Aspirin Sensitive Asthma: Provocation Tests Do Not Work in Such Patients

Abstract

In response to the impressive scientific review article by Randerath and Galetke, we want to share our own experiences with the treatment of asthma and nasal polyps, in these times of increasing funding shortages, to show that there are simpler solutions to the problem. Small practices cannot present high case numbers or evidence- based study designs. We tested the tolerability of salix (willow) and acetylsalicylic acid (ASA) in 536 patients with allergies using electroacupuncture according to the method of Voll (EAV) in 115 patients with rhinoconjunc tivitis and in 65 asthma patients with concomitant migraine or lipid metabolism disorders (1). Of those 180 patients 11 were affected, of whom two reacted to willow and ASA. They were successfully desensitized by using destructive interference (3). This method is used similarly for stimulants such as tree or grass pollen, house dust mites, eiderdown, and synthetic fibers, to prevent nasal polyps and subsequent aspirin sensitive asthma successfully. The author has been using ASA at low dosages since 1985 after testing for thrombocyte hyperaggregability (2). Platelet agglutinating factor (PAF) is released in every allergic reaction and causes microcirculatory disruptions that may manifest as pain or shortness of breath. Mast cells are activated not only by IgE but also by type III reactions (IgG). Immunocomplexes develop that activate complement pathways, thereby releasing slow reacting substances or leukotrienes. The simultaneously released heparin and similar glycosaminoglycans stimulate the matrix to release large basic proteins and arginine and lysine from eosinophils, which pro vides a stimulus to attract more eosinophils. These processes are disrupted by destructive interference, and the mast cell system can calm down. We cannot accept Randerath and Galetke’s statement: Currently there is no reliable in-vitro method to diag nose aspirin sensitive asthma, so that provocation tests are vital. Our own clinical practice has shown that prov ocation tests do not work in such patients. We there fore need leukotriene antagonists for such patients only in the initial phase of their treatment. ASA does not have to present a real problem in practice.