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 autopsies of seven patients with disseminated varicella were reviewed. Six patients had acute lymphoblastic leukemia (ALL) and the seventh had Hodgkin's disease. All the patients were on chemotherapy at the time of commencement of their varicella rash, and at autopsy only the patient with Hodgkin's disease had residual tumor. The typical anatomic lesion of varicella was one of focal necrosis (often hemorrhagic) with eosinophilic intranuclear (Cowdry type-A) inclusions. In fatal disseminated varicella the complications most commonly encountered at autopsy were interstitial pneumonitis, hepatitis, necrotizing splenitis and lymphadenitis, esophagitis, enteritis, colitis, and pancreatitis. The most significant of these complications appears to be the interstitial pneumonitis, as the major cause of death is respiratory failure.
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PMID:Disseminated varicella at autopsy in children with cancer. 632 Oct 8

We describe a very rare case in which macroamylasemia was associated with ulcerative colitis of total colitis type. The patient's serum amylase isozyme pattern by electrophoresis showed a broad abnormal peak toward the side of the positive pole compared with regular salivary and pancreatic fractions. Sephadex G-200 column chromatography showed a sedimentation coefficient of 6.6 S. Amylase activity was bound to IgG. Double diffusion experiments demonstrated that amylase activity could be precipitated in gel by an antibody to the lambda chain. Although inflammatory bowel disease is occasionally associated with hyperamylasemia due to pancreatitis, we emphasize that, when hyperamylasemia is recognized in patients with inflammatory bowel disease, macroamylasemia also should be considered.
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PMID:Macroamylasemia associated with ulcerative colitis. 754 95

We conducted a retrospective analysis of 37 children with Escherichia coli O157:H7-associated hemolytic-uremic syndrome. The infection was traced to contaminated hamburgers at a fast-food restaurant chain. Within 5 days of the first confirmed case, the Washington State Department of Health identified the source and interrupted transmission of infection. Ninety-five percent of the children initially had severe hemorrhagic colitis. Nineteen patients (51%) had significant extrarenal abnormalities, including pancreatitis, colonic necrosis, glucose intolerance, coma, stroke, seizures, myocardial dysfunction, pericardial effusions, adult respiratory disease syndrome, and pleural effusions. Three deaths occurred, each in children with severe multisystem disease. At follow-up two children have significant impairment of renal function (glomerular filtration rate < 80 ml/min/per 1.73 Hm2); both of these children have a normal serum creatinine concentration. Hemolytic-uremic syndrome is the most common cause of acute renal failure in children, and this experience emphasizes the systemic nature of this disease. Clinicians should anticipate that multisystem involvement may occur in these patients, necessitating acute intervention or chronic follow-up. This outbreak of Hemolytic-uremic syndrome also highlights the microbiologic hazards of inadequately prepared food and emphasizes the importance of public health intervention in controlling Hemolytic-uremic syndrome.
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PMID:Escherichia coli O 157:H7-associated hemolytic-uremic syndrome after ingestion of contaminated hamburgers. 793 69

Despite being a common disease in humans, little is known about the etiopathogenesis of and effective therapeutic approaches to chronic pancreatitis, due mainly to the fact that few simple animal models suitable to study inflammatory and fibrogenetic processes have been described in the pancreas. Trinitrobenzene sulfonic acid (TNBS) induces chronic colitis and cholangitis in the rat. We hypothesized that TNBS instillation into the pancreatic ducts could also result in the development of a chronic pancreatic disease. The biliopancreatic duct of rats was cannulated and tied close to the liver. TNBS [0.4 ml of 2% TNBS in phosphate-buffered saline (PBS)-10% ethanol, pH 8] was infused into the pancreas under a continuous controlled-pressure system. Control rats underwent the same procedure using vehicle only. Pathology assessment of TNBS-treated rats examined at 48 h was consistent with severe acute necrotizing pancreatitis, having a morality rate of 31% and serum amylase activity of 37.4 +/- 8.8 U/ml at 24 h and 13.3 +/- 1.7 U/ml at 48 h (p < 0.01 for both time points compared to PBS/ethanol-treated rats). Groups of 10 rats each were killed at 3, 4, and 6 week after the surgical procedure. Morphological examination revealed changes mimicking features of chronic pancreatitis in humans in 80% (32 of 40) of TNBS-treated rats, consisting in various degrees of periductal and lobular fibrosis, duct stenosis, patchy acute and chronic inflammatory cell infiltrates, and signs of gland atrophy. Animals developing chronic disease had a weight gain rate significantly lower than that of control rats. Serum amylase, fasting glucose, and a glucose tolerance test were not different in diseased or control rats. In conclusion, we were able to induce chronic fibrogenetic inflammatory disease in the pancreas after a single pulse instillation of TNBS into the pancreatic ducts. This might be a useful animal model to study the pathophysiology of inflammatory, fibrogenetic, and reparative processes in pancreatic tissue.
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PMID:Induction of chronic pancreatic disease by trinitrobenzene sulfonic acid infusion into rat pancreatic ducts. 933 99

We prospectively evaluated 139 consecutive children presenting to the Sanjay Gandhi Postgraduate Institute of Medical Sciences (Lucknow, India) with gastrointestinal (GI) bleeding from January 1991 to November 1994. Our aims were to find out whether the causes of GI bleeding in a developing country differed from developed countries and how the application of newer diagnostic techniques would help in the diagnosis of GI bleeding. Barium studies, endoscopy, technetium-99m-labelled (erythrocytes and pertechnetate) scans, selective abdominal angiography using a digital subtraction technique and rectal endoscopic ultrasonography were performed. Upper GI bleeding (n = 75) was variceal in 71 (95%) children (extrahepatic portal venous obstruction in 65, cirrhosis in six) and non-variceal in four (5%) cases (Henoch-Schonlein purpura, idiopathic thrombocytopenic purpura, drug-induced gastric erosions and pseudoaneurysm of the gastroduodenal artery due to idiopathic chronic calcific pancreatitis). Causes of lower GI bleeding (n = 64) were colitis (27 cases; 42%), colorectal polyps (26 cases; 41%), enteric fever (n = 3), solitary rectal ulcer (n = 3), portal hypertensive colopathy (n = 2), colonic arteriovenous malformation (n = 1) and internal haemorrhoids (n = 1). One patient remained undiagnosed. Angiography performed in four children was diagnostic in two. In one child with massive lower GI bleeding from portal colopathy, the bleeding site (caecum) was localized by intra-operative colonoscopy, while in the other child with portal colopathy, rectal endoscopic ultrasonography was performed to substantiate the diagnosis. We conclude that the causes of upper GI bleeding in children in developing countries are different from those in developed countries (variceal bleeding due to extrahepatic portal venous obstruction is the most common cause, while peptic ulcer is rare). However, the spectrum of lower GI bleeding is similar to that of developed countries. Application of newer diagnostic techniques is helpful and safe in the identification of the cause of GI bleeding in children.
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PMID:Gastrointestinal bleeding in children. 891 24

This paper reports two patients with catastrophic complications after marathon-type running not hitherto documented. The first, who collapsed with acute abdominal pains, was found at surgery to have infarction of the omentum and later, after a second laparotomy, acute oedematous pancreatitis. The second patient, who collapsed semi-comatose with hyperthermia, developed disseminated intravascular coagulation, rhabdomyolysis, renal shutdown and progressive hepatic failure. With regular dialysis, his condition stabilised but liver function continued to decline, associated with thrombosis of the portal vein. The spectrum of potentially life threatening disorders includes upper gastrointestinal bleeding, haemorrhagic colitis and rarely infarction of the bowel. The present two cases provide further support for ischaemia being a major contributor to the gastrointestinal catastrophes of marathon-type running.
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PMID:Gastrointestinal emergencies with marathon-type running: omental infarction with pancreatitis and liver failure with portal vein thrombosis. 967 35

Presented is a study of 15 patients (seven males and eight females ranging between 5 and 10 years of age) with hemolytic uremic syndrome (HUS) associated with hemorrhagic colitis that was caused by enterohemorrhagic Escherichia coli (EHEC) O157:H7, encountered during the outbreak in Sakai City in July, 1996. The complete form of HUS, which includes the three characteristics hemolytic anemia, thrombocytopenia and acute renal dysfunction, was noted in eight patients, while an incomplete form of HUS, which did not include all three characteristics, was noted in seven patients. Regarding treatment, intravenous gamma-globulin was administered in nine patients and dialysis was performed in five patients (two males and three females) with the complete form of HUS. In three of these five patients, plasma exchange was also performed. Weaning from dialysis was accomplished by the 15th day of disease in all patients. Some patients developed pancreatitis, central nervous system symptoms, fundal hemorrhage and elevation of transaminase, although these abnormalities subsided uneventfully. Renal biopsy, which was performed in two patients who recovered from acute renal failure but still had mild proteinuria and a decrease in creatinine clearance, showed moderate changes in the glomeruli and tubulointerstitium. One year after onset of disease, hematological and urological findings were within normal limits in all patients except one with the complete form of HUS, who still had slightly decreased creatinine clearance.
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PMID:Clinical features and treatment of children with hemolytic uremic syndrome caused by enterohemorrhagic Escherichia coli O157:H7 infection: experience of an outbreak in Sakai City, 1996. 1022 Oct 34

Failure of intestinal barrier function and subsequent translocation of bacteria from the gut are believed to play a decisive role in the development of systemic septic complications, for example, following major trauma or major abdominal surgery. This study evaluated: (a) the effect of glutamine on colonic microcirculation and electrophysiological parameters reflecting gut barrier function, (b) the translocation of live bacteria to extraintestinal organs, and (c) disease outcome in two animal models with impaired gut barrier function. Severe acute pancreatitis or colitis was induced in rats randomized for therapy with or without glutamine (0.5 g/kg daily). After 48 h one animal group was prepared for intravital microscopy of colonic capillary blood flow and electrophysiological measurement of gut permeability; another was killed after 96 h for histological and microbiological examination. In animals with pancreatitis, glutamine (Gln) supplementation significantly improved gut permeability, i.e., Gln increased colonic transmucosal resistance from 67+/-7 to 92+/-3 Omega/cm(2) and decreased mannitol flux through the epithelium by 53%. Capillary blood flow in the colonic mucosa was improved by 25%. The prevalence of pancreatic infections was reduced from 86% in animals on standard parenteral nutrition to 33% in animals given the Gln-enriched diet (P<0.05); mortality decreased by 32%. In colitis, Gln had no significant effect on these parameters except for improving colonic capillary blood flow in colon segments not adjacent to the major injury site. Glutamine supplementation improves colonic capillary blood flow, stabilizes gut permeability, and reduces secondary pancreatic infections and mortality in severe rodent pancreatitis, but it is not helpful in colitis. This confirms previous reports that glutamine stabilizes gut barrier function only in certain diseases. Our experimental data strongly suggest that acute pancreatitis (rather than colitis) is one of the diseases with gut barrier dysfunction in which glutamine substitution may be helpful to reduce bacterial translocation and should therefore be tested in a controlled clinical trial.
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PMID:Does glutamine reduce bacterial translocation? A study in two animal models with impaired gut barrier. 1046 Sep 4

Despite limited understanding of therapeutic aetiopathogenesis of ulcerative colitis and Crohn's disease, there is a strong evidence base for the efficacy of pharmacological and biological therapies. It is equally important to recognise toxicity of the medical armamentarium for inflammatory bowel disease (IBD). Sulfasalazine consists of sulfapyridine linked to 5-aminosalicylic acid (5-ASA) via an azo bond. Common adverse effects related to sulfapyridine 'intolerance' include headache, nausea, anorexia, and malaise. Other allergic or toxic adverse effects include fever, rash, haemolytic anaemia, hepatitis, pancreatitis, paradoxical worsening of colitis, and reversible sperm abnormalities. The newer 5-ASA agents were developed to deliver the active ingredient of sulfasalazine while minimising adverse effects. Adverse effects are infrequent but may include nausea, dyspepsia and headache. Olsalazine may cause a secretory diarrhoea. Uncommon hypersensitivity reactions, including worsening of colitis, pancreatitis, pericarditis and nephritis, have also been reported. Corticosteroids are commonly prescribed for treatment of moderate to severe IBD. Despite short term efficacy, corticosteroids have numerous adverse effects that preclude their long term use. Adverse effects include acne, fluid retention, fat redistribution, hypertension, hyperglycaemia, psycho-neurological disturbances, cataracts, adrenal suppression, growth failure in children, and osteonecrosis. Newer corticosteroid preparations offer potential for targeted therapy and less corticosteroid-related adverse effects. Azathioprine and mercaptopurine are associated with pancreatitis in 3 to 15% of patients that resolves upon drug cessation. Bone marrow suppression is dose related and may be delayed. The adverse effects of methotrexate include nausea, leucopenia and, rarely, hypersensitivity pneumonia or hepatic fibrosis. Common adverse effects of cyclosporin include nephrotoxicity, hypertension, headache, gingival hyperplasia, hyperkalaemia, paresthesias, and tremors. These adverse effects usually abate with dose reduction or cessation of therapy. Seizures and opportunistic infections have also been reported. Antibacterials are commonly employed as primary therapy for Crohn's disease. Common adverse effects of metronidazole include nausea and a metallic taste. Peripheral neuropathy can occur with prolonged administration. Ciprofloxacin and other antibacterials may be beneficial in those intolerant to metronidazole. Newer immunosuppressive agents previously reserved for transplant recipients are under investigation for IBD. Tacrolimus has an adverse effect profile similar to cyclosporin, and may cause renal insufficiency. Mycophenolate mofetil, a purine synthesis inhibitor, has primarily gastrointestinal adverse effects. Biological agents targeting specific sites in the immunoinflammatory cascade are now available to treat IBD. Infliximab, a chimeric antibody targeting tumour necrosis factor-or has been well tolerated in clinical trials and early postmarketing experience. Additional trials are needed to assess long term adverse effects.
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PMID:Comparative tolerability of treatments for inflammatory bowel disease. 1108 48

Disruption of the pancreatic anastomosis with resultant sepsis is the cause of nearly 50% of deaths following pancreaticoduodenectomy (PD). Traditionally, the pancreatic remnant is anastomosed to the jejunum. Pancreaticogastrostomy (PG) was introduced as an alternative by Waugh and Clagett in 1946 and by Park, Mackie, and Rhoads in 1967. The purpose of this retrospective review was to assess the safety of PG at a single institution. Between 1986 and 1998 a total of 102 patients underwent PG following PD. The indications for PD were periampullary carcinoma (n = 89), pancreatitis (n = 7), and miscellaneous (n = 6). Altogether, 80 patients underwent the traditional Whipple procedure and 22 the pylorus-preserving Whipple (PPW) procedure. The PG was performed by a single-layer invagination technique to the posterior gastric wall using interrupted silk sutures. Leaks from the pancreatic anastomosis were detected by measuring amylase in fluid obtained from surgically placed drains. Operative mortality was 3.9% (4/102). The cause of death was uncontrolled upper gastrointestinal hemorrhage, sepsis, pulmonary embolus, and cardiac failure secondary to myocardial infarction. The mean operating time was 6.8 hours. Blood transfusion was given in 43 patients (42%), and the mean amount of the transfusion was 2.6 units. Nonfatal complications occurred in 35 patients (34%), and included leaks from the pancreatic anastomosis in 9 (8.8%), leaks from the biliary-enteric anastomosis in 4 (3.9%), and gastric paresis 7 (6.9%). Other complications included abscess, wound infection, colitis, delirium tremens, and hyperbilirubinemia. Discharge occurred 6 to 47 days (median 12 days) postoperatively and was prolonged in patients suffering from a complication. PD is associated with significant morbidity. PG is a safe alternative to pancreaticojejunostomy for managing the pancreatic remnant.
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PMID:Pancreaticogastrostomy following pancreaticoduodenectomy: review of 102 consecutive cases. 1136 81


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