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

The development of the syndrome of chronic intrahepatic cholestasis in five young, black men who had systemic granulomatous disease and clinical features consistent with those of sarcoidosis is described. Clinical and biochemical aspects, similar to those of primary biliary cirrhosis, included pruritus, jaundice, hepatomegaly and striking elevations of serum levels of alkaline phosphatase and cholesterol. (One patient had skin xanthomas.) Mitochondrial antibodies were not found; and survival of the patients (7 to 18 years) exceeded the usual survival of patients with primary biliary cirrhosis. The histologic abnormalities included noncaseating granulomas, chronic intrahepatic cholestasis, increased copper in hepatocytes, progressive diminution in number of interiobular bile ducts, periportal fibrosis and the eventual development of a micronodular "biliary" cirrhosis. The histologic evolution of the disease suggests a slow, progressive destruction of the bile ducts by granulomas. Although the end stage of this syndrome resembles primary biliary cirrhosis, the characteristic nonsuppurative, destructive cholangitis of primary biliary cirrhosis was not present.
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PMID:Chronic intrahepatic cholestasis of sarcoidosis. 116 46

The jejuno-ileal bypass for weight reduction can hardly be considered a non-specific treatment: 3-4% of the patients develop chronic hepatic damage, 1-2% suffer hepatic failure due to massive fatty liver, rapidly progressing liver cirrhosis or hepatic fibrosis. Fatty liver is an invariable sequel of this operation. Once the above-mentioned symptoms set in or an incipient cirrhosis or fibrosis is diagnosed, immediate restoration of normal passage is required. The intestinal bypass syndrome observed in the patient (fem.) (viz. table 1) does not wholly coincide with the enteral bile acid loss syndrome occurring in extensive ileum resection (56) where usually there is no evidence of fatty liver, icterus, cholestasis or encephalopathy. Animal experiments seem to confirm that the blind loop in the broadest sense of the term is responsible for the sometimes fatal hepatic damage. Possibly we are confronted here with a pattern of hepatic damage due to toxic nutritive effects similar to cirrhosis as a sequel of low-protein and low-calorie intake or to the phenomenon observed in animal experiments. The cholestasis confirmed by biopsy and chemical methods is a manifestation of these hepatic disorders. The clinical aspects resemble the Reye syndrome that we know in pediatrics. Patients have to be carefully selected and informed about possible postoperative damage; a continuous clinical follow-up with biopsy of the hepatic tissue is also indicated.
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PMID:[Liver damage following intestinal by-pass surgery for weight reduction]. 122 12

From over 800 patients with chronic hepatic diseases admitted to the Institute of Internal Medicine between 1960-1969 and in whom diagnosis was assessed by hepatic biopuncture, 180 were reexamined 3-14 years later to estimate the clinical evolution and the prognostic value of the bioptic findings. The evolution was favourable in most of the cases of persistent chronic hepatitis (70%) and of moderate aggressive chronic hepatitis (59%). Severe aggressive chronic hepatitis evaluated favourably in 34% of the cases and was aggravated in 42% of the cases (26% exits). In the patients with cirrhosis the percentage of deaths reached 65 but 30% were still in a stationary form; a single exceptional case was improved 7 years after the hepatic biopuncture. The prognostic value of hepatic biopuncture is much increased if, in addition to the common histological features, other histochemical and morphological criteria such as: structural stability of collagen fibers, importance of cellular infiltrates and presence of plasma cells, nuclear changes, degree of steatosis, amount of glycogen storage, siderosis and cholestasis are also taken into consideration.
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PMID:Primary evolution of chronic hepatitis estimated 3 to 14 years after the liver biopuncture. 124 40

The activities of serum cholinesterases were determined in parallel with acetyl-, butyryl- and propionyl-thiocholiniodide in healthy persons and patients with acute and chronic hepatitis, cirrhosis of the liver, fatty liver, cholestasis, intoxication and malignant tumors. The following normal values were obtained: See Article. The correlations between the various methods, especially between butyryl- and propionylthiocholiniodide are statistically significant. Compared to healthy persons, the activity of serum-cholinesterases, determined with the three substrates, decreased significantly in patients with acute and chronic hepatitis, cirrhosis of the liver, intoxication and malignant tumors. A change of specificity of serum-cholinesterases towards acetyl-, butyryl- and propionylthiocholiniodide in normal persons and patients with endogenous or exogenous coma of the liver was not observed. In all cases a parallel decrease of activity in sera was determined.
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PMID:[Comparative methods for the determination of the activity of serumcholinesterases (acylcholin-acyl-hydrolase E.C. 3.1.1.8) and their diagnostical value (author's transl)]. 124 30

The simultaneous measurement of wedged hepatic venous pressure and portal venous pressure at 11 and 28 days following common bile duct and intrahepatic bile duct obstruction reveals a significant elevation of the portal pressure at 28 days which is due primarily to increased presinusoidal resistance to portal blood flow. Portal venograms performed prior to sacrifice revealed moderate narrowing of the portal vein radicles and delayed emptying at 11 days and severe morphological alterations at 28 days. These results confirm the findings of other investigators and help to explain why the hemodynamic alterations occur so rapidly in obstructive jaundice, well before the development of significant biliary cirrhosis.
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PMID:The location of increased resistance to portal blood flow in obstructive jaundice. 125 22

An autopsy case of mesenchymal hamartoma of the liver was reported and from the macroscopical observation and serial sections of the tumor the following findings were found: (1) macroscopically the tumor is supplied by only one large triad, (2) in the tumor hepatic lobular structure is fundamentally preserved and prolifereated bile ducts with surrounding fibrosis and many bile thrombi are mainly elongated and dilated Hering's canals, (3) the cysts connect with dilated interlobular bile ducts, (4) there are two portions, where connection of bile ducts is incomplete, that is, from Hering's canals to interlobular bile ducts and from interlobular ducts to large ducts in the large triad of (1), (5) almost all portal veins in the large triad of (2) are stenosed or obliterated by loose intimal fibrosis. From these findings it is considered that intrahepatic bile duct obstruction resulting in regional biliary cirrhosis is the fundamental process of this disease, and in addition the role of hemodynamic disturbance was discussed.
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PMID:Mesenchymal hamartoma of the liver--an autopsy case with serial sections and some comments on its pathogenesis. 127 83

The serum non-caeruloplasmin copper concentrations were measured in normal subjects and patients with various types of liver disease by a sensitive direct method involving complexing the copper and measurement by atomic absorption spectrophotometry. In normal subjects the mean concentration (+/- S.D.) was 10.1 +/- 1.6 mug/100 ml, males having a slightly higher value (10.7 +/- 1.3 mug/100 ml) than females (9.2 +/- 1.8 mug/100 ml). In patients with various non-hepatic diseases concentrations were raised (15.8 +/- 8.9 mug/100 ml), as also in hepatitis (14.7 +/- 4.3 mug/100 ml), cholestasis (16.1 +/- 6.4 mug/100 ml) and cirrhosis (16.3 +/- 8.7 mug/100 ml). Heterozygotes for Wilson's disease and patients treated for Wilson's disease had concentrations (12.9 +/- 5.9 and 9.8 +/- 3.7 mug/100 ml, respectively) which did not differ significantly from normal whereas untreated patients had very significantly raised concentrations (22.9 +/- 4.5 mug/100 ml). Direct measurement of serum non-caeruloplasmin copper is more accurate than indirect measurement and may help in assessing the effect of treatment but it is concluded that measurement of this fraction of serum copper will not enable Wilson's disease to be differentiated from other forms of liver disease.
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PMID:Direct measurement of serum non-caeruloplasmin copper in liver disease. 127 46

The authors performed 20 liver transplantations from living related donors between June 1990 and July 1991. The 20 pediatric patients (14 biliary atresia, two Budd-Chiari syndrome, one liver cirrhosis after hepatitis C viral infection (HCV hepatitis), 1 progressive intrahepatic cholestasis, 1 liver cirrhosis, 1 protoporphyria) were transplanted with 11 left lobes, eight left lateral segments, and one right lobe. The choice of donors was restricted to the parents of the recipients. The immunosuppressive treatment consisted of FK 506 and steroids. Seventeen recipients are alive, 15 of whom are well and at home. Two recipients, who underwent emergency transplantation, died of postoperative complications. Another recipient died of accidental asphyxia at 6 months after the transplantation. All 20 donors had uneventful postoperative courses and were able to resume their normal social lives. The arterial ketone body ratio (AKBR) increased to above 1.0 within 2 days after the transplantation in all cases. Relatively mild rejection episodes were encountered in only two cases transplanted with ABO-compatible grafts, and these were treated successfully with steroids and FK 506.
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PMID:An appraisal of pediatric liver transplantation from living relatives. Initial clinical experiences in 20 pediatric liver transplantations from living relatives as donors. 128 74

Liver cell functional heterogeneity has been shown to persist in toxic CCl4 cirrhosis in growing rats, but the zonation observed in cirrhotic nodules may be different in other types of cirrhosis. To investigate this possibility, we looked at the zonal activities of two microsomal enzymes, glucose-6-phosphatase and NADPH dehydrogenase, in cirrhotic nodules from growing rats with chronic cholestasis. Zonal activities were measured by quantitative cytochemistry and microdensitometry. Liver cell heterogeneity was demonstrated, and we confirmed that the metabolic zonation is the mirror image of that observed in toxic cirrhosis, with periportal activity at the nodule periphery and perivenular activity at the nodule centers. Glucose-6-phosphatase activity was 2.06 times higher at the peripheries of the nodules than at the centers, whereas NADPH dehydrogenase activity at the nodule periphery was 72% of the nodule center activity. We conclude that a liver cell functional heterogeneity persists in biliary rat cirrhosis, with zonation the reverse of that previously found in toxic CCl4 cirrhosis.
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PMID:Liver metabolic zonation in rat biliary cirrhosis: distribution is reverse of that in toxic cirrhosis. 131 72

A recent case-control study on 577 lichen planus (LP) patients and 1008 controls confirmed that LP patients may significantly associate with a chronic liver disease (CLD) which is independent from drug or alcohol intake and has some connection with hepatitis B virus (HBV) infection. The study, however, failed to define the nature of CLD. This has been investigated through the clinical and laboratory features of 50 patients with LP and impaired liver function tests. Overall, the laboratory signs of cell necrosis prevailed over those of cholestasis and a good relationship with the HBV and HCV infections was found. Ninety percent of patients with LP and CLD had antibodies to one or another of the major viruses involved in infectious hepatitis. No patient had anti-liver kidney microsomal antibodies type 1. Liver biopsies were done in 12 cases and mostly revealed a chronic active hepatitis evolving into cirrhosis. No evident cases of primary biliary cirrhosis were found. It appears that LP associated CLD is post-viral in nature.
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PMID:Clinical and laboratory presentation of lichen planus patients with chronic liver disease. 132 93


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