that some steroid hormones, as pure crystalline Progesterone (pPc) and 17-alpha-hydroxyprogesterone capronate (17 alpha HPC) heightened the cirrhogenic action produced in rat liver by carbon tetrachloride. Medroxyprogesterone (MPA), however, did not appear to promote cirrhosis, but increased just steatosis. In the present paper, we have studied the above mentioned steroid hormones for their possible capability of inducing changes in plasma fibronectin concentration. For this purpose, the soluble plasma fibronectin level was measured in female rats 45 days after CCl4-induced cirrhosis, and it was compared with the insoluble fibronectin of liver (detected by immunostaining) and the collagen content in the organ. The results obtained show that, after treatment with CCl4 and MPA, both plasma and liver fibronectin content strongly increases, whereas liver collagen content lowers. However, after treatment with CCl4 alone or in association with the other two steroid hormones, any changes in fibronectin content is not observable, but, on the contrary, is evident a heightened collagen production associated with a cirrhotic change of liver.
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PMID:Changes in fibronectin production in rat liver during cirrhotic evolution due to treatment with CCl4 and steroid hormones: correlation with plasmatic fibronectin. 146 20

The serum levels of the 7S domain of type IV collagen were measured with a radio-immunoassay in 42 patients with primary biliary cirrhosis (asymptomatic: n = 28; symptomatic: n = 14), 10 patients with chronic active hepatitis, 10 patients with liver cirrhosis and 10 healthy female controls. Serum levels of the 7S domain of type IV collagen were: 4.28 ng/mL (3.88-4.72 ng/mL; mean and range of mean +/- s.d.) in healthy controls; 5.97 ng/mL (5.07-7.02 ng/mL) in patients with chronic active hepatitis; 8.23 ng/mL (6.40-10.58 ng/mL) in patients with liver cirrhosis; and 6.79 ng/mL (4.76-9.67 ng/mL) in patients with primary biliary cirrhosis. Patients with liver cirrhosis and primary biliary cirrhosis had higher levels of serum 7S domain of type IV collagen than healthy controls (P < 0.001, respectively). Serum levels of the 7S domain of type IV collagen in patients with asymptomatic primary biliary cirrhosis, 5.83 ng/mL (4.55-7.48 ng/mL) were significantly lower than those in symptomatic primary biliary cirrhosis, 9.18 ng/mL (6.53-12.91 ng/mL; P < 0.001). Serum levels of the 7S domain of type IV collagen increased significantly along with advancement of the histological stages of primary biliary cirrhosis. Serum levels of the 7S domain of type IV collagen in the paired sera of eight patients with asymptomatic primary biliary cirrhosis (mean interval 30 months, range 12-48 months) showed significant rises during the intervals (P < 0.05), while serum levels of albumin and total bilirubin did not change significantly during these intervals.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Clinical significance of the serum levels of the 7S domain of type IV collagen in patients with primary biliary cirrhosis. 148 89

No definitive therapy exists for the treatment of hepatic fibrosis and cirrhosis. Recent evidence suggests that hepatic lipocytes (Ito cells, fat storage cells, or stellate cells of the liver) are responsible for much of the collagen hypersecretion and nodule formation that occurs during hepatic fibrosis and cirrhosis. This review describes the cellular mechanisms of hepatic fibrogenesis emphasizing new experimental data about cytokines or growth factors to suggest potential avenues of future therapeutic design.
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PMID:Pathogenesis of hepatic fibrosis and the role of cytokines. 150 Jun 64

Male Sprague-Dawley rats with CCl4-induced cirrhosis (confirmed by increased collagen content and light microscopy) were fed either ethanol (Group A, n = 9) or isocaloric carbohydrate diet (Group B, n = 8) for 4 weeks. Histologic and hemodynamic measurements were obtained in the awake state before (time 1) and after the 4 weeks of diet (time 2). Portal-systemic shunts were evaluated using radiolabelled microspheres. Liver weight was increased in Group A (16.5 +/- 0.5 vs. 14.2 +/- 0.5 g, mean +/- SE, p less than 0.005) as was the ratio of liver weight over total body weight (3.41 +/- 0.05 vs. 2.86 +/- 0.09%, p less than 0.0001, +19.2%). Hepatocytes surface area was increased in the ethanol group (357 +/- 9 vs. 294 +/- 7 microns 2, p less than 0.0001). In Group B, only 9 +/- 2% of hepatocytes had steatosis as opposed to 69 +/- 3% of centronodular and 34 +/- 3% of perinodular hepatocytes in Group A (p less than 0.001). Portal pressure remained stable in both groups (time 1 (A) 16.9 +/- 0.8, (B) 15.8 +/- 1.1 mmHg, n.s.; time 2 (A) 15.9 +/- 0.7, (B) 15.8 +/- 0.6 mmHg, n.s.). Portal-systemic shunts did not change with time or diet (time 1 (A) 10.6 +/- 3.7%, (B) 4.1 +/- 2.1%, n.s.; time 2 (A) 13.4 +/- 5.9%, (B) 10.8 +/- 4.3%, n.s.).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effect of alcohol-induced hepatomegaly on portal hypertension in cirrhotic rats. 150 55

The development of disseminated intravascular coagulation (DIC) during a controlled IV infusion of concentrated ascitic fluid was studied in a group of patients with cirrhosis and refractory ascites. Nine studies were performed on patients who had not received prophylactic antiplatelet therapy. All developed laboratory evidence of DIC. The total collagen infused, estimated by ascitic hydroxyproline concentration, correlated significantly with both the prolongation of the partial thromboplastin time with kaolin (r = 0.8628; P less than 0.005) and the decrease in platelet count (r = 0.5674; P less than 0.05). The changes in the coagulation profile were reversible on ceasing the infusion, returning to baseline levels within 12 hours. There were no changes in the coagulation profiles of four patients studied 48 hours after beginning antiplatelet therapy with aspirin and dipyridamole. It is concluded that the infusion of concentrated ascitic fluid into a peripheral vein of patients with cirrhosis results in DIC, the severity of which correlates with the amount of collagen infused and which is completely prevented by inhibiting collagen-induced platelet aggregation. The results support the hypothesis that the DIC that complicates ascites infusion into the systemic circulation is largely related to ascitic fluid collagen.
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PMID:Coagulopathy during ascites reinfusion: prevention by antiplatelet therapy. 155 39

We have investigated the effects of nontoxic doses of vitamin A on the hepatic contents of collagen and sulfated glycosaminoglycans (SGAGs) in rats chronically treated with CCl4. When the animals were treated with this retinoid before the intoxication with CCl4, liver collagen level was significantly reduced as compared with that in rats that received only CCl4 (3.31 +/- 0.40 vs 5.00 +/- 0.61 mg/gm wet liver, mean +/- SD, respectively), although no significant differences were found for the relative proportion of type III collagen related to type I collagen. The absolute increment in the total amount of liver SGAG in the vitamin A--pretreated group was followed by a more important increase in the concentration of dermatan sulfate as compared with the CCl4 group (dermatan sulfate-to-heparan sulfate ratio: 1.15 for the CCl4 group vs 1.70 for the vitamin A--pretreated group). A significant proportion of the dermatan sulfate from this last group was of higher molecular weight when compared with the dermatan sulfate found in the liver of rats that received only CCl4. Our results indicate that the pretreatment with vitamin A modifies hepatic collagen and SGAG deposition and can inhibit or delay the development of liver cirrhosis in rats chronically treated with CCl4. We speculate that this effect could be due to the changes in the fat-storing (Ito) cells phenotype induced by vitamin A.
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PMID:Effects of vitamin A administration on collagen and sulfated glycosaminoglycans contents in the livers of rats treated with carbon tetrachloride. 159 6

We report two cases of pleural effusion in which a subdiaphragmatic cause was noted. In both cases it was necessary to obliterate a defect in the diaphragm via a thoracic incision. In one case, a left chylothorax occurred in a patient with hepatic cirrhosis. In this case, it was postulated that the normal lymphatic pathway through the right hemidiaphragm could have been stopped by pleural sequelae from right lobectomy. In the other case, a right pleural effusion occurred after peritoneal dialysis. It is a well known pathological entity: the structural defect can be observed by separation of collagen bundles in the tendinous diaphragm. This type of pleuro-peritoneal communication is well known in women suffering from menstrual pneumothorax or in patients treated by peritoneal dialysis.
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PMID:[Atypical pleural effusion secondary to transdiaphragmatic communication. Apropos of two cases: a chylothorax and a hydrothorax]. 160 41

To study the liver disease of patients with cystic fibrosis, percutaneous liver biopsies were performed in 10 patients with cystic fibrosis aged 6 to 22 yr. Nine of 10 patients had high Shwachman scores, eight had normal serum levels of transaminases. Light-microscopical examination showed steatosis in seven cases and in five slight or moderate inflammatory infiltration. Eight patients showed varying degrees of fibrosis and even cirrhosis. Six patients had bile-duct proliferation and, in one case a bile plug was found. Other signs of cholestasis were not seen. Electron-microscopical investigation showed no specific signs of cholestasis such as ductal plugs or intracellular bile pigments. The canaliculi were not dilated, except in one case. Most patients had bile-duct cells with irregular shapes, protruding into the lumen, and some cases even had necrotic cells. Around the bile ducts and ductules, collagen was deposited and fat-storing cells were a common finding. Our findings do not support the view that cholestasis is the pathogenetic factor in liver disease in cystic fibrosis. A cytotoxic influence on the biliary cells, stimulating collagen deposition, seems more likely.
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PMID:Bile-duct destruction and collagen deposition: a prominent ultrastructural feature of the liver in cystic fibrosis. 163 46


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