Boudewina M. von Blomberg

Frequent delay of coeliac disease diagnosis in symptomatic patients with type 1 diabetes mellitus: Clinical and genetic characteristics

BACKGROUND Patients with type 1 diabetes mellitus (T1DM) are more prone to develop other auto-immune diseases, including coeliac disease (CD). Paediatric patients with T1DM are screened for CD, whereas in adult T1DM patients screening programs for CD are not standardised. The aim of this study was to investigate clinical and genetic characteristics of patients with both diagnoses so as to lead to better detection of CD in adult patients with T1DM. METHODS We studied 118 patients with both T1DM and CD identified in The Netherlands. We retrospectively collected data on sex distribution, age of onset of T1DM, age of CD diagnosis, CD complaints, duration of CD complaints before CD diagnosis, family history of CD or T1DM, comorbidity and HLA-DQ type. RESULTS Thirty-three percent of T1DM+CD patients reported CD related complaints for at least 5 years before CD diagnosis. Two peaks in the age of CD diagnosis in T1DM patients were observed: around 10 and 45 years of age. Women were diagnosed with CD at a younger age than men (median 25 years (IQR 9-38) versus 39 (12-55) years, respectively, P<0.05). CONCLUSION A delay of CD diagnosis is frequently found in adult T1DM patients and two peaks in the age of CD diagnosis are present in T1DM patients. This observational study emphasises that more frequent screening for CD in particularly adult T1DM patients is required, preferably by a 5 years interval.

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

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.

Antibody titers against food antigens decrease upon a gluten-free diet, but are not useful for the follow-up of (refractory) celiac disease.

Sascha Gross, Roy L.J. van Wanrooij, Greetje J. Tack, Kyra A. Gelderman, Sjoerd F. Bakker, Ingrid M.W. van Hoogstraten, Eskelina A. Neefjes-Borst, Marco W.J. Schreurs, Gerd Bouma, Chris J.J. Mulder, Boudewina M.E. von Blomberg and Hetty J. Bontkes, Medical Immunology Unit, Department of Pathology, Department of Gastroenterology, VU Medical Centre, Amsterdam and Department of Immunology, Erasmus MC, University Medical Center, Rotterdam, The Netherlands

High myeloid-derived suppressor cell frequencies in the duodenum are associated with enteropathy associated T-cell lymphoma and its precursor lesions

Enteropathy-associated T-cell lymphoma (EATL) is an extra-nodal T-cell non-Hodgkin lymphoma originating from intestinal intraepithelial T-lymphocytes (IEL). EATL is associated with coeliac disease (CD), which is a gluten sensitive enteropathy that is normally successfully treated with a gluten free diet (GFD). However, 2–3% of adult onset CD patients develop refractory CD type II (RCDII), which is characterized by clonal expansion of surface CD3 negative, cytoplasmic CD3 positive IEL (Rubio-Tapia et al, 2009). This aberrant cell population is believed to be at the origin of EATL (Daum et al, 2000), developing in c.50% of RCDII patients. Despite aggressive therapy, clinical outcome of EATL patients is poor, with a 5-year survival rate of 15%. Therefore, it is important to identify patients at risk for EATL development to justify early aggressive treatment, before EATL arises (Al-Toma et al, 2007). Myeloid-derived suppressor cells (MDSC) are immature myeloid cells that fail to terminally differentiate into granulocytes, monocytes or dendritic cells, but rather acquire immune suppressive abilities. Human granulocytic (gr-) MDSC are CD11bCD15CD33 and monocytic (mono-) MDSC are CD14HLA-DR . MDSC exert immunosuppressive capabilities via the expression of, among others,