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)

Controversial data have been reported on gastric acid secretion in patients with chronic pancreatitis. Moreover, studies on gastroduodenal morphological changes in patients with this disease and with other alcohol-related conditions have given different results. Basal and penta-gastrin-stimulated gastric secretion, histological changes of gastric and duodenal mucosa, and basal and meal-stimulated gastrin were measured in 21 patients with chronic alcoholic pancreatitis and in the following pair-matched groups: 21 chronic alcoholics and 21 control subjects (nonulcer dyspepsia), and in 19 patients with proven liver cirrhosis of alcoholic origin. No patient suffered from peptic ulcers. Moreover, gastric secretion was also measured in 51 patients with proven duodenal ulcers and in 34 healthy subjects. Basal acid output in patients with chronic pancreatitis was significantly higher (p less than 0.05) than in the other groups, except for the patients with duodenal ulcers. Peak acid output values in patient with chronic pancreatitis were similar to those measured in patients with duodenal ulcer, and they were higher than in the healthy subject group and in patients with liver cirrhosis, but statistical significance was not attained for patients with nonulcer dyspepsia. An increased frequency of duodenitis was found in patients with chronic pancreatitis, whereas an increased frequency of gastric metaplasia in the duodenal bulb was observed in all the patients with alcohol-related conditions considered. No relevant differences among the considered groups were found relating to gastric histological changes. Basal and meal-stimulated gastrin were similar in all the studied groups. This study suggests that in patients with chronic pancreatitis there is increased gastric secretion and probably an increased capacity for secretion of acid. Moreover, in patients with chronic pancreatitis, duodenitis seems to be frequent, but it probably is not directly related to chronic alcohol consumption.
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PMID:Gastric secretion, gastroduodenal histological changes, and serum gastrin in chronic alcoholic pancreatitis. 707 77

Fibrosis of chronic pancreatitis can cause obstructive jaundice by compressing the intrapancreatic portion of the common bile duct. The frequency and clinical manifestations of common bile duct stricture from symptomatic chronic pancreatitis have been evaluated in 26 patients undergoing lateral pancreaticojejunostomy for intractable pain between 1974 and 1980. Four patients (15%) had a stricture with partial obstruction of the common duct in addition to pancreatic duct obstruction. Three of the four strictures were identified prior to operation by ERCP. The fourth developed biliary obstruction six months after pancreaticojejunostomy. Slight elevation of alkaline phosphatase was common and occurred in 12 of 22 patients with chronic pancreatitis without biliary obstruction. Alkaline phosphatase was elevated greater than four times normal in three of the four patients with a biliary stricture. Elevation of total and direct serum bilirubin occurred only in patients with stricture of the distal common duct. A waxing and waning picture of jaundice was seen in these four patients. When a fixed smooth stricture of the common duct is demonstrated in a patient with symptomatic chronic pancreatitis, drainage of the biliary tree should be combined with pancreatic duct drainage in order to prevent cholangitis, biliary cirrhosis, diagnostic confusion with pancreatic carcinoma, and persistence of pain.
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PMID:common duct obstruction in patients with intractable pain of chronic pancreatitis. 711 5

Alcohol-induced chronic pancreatitis involving the head of pancreas may have profound effects on the hepatobiliary system. The natural history, complications, and management of the syndrome are presented, using selected cases to emphasize important features. Chronic pancreatitis can cause mechanical obstruction to both the distal common bile duct and the proximal pancreatic duct. In the common bile duct this will result in proximal dilatation above the stenosis with bile stasis. Possible sequelae are ascending cholangitis, cholecystitis, biliary calculi formation, and secondary biliary cirrhosis. The mechanical effects of stricture of the proximal pancreatic duct may exacerbate pancreatic dysfunction. The clinicopathological spectrum of chronic pancreatitis with biliary obstruction encompasses three clinical types--"transient," "recurrent", and "persistent." The widespread effects of the syndrome are evident from the involvement of pancreas, proximal pancreatic duct, papilla of Vater, liver, peripheral biliary tree, common bile duct, gallbladder, and reticuloendothelial system. Essential to management is surgery which should be considered when there is objective evidence of obstruction to the common bile duct. Choledochoduodenostomy is the preferred type of operation. If dilatation is mild and jaundice transient, conservative therapy with careful observation is advocated.
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PMID:Chronic pancreatitis and the hepatobiliary system. 713 42

Ethanol is easily absorbed from the intestine and diffuses quickly throughout body water. The bulk of ethanol is metabolized in the liver, where alcohol dehydrogenase, a complex mixture of isoenzymes, oxidizes ethanol to acetaldehyde. Ethanol abuse produces functional and structural changes in the gastrointestinal tract, such as in the stomach, small intestine, liver, and pancreas. Accumulating evidence suggests direct toxicity of ethanol and possibly of acetaldehyde. Fatty liver, alcoholic hepatitis, liver cirrhosis, acute and chronic gastritis, deranged structure and function of the small intestine, acute and chronic pancreatitis, and pancreatic lithiasis are some of the sequelae of ethanol abuse. Recent investigations have enhanced our understanding of the functional and structural changes of the gastrointestinal tract produced by the abuse of ethanol.
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PMID:Ethanol, the liver, and the gastrointestinal tract. 719 92

A syndrome of distal common bile duct obstruction secondary to the fibrotic effects of chronic pancreatitis has been recognized for some time. A group of ten characteristic patients, seven of whom have undergone surgery, is discussed. The diagnostic techniques and surgical procedures are presented, and the results are analyzed. Three patients with the syndrome were not operated upon and one improved spontaneously. The typical patient was a male alcoholic, average age 48 years, with a history of chronic, relapsing pancreatitis and abdominal pain. The most consistently abnormal laboratory value is a markedly elevated alkaline phosphates level. Endoscopic retrograde pancreaticocholangiography and transhepatic cholangiography are the most useful diagnostic procedures. Fifteen per cent of the most useful diagnostic procedures. Fifteen per cent of the patients operated upon required emergent surgery for acute cholangitis and sepsis. Another 29 per cent required prompt intervention for progressive hepatic failure secondary to biliary cirrhosis. The authors advocate an aggressive approach to establish biliary drainage in the presence of acute cholangitis or biliary cirrhosis. If a dilated pancreatic duct can be demonstrated and abdominal pain is the principal problem a direct procedure on the pancreas is needed.
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PMID:Biliary obstruction in chronic pancreatitis: indications for surgical intervention. 724 5

The liver histopathology in 40 liver biopsies from 24 patients with verified chronic common bile duct stenosis due to chronic alcoholic pancreatitis has been reviewed code-blinded. This represents an 8% prevalence of this complication in approximately 300 patients with alcoholic pancreatitis screened biochemically for alkaline phosphatase greater than two-fold for less than 1 month. The majority were anicteric with no symptoms other than from acute exacerbations of chronic pancreatitis. Biliary obstructive liver histopathology of varying severity was diagnosed in 19 patients (79%), seven of whom (29%) had secondary biliary cirrhosis. In 3 of these 7 cases, progression to biliary cirrhosis was documented with sequential biopsies. The remainder demonstrated this histologic picture when first diagnosed, supporting this insidious nature of this process. Stromal edema of the portal tracts, increased portal connective tissue, and marked proliferation of interlobular bile ducts and ductules were the most striking histologic features. Histologic cholangitis, although frequent, was generally mild or absent, reflecting the incomplete nature of the duct obstruction. Features of alcoholic liver disease were observed in only two cases. The results indicate that (1) chronic alcoholic pancreatitis with incomplete duct obstruction frequently causes secondary biliary cirrhosis, (2) significant alcoholic liver disease very infrequently coexists with persistent common bile duct stricture from alcoholic pancreatitis, and (3) surgical biliary decompression should be considered in any patient with documented persistent common bile duct stenosis from alcoholic pancreatitis.
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PMID:Liver histopathology in chronic common bile duct stenosis due to chronic alcoholic pancreatitis. 728 90

Alcoholism in frequently associated to inflammatory lesions of the pancreas. The changes involved have been duly depicted in necropsis studies. In this paper we have evaluated the association of pancreatic changes in patients undergoing hepatic cirrhosis due to alcoholism by means of endoscopic pancreatography. Forty four patients were studied by endoscopic pancreatography, 25 males and 19 females. Their ages varied between 22 and 81 year old. Three groups were formed; the first one by 19 patients with hepatic cirrhosis due alcoholism; the second group by 7 patients with hepatic cirrhosis in whom no alcoholic antecedents could be ascertained; the third group was formed by 18 non alcoholic, non cirrhotic individuals. Pancreatography was performed by means of a JF-B3 duodenoscope. In 12 out of 19 patients with alcoholic hepatic cirrhosis, the pancreatography showed changes such as irregularities in the ducts, sacular formations, retarded emptying with partial filling, shortening and stenosis of the ducts, changes usually present in patients with chronic pancreatitis. Both in groups II and III no pathologic changes were found in pancreatography. From the radiologic standpoint alone one cannot eestablish the diagnosis of chronic pancreatitis, although we consider that the usefulness of the pancreatography is that of making quite apparent the above said alterations in the alcoholic cirrhotics patients and stablish the adequate therapeutic conduct.
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PMID:[Pancreatic changes in patients with liver cirrhosis caused by alcoholism]. 733 64

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 diagnostic value of bile salt-dependent lipase for pancreatic diseases was tested in sera of 187 patients. Of these patients, 76 suffered from pancreatic carcinoma, 43 from nonmalignant liver diseases (cirrhosis and chronic hepatitis), 18 from acute pancreatitis, and 20 from chronic pancreatitis. The remaining subjects were controls without pancreatic pathology. Bile salt-dependent lipase was determined by a sandwich enzyme-linked immunosorbent assay using polyclonal antibodies. Amylase and CA 19-9 antigen were also determined. In sera from control patients, the mean level of bile salt-dependent lipase was 1.5 micrograms/L. This level is quite similar to that of patients with benign liver diseases (1.1 micrograms/L) and with chronic pancreatitis (1.4 micrograms/L), but it was raised to 3.5 micrograms/L in patients with acute pancreatitis and decreased to 0.5 microgram/L in subjects with pancreatic adenocarcinoma. Thirty percent of control subjects and 73% of cancer patients had a bile salt-dependent lipase serum level below the cutoff value of 0.5 microgram/L. In acute pancreatitis, 11 of 16 subjects had levels above 1.5 micrograms/L. Amylase level largely increased in acute pancreatitis but was normal in all other groups. Concerning CA 19-9 antigen, 65% of control patients and > 80% of patients with nonmalignant pancreatic or liver diseases had normal levels. In sera from cancer patients, 80% presented with high levels. Accordingly, 36 of 38 patients with pancreatic cancer had either low serum levels of bile salt-dependent lipase (< 0.5 microgram/L) or high values of CA 19-9 antigen (> 37 U/ml; sensitivity 95%).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Is bile salt-dependent lipase concentration in serum of any help in pancreatic cancer diagnosis? 750 10

The clinical significance of the measurement of c-erbB-2 oncogene product was evaluated. The subjects consisted of 404 patients, including 248 with cancer of the digestive organs and 128 with benign digestive diseases. Serum c-erbB-2 protein levels were measured by sandwich immunoenzyme assay. The positive rates of c-erbB-2 protein, at a cut-off value of 17.0 U/ml, were, for cancers: hepatocellular carcinoma 61.6%, biliary tract cancer 54.8%, pancreatic cancer 25.0%, esophageal cancer 33.3%, gastric cancer 16.9%, and colorectal cancer 5.0%. For benign digestive diseases, the rates were: liver cirrhosis 63.3%, chronic hepatitis 43.2%, acute hepatitis 42.9%, other liver diseases 42.8%, cholelithiasis 30.0%, and chronic pancreatitis 0%. Serum c-erbB-2 protein levels were significantly correlated with the markers of hepatic functional reserve, the indocyanine green retention rate and the hepaplastin test. These findings suggest that serum c-erbB-2 protein levels are greatly influenced by liver dysfunction and that their clinical usefulness as a serum tumor marker is questionable.
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PMID:Serum levels of c-erbB-2 protein in digestive diseases. 752 80


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