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)

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

The biliary complications of pancreatitis include cholestasis, secondary biliary cirrhosis, cholangitis, and pseudocyst or fistula affecting the hepatobiliary system. Of these, the most relevant for radiologists is cholestasis caused by biliary duct stenosis in an inflamed pancreatic head. Radiologic assessment of these complications is based on judicious use of ultrasound, computed tomography, and direct cholangiography. The typical imaging finding of common bile duct stenosis due to chronic pancreatitis is gradual tapered narrowing of the intrapancreatic common bile duct, which can be portrayed by carefully accomplished computed tomography, and ultrasound as well as cholangiography. When combined with clinical assessment, imaging tests can help determine strategies for treatment, which include traditional operations as well as transhepatic, endoscopic, or percutaneous interventions.
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PMID:Biliary complications of pancreatitis. 264 80

A case of multiple myeloma (Bence Jones, lambda) associated with alcoholic liver cirrhosis is reported. A 56-year-old Japanese male died of hepatic failure and hypercalcemia. Autopsy revealed alcoholic liver cirrhosis and plasma cell myeloma. Immunoelectrophoretic analysis of his reserved serum disclosed the presence of M component of lambda Bence Jones protein. IgA and lambda light chain were demonstrated in the cytoplasm of the myeloma cells. Complications such as generalized amyloidosis, metastatic calcification, myeloma kidney and hemorrhagic pancreatitis were noted. The coexistence of multiple myeloma and liver cirrhosis has rarely been reported. On the basis of a review of the reported cases, a possible association between both diseases was discussed.
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PMID:Multiple myeloma in alcoholic liver cirrhosis. 265 75

Cholestatic syndromes present symptomatically with pruritus and biochemically either with elevated levels of serum bile acid as an early manifestation of hepatocellular disease or with elevated levels of serum alkaline phosphatase if the disease originates in the biliary tree. Slow progression to cirrhosis occurs, with recurrent cholangitis and/or pancreatitis as the major problems if the obstruction is in the larger duct system. Maintenance of nutrition and relief of pruritus are important supportive measures. Colchicine and ursodeoxycholic acid administered orally have been proposed as useful therapies for delaying the progression to cirrhosis. Liver transplantation has proven successful in those patients in whom spontaneous remission does not occur.
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PMID:Cholestatic liver disease and its management. 265 62

The pathogenesis and diagnosis of cirrhotic ascites are reviewed, and the treatment options are described, focusing on pharmacologic management. The major theories on the pathogenesis of cirrhotic ascites are the underfill and overflow theories. The underfill theory states that ascites formation results in decreased plasma volume leading to renal sodium and water retention. The overflow theory states that the initial event in ascites formation is renal sodium retention. Evidence suggests that the formation of ascites is a continuum involving both overflow (early) and underfill (late) mechanisms. Although the most frequent cause of ascites is hepatic cirrhosis, analysis of the ascitic fluid is important to exclude other causes (e.g., neoplasm, peritonitis, pancreatitis). Patients who do not respond to treatment with sodium restriction and bed rest require diuretic therapy. Spironolactone is the agent of choice for treatment of the nonazotemic patient with cirrhotic ascites. Combination therapy with spironolactone and furosemide or spironolactone and metolazone may be used in those patients who do not respond to spironolactone. Patients with impaired renal function should not be treated with spironolactone because of the risk of hyperkalemia. Paracentesis with albumin replacement has been used successfully for treatment of patients with tense cirrhotic ascites. Initial management of cirrhotic ascites is conservative, with sodium restriction and bed rest. Spironolactone is a good first-choice drug for treatment of ascites. Daily weight, serum electrolytes, and renal function should be monitored to assess the effectiveness and potential adverse effects of diuretic therapy.
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PMID:Management of cirrhotic ascites. 267 16

In order to evaluate the effects of chronic alcohol consumption on pancreas morphology we reviewed the autopsy data of 530 patients: 148 with liver alcoholic cirrhosis (group I), 39 with non alcoholic cirrhosis (group II), 47 autopsies of chronic alcohol drinkers without liver cirrhosis (group III) and 296 non alcoholic patients with normal liver, age and sex-matched with group I (group IV). In the control group (group IV) lipomatosis and intralobular fibrosis were common (57 percent and 40 percent) and increased with age. The prevalence of five elementary lesions (protein plug, dilatation of duct, epithelial atrophy, canalicular regression and perilobular fibrosis) and of one pathologic diagnosis (diffuse fibrosing pancreatitis) were higher in group I than in group IV. Duct lesions (protein plugs, canalicular regression and epithelial atrophy) were also significantly higher in drinkers without cirrhosis (group III) than in group IV. Chronic calcifying pancreatitis was rare (2 cases in group I). Thirty-six cases were classified as diffuse fibrosing pancreatitis. This constituted an homogeneous histopathologic group, significantly more frequent in the group of alcoholic cirrhosis, and was always discovered incidentally at autopsy. Because diffuse fibrosing pancreatitis might easily be confused with the morphological changes of chronic calcifying pancreatitis, we suggest to include this histopathologic entity into the Marseille's classification of pancreatitis.
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PMID:Diffuse fibrosis of the pancreas: a peculiar pattern of pancreatitis in alcoholic cirrhosis. 275 5

Sixty patients with chronic alcohol-induced pancreatitis with endoscopic retrograde cholangiopancreatography evidence of common bile duct stenosis were studied to determine the clinical spectrum and natural history of this complication, as well as the indications for biliary bypass. In 17% of patients, common bile duct stenosis (CBDS) was an incidental finding at ERCP, while in the remaining cases pain and jaundice were the predominant symptoms in 35% and 48%, respectively. Biliary drainage was performed in 38% of patients for persistent or recurrent jaundice, cholangitis, and while undergoing pancreatic duct or cyst drainage procedures for pain. The benign nature of CBDS in chronic alcohol-induced pancreatitis (CAIP) in patients without persistent jaundice is emphasized. In particular, no histologically proved cases of secondary biliary cirrhosis were noted. The majority of patients with CBDS due to CAIP may be safely managed without biliary bypass but require close follow-up.
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PMID:The spectrum and natural history of common bile duct stenosis in chronic alcohol-induced pancreatitis. 281 30

Alcohol sales in Stockholm County decreased by 18 per cent from 1976 to 1981. The socioeconomic status of inpatients treated for alcohol psychosis, alcoholism, alcohol intoxication, liver cirrhosis, and pancreatitis was studied by linking data from the National Housing and Population Censuses in 1975 and 1980 with the inpatient care registers for 1976 and 1981. In both years, all rates were highest for people outside the labor market and lowest among white collar employees. The employment rate for those aged 25-44 years and treated in 1981 for alcohol psychosis, alcoholism, and alcohol intoxication--already low in 1975--had drifted further downward by 1980. Total rates of inpatient treatment for alcohol-related diagnoses generally declined but the gap between blue collar workers and white collar workers widened. We conclude that the goal for national alcohol policy, suggested by the WHO--a reduction of per capita consumption--should be combined with additional measures that will reach all social groups.
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PMID:Changes in alcohol-related inpatient care in Stockholm County in relation to socioeconomic status during a period of decline in alcohol consumption. 276 19

Infection with 100 Opisthorchis viverrini (OP) metacercariae prior to two injections of dihydroxy-di-n-propyl nitrosamine (DHPN) (1000 mg/kg body weight) brought about significant enhancement of resultant preneoplastic lesion development in Syrian hamster liver and pancreas tissue. Thus combined treatment with carcinogen and parasite was associated with pancreatic atypical (dysplastic) foci, hepatocellular nodules, cholangiofibrosis and cholangiocarcinomas. No such lesions were observed in carcinogen alone, parasite alone or untreated control groups. In addition, parasite induced hyperplastic gall bladder epithelium was found to include areas of putative preneoplastic cells only in the DHPN-OP combined group. The results strongly suggest that pancreatitis and biliary cirrhosis associated with liver fluke infestation are responsible for the observed enhancement of carcinogenesis, and that the resultant increased proliferation plays a major role in tumorigenesis.
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PMID:Enhancement of DHPN induced hepatocellular, cholangiocellular and pancreatic carcinogenesis by Opisthorchis viverrini infestation in Syrian golden hamsters. 283 5

Somatostatin is present in the gastrointestinal tract in appreciable amounts. The highest concentrations of the polypeptide are found in the stomach, the upper small intestine, and the pancreas. Within the gastrointestinal tract, somatostatin inhibits various functions, including endocrine and exocrine secretion, motility, blood flow, absorption, and growth. The polypeptide regulates these functions by endocrine, paracrine, neurocrine or luminal mechanisms. Abnormalities of endogenous somatostatin have been implicated in several gastrointestinal disorders, including the somatostatinoma syndrome, antroduodenal D-cell hyperplasia, peptic ulcer, obesity, and liver cirrhosis. Because of its potent inhibitory effects, somatostatin or somatostatin-analogues have been used as therapeutic agents in various clinical conditions, such as upper gastrointestinal haemorrhage, endocrine pancreatic tumours, gastrointestinal and pancreatic fistulas, pancreatitis, secretory diarrhoea, and dumping syndrome. The recent availability of the synthetic long-acting somatostatin-analogue SMS 201-995 (Sandostatin) has greatly facilitated the therapeutical application of somatostatin-polypeptides.
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PMID:Clinical and pathophysiological aspects of somatostatin and the gastrointestinal tract. 289 34


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