PurposeHigh prevalence of thyroid disorders is more common in type 1 diabetes compared to type 2 diabetes, due to associated autoimmunity. Hypothyroidism is the most common disorder. The objective was to assess the prevalence of thyroid dysfunction among type 2 diabetic Egyptian females and to find the correlation between metabolic syndrome components and autoimmune thyroid dysfunction.Materials and methodsThe study included 62 type 2 diabetic Egyptian females and 27 sex- and age-matched controls. All patients in the study were subjected to anthropometric measures, including HbA1c, lipid profile, serum uric acid, thyroid-stimulating hormone (TSH), free triiodothyronine, free thyroxine, anti-thyroid peroxidase (TPO), antithyroglobulin (anti-Tg), and thyroid ultrasound.ResultsHypothyroidism was found in 45.2% of patients (5.49±3.37 μIU/mL) versus 11.1% of controls (1.79±1.21 μIU/mL) (P<0.001). Anti-TPO was found in 75.8% (347.15±244.87 IU/mL) of patients versus 7.4% (32.89±33.26 IU/mL) of controls (P<0.001). Anti-Tg was found in 61.3% (508.03±369.16 IU/mL) of patients versus 0 (51.26±35.53 IU/mL) controls (P<0.001). A significant positive correlation was found between TSH and antithyroid antibodies (anti-Tg, anti-TPO; P=0.002 and P=0.043, respectively) and between TSH and thyroid-gland volume (P=0.002) in diabetic patients. No correlation was found between any components of metabolic syndrome and thyroid antibodies in diabetic patients.ConclusionAutoimmune thyroid disease is more common in Egyptian women with type 2 diabetes than nondiabetic women, and thus points to a role of autoimmunity in the pathogenesis of type 2 diabetes.

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Background: The exact relationship between the different TCF7L2 gene polymorphisms and the development of diabetic nephropathy (DN) remains unclear. Objective: To investigate the association of TCF7L2 rs12255372 (G/T) gene polymorphism and diabetic nephropathy (DN) in patients with type 2 diabetes (T2D). Methods: 100 patients with T2D (50 patients without DN and 50 patients with DN) and 50 age and sex-matched healthy controls (HC) were enrolled in the study. Genotyping for the rs12255372 (G>T) polymorphism in the TCF7L2 gene was performed by real-time PCR. Results: The rs12255372 polymorphism showed a statistically significant difference between HC and patients with and without DN in both the genotype and allele frequency. However, the rs12255372 polymorphism genotype or allele frequency was not statistically different between patients with DN and those patients without DN. The G allele was found to be higher in patients and the T allele was higher in HC suggesting that the G allele was the risk allele for developing T2D &DN and that the T allele was protective. Conclusion: rs12255372 TCF7L2 gene polymorphism was strongly associated with type 2 diabetes mellitus and DN. The association between rs12255372 polymorphism and DN was a mere reflection of a complicated diabetes mellitus rather than a direct independent association.

Background: Several cardiovascular risk factors have been recognized in patients with diabetes and vitamin D deficiency is emerging as a new risk. The aim of this study was to determine the effect of vitamin D deficiency on the incidence of premature atherosclerosis in patients with type 2 diabetes. Methods: A total of 78 patients with type 2 diabetes were subjected to history taking, physical examination, fasting glucose level, homeostasis model assessment of insulin resistance, lipid profile, 25(OH) vitamin D measurement, and carotid Doppler. Results: Patients with normal carotid intima-media thickness (CIMT) had sufficient vitamin D. Of those with increased CIMT 23.1% had insufficient vitamin D while 76.9% had sufficient vitamin D (six patients had plaques, one of them had vitamin D insufficiency, and the other five patients had sufficient vitamin D). There was a statistically significant difference in the serum level of vitamin D between patients with increased CIMT, and those with normal intima, with a decreased level in the first group. There was a significant negative correlation between vitamin D and fasting blood glucose. There was a statistically significant correlation in left CIMT between the vitamin D sufficiency group and the vitamin D insufficiency group, with higher values in the second group. There was no statistically significant difference in serum cholesterol, triglycerides, HDL cholesterol, and LDL cholesterol in patients with increased CIMT and those with normal intima. Conclusions: Decreased vitamin D levels in patients with diabetes lead to increased CIMT. The absence of a statistically significance difference in lipid profile between increased and normal CIMT groups raises the possibility of underlying causes for atherosclerosis in patients with diabetes other than dyslipidemia.

Oral hypoglycemics are a widely prescribed group of drugs for the management of type 2 diabetes mellitus. Sulfonylureas (SUs) are the cornerstone of type 2 diabetes pharmacotherapy. The enzyme cytochrome P450 2C9 (CYP2C9) is the main enzyme that catalyzes the biotransformation of SUs. It is encoded by the polymorphic gene CYP2C9 with two allelic variants namely CYP2C9*2 and CYP2C9*3 coding for variant allozymes with reportedly decreased metabolic capacity resulting in decreased SUs clearance and consequently prolonged and exacerbated action. The aim of this study was to investigate the influence of genetic polymorphisms of CYP2C9 on the response to glibenclamide, a second-generation sulfonylurea. Hundred type 2 diabetic patients were enrolled in the study. Genotyping was done on the LightCycler 2 by real-time polymerase chain reaction (PCR) hybridization probe assay. The results are the following: 53 patients were carriers of the wild genotype (CYP2C9*1/*1), 20 were heterozygous for the variant CYP2C9*2 allele (CYP2C9*1/*2), 18 were heterozygous for the variant CYP2C9*3 allele (CYP2C9*1/*3), and 9 were double heterozygous for both mutant alleles (CYP2C9*2/*3); of those double mutant genotype patients, two were also homozygous for the mutant CYP2C9*2 allele (CYP2C9*2/*2) and one patient was homozygous for the mutant CYP2C9*3 allele (CYP2C9*3/*3). Although there was no significant difference in drug dosage between the four groups, there was however a significant association of the CYP2C9*2/*3 genotype with better glycemic control. As conclusion, the better glycemic control observed can probably be attributed to slower metabolism of SUs by the carriers of the CYP2C9*2/*3 genotype and consequently longer half-life or exacerbated effect of the SUs administered.