Antibodies to tissue transglutaminase C in newly diagnosed and long-standing Type I diabetes mellitus

Diabetologia, Jun 2000

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Antibodies to tissue transglutaminase C in newly diagnosed and long-standing Type I diabetes mellitus

0 Yours faithfully, M. Iwatani, T. Wasada, K. Katsumori , C. Watanabe-Takahashi, N. Kamatani, Y. Iwamoto Fig. 1. Change in serum uric acid concentrations after treatment with troglitazone in 95 Type II diabetic patients ance in Type II diabetic and in non-diabetic subjects. These findings again support the close association between hyperuricaemia and insulin resistance or hyperinsulinaemia or both. 1. Modan M, Halkin H, Karasik A, Lusky A (1987) Elevated serum uric acid a facet of hyperinsulinaemia. Diabetologia 30: 713718 2. Facchini F (1991) Relationship between resistance to insu lin-mediated glucose uptake, urinary uric acid clearance, and plasma uric acid concentration. JAMA 266: 30083011 3. Bonora E, Kiechl S, Willeit J et al. (1998) Prevalence of insulin resistance in metabolic disorders, the Bruneck Study. Diabetes 47: 16431649 4. Quinones GA, Natali A, Baldi S et al. (1995) Effect of insulin on uric acid excretion in humans. Am J Physiol 268:E1E5 5. Muscelli E, Natali A, Bianchi S et al. (1996) Effect of insulin on renal sodium and uric acid handling in essential hypertension. Am J Hypertens 9: 746752 6. Vuorinen-Markkola H, Yki-Jarvinen H (1994) Hyperuricemia and insulin resistance. J Clin Endocrinol Metab 78: 2529 7. Galvan AQ (1995) Effect of insulin on uric acid excretion in humans. Am J Physiol 268:E1E5 8. Sironi AM, Vichi S, Gastaldelli A et al. (1997) Effects of troglitazone on insulin action and cardiovascular risk factors in patients with non-insulin-dependent diabetes. Clin Pharmacol Ther 62: 194202 Dear Sir, We read with interest the recent paper by Lampasona et al. [1] about the detection of autoantibodies to tissue transglutaminase C (tTGA) in patients with newly diagnosed Type I (insulin-dependent) diabetes mellitus to determine the extent of gluten-associated autoimmunity. Tissue transglutaminase C has been recently identified as an autoantigen target of antiendomysium antibodies (EMA), known as the serological marker of coeliac disease (CD) [2]. The authors found a prevalence of IgA antibodies to transglutaminase C [1] in about 8 % and a low level of IgG autoantibodies to transglutaminase C in a further 32 % of newly diagnosed Type I diabetic patients. This suggests that the high prevalence of autoimmunity to transglutaminase C could be due to an involvement of the gut in the pathogenesis of Type I diabetes or to a release of transglutaminase C from destroyed pancreatic beta cells. We report our results about the detection of specific IgA to tTG and IgA antiendomysium (EMA) in 68 patients with Type I diabetes (36 males and 32 females, aged between 1 and 25.7 years). Amongst patients, 31 were newly diagnosed and 37 had long-standing diabetes, with a disease duration ranging between 1.1 and 16 years. Antibodies to protein tyrosine phosphatase (IA-2A) and to glutamic acid decarboxylase (GADA) were also detected in all patients. We measured tTG-IgA by an immunoenzymatic method (Genesis Diagnostics, Cambridgeshire, UK); both intra-assay and inter-assay coefficients of variation of this test were less than 12 %. We detected EMA by immunofluorescence (Bios Labordiagnostik, Grafelfing, Germany), IA-2A and GADA by radioimmunoassay (CIS Bio International ORIS Group Cedex, F and Medipan Diagnostica, Solchow, Germany, respectively). We defined tTGIgA values higher than 14 U/ml (mean + 3SD of 56 age and sex-matched healthy control subjects) as positive. Out of 68 patients 18 (26.4 %), in particular 6 newly diagnosed (19.3 %) and 12 with long-standing diabetes (32.4 %), were positive for tTGIgA, with a higher frequency than control subjects (0/56) (Yates corrected c2 = 15.27; p = 0.000 093). The high frequency of tTG-IgA found in our newly diagnosed patients is different from the results in other reports [1, 4]. This could be due to the different method used for tTG-IgA detection (radioimmunoassay instead of enzyme-linked immunoassay) [1, 4]. Amongst 31 newly diagnosed patients, 6 (19.3 %) were positive for tTGA, and 2 of them for both tTGA and EMA. Jejunal biopsy in these 2 patients with both tTGA and EMA showed coeliac disease. Amongst 37 patients with long-standing diabetes, 12 (32.4 %) were positive for tTG-IgA and 10 of them for both tTG-IgA and EMA. Jejunal biopsy in these 10 patients showed total villous atrophy compatible with coeliac disease in 9 and partial villous atrophy compatible with latent coeliac disease in 1. Immunological markers of Type I diabetes showed a significant association between GADA positivity and antibodies associated with coeliac disease in long-standing patients (p = 0.0006, c2 test), not found in newly diagnosed patients (NS, Fisher exact test) (Table 1). It has been reported [5] that GADA detection in patients with long-standing diabetes could be due to a persistence of some residual beta cells or specific environmental factors or both, capable of sustaining the auNewly diagnosed diabetic patients (n = 31) aAbnormal biopsies a Only EMA positive p (...truncated)


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Antibodies to tissue transglutaminase C in newly diagnosed and long-standing Type I diabetes mellitus, Diabetologia, 2000, pp. 815-816, Volume 43, Issue 6, DOI: 10.1007/s001250051381