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)

Whilst the importance of mutations in a wide range of keratins in skin fragility disorders is now well established, there is much less evidence for simple epithelial keratin involvement in disease. Some simple epithelial keratin mutations have been reported in liver cirrhosis and pancreatitis patients, and recently mutations in the simple epithelial keratin K8 were identified in a group of patients with inflammatory bowel disease (Crohn disease or ulcerative colitis). In comparison with the mutations seen in epidermal keratins, these simple epithelial mutations would be predicted to have mild consequences, although analysis shows that they do have a distinct effect. This review article discusses the evidence that these mutations are a predisposing factor for inflammatory bowel disease.
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PMID:Keratin mutations and intestinal pathology. 1549 67

This article summarizes the clinical research advances in gastroenterology and hepatology that were reviewed during the Plenary Session of the American Gastroenterological Association's Annual Meeting in May 2004 in New Orleans, Louisiana. The clinical research advances included the efficacy of infliximab in the treatment of fistulizing Crohn's disease, survival after isolated intestinal transplantation, the role of endoscopic treatment of bleeding peptic ulcers and Barrett's esophagus, the recurrence of cancer after laparoscopic colectomy, the impact of microsatellite instability on the response to adjuvant chemotherapy with 5-fluorouracil (5-FU), the epidemiology of obesity and its response to low-carbohydrate diets, the potential role of gastrointestinal factors in the development of obesity, and, the newly appreciated condition, autoimmune pancreatitis with associated cholangitis. Clinical research advances will impact the management of digestive diseases.
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PMID:GIH clinical research 2003-2004: the year in review. 1562 46

According to the literature data the modern concepts of the etiological factors, the pathomorphological features, the diagnosis, the clinical features and the treatment of the drug-induced and the idiopathic pancreatitis, accompanying the IBD are reviewed. The results of a retrospective review of the clinical data of 50 patients, operated on--16 with Crohn's disease and 34 with ulcerative colitis, are shown. Postoperative hyperamylasemia was found in 2 patients with Crohn's disease and in 3 patients with ulcerative colitis. One of them also had primary sclerosing cholangitis. All patients were treated with Metronidazole and Cortizone. Nine years after the operation one of the patients with ulcerative colitis had acute pancreatitis, treated conservatively.
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PMID:[Pancreatitis accompanying inflammatory bowel diseases, and our observations]. 1570 45

Pancreatitis-associated protein I (PAP I), also known as HIP, p23, or Reg2 protein, has recently been implicated in the endogenous regulation of inflammation. Although it was initially characterized as a protein that is overexpressed in acute pancreatitis, PAP I has also been associated with a number of inflammatory diseases, such as Crohn's disease. Knowing that PAP I and IL-10 responses share several features, we have used a pancreatic acinar cell line (AR42J) to assess the extent to which their expression is reciprocally regulated, and whether the JAK/STAT and NF-kappaB signaling pathways are involved in the suppression of inflammation mediated by PAP I. We observed that PAP I is induced in epithelial cells by IL-10 and by PAP I itself. In contrast, we found phosphorylation and nuclear translocation of STAT3 and induction of suppressor of cytokine signaling 3 in response to PAP I exposure. Finally, a JAK-specific inhibitor, tyrphostin AG490, markedly prevented PAP I-induced NF-kappaB inhibition, pointing to a cross-talk between JAK/STAT3 and NF-kappaB signaling pathways. Together, these findings indicate that PAP I inhibits the inflammatory response by blocking NF-kappaB activation through a STAT3-dependent mechanism. Important functional similarities to the anti-inflammatory cytokine IL-10 suggest that PAP I could play a role similar to that of IL-10 in epithelial cells.
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PMID:Pancreatitis-associated protein I suppresses NF-kappa B activation through a JAK/STAT-mediated mechanism in epithelial cells. 1651 47

Genetic, immunological and environmental factors are involved in the pathogenesis of the gastrointestinal diseases. Situated on the short arm of the chromosome 6, the HLA system is very polymorphic and has the capacity to confer susceptibility or resistance to different diseases. The relationship HLA vs. disease differs with the disease and, sometimes, with the ethnic-racial group studied. Histocompatibility molecules could determine the age of onset, the treatment response and the clinical course for some diseases. The recent discovery of new methods to typify HLA alleles and the changes in its nomenclature has contributed to a better understanding of this system. Nevertheless, has not thoroughly widespread. The aim of this review is to discuss the HLA structure and function, methods of detection, nomenclature and its association with celiac disease, Crohn's disease, autoimmune hepatitis, autoimmune pancreatitis and oral recurrent ulcers.
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PMID:[Human histocompatibility system association with gastrointestinal diseases]. 1685 82

Push-and-Pull enteroscopy/Double balloon enteroscopy (PPE/DBE) allows enteroscopy of the entire small bowel, or at least a substantial part of it. The complication rate is acceptably low. Severe complications such as pancreatitis and perforation were encountered in the literature in approximately 1% of all diagnostic PPE/DBEs. It can be expected that the complication rate of therapeutic PPE/DBEs is higher, comparable with the conventional endoscopy. The diagnostic yield is high, at approximately 75%, as is the therapeutic yield. The option of carrying out endoscopic therapy (in approximately 40%-50% of cases in the Western hemisphere) is an important aspect. Angiodysplasias are the main bleeding source, at least in Western countries. Using the PPE/DBE device, endoscopic treatments such as endoscopic hemostasis using injection and argon plasma coagulation, polypectomy, endoscopic resection, balloon dilation, and foreign-body extraction have become feasible even in the small intestine and can generally be performed safely and without relevant technical problems. Medical therapy can be started in up to 20% of cases-e.g., after a new or changed diagnosis of Crohn's disease. Surgical therapy is required in 10-20% of cases, due to malignant tumors or complex stenoses, for example. The main indication is mid-gastrointestinal bleeding.
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PMID:Push-and-pull enteroscopy using the double-balloon technique/double-balloon enteroscopy. 1697 35

This review summarises clinical pharmacological aspects of thiopurines in the treatment of chronic inflammatory bowel disease (IBD). Current knowledge of pharmacogenetically guided dosing is discussed for individualisation of thiopurine therapy, particularly to avoid severe adverse effects. Both azathioprine and mercaptopurine are pro-drugs that undergo extensive metabolism. The catabolic enzyme thiopurine S-methyltransferase (TPMT) is polymorphically expressed, and currently 23 genetic variants have been described. On the basis of an excellent phenotype-genotype correlation for TPMT, genotyping has become a safe and reliable tool for determination of a patient's individual phenotype. Thiopurine-related adverse drug reactions are frequent, ranging from 5% up to 40%, in both a dose-dependent and -independent manner. IBD patients with low TPMT activity are at high risk of developing severe haematotoxicity if pharmacogenetically guided dosing is not performed. Based on several cost-benefit analyses, assessment of TPMT activity is recommended prior to thiopurine therapy in patients with IBD. The underlying mechanisms of azathioprine/mercaptopurine-related hepatotoxicity, pancreatitis and azathioprine intolerance are still unknown. Although the therapeutic response appears to be related to 6-thioguanine nucleotide (6-TGN) concentrations above a threshold of 230-260 pmol per 8 x 10(8) red blood cells, at present therapeutic drug monitoring of 6-TGN can be recommended only to estimate patients' compliance.Drug-drug interactions between azathioprine/mercaptopurine and aminosalicylates, diuretics, NSAIDs, warfarin and infliximab are discussed. The concomitant use of allopurinol without dosage adjustment of azathioprine/mercaptopurine leads to clinically relevant severe haematotoxicity due to elevated thiopurine levels. Several studies indicate that thiopurine therapy in IBD during pregnancy is safe. Thus, azathioprine/mercaptopurine should not be withdrawn in strictly indicated cases of pregnant IBD patients. However, breastfeeding is contraindicated during azathioprine/mercaptopurine therapy. Use of azathioprine/mercaptopurine for induction and maintenance of remission in corticosteroid-dependent or corticosteroid-refractory IBD, particularly Crohn's disease, is evidence based. To improve response rates in thiopurine therapy of IBD, comprehensive analyses including metabolic patterns and genome-wide profiling in patients with azathioprine/mercaptopurine treatment are required to identify novel candidate genes.
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PMID:Thiopurine treatment in inflammatory bowel disease: clinical pharmacology and implication of pharmacogenetically guided dosing. 1771 77

Pancreatic exocrine insufficiency with steatorrhea is a major consequence of pancreatic diseases (eg, chronic pancreatitis, cystic fibrosis, severe acute necrotizing pancreatitis, pancreatic cancer), extrapancreatic diseases such as celiac disease and Crohn's disease, and gastrointestinal and pancreatic surgical resection. Recognition of this entity is highly relevant to avoid malnutrition-related morbidity and mortality. Therapy for pancreatic exocrine insufficiency is based on the oral administration of pancreatic enzymes aiming at providing the duodenal lumen with sufficient active lipase at the time of gastric emptying of nutrients. Administration of enzymes in the form of enteric-coated minimicrospheres avoids acid-mediated lipase inactivation and ensures gastric emptying of enzymes in parallel with nutrients. Nevertheless, such factors as acidic intestinal pH and bacterial overgrowth may prevent normalization of fat digestion even in compliant patients. The present article critically reviews current therapeutic approaches to pancreatic exocrine insufficiency.
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PMID:Pancreatic enzyme therapy for pancreatic exocrine insufficiency. 1741 56

Chronic autoimmune pancreatitis is an entity distinct from all other forms of chronic pancreatitis. It is expressed by signs of acute or chronic pancreatitis, sometimes associated with cholestatic jaundice. In imaging, it may appear as diffuse (duct destructive) or pseudotumoral lesions. These 2 aspects are probably different clinical forms of chronic autoimmune pancreatitis. Some autoimmune diseases are associated with chronic autoimmune pancreatitis, but not consistently. One such disease involves a bile disorder very similar to primary sclerosing cholangitis but responsive to corticosteroid treatment. Pancreatitis may be a sign of intestinal inflammatory diseases (and vice versa): testing for Crohn's disease and ulcerative rectocolitis is justified in patients with idiopathic pancreatitis. Chronic autoimmune pancreatitis must be routinely considered in patients with a pancreatic tumor that is for a clinical, epidemiologic, serologic or imaging reason not completely consistent with pancreatic adenocarcinoma. A short corticosteroid therapy (< 4 weeks) is probably less harmful in a patient with pancreatic adenocarcinoma than pancreatectomy (or chemotherapy) in patients with chronic autoimmune pancreatitis. Diagnosis depends on a body of clinical and radiologic evidence. The diagnostic value of serologic markers and especially of autoantibodies must be clarified in the future.
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PMID:[Autoimmune pancreatitis]. 1749 Aug 50

It is well-known that physiological phenomena and certain diseases, including neonatal granulocytosis, age-associated granulocytosis, periodontitis, pancreatitis, Crohn's disease, ulcerative colitis, hemorrhoids, endometriosis, and NSADs-enteritis, are accompanied by tissue destruction and granulocytosis. We investigated what is a key factor connecting tissue destruction and granulocytosis, attention being focused on adrenergic receptors on granulocytes and stress-induced sympathetic nerve stimulation. If we introduce the concept that "granulocytosis and subsequent tissue destruction are induced by sympathetic nerve stimulation," the mechanisms underlying many physiological phenomena and the etiology of several uncurable diseases in humans can be clearly understood.
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PMID:Relationship between diseases accompanied by tissue destruction and granulocytes with surface adrenergic receptors. 1787 4


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