Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0000737 (abdominal pain)
 31,184 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Eosinophilic gastroenteritis is a heterogeneous and uncommon disorder characterized by eosinophilic inflammation of the gastrointestinal tissues. The location and depth of infiltration determine its varied manifestations, and the latter is also the basis for the proposed classification into mucosal, muscular and serosal eosinophilic gastroenteritis. Abdominal pain, vomiting, and diarrhea are each present in nearly 50% of the patients, with some overlap. Peripheral eosinophilia is seen in approximately two-thirds of patients with eosinophilic gastroenteritis. It is now clear that eotaxin, a specific eosinophil chemoattractant, plays a pivotal role in the process of eosinophil production. The differential diagnosis of eosinophilic gastroenteritis in children includes parasitic infections, inflammatory bowel disease, connective tissue diseases, some malignancies and adverse effects of drugs. Eosinophilic gastroenteritis itself has been strongly associated with food allergies, and concomitant atopic diseases or a family history of allergies is elicited in about 70% of cases. The pediatric experience is unique with respect to recognition of distinctive entities such as allergic procto-colitis, almost exclusively seen in infants, and eosinophilic esophagitis being increasingly reported among children and young adults. The gold standard for diagnosis, usually demonstrated on endoscopic biopsies, is prominent tissue eosinophilia. However, the diagnosis may be obscured by the patchy nature of the disease, and muscular and serosal eosinophilic gastroenteritis subtypes. In the latter cases, full thickness biopsies would be indicated for a definitive diagnosis. There are many reports of successful treatment of eosinophilic gastroenteritis in children, using a variety of treatment regimens including elimination diets. Corticosteroids remain the most effective agents for controlling symptoms, but unfortunately the relapsing nature of the disease would mandate prolonged corticosteroid use. Reports of favorable responses to new leukotriene inhibitors in patients with eosinophilic gastroenteritis are encouraging; these responses should stimulate future research on the pathophysiology and management of eosinophilic gastroenteritis.
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PMID:Eosinophilic gastroenteritis: epidemiology, diagnosis and management. 1217 71

BACKGROUND: Eosinophilic gastritis is related to eosinophilic gastroenteritis, varying only in regards to the extent of disease and small bowel involvement. Common symptoms reported are similar to our patient's including: abdominal pain, epigastric pain, anorexia, bloating, weight loss, diarrhea, ankle edema, dysphagia, melaena and postprandial nausea and vomiting. Microscopic features of eosinophilic infiltration usually occur in the lamina propria or submucosa with perivascular aggregates. The disease is likely mediated by eosinophils activated by various cytokines and chemokines. Therapy centers around the use of immunosuppressive agents and dietary therapy if food allergy is a factor. CASE PRESENTATION: The patient is a 31 year old Caucasian female with a past medical history significant for ulcerative colitis. She presented with recurrent bouts of vomiting, abdominal pain and chest discomfort of 11 months duration. The bouts of vomiting had been reoccurring every 7-10 days, with each episode lasting for 1-3 days. This was associated with extreme weakness and cachexia. Gastric biopsies revealed intense eosinophilic infiltration. The patient responded to glucocorticoids and azathioprine. The differential diagnosis and molecular pathogenesis of eosinophilic gastritis as well as the molecular effects of glucocorticoids in eosinophilic disorders are discussed. CONCLUSIONS: The patient responded to a combination of glucocorticosteroids and azathioprine with decreased eosinophilia and symptoms. It is likely that eosinophil-active cytokines such as interleukin-3 (IL-3), granulocyte macrophage colony stimulating factor (GM-CSF) and IL-5 play pivotal roles in this disease. Chemokines such as eotaxin may be involved in eosinophil recruitment. These mediators are downregulated or inhibited by the use of immunosuppressive medications.
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PMID:Eosinophilia in a patient with cyclical vomiting: a case report. 1514 61

Eosinophilic gastroenteritis despite its uncommon occurrence is one of the most important primary eosinophilic gastrointestinal disorders, and most commonly presents with abdominal pain. The terminology is, however, misleading because all levels of the gastrointestinal tract from the esophagus to the rectum may be affected. A history of atopy and allergies is present in 25-75% cases. The heterogeneity in the clinical presentations of EG is determined by the site and depth of eosinophilic infiltration. Eosinophilic intestinal inflammation also occurs secondarily in the gastrointestinal tract in inflammatory bowel disease, autoimmune diseases, as reactions to medications, infections, hypereosinophilia syndrome, and after solid organ transplantation. Recent investigations providing an insight into the pathogenesis of eosinophilic gastroenteritis support a critical role for allergens, eosinophils, Th-2 type cytokines, and eotaxin in mediating eosinophilic inflammation. The diagnosis is confirmed by demonstrating prominent tissue eosinophilia on histopathology. Treatment recommendations based on data extrapolated from retrospective, uncontrolled studies, and expert opinion support the use of restricted diets, corticosteroids, leukotriene receptor antagonists, and mast cell stabilizers. Many unanswered questions remain with regard to the natural history, optimal duration of therapy, safer steroid-sparing long-term treatment agents, and the means of reliable and non-invasive follow-up.
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PMID:Eosinophilic gastroenteritis. 1583 87

Cytokines are secreted immunomodulating proteins involved in pancreatic stellate cell activation and propagation of fibrosis in chronic pancreatitis. We aim to show that cytokines can be identified from pancreatic fluid by (1) collecting pancreatic fluid with the ePFT method, (2) processing the fluid for cytokine-targeted microarray analysis, and (3) comparing cytokine profiles in pancreatic fluid of chronic pancreatitis (CP) patients and of chronic abdominal pain (CAP) controls. We endoscopically collected pancreatic fluid from patients with CP and those with CAP using the ePFT method. This fluid was subjected directly to a multiplexed cytokine protein microarray assay. Six patients (3 CP, 3 CAP) underwent a secretin-stimulated ePFT. The mean peak bicarbonate concentrations [meq/L] of the CP and CAP patients were 43 and 97, respectively. Statistically significant decreases in the cytokine concentrations of EGF, IP-10, eotaxin, IL-3, MIP-1a, IL-15, PDGF-AB/BB, and IL-1a were observed in the CP specimens (p<0.05). We have successfully identified differences in the abundance of cytokines in ePFT-collected pancreatic fluid with a multiplexed microarray assay comparing CP and CAP controls. Further targeted investigation of cytokines in ePFT-collected fluid will broaden our knowledge of pancreatic immune response and pathogenesis in chronic pancreatitis.
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PMID:Cytokine profiling of pancreatic fluid using the ePFT collection method in tandem with a multiplexed microarray assay. 2156 76