Screening for coeliac disease in adult patients with type 1 diabetes mellitus: myths, facts and controversy.

Suat Simsek,Sjoerd F. Bakker,Hetty J. Bontkes,Chris J. Mulder,Boudewina M. E. von Blomberg,Maarten E. Tushuizen

doi:10.1186/s13098-016-0166-0

Suat Simsek, Sjoerd F. Bakker + Show 4 more

Open Access

https://doi.org/10.1186/s13098-016-0166-0

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Abstract

This review aims at summarizing the present knowledge on the clinical consequences of concomitant coeliac disease (CD) in adult patients with type 1 diabetes mellitus (T1DM). The cause of the increased prevalence of CD in T1DM patients is a combination of genetic and environmental factors. Current screening guidelines for CD in adult T1DM patients are not uniform. Based on the current evidence of effects of CD on bone mineral density, diabetic complications, quality of life, morbidity and mortality in patients with T1DM, we advise periodic screening for CD in adult T1DM patients to prevent delay in CD diagnosis and subsequent CD and/or T1DM related complications.

Highlights

Coeliac disease (CD) is a permanent intolerance to ingested gluten resulting in immune mediated inflammatory damage to the small intestinal mucosa and a subsequent malabsorption syndrome [1]
Genetic overlap exists between coeliac disease (CD) and type 1 diabetes mellitus (T1DM) consisting of both human leukocyte antigen (HLA) and non-HLA genes [14,15,16]. Both disorders are associated with the major histocompatibility complex (MHC) class 2 antigen DQ encoded by the alleles DQA1*05 with DQB1*02 (DQ2.5) and DQA1*03 with DQB1*03:02 (DQ8) [1, 17]
Rationale for screening for CD in adult T1DM patients CD fulfills many of the World Health Organization (WHO) criteria for screening in patients with T1DM but not all of them [83]

Summary

Background

Coeliac disease (CD) is a permanent intolerance to ingested gluten resulting in immune mediated inflammatory damage to the small intestinal mucosa and a subsequent malabsorption syndrome [1]. Genetics T1DM and CD are auto-immune, inflammatory diseases for which the major genetic contribution arises from the major histocompatibility complex [12] These so-called HLA-DQ heterodimers enable the presentation of peptides that are derived from otherwise innocuous self- or non-self antigens (proteins from insulin producing beta cells in T1DM, gliadins in CD) and activate pathogenic effector T-cells [13]. Genetic overlap exists between CD and T1DM consisting of both HLA and non-HLA genes [14,15,16] Both disorders are associated with the major histocompatibility complex (MHC) class 2 antigen DQ encoded by the alleles DQA1*05 with DQB1*02 (DQ2.5) and DQA1*03 with DQB1*03:02 (DQ8) [1, 17]. In patients with T1DM, the HLA-DQ 2.5 haplotype showed a significant association and provided the highest risk for developing double autoimmunity (OR = 1.44, p-value = 0.0003, Table 1). These studies show conflicting results [28,29,30]

Demographic characteristics

Frequency controls

Enteropathy associated T cell lymphoma ?

Australian Diabetes Society

Findings

Conclusions