Ivarsson Anneli
Epidemiology and Public Health Sciences, Department of Public Health and Clinical Medicine, Umeå University, S-901 87, Umeå, Sweden.
Best Pract Res Clin Gastroenterol. 2005 Jun;19(3):425-40. doi: 10.1016/j.bpg.2005.02.005.
Sweden has experienced an epidemic of symptomatic coeliac disease that has no likeness anywhere else in the world. This is quite unique for a disease that is genetically dependent, immune-mediated and chronic, and suggests an abrupt increase and decrease, respectively, of one or a few causal factors influencing a large proportion of Swedish infants during the period in question. We have shown that half of the epidemic was explained by an increase in the proportion of infants introduced to gluten in comparatively large amounts after breast-feeding had been ended. This was partly an effect of societal changes in national dietary recommendations and the food content of industrially produced infant foods. Thus, these changes over time in infant feeding practices had a large public health impact. In fact, when the Swedish epidemic began, the increase in incidence rate was larger in girls than in boys, as was the decrease during the post-epidemic period. Moreover, children born during summer had an increased risk for coeliac disease, possibly as they were mostly introduced to dietary gluten during winter when infections are more common. Notably, birth cohorts of the epidemic and post-epidemic periods differ considerably regarding coeliac disease occurrence at comparable ages, even when followed up to school age. A longer follow-up will reveal to what extent new cases develop later in life, and to what extent this difference in cumulative incidence remains. However, mass screening studies of both the epidemic and post-epidemic cohorts at comparable ages are also planned to determine to what extent 'silent' disease cases develop. Continuing to explore the Swedish epidemic of coeliac disease by means of an epidemiological approach provides a unique opportunity. This may include increasing our understanding of what determines the clinical expression of the disease, exploring the potentially causal role of environmental exposures, and possibly also identifying strategies for primary prevention.
瑞典经历了有症状的乳糜泻流行，这在世界其他任何地方都没有类似情况。对于一种具有遗传依赖性、免疫介导且慢性的疾病来说，这相当独特，表明在相关时期内，影响很大一部分瑞典婴儿的一个或几个致病因素分别突然增加和减少。我们已经表明，该流行病的一半可归因于在母乳喂养结束后以相对大量引入麸质的婴儿比例增加。这部分是国家饮食建议的社会变化以及工业生产的婴儿食品的食物成分所产生的影响。因此，婴儿喂养方式随时间的这些变化对公共卫生产生了重大影响。事实上，瑞典流行病开始时，发病率的上升在女孩中比在男孩中更大，流行后时期的下降情况也是如此。此外，夏季出生的儿童患乳糜泻的风险增加，可能是因为他们大多在冬季感染更常见时开始摄入饮食中的麸质。值得注意的是，即使随访至学龄期，流行期和流行后期的出生队列在可比年龄的乳糜泻发病情况也有很大差异。更长时间的随访将揭示新病例在生命后期发展的程度，以及这种累积发病率差异在多大程度上仍然存在。然而，也计划对可比年龄的流行期和流行后期队列进行大规模筛查研究，以确定“无症状”疾病病例发展的程度。通过流行病学方法继续探索瑞典的乳糜泻流行提供了一个独特的机会。这可能包括增进我们对决定该疾病临床表型的因素的理解，探索环境暴露的潜在因果作用，以及可能还包括确定一级预防策略。
