Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0001339 (acute pancreatitis)
 10,593 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This chapter reviews the therapeutic use of octreotide in a variety of pancreatic disorders, including acute pancreatitis, in the prevention of postoperative and post-ERCP pancreatitis, in the control of postoperative pancreatic fistulae, and in chronic pancreatitis for the control of pain and of pseudocysts and ascites. The review also discusses the use of octreotide in intestinal disorders of motility, gastrointestinal bleeding, intestinal fistulae and refractory diarrhoea, including the diarrhoeas of AIDS, diabetes, short gut, chemotherapy, ileostomy and gastric surgery. The use of octreotide in neuroendocrine tumours, both for therapy and diagnostic imaging, is reviewed briefly. The paucity of adequately controlled studies in many of these situations is indicated and the potential usefulness of octreotide estimated.
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PMID:Expanding uses of octreotide. 794 61

Enterokinase is a glycoprotein and is now designated enteropeptidase (E.C.3.4.4.8.). It is present in the duodenal and jejunal mucosa. Pancreatic proteolytic enzymes are secreted as proenzymes. Enterokinase converts trypsinogen to trypsin in the duodenal lumen. Duodenopancreatic reflux of duodenal enterokinase may be important in the pathogenesis of experimental and clinical acute pancreatitis. Congenital enterokinase deficiency is a distinct clinical entity characterized by diarrhea, failure to thrive, hypoproteinemia, and edema. Acquired enterokinase deficiency may occur in some diffuse small bowel diseases. Steatorrhea of celiac spruce may be due partly to the fact that deficiency of secretin and cholecystokinin may interfere with the action of enterokinase. The interrelationship between secretin, cholecystokinin, enterokinase, and bile salts is not completely understood.
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PMID:Enterokinase. 820 33

The potential therapeutic applications of somatostatin and octreotide in gastroenterology involve gut neuro-endocrine tumours, bleeding varices, bleeding peptic ulcers, gastro-intestinal fistulae, pancreatic fistulae, dumping syndrome, pancreatic pseudocysts, short bowel syndrome, acute pancreatitis, AIDS-related diarrhoea, intestinal subacute obstruction, idiopathic 'diarrhoea', irritable bowel syndrome and GIT tumours. Octreotide has a longer duration of action than somatostatin and can be administered by subcutaneous injection, thus making it suitable for long-term administration. Many of the potential gastro-intestinal indications require long-term administration and thus octreotide would be the agent of choice.
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PMID:Potential indications for octreotide in gastroenterology: summary of workshop. 835 70

Homocystinuria is frequently associated with severe multisystem involvement such as dislocated lenses, skeletal deformities, mental retardation and premature vascular occlusions. Surprisingly, gastro-intestinal involvement has not been described in this disorder. We present a 17 year old boy with homocystinuria due to cystathionine beta-synthase deficiency, who developed severe gastrointestinal involvement, manifested by chronic diarrhoea and acute pancreatitis. The diarrhoea was successfully treated with betaine. Possible pathophysiological mechanisms and suggested treatment are described.
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PMID:Gastrointestinal involvement in homocystinuria. 843 64

We report a case of acute pancreatitis with diabetic ketoacidosis associated with increased serum myoglobin concentration, acute renal failure, and disseminated intravascular coagulation. A 49-year-old man suffering from diarrhea, vomiting, and somnolence was admitted to the hospital. He had had flu-like symptoms for 4 days prior to the onset of these symptoms. He was a habitual drinker and had been consuming 360 ml-900 ml of the drink "shochu" (distilled spirits containing 28% alcohol) daily for 30 years. Laboratory data on admission revealed elevated serum levels of pancreatic enzymes, including amylase, trypsin, lipase, pancreatic secretory trypsin inhibitor (PSTI), phospholipase A2 (PLA2), and elastase-1, as well as elevated levels of glucose (373 mg/dl), ketone bodies (3675 mumol/l), and myoglobin (229.8 ng/ml). Treatment with subcutaneous insulin and intravenous administration of electrolyte fluid and the systemic protease inhibitor, gabexate mesilate, was begun immediately. Early after the initiation of treatment, there was an increase in serum creatinine (4.9 mg/dl), and thromobocytopenia (15000/microliters) was observed. The patient completely recovered from renal failure and acute pancreatitis, but required insulin therapy. Alcohol ingestion and dehydration are thought to have played a major role in the triggering of the acute pancreatitis. We examined the relationship among acute pancreatitis, diabetic ketoacidosis, and hypermyoglobinemia in the literature.
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PMID:Acute pancreatitis with diabetic ketoacidosis associated with hypermyoglobinemia, acute renal failure, and DIC. 884 91

The diagnosis of chronic pancreatitis continues to present difficulties. The nonspecific nature of the symptomatology, its low prevalence and the limited value of morphological and functional tests in the early stages are the most common causes of delay in diagnosis. Our aim was to analyze the most significant clinical manifestations and the diagnostic features of chronic pancreatitis, distinguishing between alcoholic and nonalcoholic etiologies. We studied 158 patients, 136 (86.1%) with alcoholic and 22 (13.9%) with nonalcoholic chronic pancreatitis. The initial symptomatology, the age at diagnosis, the delay in diagnosis from the onset of the clinical signs and the type of diagnosis (incidental or suspected) were considered for each patient. Men predominated in both the alcoholic and the nonalcoholic pancreatitis groups (97.8% and 68.2%, respectively). The mean ages at onset and diagnosis were 38 and 50.6 years, respectively, in alcoholic chronic pancreatitis and 44 and 55 years in the nonalcoholic group; the differences between the two parameters were statistically significant. The most common clinical signs in alcoholic chronic pancreatitis were abdominal pain (81.6%) and episodes of acute pancreatitis (64%), while patients with nonalcoholic pancreatitis presented abdominal pain (59%), diarrhea (40.9%) and weight loss (36.4%). The delay in diagnosis from the onset of the clinical manifestations was 5.8 years (6.1 years in alcoholic and 4.3 years in nonalcoholic pancreatitis. The diagnosis was incidental in 34% of cases of alcoholic chronic pancreatitis and in 50% of cases in the nonalcoholic group.
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PMID:Diagnosis of chronic pancreatitis: presenting features and diagnostic delay. 944 41

The effects of the clinical and dietetics in patient managements on the protein-energy status of hospitalized patients were retrospectively (four yr) investigated in 243 adult (49 +/- 16 yr), male (168) and female (75) patients suffering from chronic liver diseases (42%), intestinal diseases with diarrhea (14%), digestive cancers (11%), chronic pancreatitis (10%), stomach and duodenum diseases (7%), acute pancreatitis (7%), primary protein-energy malnutrition (3%), esophagus diseases (3%), intestinal diseases with constipation 14 (2%) and chronic alcoholism (2%). The protein-energy nutritional status assessed by combinations of anthropometric and blood parameters showed 75% of protein energy malnutrition at the hospital entry mostly (4/5) in severe and moderate grades. The overall average of hospitalization was 20 +/- 15 days being the shortest (13 +/- 5,7 days) for esophagus diseases and the longest (28 +/- 21 days) for the intestinal diseases with diarrhea patients which also received mostly (42%) of the enteral and/or parenteral feedings followed by acute pacreatitis (41%) and digestive cancers (31%) patients. When compared to the entry the protein-energy malnutrition rate at the discharge decreased only 5% despite the increasing of 30% found on the protein-energy intake. The main improvement of the protein-energy nutritional status were attained to those patients showing protein-energy malnutrition milder degrees at the entry which belonged mostly to primary protein-energy malnutrition, acute pancreatitis and intestinal diseases with diarrhea diseases. The later two groups showed protein-energy nutritional status improvement only after the second week of hospitalization. The digestive cancers patients had their protein-energy nutritional status worsened throughout the hospitalization whereas it happened only in the first week for the intestinal diseases with diarrhea and chronic liver diseases patients, improving thereafter up to the discharge. The protein-energy nutritional status improvement found in few patients could be attributed to some complementary factors such as theirs mild degree of protein-energy malnutrition at entry and/or non-invasive propedeutics and/or enteral-parenteral feddings and/or longer hospitalization staying. The institutional causes for the unexpected lack of nutritional responses by the patients were probably the high demand for the few available beds which favour the hospitalization of the most severed patients and the university-teaching pressure for the high rotation of the available beds. Both often resulting in early discharging. In persisting the current physical area and attendance demand one could suggest an aggressive support early at the entry preceding and/or accompanying the more invasive propedeutical procedures.
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PMID:[Protein-energy malnutrition as a consequence of the hospitalization of gastroenterologic patients]. 945 55

A 37-yr-old man underwent an open drainage operation for severe acute pancreatitis and received respiratory ventilation support for 4 mo because of respiratory failure based on disseminated intravascular coagulation (DIC) and septic shock. Under intensive care, he sometimes had bloody diarrhea for about 6 wk. Colonoscopic findings suggested that the bleeding had derived from the small intestine. The patient then gradually recovered from acute pancreatitis and was discharged from the hospital. Thereafter, he suffered relapses of ileus and his symptoms progressively worsened. The patient underwent a second operation about 2 yr after the onset of acute pancreatitis. At celiotomy, multiple stenoses of the distal ileum measuring about 60 cm in length were found and the segment was resected. The resected specimen demonstrated six separate circumferential strictures and shallow ulcerations. Histologically, multiple ulcerations were restricted to the mucosa and were accompanied by marked submucosal edema and fibrosis. The mucosa between the ulcers revealed chronic regenerative changes: intimal thickening of small mesenteric arteries causing luminal narrowing and organized thrombosis in small mesenteric veins. Therefore, these were considered to be a series of segmental ischemic lesions. Note that delayed ischemic stricture of the small intestine may occur as a chronic complication of acute pancreatitis.
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PMID:Ischemic stricture of the small intestine associated with acute pancreatitis. 987 59

Edwardsiella tarda (E. tarda) has recently become recognized as a pathogen in humans. Here we report a new case of E. tarda bacteraemia complicated by acute pancreatitis and pyomyoma. A 46-year-old female came to our emergency room complaining of sudden onset of left upper quadrant pain and vomiting for the previous few hours after drinking three bottles of wine. An abdominal computed tomography (CT) scan revealed multiple biliary stones, acute pancreatitis with extensive inflammatory change, and a large uterine myoma. Fever, watery diarrhoea, and mild suprapubic discomfort with vaginal spotting were noted soon after admission. The patient's blood cultures yielded E. tarda and symptoms subsided after antibiotic therapy. Fever and severe suprapubic pain with rebound tenderness developed 12 days later. Repeat abdominal CT scan revealed an enlarged uterine myoma with central necrosis. The patient subsequently underwent anterior total hysterectomy and bilateral salpingo-oophorectomy, revealing a uterine myoma with infarction and abscess formation. The patient recovered uneventfully and was discharged 1 week later.
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PMID:Edwardsiella tarda bacteraemia--complicated by acute pancreatitis and pyomyoma. 1034 54

Exatecan mesylate (DX-8951f) is a new hexacyclic camptothecin analogue with favorable attributes compared to topotecan and CPT-11, including watersolubility, greater potency against topoisomerase I, lack of esterase-dependent activation, broad antitumor activity, and low cross-resistance against MDR-1 overexpressing tumors. In preclinical studies, the compound demonstrated a favorable toxicology profile with hematologic dose-limiting toxicity and moderate gastrointestinal toxicity, linear pharmacokinetics, P450 hepatic metabolism (CYP3A4 and CYP1A2), and predominately fecal excretion. The results of six U.S. and European phase I clinical trials as well as two Japanese studies are presented including total DX-8951 and lactone DX-8951 pharmacokinetics. The toxicity profile was similar for all schedules of administration. Hematologic toxicity was dose-dependent and reversible. Neutropenia was dose-limiting in minimally pretreated patients, whereas neutropenia and thrombocytopenia were dose-limiting in heavily pretreated patients. Non-hematologic toxicity included moderate gastrointestinal toxicity (nausea, vomiting > diarrhea), transient elevation of hepatic transaminases, asthenia, and alopecia. Two cases of acute pancreatitis not predicted by preclinical toxicology were also observed. Antineoplastic activity was detected in several solid tumor types: non-small cell lung cancer, extrapulmonary small cell cancer, colorectal cancer, hepatocellular cancer, and sarcoma. Antitumor activity was seen in CPT-11 and topotecan-resistant tumors. Pharmacokinetics were linear within the dose range tested. A pharmacokinetic/pharmacodynamic model predictive of DX-8951f-induced neutropenia in individual patients was developed. The daily x5, every 3-week schedule with the drug administered as a 30-minute intravenous infusion was selected for future phase II clinical trials based on its superior antitumor activity.
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PMID:DX-8951f: summary of phase I clinical trials. 1119 1


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