Endocrine Abstracts

Objective: Graves’ Disease (GD) is one of the most common autoimmune disorders. Some SNP in pro-inflammatory cytokines have already been linked to an increased susceptibility of developing GD. Thyroid hormones are crucial modulators of lipid metabolism. A pro-inflammatory state, may contribute several metabolic changes, including disturbances in lipid metabolism. Our aim was to evaluate if SNP in pro-inflammatory cytokines also contribute to disturbances of lipid profile in GD patients.

Methods: Lipid profiles (total cholesterol [TC], high density lipoprotein [HDL], low-density lipoprotein [LDL] and triglycerides [TG], apolipoprotein A-I [Apo A-I], apolipoprotein B [ApoB] and lipoprotein (a)) were assessed in a case-control study comprising 98 Graves’ disease patients treated with methimazole. Genetic variants in IL6-174 G/C (rs1800795), TNFA-308 G/A (rs1800629), IL1B-511 C/T (rs16944), and IFNGR1-56 T/C (rs2234711) were discriminated by real-time PCR using TaqMan SNP genotyping assays. The associations of genetic variants with lipid profile were evaluated with analysis unadjusted and adjusted for age and sex.

Results: Within our sample of 97 patients with GD, 91.8% were females, with a mean age of 44.4 ± 15.1 years. The mean TSH level of our population was 0.4 (0.0-1.3) μUI/l, and the mean levels of FT3 and FT4 were 3.0 (2.6-3.5) ng/ml and 1.1 (0.9-1.4) μg/mL, respectively. Seven subjects (9.2%) had diabetes and thirty-three patients (43.4%) had prediabetes. The mean level of total cholesterol was 193.7 (149.1-238.3) mg/dL, the mean level of HDL cholesterol was 59.9 (43.5-76.3) mg/dL and the of LDL cholesterol’s level was 117.1 (84-150.2) mg/dL. The A allele in TNFA-308 G/A was associated with significant lower levels of HDL cholesterol (P = 0.037). TNF-α A allele also had higher levels of fasting insulin (0.042). IL1B-511 C/T (rs16944), IL6-174 G/C (rs1800795) and IFNGR1-56 T/C (rs2234711) polymorphisms showed no association with lipid profile.

Conclusions: In patients with GD, we found lower levels of HDL among those with A allele in TNFA-308 G/A. This polymorphism may contribute to a higher atherogenic risk in patients with GD.