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)

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

Dyspepsia can describe a subset of children with episodic or persistent abdominal symptoms--often related to feeding--that are thought to be caused by disorders of the proximal part of the digestive tract. Symptoms, such as vomiting, early satiety, postprandial epigastric abdominal pain, heartburn, abdominal fullness, poor weight gain, and/or anorexia, have been incorporated into the definition of dyspepsia. Unfortunately, presenting signs and symptoms in children with dyspepsia are nonspecific and can occur as a result of many diseases, such as parasitic infections, esophagitis, eosinophilic gastroenteritis, Helicobacter pylori infection, Crohn's disease, biliary tract or hepatic disease, pancreatitis, and lactose intolerance. This lack of specificity makes the evaluation of dyspepsia more difficult. Here, we describe an approach for the evaluation of dyspepsia that correlates in part with the child's presenting symptoms.
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PMID:Techniques for the evaluation of dyspepsia in children. 1141 83

As a result of extensive clinical and basic research, the pivotal role of tumour necrosis factor (TNF) in the pathogenesis of chronic inflammatory diseases such as inflammatory bowel disease (IBD) has now generally been acknowledged. This has led to promising clinically effective anti-TNF-strategies. Of note, there is more and more evidence that TNF seems to play a key role in other gastrointestinal diseases including Helicobacter pylori infection, pancreatitis, viral hepatitis and toxic liver damage, too. The action of TNF at the cellular level is mediated by two cell surface receptors, TNF-R1 (p60) and TNF-R2 (p80). The function of these receptors and the downstream intracellular signal transduction pathway have been extensively studied in vitro and it can be expected, that there are critically important steps in TNF-signal transduction that might be dysregulated in these disease states. Their elucidation could lead to a better understanding of the pathogenesis of these diseases, in particular IBD and potentially reveal new, more specific therapeutic targets. Objective of this review is to give an overview about the current knowledge on TNF signal transduction in relationship to selected examples of important gastrointestinal disorders with special focus on IBD. Finally, the implications for future research efforts will be discussed.
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PMID:Functional relevance of soluble TNF-alpha, transmembrane TNF-alpha and TNF-signal transduction in gastrointestinal diseases with special reference to inflammatory bowel diseases. 1229 83

Autoimmune pancreatitis is a recently defined nosological entity, which accounts for 4.6-6% of all forms of chronic pancreatitis and is often associated with other autoimmune diseases, particularly Sjogren's syndrome. Possession of the HLA DRB1*0405-DQB1*0401 genotype confers a risk for the development of autoimmune pancreatitis. Autoantibodies against carbonic anhydrase II and lactoferrin are frequently present in affected subjects and are suspected to have a pathogenic role. A link between gastric infection by Helicobacter pylori and autoimmune pancreatitis has been hypothesized. We used in silico protein analysis and search for HLA binding motifs to verify this hypothesis. We found a significant homology between human carbonic anhydrase II and alpha-carbonic anhydrase of Helicobacter pylori, an enzyme which is fundamental for the survival and proliferation of the bacterium in the gastric environment. Moreover, the homologous segments contain the binding motif of the HLA molecule DRB1*0405. Our data strengthen the hypothesis that gastric Helicobacter pylori infection can trigger autoimmune pancreatitis in genetically predisposed subjects.
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PMID:Helicobacter pylori and autoimmune pancreatitis: role of carbonic anhydrase via molecular mimicry? 1620 23

We review key sessions on pharmacological treatment, including four on irritable bowel syndrome and others on pancreatitis and Helicobacter pylori infection.
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PMID:Digestive Disease Week. 2618 7

Changes in diet, lifestyle, and exposure to environmental risk factors account for the increased incidence of pancreatic disorders, including acute and chronic pancreatitis, and pancreatic cancer. The role of the microbiota in the development of pancreatic disorders is increasingly acknowledged. The translocation of gut bacteria and endotoxins following gut barrier failure is a key event contributing to the severity of acute pancreatitis, while small intestine bacterial overgrowth is common in patients with chronic pancreatitis and further worsens their symptoms and malnutrition. Specific molecular mimicry link the microbiota and Helicobacter pylori with autoimmune pancreatitis. Changes in the oral microbiota typical of periodontitis seem to be associated with an increased risk of developing pancreatic cancer. The composition of the gut microbiota is also unbalanced in the presence of risk factors for pancreatic cancer, such as obesity, smoking and diabetes. Helicobacter pylori infection, atrophic body gastritis and related decreased gastric acid secretion also seem associated with the risk of pancreatic cancer, although this area needs further research. The link between dysbiosis, immune response and proinflammatory status is most likely the key for these associations. The present review article will discuss current available evidence on the role of gut microbiota in pancreatic disorders, highlighting potential areas for future research.
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PMID:Gut microbiota and pancreatic diseases. 2824 4