Evaluation of Anti-GAD, IAA Presence and Measurement of C- Peptide Level in T2DM Patients, 60 and above 60 years old in Nasiriyah City / South of Iraq

Authors

  • Mahdi Murshud Thuwaini
  • Hussain Ali Kareem
  • Talib Hassan Ali

Keywords:

T2DM, IAA, anti-GAD, C peptide, Nasiriyah, Iraq

Abstract

Background: The study aimed to estimate the prevalence of positive autoantibodies (Anti-GAD, IAA) among (T2DM) as T1DM especially in elderly DM patients in a sample of the Iraqi population, and to compare some metabolic and inflammatory markers to those of patients having negative autoantibodies. Methods. 65 Patients with T2DM and 21 control participants 60 or older than 60 years were enrolled in this study. Antiglutamic acid decarboxylase GAD, and insulin autoantibody IAA, and C peptide, were evaluated by ELISA. Fasting blood sugar, Random blood sugar, BMI, cholesterol concentration, triglyceride concentration systolic and diastolic blood pressure were assessed, in addition to considering demographic characteristics. Results. 3% of patients with T2DM had both anti-GAD and anti-IAA autoantibodies, 10(15%) and 7(10.8%) of the patient were positive for two antibodies respectively, however, none of healthy control group have one of them. The mean duration of initiation insulin up taking by bearing autoantibody group, was (60±38.7 months) and in -ve antibody, group was (48 ±53 months) but these differences were not significant (P=0.56).  there are no significant differences in the median age (P =0.80), BMI (p=0.4218), main cholesterol concentration. (p=0.57) and C peptide (p=0.091) between +ve and -ve autoantibody bearing T2DM. +ve patients had lower body mass index (p=0.014) than those in -ve autoantibodies cases. Conclusion. Prevalence of having positive autoantibodies within Iraqi T2DM patients 60 and over 60 years old was 3%. They shared common clinical and metabolic features with subjects with non antiGAD, and IAA autoantibody bearing subjects.

References

Emanuela Tsvetkova Zaharieva, Tsvetelina Veselinova Velikova, Adelina Dimitrova Tsakova, and Zdravko Asenov Kamenov (2017) Prevalence of Positive Diabetes-Associated Autoantibodies among Type 2 Diabetes and Related Metabolic and Inflammatory Differences in a Sample of the Bulgarian Population, Journal of Diabetes Research Volume, Article ID 9016148, 6 pages https://doi.org/10.1155/2017/9016148

Bonifacio E. Predicting type 1 diabetes using biomarkers. Diabetes Care 2015; 38:989–996

Tuomi, T.; Groop, L.C.; Zimmet , P.Z.; Rowley, M.J.; Knoweles, W.&Mackay, I.R. (1993). Autoantibobies to glutamic acid decarboxylase reveal latent autoimmune diabetes mellitus in adults with non-insulin dependent onset of diabetes. Diabetes. 42: 359-362.

J. P. Palmer and I. B. Hirsch, (2003) “What’s in a name: latent autoimmune diabetes of adults, type 1.5, adult-onset, and type 1 diabetes,” Diabetes Care, vol. 26, no. 2, pp. 536– 538.

G. Stenström, A. Gottsäter, E. Bakhtadze, B. Berger, and G. Sundkvist, (2005) “Latent autoimmune diabetes in adults: definition, prevalence, beta-cell function, and treatment,” Diabetes, vol. 54, Supplement 2, pp. S68–S72.

Wentworth JM, Fourlanos S, Harrison LC: (2009) Reappraising the stereotypes of diabetes in the modern diabetogenic environment. Nat Rev Endocrinol; 5: 483–489.

Fourlanos S, et al: (2006) A clinical screening tool identifies autoimmune diabetes in adults. Diabetes

Care; 29: 970–975.

Turner R, et al: (1997) UKPDS 25: autoantibodies to islet-cell cytoplasm and glutamic acid decarboxylase

for prediction of insulin requirement in type 2 diabetes. UK Prospective Diabetes Study Group. Lancet; 350: 1288– 1293.

M. Maioli, G. M. Pes, G. Delitala et al., (2010) “Number of autoantibodies and HLA genotype, more than high titers of glutamic acid decarboxylase autoantibodies, predict insulin dependence in latent autoimmune diabetes of adults,” European Journal of Endocrinology, vol. 163, no. 4, pp. 541–549.

Lupi R, et al: Prolonged exposure to free fatty acids has cytostatic and pro-apoptotic effects on human pancreatic islets: evidence that β-cell death is caspase mediated, partially dependent on ceramide pathway, and Bcl-2 regulated. Diabetes 2002; 51: 1437–1442.

Bianca K. Itariu a, b Thomas M. Stulnig. Autoimmune Aspects of Type 2 Diabetes Mellitus – A Mini-Review, Gerontology 2014;60:189–196

Tiberti C, Giordano C, Locatelli M, et al. (2008) Identification of tyrosine phosphatase 2(256-760) construct as a new, sensitive marker for the detection of islet autoimmunity in type 2 diabetic patients: the non-insulin requiring autoimmune diabetes (NIRAD) study 2. Diabetes; 57:1276–1283

Brooks-Worrell BM, Boyko EJ, Palmer JP. (2014) Impact of islet autoimmunity on the progressive b-cell functional decline in type 2 diabetes. Diabetes Care; 37:3286–3293

The Expert Committee on the Diagnosis and Classification of Diabetes Mellitus. Report of the Expert Committee on the Diagnosis and Classification of Diabetes Mellitus. Diabetes Care. 2002;25(Suppl 1): S5- 20.

Agardh CD, Cilio CM, Lethagen A, et al. Clinical evidence for the safety of GAD65 immunomodulation in adult-onset autoimmune diabetes. J Diabetes Complications. 2005;19(4): 238-46.

Vehik K, Lynch KF, Schatz DA, et al.; TEDDY Study Group. Reversion of b-cell autoimmunity changes risk of type 1 diabetes: TEDDY study. Diabetes Care 2016; 39:1535–1542

E. Laugesen, J. A. Østergaard, and R. D. Leslie, (2015) “Danish diabetes academy workshop and workshop speakers. Latent autoimmune diabetes of the adult: current knowledge and uncertainty,” Diabetic Medicine, vol. 32, no. 7, pp. 843–852.

Borg H, et al: A 12-year prospective study of the relationship between islet antibodies and β-cell function at and after the diagnosis in patients with adult-onset diabetes. Diabetes 2002; 51: 1754–1762

Chan JM, Rimm EB, Colditz GA, Stampfer MJ, Willett WC. (1994) Obesity, fat distribution, and weight gain as risk factors for clinical diabetes in men. Diabetes Care; 17:961–969

Colditz GA, Willett WC, Rotnitzky A, Manson JE. (1995) Weight gain as a risk factor for clinical diabetes mellitus in women. Ann Intern Med; 122:481– 486

Donath MY, Shoelson SE: (2011) Type 2 diabetes as an inflammatory disease. Nat Rev Immunol; 11: 98–107.

Eberhart MS; Ogden C; Engelgau M; Cadwell B; Hedley AA; Saydah SH (2004). "Prevalence of overweight and obesity among adults with diagnosed diabetes—United States, 1988-1994 and 1999-2002". MMWR Morb. Mortal. Wkly. Rep. 53 (45): 1066–8.

A. W. Deutekom, R. J. Heine, and S. Simsek, (2008) “The islet autoantibody titres: their clinical relevance in latent autoimmune diabetes in adults (LADA) and the classification of diabetes mellitus,” Diabetic Medicine, vol. 25, no. 2, pp. 117– 125.

T. M. Davis, A. D. Wright, Z. M. Mehta et al., (2005) “Islet autoantibodies in clinically diagnosed type 2 diabetes: prevalence and relationship with metabolic control (UKPDS 70),” Diabetologia, vol. 48, no. 4, pp. 695–702.

Matzinger P: The danger model: a renewed sense of self. Science 2002; 296: 301–305.

Mansour AA, & Al-Jazairi MI. (2007) Cut-off values for anthropometric variables that confer increased risk of type 2 diabetes mellitus and hypertension in Iraq. Arch Med Res. 38(2):253-8.]

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2021-02-26

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