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)

Endoscopic retrograde cholangiopancreatography (ERCP) is essential in the diagnosis of pancreatic disease, jaundice and in post-cholecystectomy syndromes, as well as in cases where cholecystography and i.v. cholangiography fail to explain disturbances that strongly suggest bile duct involvement. Its confirmation of clinically established pancreatic disease is much more positive than that given by scintiscanning and multiple superselective arteriography. Unlike the latter, it also permits the differential diagnosis of chronic pancreatitis, cancer of the pancreas, pseudocysts, etc. and distinguishes medical and surgical pancreatitis (stenosis, proteinaceous calculi, and obstructing pseudocysts). Differential diagnosis of progressive jaundice on clinical grounds or with the aid of ordinary means of examination is sometimes unsatisfactory. ERCP clearly distinguishes medical and surgical forms, so that exploratory laparotomy is not needed in subjects with liver-cell forms. It also shows the nature, site and extent of extrahepatic obstruction, and points to the organic cause in 79% of cases of postcholecystectomy syndrome. Right hypochondrial pain or intermittent jaundice and negative cholecystography and i.v. cholangiography is a further indication, since ERCP will reveal disease of the pancreas or bile ducts (cholelithiasis, choledocholithiasis, sclerosing cholangitis, etc). It is also useful in the diagnosis of cirrhosis, abscess, echinococcus cyst and primary or secondary cancer in cases where needle biopsy and-or arteriography are either contra-indicated or inconclusive.
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PMID:[Diagnostic value of retrograde cholangiopancreatography by transendoscopic route]. 66 74

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.
Pancreas 1990 Sep
PMID:Serum apolipoprotein A-I in alcoholic patients with chronic calcifying pancreatitis. 212 44

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)
Pancreas 1993 Sep
PMID:Is bile salt-dependent lipase concentration in serum of any help in pancreatic cancer diagnosis? 750 10

This study compared diet, type of alcoholism, and smoking in three groups of alcoholic men, with chronic pancreatitis (n = 56), with histological cirrhosis (n = 50), and without pancreatitis or cirrhosis (controls; n = 50) by a multidimensional analysis. Only patients in whom the first symptom of pancreatitis or cirrhosis was present for < 1 year before the interview were included. Patients with pancreatitis consumed more nonalcohol calories than cirrhotics (p < 0.05). The percentage of calories taken as proteins (p < 0.0003) and lipids (p < 0.0001) was higher and the percentage of calories taken as alcohol (p < 0.0003) was lower in patients with pancreatitis than in cirrhotics and control patients. There was no difference among the three groups for total calories/basal energy expenditure ratio, total nonalcohol calories/basal energy expenditure ratio, mineral and vitamin intake, or tobacco consumption. The duration of excessive alcohol consumption and the total alcohol consumption in patients with pancreatitis was similar to that of controls but lower than that of cirrhotics (p < 0.002 and p < 0.05, respectively). Three parameters were found to be independently different in the three groups by discriminant analysis: percentage of calories taken as lipids (p < 0.0001), duration of excessive alcohol consumption (p < 0.002), and percentage of calories taken as proteins (p < 0.08). These three parameters explained 24% of the variance. We conclude that the reasons alcoholic men develop chronic pancreatitis may be explained partly by dietary habits.(ABSTRACT TRUNCATED AT 250 WORDS)
Pancreas 1995 Apr
PMID:A multidimensional case-control study of dietary, alcohol, and tobacco habits in alcoholic men with chronic pancreatitis. 762

The distribution and clinicopathologic features of pancreatic fibrosis were studied histopathologically in 137 autopsy cases of chronic alcohol abuse. Fibrosis was observed in 90 of the cases and was classified as perilobular sclerosis (PS) and intralobular sclerosis (IS). Fibrosis of the PS type was irregular and sometimes patchy and extended into the intralobular area in advanced cases. In some advanced cases, complete replacement of the pancreatic tissue by extensive fibrosis was seen. Fibrosis of the IS type was uniformly distributed. The tissues in some cases showed prominently periacinar fibrosis. In these cases, the pancreatic parenchyma had not been completely replaced by extensive fibrosis. Clinicopathologic comparisons revealed the following results: accompanying liver cirrhosis was greater in the IS than in the PS of fibrosis. However, a higher frequency of protein plugs, pancreatic stones, extensive fibrosis replacement, peripancreatic fibrosis, splenic vein involvement, choledochus involvement, pseudocyst, and ductal hyperplasia was found in the PS type compared to the IS type. In conclusion, the findings on the perilobular and intralobular distribution of fibrosis and differences in various components or accompanying diseases in pancreatic fibrosis suggest that this entity shows two distinct pathologic patterns with differing mechanisms.
Pancreas 1996 May
PMID:Histopathologic study of coexistent pathologic states in pancreatic fibrosis in patients with chronic alcohol abuse: two distinct pathologic fibrosis entities with different mechanisms. 874 Apr 4

The treatment recommendations for intracystic hemorrhage in pancreatic pseudocysts are various. We have used a defined treatment protocol in these difficult cases. The experiences gained are reported here. Patients with clinical signs of ongoing bleeding and with hemorrhagic pancreatic pseudocyst in ultrasonography and computed tomography (CT) were studied with urgent angiography. Patients showing a pseudoaneurysm were treated with immediate embolization and delayed elective surgery whenever candidates for surgery. During a 5-year period 10 patients were treated according to the protocol. Pseudoaneurysm was demonstrated and subsequent embolization performed in six. Angiography was negative in four patients. During the study period two additional patients were treated conservatively without angiography because the bleeding had stopped 2 weeks prior to the referral to our institution. Two patients were electively operated on and the remaining 10 patients were treated conservatively. Fever and elevated transaminases developed in one of the six patients after the embolotherapy. One of the four embolized patients who were not operated on developed pseudocyst infection 4 months after the embolization. One of the 10 conservatively treated patients died (1/10 = 10%; total mortality, 1/12 = 8%) during the follow-up for infection complications of necrotizing pancreatitis 2 months after the initial bleeding. Another conservatively treated patient with negative angiography had recurrent bleeding during the follow-up but could not be operated on due to severe liver cirrhosis. In the remaining eight patients pseudocysts resolved during the 3-month to 3.5-year follow-up as confirmed by CT. The low rates of mortality and rebleeding support a fairly conservative approach for hemorrhagic pancreatic pseudocysts.
Pancreas 1997 Mar
PMID:Intracystic hemorrhage in pancreatic pseudocysts: initial experiences of a treatment protocol. 905 92

The salivary glands are structurally similar to the exocrine pancreas and may be involved in the course of diseases of autoimmune origin (sclerosing cholangitis, ulcerative rectocolitis, primary biliary cirrhosis). For a not-yet-quantified proportion of chronic pancreatitis (CP) cases, a possible autoimmune pathogenesis has been postulated. The aim of the study was to assess the frequency of salivary ductal system abnormalities in patients with CP. Fifty-one patients with CP consecutively admitted to our center were studied (44 men, seven women; mean age, 48.2 +/- 10.8 years). The mean duration of disease was 11.7 years (range, 1-37 years); 44 (86%) of 51 patients had pancreatic calcifications, 25 (49%) of 51 diabetes, 25 (52%) of 48 steatorrhea, and 32 (63%) of 51 underwent pancreatic surgery. As a control group, we studied 10 patients of whom four with liver cirrhosis (three alcoholic and one posthepatitis; three men, one woman; mean age, 57 +/- 12.5 years), and six with temporomandibular pain (five men and one woman; mean age, 42 +/- 10.3 years). The patients were given parotid sialography, the findings being read by two independent observers. In two CP patients, parotid sialography was unsuccessful. Fifteen (31 %) of 49 patients and none of the 10 control patients exhibited abnormalities of the glandular ducts compatible with chronic inflammation of the salivary ducts (p = 0.039). None of the CP patients had salivary intraductal calcifications. Findings of parotid ductal abnormalities are frequent in the course of CP and may indicate a common pathogenetic mechanism, even of an immune type.
Pancreas 1999 Jul
PMID:Salivary gland involvement in patients with chronic pancreatitis. 1041 89

We report about our experience with combined en-bloc liver-pancreas transplantation in 14 patients with liver cirrhosis and insulin dependent type 2 diabetes mellitus. Exocrine drainage was achieved by duodeno-duodenostomy. Median posttransplant follow-up is currently 92.5 months. All patients were rendered independent from insulin therapy shortly after transplantation. Levels of glycosylated hemoglobin normalized in all recipients. Mean fasting C-peptide values increased from pretransplant 7.0+/-1.7 ng/mL to 10.5+/-2.9 ng/mL 3 months posttransplantation (P<0.001). One recipient (7.1%) developed recurrent exogenous insulin dependence 7 years after transplantation. Pancreas allograft rejection was confirmed by endoscopic biopsy of donor duodenum mucosa in two patients (14.3%). Calculated 5- and 7-year survival is currently at 64.3% and 64.3%, respectively. Our results indicate that combined en-bloc liver-pancreas transplantation using duodeno-duodenostomy is technically feasible and leads to excellent long-term control of glucose metabolism in patients with liver cirrhosis and insulin-dependent type 2 diabetes.
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PMID:Combined en-bloc liver-pancreas transplantation in patients with liver cirrhosis and insulin-dependent type 2 diabetes mellitus. 1930 91

Kidney-pancreas transplantation is a valid therapeutic option for patients with insulin-dependent diabetes mellitus. However, vascular complications associated with pancreas transplantation are not uncommon. Herein we have reported a 32-year-old woman with a history of insulin-dependent diabetes mellitus and celiac disease. She underwent liver transplantation for acute hepatitis. After 7 years, the patient developed end-stage kidney disease beginning hemodialysis and being listed for a kidney-pancreas transplantation, which was successfully performed when she was 29 years old with enteric diversion (Roux intestinal loop reconstruction). Five years after kidney-pancreas transplantation, she was admitted to our hospital with serious intestinal bleeding and poor liver function. The ultrasound showed a pattern like a arteriovenous fistula near the head of the pancreas. Computed Tomography was not diagnostic; an arteriogram showed the presence of a mesenteric varix and a mesenteric-caval shunt through the duodenum of the pancreatic graft. The liver biopsy and portal pressure gradient showed portal hypertension and liver cirrhosis. To obtain time a waiting a new liver, the patient underwent percutaneous embolization of the mesenteric varix through jugular access. The procedure was uneventful. The patient was successfully transplanted 2 months later. Pancreas function was always satisfactory.
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PMID:Percutaneous embolization of periduodenal varix due to portal hypertension in a patient with kidney-pancreas transplantation: a case report. 2069 34