[Therapy of allergic rhinitis]

Abstract

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)