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)

Elevated circulating CEA levels occur in patients with benign gastrointestinal and hepatic disorders. These are usually less than 10 ng/ml. Of clinical importance is the influence of liver disease on the interpretation of CEA. At least 50% of patients with severe benign hepatic disease have elevated CEA levels, most often active alcoholic cirrhosis, and also chronic active and viral hepatitis, and cryptogenic and biliary cirrhosis. Patients with benign extrahepatic biliary obstruction may have increased plasma CEA, the highest in patients with co-existent cholangitis and especially liver abscess. The liver appears to be essential for the metabolism and/or excretion of CEA. Hence, liver work-up is needed to assess any patient with an elevated CEA. A damaged liver may further augment elevated CEA levels due to cancer. The increased circulating CEA observed in some patients with active ulcerative colitis tends to correlate with severity and extent of disease and usually returns to normal with remission. CEA levels also may be mildly elevated in patients with pancreatitis and in adults with colonic polyps. Smoking may contribute to the increased CEA levels seen in patients with alcoholic liver disease and pancreatitis. Therefore, in interpreting mildy elevated circulating CEA levels in patients with GI tract diseases, one must consider benign as well as malignant etiologies.
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PMID:Carcinoembryonic antigen (CEA) levels in benign gastrointestinal disease states. 36 Dec

The diagnosis of viral hepatitis was not confirmed in 2976 (22.79%) out of the admitted to the hospital patients for a period of 15 years. What impresses is the percentage growth for the last several years, reaching to 30. This, on one hand is associated with the greater exigence of HEI and with the strong fear of that disease as well as with the improved diagnostic possibilities of the infectious diseases wards on the other. In fact, almost all patients with icterus were admitted to infectious diseases wards, where the differential diagnosis of icterus was made. The first place among the false diagnoses is occupied by liver-bile diseases, progressing with icterus-50.81%, (cholelithiasis-29%, carcinoma-11%, cirrhosis, chronic hepatitis, steatosis, cholangiohepatitis, pancreatitis, etc-10.8%). Second, according to incidence, come the gastrointestinal diseases-13.51%, grippe and grippe-like diseases-13.44%, lung diseases-5.21%, blood-3.80%, heart-3.16%, toxic hepatitis 3.26%, etc. Thirty cases of infectious mononucleosis with icterus are reported as well as 17 patients with liver etzymopathies, syndrome of Dublin--Johnson--6 and Gilbert--Meulengracht syndrome--11. Viral hepatitis diagnosis is not always easy and in many cases it requires a complex of laboratory and other investigations and many years of experience. However, the false diagnosis could be reduced with more than a half with the careful consideration of the epidemic situation, anamnestic and clinical data.
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PMID:[Diagnostic problems of viral hepatitis]. 89 23

The etiology of acute pancreatitis is diverse, and unusual causes include several common viral infections. Although pancreatitis has been found at autopsy in patients with fulminant hepatic failure, there have been only a few reports of an association between mild to moderate acute viral hepatitis and acute pancreatitis. A case of acute hepatitis A complicated by acute pancreatitis is presented, and the relevant literature regarding this unusual association is reviewed.
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PMID:Acute pancreatitis associated with acute hepatitis A. 144 93

We report on a case of acute pancreatitis in a 9 year-old girl suffering from steroid resistant nephrotic syndrome. Acute abdominal pains revealed pancreatitis whose outcome was favorable after 5 days of total parenteral nutrition. None of the usual causes of pancreatitis was recognized. A serologic profile of hepatitis B, compatible with a chronic carriage of the virus B was found. The possible relationships between pancreatitis, viral hepatitis and the nephrotic syndrome are discussed.
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PMID:[Nephrotic syndrome, pancreatitis, hepatitis B. Report of a case]. 166 3

Significant differences exist in the prevalence of most gastroenterological emergencies in tropical compared with temperate countries. Both ethnic and environmental (often clearly defined geographically) factors are relevant. The major oesophageal lesions which can present acutely in tropical countries are varices and carcinoma; bleeding and obstruction are important sequelae. Peptic ulcer disease (and its complications), often associated (not necessarily causally) with Helicobacter pylori infection, has marked geographical variations in incidence. Emergencies involving the small intestine are dominated by severe dehydration, and its sequelae, resulting from secretory diarrhoea, most notably cholera. However, enteritis necroticans ('pig bel' disease), paralytic ileus (sometimes caused by antiperistaltic agents) and obstruction (secondary to luminal helminths, volvulus and intussusception) are other important problems, especially in infants and children. Enteric fever is occasionally complicated by perforation and haemorrhage; the former (which is notoriously difficult to manage) is accompanied by significant mortality. Ileocaecal tuberculosis is a major cause of right iliac fossa pathology--sometimes associated with malabsorption; amoeboma is an important clinical differential diagnosis. The colon can be involved in invasive Entamoeba histolytica infection (which, like complicated enteric fever, is difficult to manage if the fulminant form, with perforation, ensues), shigellosis, volvulus and intussusception. Acute colonic dilatation occasionally follows Salmonella sp., Shigella sp., Campylobacter jejuni, Yersinia enterocolitica and rarely E. histolytica infections. Acute hepatocellular failure is a major cause of morbidity and mortality in the tropics and subtropics. It usually results from viral hepatitis (HBV, sometimes complicated by HDV, and HCV), but there is a long list of differential diagnoses. Hepatotoxicity resulting from herbs, chemotherapeutic agents or alcohol also occurs not infrequently. Chronic liver disease and its sequelae (often long-term results of viral hepatitis) are commonplace. Haematemesis and hepatocellular failure are usually very difficult to manage due to a lack of sophisticated support techniques in developing countries. Invasive hepatic amoebiasis usually responds well to medical management; however, spontaneous perforation can occur and the consequences of this are serious. Pyogenic liver abscess, although far less common than amoebic 'abscess', carries a bad prognosis whatever the method(s) of management. Hydatidosis and schistosomiasis also involve the liver, and helminthiases are important in the context of biliary tract disease. Gall stones are unusual in most tropical settings. Acute pancreatitis is overall unusual, but chronic calcific pancreatitis can present as an acute abdominal emergency.
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PMID:Gastroenterological emergencies in the tropics. 176 26

Alcoholic liver disease includes steatosis, alcoholic hepatitis and cirrhosis. Other liver diseases of genetic origin, but with a curious association with alcohol intake, are hemochromatosis and porphyria cutanea tarda. The attribution of chronic hepatitis to alcohol intake remains speculative, and the association may reflect hepatitis C infection. Hepatic injury attributed to alcohol includes the changes reported in the fetal alcohol syndrome. Steatosis, the characteristic consequence of excess alcohol intake, is usually macrovesicular and rarely microvesicular. Acute intrahepatic cholestasis, which in rare instances accompanies steatosis, must be distinguished from other causes of intrahepatic cholestasis (e.g., drug-induced) and from mechanical obstruction of the intrahepatic bile ducts (e.g., pancreatitis, choledocholithiasis) before being accepted. Alcoholic hepatitis (steatonecrosis) is characterized by a constellation of lesions: steatosis, Mallory bodies (with or without a neutrophilic inflammatory response), megamitochondria, occlusive lesions of terminal hepatic venules, and a lattice-like pattern of pericellular fibrosis. All these lesions mainly affect zone 3 of the hepatic acinus. Other changes, observed at the ultrastructural level, are of importance in progression of the disease. They include widespread cytoplasmic shedding, and capillarization and defenestration of sinusoids. Progressive fibrosis complicating alcoholic hepatitis eventually leads to cirrhosis that is typically micronodular but can evolve to a mixed or macronodular pattern. Hepatocellular carcinoma occurs in 5 to 15% of patients with alcoholic liver disease. The clinical syndrome of alcoholic liver disease is the result of three factors--parenchymal insufficiency, portal hypertension and the clinical consequences of extrahepatic damage produced by alcohol. At the several phases of the life history of alcoholic liver disease, the individual factors play a different role. The clinical manifestations of alcoholic steatosis are mainly extrahepatic in origin. Those of alcoholic hepatitis reflect mainly parenchymal insufficiency and those of cirrhosis are mainly those of portal hypertension. Alcoholic liver injury appears to be generated by the effects of ethanol metabolism and the toxic effects of acetaldehyde, perhaps the immune responses to alcohol- or acetaldehyde-altered proteins, and questionably enhanced by viral hepatitis. Alcoholic hepatitis may be mimicked histologically, and to a varying degree clinically, by a number of conditions (obesity, diabetes, several drug-induced injuries, jejunoileal bypass, and related "shortcircuiting" of the bowel). Perhaps the most important facet of the hepatotoxicity of alcohol is its enhancement of the effects of a number of other hepatotoxic agents, among which acetaminophen is the prime example.
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PMID:Alcoholic liver disease: pathologic, pathogenetic and clinical aspects. 205 45

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

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

A large retrospective autopsy study of patients was analyzed to evaluate the major etiologic and pathologic factors contributing to fatal acute pancreatitis (AP). From an autopsy population of 50,227 patients, 405 cases were identified where AP was defined as the official primary cause of death. AP was classified according to morphological and histological, but not biochemical, criteria. Patients with AP died significantly earlier than a control autopsy population of 38,259 patients. Sixty percent of the AP patients died within 7 days of admission. Pulmonary edema and congestion were significantly more prevalent in this group, as was the presence of hemorrhagic pancreatitis. In the remaining 40% of patients surviving longer than 7 days, infection was the major factor contributing to death. Major etiologic groups in AP were chronic alcoholism; postabdominal surgery; common duct stones; a small miscellaneous group including viral hepatitis, drug, and postpartum cases; and a large idiopathic group comprising patients with cholelithiasis, diabetes mellitus, and ischemia. The prevalence of established diabetes mellitus in the AP group was significantly higher than that observed in the autopsy control series, suggesting that this disease should be considered as an additional risk factor influencing survival in AP. Pulmonary complications, including pulmonary edema and congestion, appeared to be the most significant factor contributing to death and occurred even in those cases where the pancreatic damage appeared to be only moderate in extent. Emphasis placed on the early recognition and treatment of pulmonary edema in all cases of moderate and severe AP should contribute significantly to an increase in survival in this disease.
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PMID:Death due to acute pancreatitis. A retrospective analysis of 405 autopsy cases. 389

The histological features of 24 pancreases obtained from patients who died of causes other than hepatitis, pancreatitis or pancreatic tumors, included a variable degree of autolysis, rare foci of inflammatory reaction but no hemorrhagic fat necrosis or destruction of elastic tissue in vessel walls (elastolysis). Assays of elastase in extracts of these pancreases showed no free enzyme, but varying amounts of proelastase.A review of autopsy findings in 33 patients with fatal liver necrosis attributed to halothane anesthesia, demonstrated changes of acute pancreatitis only in two. On the other hand, a review of 16 cases of fulminant viral hepatitis revealed changes characteristic of acute pancreatitis in seven - interstitial edema, hemorrhagic fat necrosis, inflammatory reaction and frequently elastolysis in vessel walls. Determination of elastase in extracts of one pancreas showed the bulk of the enzyme in free form. Furthermore, assays of urinary amylase in 44 patients with viral hepatitis showed increased levels of this enzyme (2583 +/- 398 mean value +/- standard error, Somogyi units per 100 ml in 13, or 29.5 percent). The evidence suggests that acute pancreatitis may at times complicate viral hepatitis. Although direct proof of viral pancreatic involvement is not feasible at present, a rational hypothesis is advanced which underlines similar mechanisms of tissue involvement in both liver and pancreas that may be brought about by the hepatitis viruses.
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PMID:The association of viral hepatitis and acute pancreatitis. 507 Jun 94


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