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)

The endoscopic retrograde cholangiogram and pancreatogram of 22 patients with primary biliary cirrhosis, 33 patients with other forms of chronic liver disease and 28 'normal' controls were compared. The incidence of radiological intrahepatic duct abnormality is similar in patients with primary biliary cirrhosis and in other forms of liver disease, but is present in only a minority of both groups. A 'notch' or smooth indentation on the extrahepatic bile ducts at the porta hepatis was present in 58% of patients with primary biliary cirrhosis but in none in either of the other two groups. Three out of seven patients with sclerosing cholangitis showed minimal-change pancreatitis. Pancreatic abnormalities were otherwise infrequent.
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PMID:The endoscopic retrograde cholangiogram and pancreatogram in chronic liver disease. 687 47

Forty patients with chronic liver disease and portal hypertension but without clinical signs of portasystemic encephalopathy (15 patients with nonalcoholic cirrhosis, 15 patients with alcoholic cirrhosis, and 10 patients with minimal EEG changes) and a control group of 12 patients with chronic alcohol pancreatitis were studied using an extensive psychometric program, which, in the same form, is used for expert reports on driving capacity. Of the cirrhotic patients, 60% were considered unfit to drive; in 25% driving capacity was questionable, 15% (only nonalcoholic cirrhotics) were considered fit to drive. In contrast 75% of the patients with alcoholic pancreatitis were considered fit to drive. Major defects were found only in three heavy alcoholics. Patients with alcoholic cirrhosis scored lower than patients with nonalcoholic cirrhosis. This was due to differences in liver function rather than to the effect of alcohol consumption. Patients with minimal EEG changes were practically all considered unfit to drive.
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PMID:Latent portasystemic encephalopathy. I. Nature of cerebral functional defects and their effect on fitness to drive. 724 98

An unusual complication of pancreatic pseudocyst is reported. A 47-year-old woman with chronic liver disease and a history of recurrent pancreatitis died of fulminant, gram-negative septic shock. Acute, bilateral thigh cellulitis with tissue culture positive for Escherichia coli was the only potential infectious source identified. Autopsy revealed a pseudocyst in the head of the pancreas that had eroded into the portal vein, with embolization of mucoid cyst material into intrahepatic portal vein branches. Fibrous organization and recanalization of some of the occluded portal vein branches indicated that this process had been present for weeks to months and was therefore not the direct cause of death. The literature on this unusual complication of pancreatic pseudocyst is also reviewed.
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PMID:Spontaneous rupture of a pancreatic pseudocyst into the portal vein. 755 73

One hundred and fourteen consecutive patients with unresectable hepatocellular carcinoma were treated by chemoembolization using ethiodized oil (Lipiodol), anticancer agents. Ninety patients had concomitant chronic liver disease. Hepatocellular carcinoma (HCC) was diagnosed by US, contrast enhanced CT, fine needle biopsy and alpha-feto-protein level. Admission criteria were as follows: tumor confined to the liver with or without hilar nodal involvement, Child class A or B, white blood cell count above 2.000/mmc and platelet count above 75,000/mmc. All the patients underwent angiographic chemoembolization with Lipiodol and anticancer agents. In 98 patients we performed transcatheter hepatic arterial embolization (TAE) with Gelfoam or for Ivalon sponge. In 16 patients TAE was not performed because of portal thrombosis (7 cases) or technical reasons (9 cases). Mitomycin was used in 40 patients and dihydroxyanthracenedione (DADH) in 58 patients. In the TAE group 83 patients were Child A and 15 Child B. In 27 patients HCC was mononodular whereas in 71 it was multinodular. In 41 patients the tumor was more than 5 cm in diameter (in multinodular tumors only the larger lesion was taken into account). In 56 patients chemoembolization plus TAE was repeated. Seven patients died within one month after treatment: two from myocardial infarction, two from liver failure, two from digestive haemorrhage and one from necrotizing pancreatitis. Long-term survival rates were investigated in relation to prognostic factors: anti-cancer agent, number of nodes, tumor size and Child stage using Kaplan-Meier method. Survival rate at 12, 24 and 36 months are 64%, 38%, and 30% respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The treatment of hepatocellular carcinoma by chemoembolization]. 802 66

The clinical histories of 46 adult patients (24 men and 22 women, mean age 20.6 +/- 5.1 years) diagnosed of cystic fibrosis were reviewed evaluating the digestive alterations. The age at diagnosis of cystic fibrosis was 5.63 +/- 5.3 years (range: newborns-19 years). The initial diagnosis was established by ileus meconium, in four, lung disease in 15, steatorrhea in 12, lung disease and steatorrhea in 13 and following the diagnosis of cystic fibrosis in siblings in two. Four patients presented ileus meconium, nine occlusive syndrome of the distal intestine, 42 steatorrhea (20 severe, 12 moderate and 10 mild), with the severity of the steatorrhea not being associated with the severity of the respiratory insufficiency. Two patients presents rectal prolapse, five gastroesophageal reflux syndrome (four with hiatal hernia), six cholelithiasis, one recurrent pancreatitis without detection of biliary lithiasis, one neonatal cholestasis and 10 malnutrition (five severe and five moderate) fundamentally in relation to the severity of the lung disease and, to a lesser degree, liver disease. In 10 patients chronic liver disease was diagnosed corresponding to established cirrhosis in seven, indicating liver transplantation in two. In most cases, the liver disease was already manifest in adolescence even in the cirrhotic stage. Cholangiography by magnetic resonance was useful in the study of liver disease showing abnormalities which imitated primary sclerosing cholangitis. Treatment with ursodesoxicholic acid at a dosis of 20 mg/kg/day led to a significant decrease in the transaminase values and overall of gammaglutamyltranspeptidase but did not avoid complications in the cirrhotic stages. Genetic studies performed in 36 patients detected the delta F508 mutation in 69.4%, being found in almost all of the patients with ileus meconium, occlusive syndrome of the distal intestine, liver disease, cholelithiasis and malnutrition.
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PMID:[Digestive alterations in cystic fibrosis. Retrospective study of a series of 46 adult patients]. 1019 90

To understand recent temporal trends in acquired immunodeficiency syndrome (AIDS) mortality in the era of highly active antiretroviral therapy (HAART), trends in causes of death among persons with AIDS in San Francisco who died between 1994 and 1998 were analyzed. Among 5234 deaths, the mortality rate for human immunodeficiency virus (HIV)-related or AIDS-related deaths declined after 1995 (P<.01), whereas the mortality rate for non-HIV- or non-AIDS-related deaths remained stable. The proportion of deaths of persons with AIDS associated with septicemia, non-AIDS-defining malignancy, chronic liver disease, viral hepatitis, overdose, obstructive lung disease, coronary artery disease, and pancreatitis increased (P<.05). The standardized mortality ratio was high for these causes in both pre- and post-HAART periods, except for pancreatitis, a possible complication of HAART, which demonstrated an increasing standardized mortality ratio trend after 1996. With increasing AIDS survival, prevention of chronic diseases, assessment of long-term toxicity from HAART, and surveillance for additional causes of mortality will become increasingly important.
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PMID:Trends in causes of death among persons with acquired immunodeficiency syndrome in the era of highly active antiretroviral therapy, San Francisco, 1994-1998. 1223 45

Common to both acute and chronic disease are disturbances in energy homeostasis, which are evidenced by quantitative and qualitative changes in dietary intake and increased energy expenditure. Negative energy balance results in loss of fat and lean tissue. The management of patients with metabolically-active disease appears to be simple; it would involve the provision of sufficient energy to promote tissue accretion. However, two fundamental issues serve to prevent nutritional demands in disease being met. The determination of appropriate energy requirements relies on predictive formulae. While equations have been developed for critically-ill populations, accurate energy prescribing in the acute setting is uncommon. Only 25-32% of the patients have energy intakes within 10% of their requirements. Clearly, the variation in energy expenditure has led to difficulties in accurately defining the energy needs of the individual. Second, the acute inflammatory response initiated by the host can have profound effects on ingestive behaviour, but this area is poorly understood by practising clinicians. For example, nutritional targets have been set for specific disease states, i.e. pancreatitis 105-147 kJ (25-35 kcal)/kg; chronic liver disease 147-168 kJ (35-40 kcal)/kg, but given the alterations in gut physiology that accompany the acute-phase response, targets are unlikely to be met. In cancer cachexia attenuation of the inflammatory response using eicosapentaenoic acid results in improved nutritional intake and status. This strategy poses an attractive proposition in the quest to define nutritional support as a clinically-effective treatment modality in other disorders.
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PMID:Nutritional demands in acute and chronic illness. 1501 75

A 7-year-old, male, castrated, Labrador Retriever with a history of pancreatitis and inflammatory bowel disease presented for vomiting and anorexia. Serum biochemistry findings were indicative of cholestasis, hepatocellular insult, and decreased hepatic function. Ultrasound examination showed sediment and gas within the gallbladder, and a diagnosis of emphysematous cholecystitis was made. Emergency gallbladder resection was performed. Cytologic examination of bile fluid collected at surgery showed a mixed population of bacteria (bactibilia) together with fungal organisms consistent with Cyniclomyces guttulatus (previously known as Saccharomycopsis guttulatus). Similar fungal organisms were seen on a fecal smear. Bacteria cultured were normal gastrointestinal flora, supporting ascending infection; the fungal organisms were interpreted as incidental. Histopathology of the gallbladder indicated active (suppurative) and chronic (lymphocytic) cholecystitis and sections of liver tissue had evidence of chronic liver disease. A positive liver culture indicated concurrent bacterial hepatitis or cholangiohepatitis. Despite supportive care, the dog continued to decline and was euthanized 30 days later. Necropsy results confirmed end stage liver disease, but an initiating cause was not found. This case highlights the role of bactibilia in the development of acute cholecystitis and the unique cytologic appearance of C guttulatus as an incidental finding in bile fluid.
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PMID:Gallbladder aspirate from a dog. 1712 57

Direct hyperbilirubinemia, may result from a variety of pathologies, including structural obstructions with biliary tract occlusions (as in cholelithiasis), infections (e.g. hepatitis) and genetic disorders (Rotor's and Dubin-Johnson's syndrome). One of the less common and probably more frequently underdiagnosed causes is benign recurrent intrahepatic cholestasis (BRIC). First described in 1959, BRIC was further classified into two subgroups which differ in their pathogenesis and clinical manifestation. Both BRIC types originate from impaired function bile salt excretion from hepatocytes to the canaliculi which is mediated by the bile salt export pump (BSEP) which is located on the hepatyocyte membrane, unevenly distributed within the membrane lipid bilayer. In BRIC type-I, a mutation impairs the asymmetrical distribution of BSEP. In BRIC type-II, a mutation occurs directly damaging the BSEP. Apart from cholestasis, clinical manifestations of BRIC type-I include extra-hepatic symptoms such as watery diarrhea, pancreatitis and hearing impairment. Patients with BRIC type-II present mainly with hepatobiliary disease such as colelithiasis. In the past, BRIC was conventionally considered to result in no more than canalicular cholestasis, however several reports have associated BRIC with fibrosis and porto-portal septa formation. Disease course may last between weeks and months, more common in females, at any age, and usually resolves spontaneously, although chronic liver disease has also been described. Treatment modalities range from expectant management, medication (cholestyramine, ursolit) or even surgery (biliary bypass/liver transplantation). This report describes a patient with BRIC type-II and reviews the relevant literature.
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PMID:[Benign recurrent intrahepatic cholestasis type-II--a rare cause of direct hyperbilirubinemia exacerbations with hepatic fibrosis]. 1877 Sep 56

Acute viral hepatitis has been reported to cause acute pancreatitis. It was also reported that exocrine pancreatic function is damaged in chronic liver disease (CLD). Growth factors stored in the extracellular matrix and released in the course of pancreatic degradation are major mediators of inductive processes. The immunostaining technique was used to evidence the changes of the expression of the growth factors in different pancreatic cells. VEGF and FGF-beta are involved in the angiogenesis processes and in the evolution of the pancreatic interstitial tissue in case of chronic pancreatitis. Theses markers can also be used for the diagnosis of pancreatitis, but their value is variable. They stimulate the pancreatic star cells, the myofibroblasts and play an important role in the genesis of the extracellular matrix and in the repairing of the tissue after the aggression. TGF beta is important for its role in cellular differentiation and growth and in the development of the fibrosis in liver and other organs. The present paper studies the immunohistochemical expression of these growth factors in pancreatic cells.
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PMID:Immunohistochemical expression of growth factors in the exocrine pancreas of patients with chronic liver diseases. 2049 48


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