4.7 Article

Risk of endometriosis in 11 000 women with celiac disease

Journal

HUMAN REPRODUCTION
Volume 26, Issue 10, Pages 2896-2901

Publisher

OXFORD UNIV PRESS
DOI: 10.1093/humrep/der263

Keywords

autoimmunity; celiac disease; inflammation; endometriosis

Funding

  1. Swedish Society of Medicine
  2. Orebro University Hospital
  3. Swedish Research Council-Medicine [522-2A09-195]
  4. Sven Jerring Foundation
  5. Orebro Society of Medicine
  6. Karolinska Institutet
  7. Clas Groschinsky Foundation
  8. Juhlin Foundation
  9. Majblomman Foundation
  10. Uppsala-Orebro Regional Research Council
  11. Swedish Celiac Society

Ask authors/readers for more resources

BACKGROUND: Endometriosis is a common cause of infertility. Whereas celiac disease (CD) is present in similar to 1% of individuals in Western Europe, the prevalence in women undergoing investigation for infertility is often >2%. Still, the relationship between CD and endometriosis is unclear. METHODS: We identified 11 097 women with CD (Marsh 3: villous atrophy) through biopsy data from all 28 pathology departments in Sweden. Biopsies had been performed between 1973 and 2008. Data on inpatient and outpatient diagnoses of endometriosis were retrieved from the National Patient Register. We then used the Cox regression to estimate the hazard ratios (HRs) for endometriosis in women with CD to compare with those in 54 992 age-matched control women. RESULTS: During the follow-up, 118 individuals with CD and 399 matched controls developed endometriosis. Hence, patients with CD were at increased risk of subsequent endometriosis [HR = 1.39; 95% confidence interval (CI) = 1.14-1.70]. The absolute risk of endometriosis in patients with CD was 112/100 000 person-years with an excess risk of 31/100 000. Risk estimates were highest in the first year after diagnosis (HR = 1.49; 95% CI = 0.83-2.67) and gradually decreased (>5 years after CD diagnosis, HR = 1.33; 95% CI = 1.00-1.79). CONCLUSION: Endometriosis seems to be associated with prior CD. Potential explanations include shared etiological factors and CD-mediated inflammation.

Authors

I am an author on this paper
Click your name to claim this paper and add it to your profile.

Reviews

Primary Rating

4.7
Not enough ratings

Secondary Ratings

Novelty
-
Significance
-
Scientific rigor
-
Rate this paper

Recommended

No Data Available
No Data Available