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)

Nasal allergy is due to a change in the immunoreactivity of an individual. B-lymphocytes produce allergen-specific IgE antibodies after the antigen is presented to T-helper cells. IgE bound to mast cells leads to mast cell activation in the case of antigen contact. Mast cells release mediators and induce local inflammation. The symptoms of allergic rhinitis are caused by various factors and are different in individuals, and hence therapy must be in accordance with the necessities in the individual. There are four principles of therapy in allergic rhinitis. The first and best is allergen avoidance. It is the first choice in animal allergy and important in mite allergy. It is difficult for mold allergy and impossible for pollen allergy. The second is immunotherapy. Immunotherapy is a specific form of controlled allergen admission that changes immunoreactivity into allergen tolerance in a major part of patients. Immunotherapy is a very important tool if performed by a physician with experience. The third principle is drug therapy. With todays drugs, it is still symptomatic. alpha-sympathomimetic vasoconstrictors administered systemically (and, still better, locally) relieve nasal stuffiness. Parasympatholytic drugs can abort pathological secretions. Cromoglycate (DNCG) is a local prophylactic drug improving all symptoms of allergic rhinitis. DNCG is the first choice in pollinosis. Antihistamines are usually given systemically, and the modern drugs have no sedative effect. Clinical effects are comparable to DNCG, and there are new substances available for local therapy. Steroids given systematically improve all symptoms of allergy and inflammation after a certain delay. Due to side effects, local steroids are preferred today.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Therapy of allergic rhinitis]. 810 4

Eosinophilic gastrointestinal disorders, including eosinophilic esophagitis, gastroenteritis, and colitis, refer to a spectrum of clinical diseases that present with variable degrees of infiltration of the gastrointestinal tract by eosinophils in the absence of other known causes of tissue eosinophilia. Clinical symptoms and laboratory findings are usually non-specific and may or may not be accompanied by peripheral blood eosinophilia. The extent of eosinophilic infiltration of the gastrointestinal wall varies from mucosal to transmural and serosal involvement. Diagnosis requires presence of gastrointestinal symptoms, demonstration of gastrointestinal eosinophilia by biopsy, and exclusion of other known causes of tissue eosinophilia. Many studies have pointed toward the eosinophil as the major offender; however, the exact functional role of the eosinophil in the pathogenesis of eosinophilic gastrointestinal disorders remains unclear. The roles of T-helper-2 cytokines and other mediators, such as eotaxin-1 and interleukin-5, have gained significant importance in the pathobiology of eosinophilic gastrointestinal disorders. Current understanding of treatment is based on case reports and a few case series, as there is a lack of large prospective studies. Steroids are currently the mainstay of therapy, but the roles of other drugs such as leukotriene inhibitors, mast cell stabilizers, interleukin-5 inhibitors, and anti-immunoglobulin E, along with other targets in the immune pathway, are currently being explored.
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PMID:Eosinophilic Gastroenteritis and Colitis: a Comprehensive Review. 2605 22