Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2011) 26 OC4.6

ECE2011 Oral Communications Diabetes/Thyroid (6 abstracts)

No causal relationship between Yersinia enterocolitica infection and autoimmune thyroid disease: evidence from a prospective study

G Effraimidis , J G P Tijssen & W M Wiersinga


Academical Medical Centre, University of Amsterdam, Amsterdam, The Netherlands.


Objective: To evaluate prospectively the relationship between Yersinia Enterocolitica (YE) infection and the development of overt autoimmune hypo- or hyperthyroidism (study A) and the de novo occurrence of thyroid antibodies (study B).

Subjects and methods: Prospective cohort study of 790 euthyroid women who were 1st or 2nd degree relatives of AITD patients. Follow-up was 5 years, with annual assessments.

Study A. Nested case–control study in which YE serological status was measured between cases (subjects who developed overt hypothyroidism (TSH>5.7 mU/l and FT4<9.3 pmol/l) or overt hyperthyroidism (TSH<0.4 mU/l and FT4>20.1 pmol/l)) and matched controls.

Study B. Three hundred and eighty-eight euthyroid women without thyroid antibodies at baseline were enrolled. The YE serological status was compared between subjects who developed TPO-Ab and/or Tg-Ab at 4-year follow-up and those who remained negative.

Results: Study A. The proportion of subjects positive for YOP-IgG or YOP-IgA did not differ between cases and controls at baseline. One year before the development of overt hypo- or hyperthyroidism, the proportion of subjects with YOP-IgG was not different between cases and controls, but YOP-IgA were less prevalent in cases.

Study B. De novo occurrence of TPO (or TPO-Ab and/or Tg-Ab) did not differ between subjects in whom at baseline YOP-IgG were positive or negative. Neither persistence nor emergence of YOP-IgG at 4-year follow-up was associated with the occurrence of TPO-Ab or Tg-Ab. Similar results were observed with respect to YOP-IgA.

Conclusions: Yersinia enterocolitica infection does not contribute to an increased risk of thyroid autoimmunity.

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