Background: Celiac disease, a permanent gluten sensitive enteropathy, is the most common genetic disorder, although largely underestimated public health problem worldwide. The wide spectrum of its multifaceted manifestations is a continuum representing the outcome of a complex interplay of genetic and environmental factors with immunological processes suggesting its multifactorial etiopathogenesis and also involves the risk of malignancy. Despite of the new insights gained by recent advances in knowledge, etiopathogenesis still remains to be elucidated completely. Investigating the Swedish epidemic of CD by epidemiological approach has revealed the possible associations of CD with some environmental factors. Emphasizing the significance of events in early infancy in view of current CD aetiopathogenesis concepts and with relevance to the unique pattern of CD incidence trends in Swedish children, early infectious episodes emerge as seemingly important clue in etiology of CD. This study investigates the possible contribution to the risk from early infectious episodes to development of Celiac disease. Objectives: This study aims to investigate possible contribution by early infectious episodes to the risk of development of celiac disease and discusses the findings in view of current concepts of CD aetiopathogenesis. Methods: Literature-review. A review of available knowledge from studies in the aetiopathogenesis of celiac disease was done to understand the possible association with environmental factors, in particular role of infectious episodes. Study-design and data-analysis: Data from a Swedish population-based incident case-referent study with 627 confirmed cases of celiac disease and 1254 referents was analyzed to investigate a possible predisposition caused by early infections to celiac disease. Results: Current literature suggests that infections may induce, trigger the development of CD (Gl infectious episodes to the major extent) or may activate already latent CD by different mechanisms. However, our study concludes statistically significant risk associated with early infectious episodes of all types to the development of celiac disease. Besides, findings suggest higher risk associated with the combined effect of consumption of larger amounts of gluten and frequent infectious episodes. Conclusion: This study presents the first epidemiological findings concluding increased risk to development of celiac disease associated with occurrence of infectious episodes during early infancy (before the age of 6 months), and suggests possible involvement of molecular mimicry or other mechanism. The findings also suggest focusing on early infancy and to the events that precede immunopathogenetic processes. Thus, it provides implication for the further exploration of complete immunolopathogenetic mechanisms involved in pathogenesis of celiac disease and it may prove rewarding in designing innovative preventive, immunomodulatory and antigen-centered therapeutic strategies. / digitalisering@umu
| Identifer | oai:union.ndltd.org:UPSALLA1/oai:DiVA.org:umu-188790 |
| Date | January 2006 |
| Creators | Joshi, Himanshu |
| Publisher | Umeå universitet, Epidemiologi och folkhälsovetenskap, Umeå : Umeå universitet |
| Source Sets | DiVA Archive at Upsalla University |
| Language | English |
| Detected Language | English |
| Type | Student thesis, info:eu-repo/semantics/bachelorThesis, text |
| Format | application/pdf |
| Rights | info:eu-repo/semantics/openAccess |
| Relation | Public health report series, 1651-341X ; 2006:15 |
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