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 68-year-old man without previous hepatobiliary or pancreatic disease was admitted after five attacks of nausea, vomiting, abdominal pain and high fever. Laboratory investigations indicated cholestatic liver disease and pancreatitis. For 1.5 years the patient had occasionally been taking a non-steroidal anti-inflammatory drug, sulindac (clinoril, MSD, New York), for osteoarthritis. On suspicion of a drug-associated disease, a rechallenge experiment was performed with sulindac. Five hours after drug administration symptoms recurred. There was a pronounced increase in serum alkaline phosphatase and amylase. A liver biopsy 3 d later showed portal tract inflammatory infiltration and abnormal interlobular bile ducts with degeneration and necrosis of the epithelium and neutrophilic infiltration of the ducts. Sulindac-induced cholangitis has not been described previously. The pathogenetic mechanism is considered to be an immunoallergic idiosyncratic reaction to the active metabolite of sulindac absorbed by the bile duct epithelium. The lesion is apparently reversible.
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PMID:Acute cholangitis and pancreatitis associated with sulindac (clinoril). 362 32

Spontaneous bacterial peritonitis (SBP), a fascinating disease that had been reported perhaps 50 times in varying guises over the preceding century, suddenly burst forth in the 1960s and was recognized in clusters of cases almost simultaneously in Paris, London, and West Haven, Connecticut. The spectrum of the disease has broadened. Initially, it was associated almost exclusively with alcoholic cirrhosis, but it has now been found in association with posthepatitic cirrhosis, cryptogenic cirrhosis, chronic active liver disease, and, occasionally, in biliary cirrhosis and cardiac cirrhosis. Recently, it has been reported in alcoholic hepatitis and acute viral hepatitis. It occurs occasionally in malignant ascites and in pancreatitis in the absence of cirrhosis. It is surprisingly common in disseminated lupus, in which it occurs relatively more commonly than in alcoholic cirrhosis. A similar syndrome, primary peritonitis, occurs frequently in children with nephrotic ascites. The clinical pattern of SBP has broadened. Initially it consisted of abdominal pain, fever, rebound tenderness, hypoactive bowel sounds, hypotension, encephalopathy, and cloudy ascites with large numbers of polymorphonuclear leukocytes in ascitic fluid. Each and every symptom, sign, and laboratory abnormality may be absent; indeed, the syndrome can be completely silent. Initially, the causative bacteria appeared to be almost exclusively enteric, but now the list of bacteria isolated in cases of SBP looks like a bacteriology textbook. Anaerobes are rare. Multiple organisms usually suggest nonspontaneous origin such as perforation or vasopressin induction. The differentiation between spontaneous and nonspontaneous bacterial peritonitis is crucial in the differential diagnosis. The great majority of cases of SBP develop in the hospital, 80% more than one week after admission. It is therefore a nosocomial disease that may be precipitated by procedure-induced bacteremia, gastrointestinal bleeding, or diarrhea, and it tends to occur in patients with low ascitic fluid protein (complement) concentrations and severe portal-systemic shunting.
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PMID:Spontaneous bacterial peritonitis: variant syndromes. 368 33

Isolated obstruction of the splenic vein leads to segmental portal hypertension, which is a rare form of extrahepatic portal hypertension, but it is important to diagnose, since it can be cured by splenectomy. In a review of the English literature, 209 patients with isolated splenic vein obstruction were found. Pancreatitis caused 65% of the cases and pancreatic neoplasms 18%, whereas the rest was caused by various other diseases. Seventy-two per cent of the patients bled from gastroesophageal varices, and most often the bleeding came from isolated gastric varices. The spleen was enlarged in 71% of the patients. A correct diagnosis in connection with the first episode of bleeding was made in only 49%; 22% were operated on because of gastrointestinal bleeding, but the cause of bleeding was not found. The diagnosis should be suspected in patients with gastroesophageal varices, but without signs of a liver disease, especially if isolated gastric varices are found. The diagnosis is confirmed by portography.
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PMID:Segmental portal hypertension. 372 85

Pathogenetic associations between benign hepatic tumours and liver damage were studied in an autopsy series of 91 males with high incidence of alcoholism. Information on the consumption of alcohol was obtained by interviewing a family member or a close friend of the deceased. The reported use of alcohol correlated well with the increase of fatty and fibrotic changes and with the occurrence of liver cirrhosis, alcoholic hepatitis or pancreatitis. Benign bile duct tumours (bile duct adenomas and von Meyenburg's complexes) (n = 26) were associated with the occurrence of bridging (P less than 0.0005) and periportal (P less than 0.025) fibrosis of the liver and, independently from these, with chronic pancreatitis (P less than 0.05) and with non-parasitic liver cysts (n = 14) (P less than 0.01). The weight of the liver was greater (P less than 0.01) in males with focal nodular hyperplasia (n = 3). Cavernous hemangioma (n = 19) occurred independently of the parameters studied. None of the tumours showed significant correlation to liver cirrhosis, alcoholic hepatitis, fatty liver or diseases of the gallbladder. The results are in line with observations on the reactive nature and connections to fibropolycystic liver disease of benign bile duct tumours in laboratory animals and in man. Their presence in human liver specimens should be taken into account as a sign of liver damage, in this study related to heavy use of alcohol or to chronic inflammation of the pancreas.
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PMID:Benign bile duct tumours, non-parasitic liver cysts and liver damage in males. 395 Mar 64

The ability to recognize diverse clinical forms of xanthomas, such as tuberous, planar, eruptive and tendinous, is important in the detection of underlying systemic disease. A variety of primary genetic disorders, as well as numerous secondary conditions such as diabetes, obstructive liver disease, thyroid disease, renal disease, and pancreatitis, can lead to hyperlipoproteinemia that results in the formation not only of xanthomas but also of life-threatening vascular atherosclerosis. An understanding of the pathogenesis of the underlying lipoprotein alterations provides a rational approach to therapy utilizing dietary manipulations and drugs. Such treatment is capable of correcting most disorders of lipid metabolism, and, if appropriate therapy is initiated at the first sign of xanthoma evolution, it may prevent progression of atherosclerosis, provide resolution of xanthomas, and in some instances prevent serious pancreatitis.
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PMID:Xanthomas and hyperlipidemias. 403 Nov 42

Carcinoembryonic antigen (CEA) was measured in whole serum and in serum extracted with perchloric acid by microradioimmunoassay in patients with benign and malignant diseases of the liver and pancreas. The level of detectability was 5 ng per ml. This level or greater was present in the serum of 50% of patients with chronic diffuse liver disease, 64% with pancreatitis, 94% with cancer of the digestive system, and 3% of controls. The incidence of levels of CEA of 5 ng/ml or more differed for various categories of chronic liver disease: from 22% in active chronic hepatitis, 46% in primary biliary cirrhosis, 63% in hepatoma, 78% in cryptogenic cirrhosis, and 88% in alcoholic cirrhosis; levels of CEA correlated with degrees of impairment of liver function as judged by bromsulphalein retention and serum levels of alkaline phosphatase and transaminase. In pancreatitis, 64% of cases had levels of CEA ranging from 5 to 20 ng/ml and in cancer of the pancreas 94% had levels above 5 ng/ml and 50% above 20 ng/ml.
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PMID:Carcinoembryonic antigen in serum in diseases of the liver and pancreas. 472 56

In order to assess insulin sensitivity for glucose utilization in the other type of diabetes, insulin sensitivity tests were performed in subjects with pancreatitis, liver disease, steroid treatment and hyperthyroidism. Insulin sensitivity for glucose utilization decreased in subjects with liver disease, steroid treatment and hyperthyroidism irrespective of the presence or absence of glucose intolerance. Hyperinsulinism was associated in most of the subjects with liver disease and steroid treatment, but even in normo-insulinemic subjects, insulin insensitivity was observed. Obesity was associated with only 2 cases in both pancreatitis and liver diseases and therefore was excluded as a major cause for insulin insensitivity in subjects studied. In subjects with pancreatitis, insulin sensitivity was not significantly decreased. It is to be noted that 4 out of 5 subjects with diabetic OGTT (oral glucose tolerance test) exhibited normal insulin sensitivity. The results indicate that in pancreatitis, tissue insulin sensitivity for glucose metabolism is not altered and therefore can be used as a marker to differentiate the other type of diabetes due to pancreatitis from type 1 or 2 diabetes. Although hyperinsulinemia may be attributable to insulin insensitivity in subjects studied at least in part, steroid and thyroid hormone are thought to act directly antagonistically with insulin for glucose metabolism.
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PMID:Insulin sensitivity in pancreatitis, liver diseases, steroid treatment and hyperthyroidism assessed by glucose, insulin and somatostatin infusion. 614 89

Many hepatic lesions, ranging from subcellular alterations to malignant tumors, have been attributed to the use of anabolic steroids (AS) and contraceptive steroids (CS). These lesions that have been attributed to AS and CS are discussed with focus on the following: biochemical changes; subcellular alterations; intrahepatic cholestasis; vascular complications (sinusoidal dilatation, peliosis hepatitis, Budd-Chiari syndrome); hyperplasia and neoplasia (diffuse hyperplasia, nodular transformation, focal nodular hyperplasia, hepatocellular adenoma, hepatocellular carcinoma, and miscellaneous malignant tumors); and miscellaneous effects (effects of preexisting liver disease, cholelithiasis, and pancreatitis). OCs have a number of physiologic effects on the liver. These include decreased bile flow, diminished secretion of organic anions, and decreased synthesis and secretion of bile acids. Retention of bromosulfophthalein has been noted with AS during late pregnancy and in the puerperium. It is well established that the CS can lead to elevations of serum ceruloplasmin and copper levels. Subcellular alterations have been reported in both humans and rats on AS or women on CS and involve multiple organelles of the several systems of the liver. Both AS and CS have been implicated in intrahepatic cholestasis. Jaundice usually develops after 2-5 months of therapy with AS or after 3 months of OC use. The lesions attributed to CS and AS can involve any of the systems of the liver. At times more than 1 system is affected simultaneously. Most of the steroid related lesions resemble similar ones caused by other etiologies. Some, such as peliosis hepatitis, are rarely related to other etiologies, but others can be termed steroid specific. A number of diseases associated with the CS or AS also occur in pregnancy. Acute fatty metamorphosis of pregnancy and the periportal hemorrhagic necrosis characteristic of eclampsia have not been reported in patients on CS. Spontaneous rupture of the liver during pregnancy has not been attributed to the CS.
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PMID:Hepatic lesions caused by anabolic and contraceptive steroids. 628 45

It has been our impression that clinical deterioration and worsening of liver tests of patients with alcoholic liver disease (ALD) is common immediately following hospitalization and cessation of ethanol intake. In order to determine the frequency of such deterioration and characterize features which may identify those patients who initially deteriorate, we analyzed the standard liver tests and clinical parameters of liver function following hospitalization of 273 cases of ALD, and correlated these with histologic patterns and hospital course. We found that moderate liver test worsening following hospitalization is frequent in patients with ALD, especially alcoholic hepatitis. The presence of alcoholic hyalin in patients with alcoholic hepatitis did not correlate with liver function or frequency of biochemical worsening, but did correlate with mortality. Biochemical deterioration did not correlate with clinical deterioration or mortality, unless complications such as bleeding, sepsis, or pancreatitis occurred. Spontaneous clinical deterioration of our patients in the absence of precipitating factors was rare. We conclude that worsening of liver tests following hospitalization frequently occurs in patients with ALD, does not necessarily imply presence of complications (e.g., biliary obstruction, sepsis, other liver injury), but should suggest the presence of alcoholic hepatitis.
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PMID:Clinical and biochemical course of alcoholic liver disease following sudden discontinuation of alcoholic consumption. 635 82

Rapid inhibition of tissue-type plasminogen activator (t-PA) in human plasma was measured by addition of 5 IU (50 ng) of purified t-PA per ml plasma and measurement of residual t-PA in the euglobulin precipitate after 5 min incubation at 37 degrees C. The recovery of both t-PA activity and t-PA related antigen in pooled plasma from healthy individuals was approximately 90 percent, indicating that one ml of pooled normal plasma inhibits less than 1 IU or 10 ng of t-PA within 5 min. Of 20 control subjects 13 had less than 1 IU inhibitor activity; 5 subjects inhibited between 1 and 3 IU of t-PA and 2 subjects inhibited around 4.5 IU. The inhibitor titer in the latter two had however decreased to 1.8 and 2.7 IU after two days. Markedly increased rapid inhibition of t-PA (greater than 4 IU per ml) was found in plasma of patients with severe liver disease (3 of 8), pancreatitis (4 of 8), malignancy (5 of 26), but only very occasionally and transiently in that of patients with myocardial infarction (5 of 28) or deep vein thrombosis (2 of 9). Increased inhibition was observed on the first day following coronary bypass (22 of 42) or open heart (16 of 27) surgery but this had disappeared in 15 of 16 patients on the fifth postoperative day. Titration of inhibitor levels revealed maximal amounts of 30 to 50 IU per ml plasma.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Plasma levels of a specific inhibitor of tissue-type plasminogen activator (and urokinase) in normal and pathological conditions. 642 82


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