Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P15088 (mast cell)
 14,925 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The gut wall is one of the conspicuous sites of eosinophil accumulation, presumably because of local chemotactic stimuli. It is reasonable to assume that one chemotactic factor is released by the mast cell, which is often found in proximity to the eosinophil. The association of eosinophils and eosinophilia with allergic disorders has long been recognized, and recent work has shown that increased eosinophil production is mediated by the lymphocyte. That process shares characteristics with other immunological actions. An increased rate of eosinophil tissue accumulation and destruction may be the factor which initiates the mechanism for increased production. None of many hypotheses about the 'function' of the eosinophil is substantiated; nevertheless it seems likely that this member of the immunological apparatus, which tends to be distributed in the front line (mucosal and cutaneous tissues), fulfils some normal protective or homeostatic function. Aside from that assumed normal function, there is growing clinical evidence that eosinophils can at times cause host injury, for example in such states as eosinophilic gastroenteritis and endomyocarditis.
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PMID:Immunology of the gut: role of the eosinophil. 34 22

A surgical case of a middle-aged Japanese with eosinophilic gastroenteritis is described. This 50-year-old man presented protein-losing gastroenteropathy, iron-deficiency anemia, and marked elevation of serum IgE, in whom the lesion formed a diffuse thickening of almost the entire portion of the stomach. Microscopically, there was an intense infiltration of eosinophils throughout the whole thickness of the gastric wall, interspersed with plasma cells and lymphocytes. On the affected area, an increased number of IgE-positive plasma cells and surface IgE-positive mast cells, some of which are degranulated, were identified. These immunohistochemical findings provide a strong evidence for IgE mast cell-mediated allergy concerning this disorder.
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PMID:Eosinophilic gastroenteritis. Immunohistochemical evidence for IgE mast cell-mediated allergy. 389 14

A 24-yr-old female presented with a giant gastric ulcer and anemia. She suffered from a transient infantile malabsorption syndrome with eosinophilia. The diagnosis of eosinophilic gastroenteritis associated with the gastric ulcer was made by endoscopic biopsy. Ulcer healing was refractory to medical therapy and partial gastrectomy was performed. Histologic examination revealed transmural eosinophilic infiltrates with mast cell infiltrates in the gastric wall. This case illustrates (1) an extremely rare presentation of eosinophilic gastroenteritis--giant, refractory, gastric ulcer; (2) a potential pathogenic role for mast cells in this syndrome; and (3) the chronic and relapsing nature of the syndrome.
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PMID:Giant antral ulcer: a rare presentation of eosinophilic gastroenteritis--case report and review of the literature. 921 1

Eosinophils contribute to the inflammatory process in a variety of chronic inflammatory bowel diseases. Ketotifen is beneficial in experimental models of colitis and in patients with eosinophilic gastroenteritis. Therefore, we investigated the efficacy of ketotifen therapy for the treatment of active ulcerative colitis. Children with newly or previously diagnosed ulcerative colitis with mild-moderate disease activity were treated with ketotifen at a dosage of 4 mg daily for eight weeks. Efficacy was determined by a physician disease severity index and by endoscopic and histologic examinations. Ten patients were enrolled. Symptoms improved in four patients and resolved completely in one patient. There was endoscopic improvement in three patients and histologic improvement in one. Increased eosinophils on rectal biopsy at entry were present in two of the responders. Five patients withdrew due to a lack of symptomatic improvement. No adverse events were identified. Low-dose ketotifen offers a limited therapeutic advantage in active ulcerative colitis that may be enhanced in the subgroup of patients with a high eosinophil count in the colonic mucosa. Further study of therapeutic efficacy with increased dosages of the mast cell stabilizer for acute and maintenance therapy is warranted.
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PMID:Ketotifen therapy for acute ulcerative colitis in children: a pilot study. 953 58

There are no evidence-based studies of the treatment of patients with eosinophilic gastroenteritis. Treatment decisions depend on experience gained from observations linking causative entities, principal clinical manifestations, and anticipated natural history of the disease. Because clinical symptoms and organ involvement probably vary with etiology, classification as to the likely cause (eg, food allergy or other dietary intolerance, idiosyncratic drug reaction, occult infection, idiopathic) determines the decisions made about dietary, pharmacologic, and surgical treatment. Elimination of foods and the use of elemental diets, corticosteroids, and mast cell inhibitors (eg, cromolyn sodium, ketotifen), alone or in combination, all have their place, depending on the age of the patient, organ involved, clinical presentation, and clinical urgency. Isolated cases are diagnosed only at surgical exploration for acute abdominal catastrophes; in these instances, further therapy depends on whether resection is done, but most patients remain in remission after surgery. Occult parasitism remains an elusive and unrecognized cause of an unknown number of cases, suggesting that empiric antihelminthic therapy should be tried in some patients. Individual reports of success with nonsystemic steroids and leukotriene inhibitors have been published.
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PMID:Eosinophilic Gastroenteritis. 1179 33

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

Systemic mastocytosis (SM) is characterized by the accumulation of neoplastic mast cells in bone marrow and other organs. Gastrointestinal (GI) symptoms are common in both SM and cutaneous mastocytosis [urticaria pigmentosa (UP)], and are usually caused by the release of histamine and other inflammatory mediators. Occasionally, neoplastic mast cells may also directly infiltrate the GI tract. Previous studies have suggested that enumeration of the mast cells in GI biopsies may help establish the diagnosis of SM. However, mast cells have been reported to be increased in various inflammatory diseases, and mast cell density has not been systematically evaluated in other GI disorders. Recently, expression of CD25 by mast cells in bone marrow has been shown to be specific for SM. The purpose of this study was (1) to quantitate and compare mast cells in mucosal biopsies from patients with SM involving the GI tract, UP with GI symptoms, and a control group of diverse inflammatory disorders, and (2) to determine whether immunostaining for CD25 can be used to distinguish neoplastic from reactive mast cells in GI biopsies. Seventeen GI biopsies from 6 patients with SM; 17 GI biopsies from 5 patients with UP; and 157 control cases including 10 each normal stomach, duodenum, terminal ileum, and colon, Helicobacter pylori gastritis, bile reflux gastropathy, peptic duodenitis, celiac disease, Crohn disease, ulcerative colitis, lymphocytic colitis, and collagenous colitis, 20 biopsies from 16 patients with irritable bowel syndrome, 8 biopsies from 5 patients with parasitic infections, and 9 biopsies from 7 patients with eosinophilic gastroenteritis were immunostained for mast cell tryptase, c-kit (CD117), and CD25. Mucosal mast cells were quantitated, and the presence or absence of CD25 expression on mast cells was determined. In SM patients, mast cells in the small intestine and colon numbered >100/high-power field (HPF) in nearly all cases (mean 196/HPF; range 74 to 339). This was significantly higher than in GI biopsies from UP patients (mean 17/HPF; range 8 to 32, P<0.0001) and all inflammatory diseases (P<0.01). Mast cell density in other disorders ranged from a mean of 12/HPF in H. pylori gastritis to 47/HPF in parasitic infections. Interestingly, all SM biopsies (and none of the other cases) contained aggregates or confluent sheets of mast cells. In addition, mast cells in all SM cases were positive for CD25, whereas GI mucosal mast cells in UP and all other control cases were negative. In conclusion, quantitation of mast cells can be helpful to diagnose SM in GI mucosal biopsies, although mast cells are also markedly increased in parasitic infections. Aggregates or sheets of mast cells are only seen in SM. Immunoreactivity for CD25 in GI mucosal mast cells is specific for SM and can be used to confirm the diagnosis.
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PMID:Immunoreactivity for CD25 in gastrointestinal mucosal mast cells is specific for systemic mastocytosis. 1805 23