Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030305 (pancreatitis)
 16,014 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 33-year-old man, vaccinated against hepatitis B virus, working in an hemodialysis unit, pricked himself with a needle used in a patient. Four weeks later he developed acute hepatitis along with acute pancreatitis. The pancreatitis resolved, but the liver disease ran a chronic course. The diagnosis of hepatitis non-A-non-B (NANB) was made on the following criteria: (a) epidemiologic circumstances, (b) exclusion of other causes of acute and/or chronic liver disease, (c) chronic indolent course, and (d) compatible histological features. The diagnosis of acute pancreatitis was made with clinical, biological, and radiological data. We believe that the pancreatitis was related to the NANB viral infection, as they began simultaneously and other causes of pancreatitis were eliminated. Such an association has been reported mainly with hepatitis B and exceptionally with hepatitis A. It has also been observed in the course of fulminant NANB viral hepatitis, but we believe this to be the first case associated with a benign form of NANB.
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PMID:Acute pancreatitis associated with non-A-non-B hepatitis. Report of a case. 210 6

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

The relation between various aspects of medical history, selected indicator foods and the risk of pancreatic cancer was analyzed in a hospital-based case-control study conducted in Northern Italy on 247 patients with cancer of the pancreas, and 1,089 controls in hospitals for acute, nonneoplastic or digestive conditions. There was a significant association with history of pancreatitis (relative risk, RR 3.2, 95% confidence interval = 1.3-7.9), which was however reduced when the condition was first diagnosed at least 5 years previously. The point estimates were slightly, but not significantly, above unity for diabetes (RR = 1.5), gastrectomy (RR = 1.1) and cholelithiasis (RR = 1.3), and no association was found with liver disease or drug allergy. In relation to diet, there was some tendency for the risk to decrease with more frequent fruit consumption, but the results were largely inconsistent in relation to various indicators of meat, animal protein or fat intake. Although no important associations were found in this study with various aspects of medical history or diet indicators and pancreatic cancer risk, on account of the size of the dataset and the statistical power, this study contributes usefully to the debate on a common cancer whose causes are still largely undefined.
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PMID:Medical history, diet and pancreatic cancer. 224 64

One hundred five patients receiving concurrent aminoglycoside and vancomycin therapy of at least 5 days' duration were retrospectively reviewed for development of nephrotoxicity. All had their vancomycin and aminoglycoside serum concentrations controlled by a clinical pharmacokinetics service. Nephrotoxicity occurred in 28 (27%) of the patients. Twenty-two of the 28 had other factors that are known to contribute to renal failure (amphotericin B therapy, sepsis, liver disease, obstructive uropathy, pancreatitis, anesthesia). The remaining six developed nephrotoxicity without other known contributing factors. Logistic regression analysis revealed associations between nephrotoxicity and age, sex, aminoglycoside trough and vancomycin peak and trough serum concentrations, length of aminoglycoside and vancomycin therapy, concurrent amphotericin B therapy, liver disease, neutropenia, and peritonitis (p less than 0.05). In addition to factors previously reported, this study found that neutropenia and peritonitis are associated with an increased risk of nephrotoxicity. Patients with one or more risk factors warrant close monitoring of renal function as well as vancomycin and aminoglycoside serum concentrations.
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PMID:Risk of nephrotoxicity with combination vancomycin-aminoglycoside antibiotic therapy. 228 56

Elevated values of pancreatic-type amylase activity in serum were found in 59% of patients with liver cirrhosis not complicated with renal failure, in 67% of patients with chronic renal failure not complicated with hepatopathy and in 95% of patients with chronic renal failure complicated with hepatopathy. In all the three groups, a significant positive correlation was found between the pancreatic-type amylase and intestinal isoenzyme of serum alkaline phosphatase which is an asialoglycoprotein. However, in pancreatitis a prevalence of an increase in pancreatic-type amylase with respect to intestinal alkaline phosphatase was found. A multivariate analysis showed that in chronic renal failure not complicated with hepatopathy, and in chronic renal failure complicated with chronic liver disease, the changes in calcium homeostasis and also the liver disorder, respectively, contribute significantly to the above-normal values for pancreatic-type amylase.
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PMID:Role of secondary hyperparathyroidism and liver function in hyperamylasemia in chronic renal failure. 241 93

Since 1981, when the liver transplantation program was initiated at the University of Pittsburgh, we have been impressed with the prevalence of pancreatitis occurring following liver transplantation in patients transplanted for hepatitis B-related liver disease. To either confirm this clinical impression or refute it, the records of the 27 HbsAg+ patients and those of an additional 24 HbsAg- but HbcAb and/or HbsAb+ patients who underwent orthotopic liver transplantation were reviewed to determine the prevalence of clinical pancreatitis and hyperamylasemia (biochemical pancreatitis) following liver transplantation (OLTx). Post-OLTx hyperamylasemia occurred significantly more frequently in HbsAg+ patients (6/27) than it did in the HbsAg- patients (0/24) (P less than 0.05). More importantly, clinical pancreatitis occurred in 14% (4/27) of the HbsAg+ patients and 0% (0/24) of the HbsAg- patients. Interestingly, in each case, the pancreatitis was associated with the occurrence of acute hepatitis B infection of the allograft. Based upon these data, we conclude that pancreatitis occurring after liver transplantation is more common in patients transplanted for active viral liver disease caused by hepatitis B than in those with inactive viral liver disease. These observations suggest that pancreatitis occurring in, at least some cases following liver transplantation for viral liver disease, may result from hepatitis B virus infection of the pancreas.
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PMID:Pancreatitis following liver transplantation. 245 20

Some patients with extrahepatic biliary occlusion present high levels of serum aminotransferases indicating parenchymatous liver disease. The levels, usually in the range of 400-500 U/l, may sometimes exceed 1,000 U/l. Most of these patients have stones in the bile ducts, but the causes may occasionally be pancreatic tumours and pancreatitis. Typically the maximum enzyme levels are reached within 1-2 days, followed by a rapid fall--whether the gallstones have passed or not. The alkaline phophatase levels are initially normal or slightly elevated, usually increasing slowly to about twice the upper reference level. The pathogenesis of this rapid elevation of the aminotransferases has yet not been fully elucidated. However, the main mechanisms are probably increased permeability of the hepatocyte membrane caused by elevated pressure in the bile ducts, combined with a direct toxic effect of retinated bile acids. Increased enzyme synthesis may also be a contributory factor. Further knowledge of this not unusual enzyme pattern in acute (and sometimes also chronic) biliary obstruction will help to establish a correct diagnosis at an early stage of the disease, and thus avoid a need for invasive, potentially dangerous investigations.
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PMID:[Biliary duct obstruction presenting with laboratory levels indicating liver cell damage]. 247 42

We report a patient who was admitted to hospital with acute pancreatitis but who also had malignant phase hypertension. Whilst his alcohol intake was high, there was no objective evidence of alcoholic liver disease and no other underlying cause for pancreatitis was found. The pancreatitis may therefore have been due to pancreatic infarctions associated with fibrinoid necrosis. In all patients with acute pancreatitis, the diagnosis of malignant hypertension should be considered.
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PMID:Malignant hypertension presenting as acute pancreatitis. 260 24

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

Between 1979 and 1984, 21 male cirrhotic patients with advanced liver disease, cholecystitis, and jaundice were seen. Eight patients had persistent symptoms of acute cholecystitis despite intense symptoms of acute cholecystitis despite intense medical management. Of these patients, five underwent cholecystostomy and survived. The other three patients had cholecystectomy and one died. Thirteen patients presented with jaundice. Twelve patients underwent endoscopic retrograde cholangiography which revealed gallbladder stones in four but no stones in the common bile duct. They did not undergo further surgical procedures. One patient presented with jaundice, cholangitis, and pancreatitis was found to have stones in the common bile duct and underwent endoscopic sphincterotomy with removal of multiple small, pigmented stones. This patient died from sepsis and renal failure 37 days after sphincterotomy. Endoscopic retrograde cholangiography was unsuccessful in four patients who later underwent percutaneous transhepatic cholangiography which revealed stones in one and cirrhotic ductal changes in three. The remaining jaundiced patient underwent cholecystectomy and common bile duct exploration which revealed no ductal stones. This patient died 21 days after operation from sepsis and multiple organ system failure. Three of five patients with gallstones on endoscopic retrograde cholangiography or percutaneous transhepatic cholangiography died, but none of the deaths were due to biliary tract disease. At last follow-up the two surviving patients were asymptomatic. The overall mortality rate was 14 percent (3 of 21 patients). Cholecystostomy in cirrhotic patients with advanced liver disease and acute cholecystitis is associated with minimal mortality and morbidity. Cirrhotic patients with jaundice are probably best evaluated initially by endoscopic retrograde cholangiopancreatography which is safe, diagnostic, and sometimes therapeutic.
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PMID:Therapeutic options for biliary tract disease in advanced cirrhosis. 334 96


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