4.3 Article

HLA-DQ types of celiac disease in Libyan children with type 1 diabetes mellitus

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LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/MEG.0b013e32834d09d4

Keywords

celiac disease; endomysium antibody; human leukocyte antigen; tissue transglutaminase antibody; type 1 diabetes mellitus

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Objective To determine the genetic profile of celiac disease (CD) in Libyan children with type 1 diabetes as there are no data on the frequency of human leukocyte antigen (HLA)-related CD-predisposing genes in diabetic patients in Libya. Methods We randomly studied 218 Libyan type 1 diabetic children. The mean age was 12.2 +/- 4.6 years; 56% were female patients. The mean duration of diabetes was 4.7 +/- 4.0 years. All patients were screened for CD with IgA tissue-transglutaminase (tTG) and endomysium antibodies. Patients with positive immunological screen were programmed for a small-bowel biopsy. HLA-DRB1* and HLA-DQB1* were genotyped in all tTG-positive patients. Results Twenty-seven (12.4%) out of 218 patients with type1 diabetes had positive tTG, and 20 (9.2%) of these patients were positive for endomysium antibodies. Five patients (5/27) were already known cases of biopsyproven CD. Biopsy was not performed in two patients. One biopsy result was normal, whereas 19 biopsies demonstrated morphological changes consistent with CD. Forty-eight percent of the anti-tTG-positive group were homozygous for HLA-DQ2, whereas 75% of biopsy-proven CD patients had HLA-DQ2, 21% had HLA-DQ2/DQ8, and 4% had HLA-DQ8. In addition, the majority (70%) carried HLA-DQ2 linkage with HLA-DRB1*03. Conclusion Overall, biopsy-confirmed prevalence of CD was 11% (24 of 218). The present study confirms that CD in the Libyan type 1 diabetic population is high when compared with European and US studies, and for the first time we document that this population shares similar HLA-DQ2 genotype. This supports the theory regarding the role of the environment as an important factor in CD development in this part of the world. Eur J Gastroenterol Hepatol 24: 59-63 (C) 2011 Wolters Kluwer Health | Lippincott Williams & Wilkins.

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