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)

Hepatobiliary disorders are well known complications in patients with ulcerative colitis but it is not possible to predict those patients with ulcerative colitis who will eventually develop liver disease. In this study, liver biopsies from 74 patients with ulcerative colitis have been reevaluated. None of the patients showed clinical or biochemical signs of liver disease at the time of biopsy. Thirty seven (50%) had a completely normal liver biopsy. The others showed minimal portal inflammation or fatty infiltration. The biopsies of three patients displayed concentric, periductular fibrosis, or so called 'onion skin' lesions. None showed other signs of fibrosis or cirrhosis. The histological findings were unrelated to either activity or extent of colitis, except for the onion skin lesions which were seen exclusively in biopsies of patients with involvement of the total colon. Sixty eight of the 74 patients were reviewed after a mean interval of 18 years. The majority had no symptoms of hepatobiliary disorders and only two had developed liver disease; one suffered from cryptogenic cirrhosis, possibly due to non-A, non-B hepatitis and the other of an autoimmune liver disease and later developed a bile duct carcinoma. Both were women with total colonic involvement. At the time of the first liver biopsy one showed no histological abnormalities and the other only minor fatty infiltration. Thus, minor abnormalities in liver tissue are common in patients with ulcerative colitis without biochemical evidence of liver disease. The morphological changes are of little help in predicting the future risk of a patient with ulcerative colitis developing a clinically relevant hepatobiliary complication. The absence of biochemical parameters for liver disease during the early years of ulcerative colitis predict a favourable longterm diagnosis as regards hepatobiliary complications.
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PMID:Liver histology and follow up of 68 patients with ulcerative colitis and normal liver function tests. 233 76

Musculoskeletal disease occurs in association with inflammatory bowel disorders including Crohn's disease and ulcerative colitis, as well as with Whipple's disease; with enteritis caused by Salmonella, Shigella, and Yersinia; and also following intestinal bypass surgery. Extraintestinal causes of musculoskeletal alterations include Laennec's and biliary cirrhosis and pancreatitis. Three types of musculoskeletal abnormalities are recognized in patients with inflammatory bowel diseases: peripheral joint arthritis, sacroiliitis and spondylitis identical to ankylosing spondylitis, and rarely, miscellaneous changes such as digital clubbing and hypertrophic osteoarthropathy.
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PMID:Enteropathic arthropathies. 243 70

Primary sclerosing cholangitis is an idiopathic disease characterized by progressive diffuse stricture of extrahepatic and intrahepatic bile ducts. Eighteen patients with end-stage symptoms of primary sclerosing cholangitis were evaluated during a 10-year period from 1976 to 1986. Nine patients presented with disease amenable to intrahepatic cholangiojejunostomy. All patients presented with elevated liver function test results, and six of nine patients had a history of ulcerative colitis. The mean survival after intrahepatic cholangiojejunostomy was 3.9 years (range, 4 months to 10 years). Two of three of the patients with biliary cirrhosis died within 1 year after surgery. Four of nine patients remain alive today, with a mean survival of 4.7 years. For patients with end-stage primary sclerosing cholangitis, intrahepatic cholangiojejunostomy provides effective surgical palliation in those without secondary biliary cirrhosis.
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PMID:Intrahepatic cholangiojejunostomy as a palliative procedure in primary sclerosing cholangitis. 246 9

Sulfasalazine has been associated with bronchopulmonary complications of inflammatory bowel disease (IBD) in adults. We describe a 12-year-old boy who developed desquamative interstitial pneumonitis and hepatic cirrhosis several years following the onset of ulcerative colitis. The restrictive lung disease progressed despite cessation of sulfasalazine and initiation of corticosteroid therapy. We discuss a variety of bronchopulmonary complications of IBD and their association with sulfasalazine.
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PMID:Desquamative interstitial pneumonitis complicating inflammatory bowel disease of childhood. 286 42

As an initial step in testing the hypothesis that immunoregulatory abnormalities are important in the pathogenesis of primary sclerosing cholangitis, we determined the number and percentage of lymphocyte subsets in the peripheral blood of 33 patients with primary sclerosing cholangitis. In these patients, when compared with normal and diseased controls, there was a significant reduction in the total number of circulating T cells because of a disproportionate decrease in Leu-2a (suppressor/cytotoxic) cells. This decrease resulted in a significantly increased ratio of Leu-3a to Leu-2a cells. Patients with cirrhosis had significantly higher Leu-3a/Leu-2a (helper/suppressor) ratios than did noncirrhotic patients; both disease groups, however, had ratios that were significantly higher than controls. The number and percentage of B cells were significantly increased. Alterations in the percentage of B cells correlated significantly with histologic stage and concentrations of gamma globulin, serum IgG, and bilirubin. We conclude that these abnormalities are suggestive of a defect in immunoregulation in primary sclerosing cholangitis, which is not secondary to advanced liver disease alone and appears to be independent of chronic ulcerative colitis or obstructive jaundice.
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PMID:Lymphocyte subsets in primary sclerosing cholangitis. 295 97

The Portland experience with patients requiring proctocolectomy for chronic ulcerative colitis in association with primary sclerosing cholangitis has been reported. Nineteen patients had conventional ileostomy reconstruction, 5 of whom had development of stomal varices with recurrent hemorrhage due to cirrhosis and portal hypertension. When this combination of conditions exists, the therapeutic options must be carefully weighed. Perhaps ileal pouch to anal anastomosis should be considered when proctocolectomy becomes mandatory. Ileostomy is presently a contraindication to liver transplantation. In patients with ileostomies, control of hemorrhage by local measures, including ileostomy revisions, proved to be of only temporary value, yet it should be the preferred management of patients with a severely limited life expectancy. Successful shunts directed at portal decompression have always prevented further ileostomy hemorrhage, however, they have commonly accelerated liver failure and thus death. Furthermore, such shunts seriously complicate liver transplantation if it is considered.
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PMID:Exigent ileostomy hemorrhage. A complication of proctocolectomy in patients with chronic ulcerative colitis and primary sclerosing cholangitis. 316 Feb 51

Human alkaline phosphatase isozymes--the tissue-unspecific, the intestinal, and the placental alkaline phosphatases--were determined in sera by use of isozyme-specific monoclonal antibodies. The clinical utility of serum determinations of alkaline phosphatase isozymes was evaluated in patients with diseases of the gastrointestinal tract and the liver. No elevations of the different serum isozymes were observed in the intestinal diseases investigated (active Crohn's disease and ulcerative colitis). For non-malignant diseases of the liver the alkaline phosphatase isozymes presented characteristic patterns. Patients with cirrhosis due to hepatocellular diseases had markedly elevated levels of intestinal alkaline phosphatase and moderate serum activities of tissue-unspecific and placental alkaline phosphatases. In patients with liver disease with cholestatic features tissue-unspecific and placental isozyme levels were high, but the intestinal isozyme remained normal, whereas primary biliary cirrhosis was associated with high levels of the tissue-unspecific enzyme and moderate elevations of intestinal and placental alkaline phosphatases. It can be concluded that, in addition to tissue-unspecific alkaline phosphatase, intestinal and placental isozymes contribute to the total alkaline phosphatase activity for patients with liver disease. The results suggest that specific methods for the identification of alkaline phosphatase isozymes could be of value.
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PMID:Alkaline phosphatase isozymes in non-malignant intestinal and hepatic diseases. 322 93

PSC is an unusual disease of unknown etiology. In fact, sclerosis of the bile ducts may be the result of multiple factors, including autoimmune, bacterial, congenital, drug, or viral agents. The most commonly associated diseases are ulcerative colitis and chronic pancreatitis. Except for the earliest stages of the disease, liver histology is not specific. Most patients present with jaundice, pain, and pruritus, although an increasing number of asymptomatic patients with inflammatory bowel disease and abnormal liver function are being diagnosed. Cholangiography is the key to the diagnosis and is usually pathognomonic except in the unusual case where PSC is confused with cholangiocarcinoma. Multiple forms of medical therapy have been tried, including steroids, azothiaprine, D-penicillamine, colchicine, cholestyramine, and antibiotics. To date, however, none of these medications has altered the course of this disease. In recent years, balloon dilation of biliary strictures has been accomplished via endoscopic and percutaneous transhepatic approaches. However, in patients with PSC these nonoperative manipulations must be done repeatedly, may require multiple general anesthetics, and are difficult to perform. A direct surgical approach to the biliary tree with prolonged transhepatic stenting is indicated in patients with severe hilar or extrahepatic stricturing, persistent jaundice and/or recurrent cholangitis, and no evidence of cirrhosis. Hepatic transplantation should be reserved for patients with PSC who have well-established cirrhosis and in whom other therapeutic options have failed.
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PMID:Sclerosing cholangitis. 331 16

Hepatobiliary diseases are certainly not very frequent extraintestinal complications of chronic intestinal inflammatory diseases, however, they are an important prognostic factor. 2% of patients with ulcerative colitis develop liver cirrhosis but 10% of those die as a direct result of liver failure. Other associated severe hepatobiliary diseases include primary sclerosing cholangitis, carcinoma of the bile duct and amyloidosis. The present review attempts to divide the associated hepatobiliary diseases into three groups. 1. those that are the result of therapy. 2. those that are the result of the pathophysiological mechanisms of the underlying disease and 3. those of unknown etiological origin. This division might serve not only for a better understanding of the various mechanisms but should have some impact on therapeutic regimens.
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PMID:[Hepatobiliary diseases in Crohn disease and ulcerative colitis]. 356 Nov 41

Peptide YY has been localized within human ileocolonic endocrine cells and may contribute to the regulation of gastric secretion and gastric emptying in man. Since our previous studies had shown decreased colonic concentrations of peptide YY in the idiopathic inflammatory bowel diseases, a specific radioimmunoassay was used to measure fasting serum concentrations of peptide YY in healthy controls and in patients with adenocarcinoma of the rectum, idiopathic chronic active liver disease and hepatic cirrhosis, ulcerative colitis, and Crohn's disease. In healthy controls and in patients with adenocarcinoma of the rectum, serum concentrations of peptide YY ranged from 50 to 260 pg/ml. Serum concentrations of peptide YY in patients with hepatic cirrhosis ranged from 59 to 717 pg/ml. Serum concentrations of peptide YY in patients with ulcerative colitis were similar to healthy controls. In patients with Crohn's disease, serum concentrations of peptide YY were less than 50 pg/ml in three patients who had had a previous proctocolectomy, and were more than 260 pg/ml in 14 patients who had had previous resection of more than 48 cm of ileum or presently had symptomatic Crohn's disease subsequently requiring surgical resection of a total of more than 75 cm of ileum. These results suggest that most circulating peptide YY is released from the colorectal region. Hepatic cirrhosis, previous ileal resection, and symptomatic Crohn's disease were associated with elevation of fasting serum peptide YY. The mechanism of increased fasting serum peptide YY in patients with Crohn's disease could be the loss of an ileal inhibitory factor or possibly an increased release of colonic peptide YY in response to fat malabsorption. The effect of alteration of serum peptide YY concentrations on the pathophysiology of Crohn's disease is yet unknown.
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PMID:Abnormalities of fasting serum concentrations of peptide YY in the idiopathic inflammatory bowel diseases. 356 36


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