Recent Advances in Bronchial Asthma

Abstract

\s=b\Bronchial asthma in childhood is a major pediatric problem for the physician, both as an acute emergency and as a chronic disease. To adequately manage asthma, one must have a firm understanding of its pathogenesis, and the clinical aspects of diagnosis and therapy. We review important developments in the area of the basic mechanisms causing bronchial obstruction, and methods of measuring the abnormalities present. This presentation includes the fields of neuropharmacology, biochemistry, immunology, and pulmonary physiology. With this background, the clinical aspects of diagnosis and therapy are explored. The role of the allergy history, skin testing, measurement of serum IgE antibodies, and target organ provocation testing are placed in perspective. Therapy involving avoidance measures, use of pharmacologic agents and injection therapy with inhalant allergens are discussed in detail.(Am J Dis Child 130: [890][891][892][893][894][895][896][897][898][899] 1976) Many new and exciting advances in the understanding of bron¬ chial asthma have been made in the last decade. These developments have resulted in a more rational approach to the asthmatic child. The review presented here summarizes this new information by considering the basic scientific aspects of the pathogenesis of asthma, followed by discussion of the recent developments in diagnosis and therapy. PATHOGENESIS OF BRONCHIAL ASTHMA NeuropharmacologyBronchial asthma can no longer be viewed solely as an immunologie disease. The clinical observation that several stimuli, including chemical mediators, irritants, certain respira¬ tory infections, emotional and physi¬ cal factors, as well as allergen chal¬ lenge, can result in bronchospasm, created the need for a broader concept in underlying abnormality.In the early 1960s, Szentivanyi1 advanced the theory of /3-adrenergic blockade as a possible unifying path¬ ogenic mechanism in asthma. This theory proposes that many of the stimuli that result in the clinical syndrome of asthma do so by causing release of potent chemical mediators of inflammation such as the kinins, slow-reacting substance of anaphy¬ laxis (SRS-A), histamine, serotonin, and acetylcholine. The mediators, in turn, cause both bronchoconstriction and secretion of epinephrine as a homeostatic response. If /5-adrenergic receptors are normally responsive, activation by epinephrine will balance concurrent a-adrenergic and cholinergic receptor stimulation, and airway patency will be maintained. However, if /3-receptors are defective, bronchoconstriction will result.Evidence for generalized /^-blockade in asthma includes metabolic, pulmo¬ nary, and hématologie changes. There is less elevation of serum glucose, lactate, and pyruvate levels following administration of the ß-adrenergic stimulants, isoproterenol hydrochloride and epinephrine hydrochloride, in asthmatics than in normal subjects.2 ;' Administration of the /5-blocking agent, propranolol hydrochloride, leads to increased airway resistance in asthmatic patients'; in patients with allergic ...