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)

Organ antibodies were studied after immunothermistometry treatment in 205 patients with chronic diseases of the liver. One group of patients was treated by routine methods in accordance with the diagnosis, while the second group of patients was additionally given hemodes. Before treatment organ antibodies were revealed in 31 patients (70.4%) with liver cirrhosis, in 44 (55%) with chronic hepatitis and 45 (55.5%) in chronic pancreatitis. After treatment these were respectively 9 (20.5%), 15 (18.7%) and 15 (18.5%). Depending on the treatment antibodies were more frequently eliminated in the first group of patients in chronic hepatitis. In liver cirrhosis and chronic pancreatitis there was no significant difference between the two groups of patients.
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PMID:[The dynamics of the organic antibodies during treatment in patients with chronic diseases of the liver and the pancreas]. 208 5

Serum apolipoprotein A-I measurement was compared in alcoholic patients according to presence or absence of chronic pancreatitis and liver fibrosis. Among alcoholic patients without liver disease, apolipoprotein A-I was significantly lower in patients with chronic pancreatitis (157 +/- 70 mg/dl) than in patients without pancreatitis (209 +/- 74 mg/dl, p less than 0.001). In cirrhotic patients, apolipoprotein A-I was lower in patients with chronic pancreatitis (82 +/- 35 mg/dl) than in patients without pancreatitis (102 +/- 45 mg/dl), but this difference was not significant. The decrease of serum apolipoprotein A-I was independent of nutritional parameters whether or not there was cirrhosis. Immunohistochemical study of pancreatic samples with chronic pancreatitis showed that apolipoprotein A-I was located in the pancreatic fibrosis whereas lobules were unstained. This study suggests that apolipoprotein A-I is trapped by the pancreatic extracellular matrix and that this sequestration might explain, in part, the decrease of the serum apolipoprotein A-I.
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PMID:Serum apolipoprotein A-I in alcoholic patients with chronic calcifying pancreatitis. 212 44

Serum CA 19-9 was determined in 83 control subjects, 99 patients with pancreatic cancer, 104 with chronic pancreatitis and 137 with extra-pancreatic diseases mainly of gastrointestinal origin in order to evaluate whether hepatic factors can influence circulating CA 19-9 in pancreatic cancer. Sensitivity, specificity and accuracy of this test in determining pancreatic malignancy were: 74%, 83% and 57%. We divided patients into two groups: group A (159 cases) and group B (181 cases) with and without anatomical liver damage (presence of primary or metastatic cancer, cirrhosis, hepatitis, steatofibrosis, cholangitis). Group A presented higher CA 19-9 values as compared to group B. Significant correlations were found in group B but not in group A between CA 19-9 and ALT, ALP and total bilirubin. Multiple regression analysis (CA 19-9 dependent and ALT, ALP and total bilirubin predictor variables) was significant only in group B. The standardized partial regression coefficients found to be significant were those of ALP and total bilirubin. We can conclude that CA 19-9 is an index of pancreatic cancer with satisfactory sensitivity and specificity. The presence of anatomical liver damage seems to increase the value of this index, probably releasing CA 19-9 into the bloodstream. Extra-hepatic cholestasis may also be an important factor in elevating CA 19-9 probably by reducing the hepatic catabolism of this glycoprotein.
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PMID:How does liver dysfunction influence serum CA 19-9 in pancreatic cancer? 213 20

Primary sclerosing cholangitis is a rare disease of unknown etiology. Sclerosis of the bile ducts may actually be the final result of multiple factors such as autoimmune, bacterial, congenital, drug, or viral injury. The most commonly associated diseases are ulcerative colitis and chronic pancreatitis. Except in the earliest stages of the disease, liver histologic findings are 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 identified. Cholangiography is key to the diagnosis and is usually pathognomonic except in the unusual case where primary sclerosing cholangitis is confused with cholangiocarcinoma. Many forms of medical therapy have been tried, including antibiotics, azathioprine, cholestyramine, colchicine, cyclosporine, D-penicillamine, steroids, and ursodeoxycholic acid. To date, none of these medications has been proved to alter the course of this disease. Recent reports of ursodeoxycholic acid trials have been encouraging, but long-term results of ongoing randomized trials have yet to be published. In recent years, balloon dilatation of biliary strictures has been accomplished via endoscopic and percutaneous transhepatic approaches. However, in patients with primary sclerosing cholangitis, these nonoperative manipulations must be done repeatedly, may entail multiple general anesthetics, and are difficult to perform. We believe that a direct surgical approach to the biliary tree with long-term transhepatic stenting is indicated in selected patients with severe hilar or extrahepatic stricturing, persistent jaundice or recurrent cholangitis, and no evidence of cirrhosis. Hepatic transplantation should be reserved for patients with primary sclerosing cholangitis who have well-established cirrhosis and have not responded to other therapeutic measures.
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PMID:Primary sclerosing cholangitis. 224 21

This report describes a variant form of lipase found in a patient with cryptogenic liver cirrhosis. Serum lipase in this patient showed persistently increased activity with simultaneously normal activity of amylase. Results of exclusion chromatography demonstrate that the lipase activity in the serum of this patient eluted as a macromolecule. Since macromolecular complexes were not fixed by protein A, it seems unlikely that lipase is attached to IgG. Tests of the sera from 20 patients with raised serum lipase activity in acute pancreatitis or an acute episode of chronic pancreatitis revealed, in two patients, that a small but reproducible proportion of the total lipase activity eluted in the region of the macrolipase. In addition, 10% and 18% of the total lipase activity was found in the elution region of the macrolipase in two commercial pooled sera used for quality control. The results show that, in rare cases, macrolipasemia must be considered a possible cause of raised serum lipase activity.
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PMID:Macrolipasemia: a rare cause of persistently elevated serum lipase. 232 84

In patients with chronic pancreatitis, common bile duct obstruction is reported in 3.2-45.6% of patients; however, only 5-10% of all patients with chronic pancreatitis require operative decompression of the bile duct. The cause of the intrapancreatic stricture of the common bile duct may be either a fibrotic inflammatory restriction, or compression by a pseudocyst. Obstruction of the duodenum is much less common than common bile duct obstruction in chronic pancreatitis occurring in less than 1-2% of patients with chronic pancreatitis. Colonic obstruction secondary to pancreatitis is very infrequent. The intrapancreatic strictures of chronic pancreatitis are characteristically smooth and tapering on endoscopic retrograde cholangiopancreatography (ERCP), but in some patients, they may have a sharp cut-off and closely resemble the appearance of carcinoma of the pancreas invading the bile duct. The natural history of these intrapancreatic strictures is variable. They may progress and be associated with cholangitis, biliary cirrhosis, common duct stones, or may remain stable for years or regress. Prior pancreaticojejunostomy is not protective against the development of intrapancreatic biliary strictures which may follow in 5-30% of patients, with most authors reporting an incidence of less than 10%. Evaluation of alkaline phosphatase, bilirubin, the presence of jaundice, or the appearance of an intrapancreatic stricture on ERCP is not predictive of whether cholangitis or biliary cirrhosis may or may not develop. The incidence of cholangitis and biliary cirrhosis in patients with intrapancreatic stricture is 9.4% and 7.3%, respectively. Laennec's cirrhosis occurs in a similar number of patients. Operation is indicated in patients with intrapancreatic strictures of the common bile duct in association with chronic pancreatitis in patients developing cholangitis, biliary cirrhosis, common duct stones, progression of the stricture, persistent high elevations of alkaline phosphatase and/or bilirubin for over a month or inability to rule out cancer of the pancreas or periampullary region. The operation of choice is choledochoduodenostomy or Roux-en-Y choledochojejunostomy to bypass the obstructed intrapancreatic portion of the common bile duct. Persistent duodenal obstruction for over 3 or 4 weeks is an indication for gastrojejunostomy. Pain is not a feature of common bile duct obstruction in the absence of cholangitis. In the presence of pain associated with chronic pancreatitis, longitudinal pancreaticojejunostomy is the operation of choice combined with Roux-en-Y choledochojejunostomy. Some of the newer operations, e.g., the Beger and Frey procedures, may make the necessity of a separate operation for biliary decompression superfluous.
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PMID:Treatment of chronic pancreatitis complicated by obstruction of the common bile duct or duodenum. 240 39

Insulin-like growth factor II is secreted primarily by the liver and is reported to be transcribed in many primary hepatocellular carcinoma (PHC) cell lines. We have studied diagnostic significance of serum IGF-II in chronic liver diseases using specific enzyme immunoassay. Serum IGF-II levels (mean +/- SE) were decreased in chronic hepatitis (538 +/- 51 ng/ml; N = 29), liver cirrhosis (427 +/- 45; 50) and PHC (260 +/- 41; 17) compared to controls (830 +/- 49; 57). Serum IGF-II was not different from controls in any of nonhepatic diseases such as diabetes (1032 +/- 97; 19) pancreatic cancer (1413 +/- 282; 8), chronic pancreatitis (999 +/- 126; 17), peptic ulcer (1186 +/- 43; 11), irritable bowel syndrome (1002 +/- 109; 12), gastrointestinal tract cancer (1250 +/- 216; 21) and chronic renal failure (733 +/- 135; 14). In liver diseases serum IGF-II showed a significant correlation with liver function test (negative with retention of indocyanine green and total bile acids; positive with albumin, thrombo-test, and cholinesterase). These results suggest that serum IGF-II reflects a reduced production of IGF-II in the liver and that it can be an index for the residual capacity of liver function.
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PMID:Serum insulin-like growth factor II in chronic liver disease. 253 15

Plasma pancreastatin (PST)-like immunoreactivity in normal subjects and patients with various diseases was estimated by a RIA, using antiserum raised against a synthetic C-terminal peptide of human PST deduced from the sequence of human chromogranin-A. The mean level +/- SEM was 13.2 +/- 0.6 pmol/L in normal subjects, but was significantly higher in patients with chronic renal failure (526.7 +/- 48.5). An immunoreactive form corresponding to a human PST-like sequence [human chromogranin-A-(250-301)] and a larger form were detected by gel filtration of plasma from these patients, suggesting accumulation of the larger molecular form in these patients. A significant increase in PST-like immunoreactivity was also found in patients with liver cirrhosis (20.8 +/- 3.0 pmol/L), but not in patients with noninsulin-dependent diabetes mellitus, chronic pancreatitis, or pancreatic cancer. Elevated levels were found in 16 of the 21 patients with small cell lung carcinoma examined. High levels were also found in 3 of 11 patients with islet cell tumor.
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PMID:Plasma pancreastatin-like immunoreactivity in various diseases. 255 88

Recently a glycolipid antigen known as gastrointestinal cancer antigen (GICA) has been proposed as a new seral marker of gastrointestinal and pancreatic tumours. This antigen is specifically recognised by a monoclonal antibody and biologically and immunologically distinguished by carcinoembryonic antigen (CEA). Out of 438 subjects including: 60 blood donors, 205 patients suffering from digestive tract tumours, subdivided into different organs 21 gastric ca's, 60 colon ca's, 100 pancreatic ca's and 24 liver cancers) 173 subjects with inflammatory gastrointestinal complaints, also divided by organ 18 gastric ulcers, 45 inflamed colons, 60 chronic pancreatitis and 50 liver cirrhosis). GICA and CEA radioimmunoassays were carried out (Sorin GICAK and CEAK) to evaluate sensitivity, specificity and predictive accuracy. Normal threshold levels were set at 30 ng/ml for CEA and 40 mu/ml for GICA. These levels represent the mean + 2DS of levels measured in 260 patients hospitalised for various benign and functional complaints and differ from cancer patient results by the largest amount. All blood donors, whether smokers or not, give lower values than these. Results show GICA gives a lower overall number of false positives than CEA (20% as against 9.6%). GICA diagnostic results were more accurate overall for the entire case sample examined. GICA gave higher percentage positives than CEA for individual tumour types: pancreatic ca (82% v 52%), liver cancer (70.8% v 20.8%) and gastric ca (47.6% v 33%). CEA appears to work better than GICA in the case of colorectal ca's (56% v 41%). Both markers were found to be more sensitive in the presence of tumours with metastases. GICA is the best currently available marker of pancreatic tumours thanks to its sensitivity, specificity and predictive accuracy. Although GICA gave good results in cases of liver cancer, these did not exceed those obtained with alpha foetoprotein. In the other cases of digestive tumours examined, a combination of GICA and CEA investigation techniques appears to be the best non-invasive method currently available for patient follow-up.
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PMID:[Comparison between the gastrointestinal tumor antigen and the carcinoembryonic antigen in diseases of the digestive tract]. 258 13

We report the case of a 60 year old lady suffering from celiac disease and autoimmune cirrhosis who developed exocrine pancreatic insufficiency with canalicular lesions consistent with chronic pancreatitis. Celiac disease is known to be associated with either pancreatic insufficiency or liver disease, but association of all three diseases has not yet been described. We suggest that chronic pancreatitis be added to the list of idiopathic inflammatory pancreatitis of possible autoimmune origin, enabling to explain the pathophysiology of all three disorders with one hypothesis.
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PMID:[Celiac disease, autoimmune cirrhosis, chronic pancreatitis: apropos of a triple association]. 262 89


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