Turner K J
P N G Med J. 1978 Mar;21(1):86-104.
Nothwithstanding difficulties associated with the limitations of survey techniques and methodology employed to define asthma, the evidence accumulated to date suggests that the reported differences in the prevalence rates of this disease from country to country and within local populations of the one country are real. It is accepted that allergy is not the sole cause of asthma but nonetheless hypersensitivity to environmental allergens is a significant triggering factor in most countries of the world. Comparisons between countries might therefore be influenced by the time of the year when the survey is taken since the prevalence of seasonal asthma would be higher in the period of pollinosis. Environmental factors, and in particular the relative atmospheric concentrations of pollens and the density of house dust mite (D. pteronyssinus and D. farinae) in dwellings, must therefore be considered when accumulating prevalence data. The prevalence rate for childhood asthma is high in Australia, United Kingdom, United States of America and New Zealand, and medium to low in the Scandinavian countries and Switzerland. It is not clear what factors contribute toward these differences since several studies indicate that racial characteristics per se are not pre-eminent in defining susceptibility to asthma. Most surveys indicate that the prevalence of childhood asthma is low to very low among low-income populations living in tropical areas. While it is possible to implicate inadequate diagnosis, genetic factors, nutritional status and allergen exposure as factors contributing towards the low prevalence, it has become fashionable to attribute this observation to the influence of certain helminthic infections. Parasites stimulate the production of high levels of serum IgE, the bulk of which has as yet an undetermined specificity. The suggestion that this IgE blocks mast cell receptors leaving insufficient sites available for sensitization by allergen-specific IgE antibody is attractive. However, since the kinetics of binding to mast cell receptors is unlikely to be the same for all IgE molecules, irrespective of their specificity, this hypothesis appears to be an oversimplification of the problem. It is more likely that parasitic infections repress the synthesis of IgE antibody to environmental allergens, although the mechanism for this is unclear. Circumstantial evidence suggests that the time course of exposure to parasites versus sensitization by environmental allergens may be critical. Another possibility is that parasitic infections in some way nullify the effect of allergens at the level of the target organ, perhaps through the modulating role of eosinophils. If it is established that parasitic infections, particularly in early childhood, suppress the capacity of potentially atopic children to develop asthma and other allergic disorders, there would be some justification in attempting to circumvent allergic disorders in susceptible individuals by a harmless preparation of parasite antigens.
尽管用于定义哮喘的调查技术和方法存在局限性，但迄今积累的证据表明，各国之间以及一国国内不同地区报告的这种疾病患病率差异是真实存在的。人们公认过敏不是哮喘的唯一病因，但对环境过敏原的超敏反应在世界上大多数国家仍是一个重要的触发因素。因此，各国之间的比较可能会受到调查时间的影响，因为在花粉症期间季节性哮喘的患病率会更高。在积累患病率数据时，必须考虑环境因素，特别是花粉的相对大气浓度以及住宅中屋尘螨（粉尘螨和户尘螨）的密度。澳大利亚、英国、美国和新西兰儿童哮喘的患病率较高，而斯堪的纳维亚国家和瑞士则为中低水平。目前尚不清楚导致这些差异的因素是什么，因为多项研究表明种族特征本身在确定哮喘易感性方面并非首要因素。大多数调查表明，生活在热带地区的低收入人群中儿童哮喘的患病率很低甚至极低。虽然可以将诊断不足、遗传因素、营养状况和过敏原暴露视为导致低患病率的因素，但将这种现象归因于某些蠕虫感染的影响已成为一种时尚观点。寄生虫会刺激产生高水平的血清IgE，其中大部分的特异性尚未确定。认为这种IgE会阻断肥大细胞受体，从而使可供过敏原特异性IgE抗体致敏的位点不足，这一观点很有吸引力。然而，由于所有IgE分子（无论其特异性如何）与肥大细胞受体结合的动力学不太可能相同，所以这一假设似乎过于简化了问题。更有可能寄生感染会抑制针对环境过敏原的IgE抗体的合成，尽管其机制尚不清楚。间接证据表明，接触寄生虫与环境过敏原致敏的时间进程可能至关重要。另一种可能性是，寄生感染可能以某种方式在靶器官水平抵消过敏原的作用，也许是通过嗜酸性粒细胞的调节作用。如果确定寄生感染，尤其是在幼儿期，会抑制潜在特应性儿童患哮喘和其他过敏性疾病的能力，那么尝试通过无害的寄生虫抗原制剂来规避易感个体的过敏性疾病就有一定的合理性。
