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Atopy and current intestinal parasite infection: a systematic review and meta-analysis

Authors


  • Edited by: Hans-Uwe Simon

Johanna Feary, Division of Epidemiology and Public Health, University of Nottingham, City Hospital, Hucknall Road, Nottingham NG5 1PB, UK.
Tel.: +44 115 8231388
Fax: +44 115 8231337
E-mail: jofeary@doctors.org.uk

Abstract

To cite this article: Feary J, Britton J, Leonardi-Bee J. Atopy and current intestinal parasite infection: a systematic review and meta-analysis. Allergy 2011; 66: 569–578.

Abstract

Background:  The rate of increase in prevalence of allergic disease in some countries implies environmental exposures may be important etiological factors. Our aim was to undertake a systematic review and meta-analysis of epidemiological studies to quantify the association between current intestinal parasite infection and the presence of atopy and to determine whether this relation is species specific.

Methods:  We searched MEDLINE, EMBASE, LILIACS and CAB Abstracts (to March 2009); reviews; and reference lists from publications. No language restrictions were applied. We included studies that measured current parasite infection using direct fecal microscopy and defined atopy as allergen skin sensitization or presence of specific IgE. We estimated pooled odds ratios (OR) and 95% confidence intervals (95% CI) using data extracted from published papers using random-effects model.

Results:  Twenty-one studies met our inclusion criteria. Current parasite infection was associated with a reduced risk of allergen skin sensitization OR 0.69 (95% CI 0.60–0.79; P < 0.01). When we restricted our analyses to current geohelminth infection, the size of effect remained similar OR 0.68 (95% CI 0.60–0.76; P < 0.01). In species-specific analysis, a consistent protective effect was found for infection with Ascaris lumbricoides, Tricuris trichuria, hookworm and Schistosomiasis. There were insufficient data to pool results for atopy defined by the presence of specific IgE.

Conclusion:  Intestinal parasite infection appears to protect against allergic sensitization. Work should continue to identify the mechanisms of this effect and means of harnessing these to reduce the global burden of allergic disease.

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