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)

Common bile duct stricture secondary to chronic pancreatitis is difficult to detect clinically. Surgical bypass is necessary if complications from biliary obstruction develop. In 21 patients operated on between 1968 and 1979, the earliest typical biochemical finding was a persistently elevated serum alkaline phosphatase level. The SGOT level was minimally elevated in seven patients, but did not correlate with changes in the stricture. An increased bilirubin level was noted either during an acute exacerbation of pancreatitis or late in the course of the stricture development, when obstruction was almost complete. Operative cholangiograms taken in 12 of these patients and transhepatic cholangiograms taken in nine demonstrated a stricture of the intrapancreatic bile duct more than 2 cm long. Operations were performed for treatment of obstructive jaundice (11), ascending cholangitis (three), suspected pancreatic cancer (three), and progressive biliary cirrhosis (two). Sphincteroplasty, initially attempted in four patients, uniformly failed to relieve the obstruction due to the length of strictured duct. Satisfactory drainage was obtained for up to ten years with choledochoduodenostomy (12), choledochojejunostomy (three), and cholecystojejunostomy (six).
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PMID:Common duct stricture from chronic pancreatitis. 737 60

The mechanisms of vitamin D deficiency already described are triggered off by a variety of causes. Confinement indoors leads to defective photosynthesis and dietary restrictions to insufficient intake. Malabsorption results from digestive tract diseases: mainly adult coeliac disease, but also sequelae of gastrectomy, exocrine pancreatic insufficiency, chronic biliary obstruction and all other causes of steatorrhoea. Practically, osteomalacia of digestive origin usually results from multifactorial hypovitaminosis D. The same applies to primary or nutritional biliary cirrhosis, which frequently entails low vitamin D blood levels despite subnormal 25-hydroxylation. Osteomalacia is also found in renal osteodystrophy, where it is partly due to inhibition of 1,25-hydroxylase and subsequent deficiency of 1,25-dihydrocholecalciferol, though other, non vitaminic substances may also be involved. Two misleading forms of the disease must be borne in mind: one with renal tubular lsions, the other associated with functional pseudo-hypoparathyroidism. The aetiology of most cases of osteomalacia due to vitamin D deficiency can be elucidated by a few simple tests.
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PMID:[Osteomalacia due to vitamin D deficiency. Part two: Aetiology (author's transl)]. 742 86

Hepatic copper concentrations were compared with staining grades of copper associated protein (CAP) and histochemical copper in liver sections from 44 patients (one fetus, one pre-term infant, four term infants, eight normal children, 16 children with various liver diseases, and 14 patients with intrahepatic cholestasis of childhood (IHCC)). A similar comparative study of hepatic copper concentration with CAP and histochemical copper was performed in 21 patients with Wilson's disease. CAP occurred in the fetus, pre-term infant, and term infants without liver disease. This suggests that CAP is a normal constituent of the hepatocyte and is not a consequence of liver disease or biliary obstruction. CAP was not seen when hepatic copper concentration was normal; it was absent in eight children with no evidence of liver disease, eight children with non-cirrhotic liver disease, and seven of eight children with cirrhosis. When hepatic copper concentration exceeded 4.0 mumol/g dry liver weight grade 2 or grade 3 staining for CAP and histochemical copper was found in the fetus, pre-term infant, infants, and IHCC. CAP was found in IHCC only in the presence of raised hepatic copper levels, supporting evidence of a relationship between copper and CAP. In 17 of 21 patients with Wilson's disease hepatic copper concentrations exceeded 4 mumol/g. Positive staining for CAP was seen in seven of these patients being usually grade 1. CAP is a normal associated protein, present when hepatic copper concentrations are increased in normal liver cells. It is usually absent in hepatocytes from Wilson's disease despite similar hepatic copper levels. CAP may represent material which protects the hepatocyte from the toxic effects of copper.
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PMID:Observations on copper associated protein in childhood liver disease. 745 May 63

The finding of epithelioid cell granulomas within liver biopsies is a not uncommon occurrence. We undertook this study to investigate the underlying conditions responsible for a diagnosis of granulomatous hepatitis in Northern Ireland during the thirteen year period 1980-1992. One hundred and sixty-three patients with hepatic granulomas were identified, accounting for 4% of all liver biopsies undertaken during the period of the study. In 145 cases (89%) a definite clinical diagnosis was established. The most common clinical diagnoses were primary biliary cirrhosis which accounted for 90 cases (55%) and sarcoidosis which accounted for 30 cases (18%). Other less common conditions associated with hepatic granulomas included tuberculosis (3 cases), Crohn's disease (3 cases), chronic active hepatitis (2 cases), drug hypersensitivity (2 cases) and extra-hepatic biliary obstruction (2 cases). Six patients were identified with a clinical diagnosis of psoriasis. Other miscellaneous conditions accounting for single examples of granulomatous inflammation were schistosomiasis, gout, Hodgkin's disease, secondary adenocarcinoma, collapse and necrosis of tumour following radiotherapy and chemotherapy, granulomatous inflammation within the wall of an abscess cavity and idiopathic cirrhosis. Only eighteen cases (11%) remained idiopathic with no definite diagnosis established after detailed investigation. The findings confirm the wide range of clinical conditions which can result in hepatic epithelioid cell granulomas. This has been emphasised in several previous major studies which are reviewed in this paper.
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PMID:Hepatic granulomas in Northern Ireland: a thirteen year review. 782 89

A 7-year-old child had unusual manifestation of cryptococcosis; liver and lymph node involvement predominated. There was evidence of cryptococcal hepatitis, extrahepatic biliary obstruction, and subsequent cirrhosis of the liver. Despite widespread dissemination, underlying immune disturbance was not evident. The patient was treated with two courses of amphotericin and 5-flucytosine.
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PMID:Hepatic involvement culminating in cirrhosis in a child with disseminated cryptococcosis. 788 81

Endotoxin sensitivity varies among animal species and appears to correlate with the presence of pulmonary intravascular macrophage (PIM). In rats, which lack PIM, we investigated the hypothesis that chronic cholestatic liver injury leads to induction of PIM and endotoxin sensitivity. Rats were randomized to either common bile duct ligation (BDL) or sham-surgery and studied at 1 wk (acute cholestasis), 2 wk (cholestasis, early cirrhosis), and 4 wk (cholestasis, established cirrhosis) after surgery. Intravascularly injected fluorescent latex microspheres (1 micron diameter) were taken up by large phagocytic cells in lung parenchyma of BDL rats (at 2 and 4 wk), while no uptake was observed in lungs from control rats. Electronmicroscopy revealed accumulation of large, mononuclear, macrophage-like cells containing ingested latex particles within the pulmonary capillaries. Pulmonary intravascular phagocytosis, as reflected in lung uptake of 99mTc microaggregated albumin (Microlite, mean particle diameter = 1 micron), averaged 0.7 +/- 0.1% (mean +/- SEM) of total injected dose in 13 control rats and progressively increased with time after BDL (1 wk, 1.7 +/- 0.2%; 2 wk, 10.0 +/- 3.0%; 4 wk 35.1 +/- 5.9%). Rats with biliary cirrhosis were markedly sensitive to the lethal effects of low dose endotoxin and demonstrated marked lung edema at the time of death. Furthermore, the lung uptake of intravascular 125I-lipopolysaccharide was increased five-fold in cirrhotic rats. We conclude that chronic biliary obstruction leads to the induction of pulmonary intravascular phagocytes and enhances endotoxin sensitivity in rats. Pulmonary intravascular phagocytosis in patients with advanced cirrhosis may account for their increased susceptibility to sepsis-induced adult respiratory distress syndrome.
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PMID:Chronic biliary obstruction induces pulmonary intravascular phagocytosis and endotoxin sensitivity in rats. 796 47

In human and experimental CCl4-liver damage, S-adenosyl-l-methionine-synthetase and/or the intrahepatic content of S-adenosyl-l-methionine, are diminished and in human cirrhosis phospholipid methyltransferase is markedly reduced. Therefore the aim of this study was to investigate the effect of S-adenosyl-l-methionine administration on liver damage induced by 15-day bile duct ligation. Liver damage was analyzed by histological, ultrastructural and biochemical techniques. Biliary obstruction produced an increase in collagen content, dilation of the bile canaliculi and disorganization of mitochondria. These effects were not observed in the bile-duct-ligated group receiving S-adenosyl-l-methionine. Biochemical results showed that bile duct ligation increased serum bilirubins, and alkaline phosphatase and gamma-glutamyl transpeptidase activities. These effects were prevented significantly by S-adenosyl-l-methionine. On the other hand, glycogen content in the liver was depleted while lipid peroxidation was increased by biliary obstruction, S-adenosyl-l-methionine administration prevented these effects. In the bile-duct-ligated group, hepatocyte and erythrocyte plasma membrane Na+/K+ and Ca(2+)-ATPase were lower than in the control group (p < 0.05). Administration of S-adenosyl-l-methionine preserved ATPase activities. The exogenous S-adenosyl-l-methionine supply is probably responsible for restoring transmethylation lost in liver diseases.
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PMID:Protective effect of S-adenosyl-l-methionine on liver damage induced by biliary obstruction in rats: a histological, ultrastructural and biochemical approach. 796 28

The expression of Lewis Y antigen (a blood group-related antigen containing type 2 chain) in hepatocytes was examined immunohistochemically, using the monoclonal antibody F-3, in a total of 530 liver specimens consisting of normal livers and various hepatobiliary diseased livers. Lewis Y was rarely expressed in the hepatocytes in histologically normal livers (20 cases) or in livers from patients with nonspecific reactive change or chronic persistent hepatitis, in viral livers (19 cases), autoimmune etiology livers (3 cases), or acute hepatitis-like change of autoimmune etiology livers (7 cases). In chronic active hepatitis of viral (132 cases) and autoimmune etiology livers (20 cases) with or without cirrhosis, the incidence of membranous expression of Lewis Y in clustered hepatocytes of viral and autoimmune etiology livers was 21 and 0% of mild chronic active hepatitis; 69 and 25% of moderate degree; 85 and 50% of severe degree; and 87 and 100% of cirrhosis, respectively. In alcoholic liver disease (27 cases), the incidence of membranous expression of Lewis Y in clustered hepatocytes was 18, 75, and 100% in mild fibrosis, moderate fibrosis, and cirrhosis, respectively. Such membranous expression of Lewis Y was not found in the early or late stages of the biliary diseases examined, primary biliary cirrhosis (226 cases), primary sclerosing cholangitis (8 cases), or extrahepatic biliary obstruction (22 cases).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Membranous expression of Lewis Y antigen in clustered hepatocytes in chronic viral, autoimmune, and alcoholic liver diseases but not in biliary diseases. 805 6

The peribiliary vascular plexus (PVP) plays an important role in the pathophysiology of the biliary tree. We histologically examined vascular endothelial cells of the intrahepatic PVP in various hepatobiliary diseases by immunohistochemistry and lectin histochemistry with antibodies to factor VIII-related antigens (F-VIII-R-Ag) and Ulex europaeus agglutinin I (UEA-I). The PVP around the intrahepatic large bile ducts (LBDs) and septal bile ducts (SBDs) in normal livers consists of three layers: inner layer vessels immediately adjacent to the epithelium, intermediate layer vessels within the ductal wall, and outer layer vessels outside the ductal wall. In some bile ducts that show active inflammation in hepatolithiasis, primary biliary cirrhosis (PBC), primary sclerosing cholangitis (PSC), and extrahepatic biliary obstruction (EBO), vessels in the intermediate layer and, to a lesser degree, in the inner layer, are increased in number. In sclerotic bile ducts of PSC, EBO, and hepatolithiasis, the number of inner and intermediate layer vessels are markedly and variably reduced, respectively. In liver cirrhosis or chronic advanced liver diseases, the vessels in all three layers, particularly those in the outer layer, are increased in number and dilated, probably reflecting intrahepatic microcirculatory disturbance. The PVP showed several types of numerical and luminal changes, each of which may be related to disease processes in the intrahepatic biliary tree as well as to intrahepatic microcirculatory disturbance.
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PMID:Intrahepatic peribiliary vascular plexus in various hepatobiliary diseases: a histological survey. 808 71

The histologic diagnosis of extrahepatic biliary obstruction in the setting of orthotopic liver transplantation (OLT) may be complicated by nonobstructive factors, such as rejection, preservation injury, drug effects, and infection. Indeed, biopsy specimens from OLT patients frequently exhibit early posttransplant cholestasis, which is likely the result of several of these factors acting in concert. We reviewed the clinicopathologic features of 14 OLT patients whose biopsy specimens displayed prominent cholangitis with "obstructive"-type features. Cholangiograms, Doppler ultrasound examinations, and bacterial cultures were obtained in conjunction with all biopsy specimens. Despite histologic evidence of biliary obstruction, cholangiography revealed obstruction in only one case, leaks in four cases, and nine normal studies. Ten patients had severe systemic bacterial or cytomegalovirus infections. Biliary infection was documented in two cases. Hepatic artery occlusion was diagnosed in one case. The cholangitic pattern persisted in patients with unremitting infections, and two patients developed secondary biliary cirrhosis despite having consistently normal cholangiograms. Features of acute rejection or viral hepatitis were not observed on any biopsy specimen. The presence of this clinicopathologic spectrum was associated with a poor prognosis. Nine patients died and only four patients who responded to antibiotics survived. These findings demonstrate a striking cholangitic response to systemic infections in OLT grafts. The diagnosis of biliary obstruction in OLT liver biopsy specimens cannot be rendered without cholangiographic verification.
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PMID:Rejection-independent cholangitis and cirrhosis following orthotopic liver transplantation. 825 64


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