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Κυριακή 27 Ιανουαρίου 2019

Population based study: atopy and autoimmune diseases are associated with functional dyspepsia and irritable bowel syndrome, independent of psychological distress

Summary

Background

The pathogenesis of functional GI disorders (FGIDs) is uncertain. However, underlying immune activation and psychological distress has been documented in irritable bowel syndrome (IBS) and functional dyspepsia (FD). Epidemiological data from the UK suggest that FGIDs are linked to atopy and certain autoimmune diseases but this has not been confirmed.

Aim

To test if allergic or autoimmune diseases are independently associated with FGIDs, irrespective of psychological distress in a large population based study.

Methods

A total of 3542 people (mean age 57.9 years and 52.7% females) randomly selected from the Australian population, returned a mail survey (response rate = 43%). The survey asked about a physician diagnosis of autoimmune disease (scleroderma, psoriasis, rheumatoid arthritis and diabetes mellitus) or allergic conditions (asthma, food, pollen and/or animal allergy). The questionnaire assessed psychological distress and Rome III criteria for FD and IBS.

Results

Asthma, food, pollen and animal allergies, psoriasis and rheumatoid arthritis were univariately significantly associated with IBS and FD. Food allergy (OR = 1.66; 95% CI = 1.15‐2.40, P = 0.007), psoriasis (OR = 1.81; 95% CI = 1.19‐2.74, P = 0.006) and rheumatoid arthritis (OR = 1.68; 95% CI = 1.15‐2.4, P = 0.007) were independent risk factors for IBS, controlling for age, gender and psychological distress. In FD, asthma (OR = 1.32; 95% CI = 1.04‐1.68, P = 0.025) and food allergy (OR = 1.78; 95% CI = 1.28‐2.49, P = 0.001) were independent predictors, controlling for age, sex and psychological distress.

Conclusions

There is evidence that both atopic and autoimmune diseases are risk factors for FGIDs, independent of psychological distress, differing in IBS and FD. This provides evidence that different peripheral pathways may be involved in the pathogenesis of certain FGIDs.



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