Clinical signs of type 1 diabetes are associated with type 2 diabetes marker transcription factor 7-like 2 polymorphism.

AIMS/INTRODUCTION: We aimed to assess the distribution of transcription factor 7-like 2 gene TCF7L2 (rs7903146) polymorphism and to find possible associations between TCF7L2 and the characteristics of type 1 diabetes. MATERIALS AND METHODS: We studied 190 newly diagnosed type 1 diabetes patients (median age 12.7 years, range 2.0-72.5) and 246 controls (median age 23.8 years, range 1.4-81.5) for TCF7L2 single nucleotide polymorphism. We determined anti-islet autoantibodies, random C-peptide levels, diabetes associated HLA DR/DQ haplotypes and genotypes in all patients. RESULTS: There were no differences in the distribution of TCF7L2 single nucleotide polymorphism between patients and controls. However, patients with in type 1 diabetes, after adjusting for age and sex, subjects carrying C allele were at risk for a C-peptide level lower than 0.5 nmol/L (OR 5.65 [95% CI: 1.14-27.92]) and for zinc transporter 8 autoantibody positivity (5.22 [1.34-20.24]). Participants without T allele were associated with a higher level of islet antigen-2 autoantibodies (3.51 [1.49-8.27]) and zinc transporter 8 autoantibodies (2.39 [1.14-4.99]). CONCLUSIONS: The connection of TCF7L2 polymorphism with zinc transporter 8 and islet antigen-2 autoantibodies and C-peptide levels in patients supports the viewpoint that TCF7L2 is associated with the clinical signs and autoimmune characteristics of type 1 diabetes. The mechanisms of the interaction between the TCF7L2 risk genotype and anti-islet autoantibodies need to be studied further.

IgA-Type Enterovirus Antibodies Are Increased among Adults and Children with Recently Diagnosed Type 1 Diabetes.

Enteroviruses (EV) are among the leading environmental triggers of childhood-onset type 1 diabetes (T1D). Our aim was to determine the prevalence of antibodies against EV and their association with T1D in different age groups (n = 62), including young adults, and to compare these data with results from HLA-matched control participants (n = 62). IgA, IgG, and IgM antibodies against EV were detected. IgA EV antibodies were present in 46.8% of participants with T1D (median level 10.9 EIU) and in 11.3% of controls (median level 3.4 EIU). IgA EV positivity and higher level of IgA EV antibodies were both significant risk factors for T1D (odds ratio (OR) 8.33; 95% confidence interval (CI) 2.52-27.6; p = 0.0005 and OR 1.04; 95% CI 1.01-1.06; p = 0.0105, respectively). Importantly, the prevalence of IgA EV antibodies in the subgroups of both children and young adults was also significantly different between participants with T1D and their matched controls (p = 0.0089 and p = 0.0055, respectively). Such differences were not seen for IgG and IgM EV antibodies. However, IgG EV antibodies were associated with 65 kDa glutamic acid decarboxylase antibodies, but not with zinc transporter 8 and protein tyrosine phosphatase IA2 antibodies. The genotype frequency of PTPN22 (rs2476601) and IFIH1 (rs1990760) was not associated with EV positivity. This study showed that EV infections may be an important disease-promoting factor of T1D not only in childhood-onset but also in adult-onset T1D. However, to further confirm this association, direct virological studies are needed in the latter T1D group.

Magnesium supplementation does not affect blood calcium level in treated hypoparathyroid patients.

CONTEXT: Magnesium is involved in the homeostasis of calcium metabolism, and magnesium deficiency may lead to clinically significant hypocalcemia. We have had two cases in our department in which treated hypoparathyroid patients with stable calcium levels developed hypercalcemia in conjunction with supplementary magnesium use. To our knowledge, there has been no prospective study looking at the effect of supplementary magnesium on calcium homeostasis in hypoparathyroid patients. OBJECTIVE: The aim of this pilot study was to evaluate whether magnesium treatment affects plasma calcium levels in hypoparathyroid patients. DESIGN AND SETTING: We conducted a prospective, two-phase, uncontrolled treatment trial at a referral center of endocrine disorders. PARTICIPANTS: We enrolled treated (calcium + vitamin D analog) hypoparathyroid patients with normal plasma magnesium levels. INTERVENTION: Three weeks of treatment with oral magnesium (350 mg/d) were followed by 2 wk off treatment. MEASURES: We compared the plasma ionized calcium level after 3 wk of treatment to the pretreatment value. Plasma calcium, phosphate, magnesium, and creatinine levels were measured before treatment, after 3 wk on magnesium, and 2 wk after stopping magnesium treatment. RESULTS: Ten patients completed the trial. Supplementary treatment with magnesium for 3 wk did not change calcium levels in these patients. Magnesium supplementation induced a small but statistically significant increase in the plasma magnesium level, but levels of phosphate and creatinine remained stable. CONCLUSIONS: Magnesium supplementation did not influence plasma calcium levels in treated hypoparathyroid patients.