Cardiovascular risk factors in autoimmune thyroiditis: role of adiponectin, resistin, inflammation and auto-immunity...

Autoimmune thyroiditis (AIT) has been associated with an increased cardiovascular risk. Whether adipokines, inflammation and auto-immunity contribute to this increased risk is uncertain. Our aim was to evaluate the interrelationships of adipokines, inflammation, auto-immunity, and thyroid function with cardiovascular risk in autoimmune thyroiditis.

Sixty-two patients with AIT, with normal free T4 (FT4) and free T3 (FT3), without other comorbidities were studied. Patients were divided into two groups: AIT with thyroid-stimulating hormone (TSH) ≤2.5 mU/L and AIT with TSH >2.5 mU/L. Parameters of thyroid function tests, serum lipid, high sensitivity C-reactive protein (hs-CRP) and homocysteine levels, anti-thyroglobulin antibodies, anti-thyroid peroxidase (TPO) antibodies, adiponectin and resistin were measured.

Patients with TSH >2.5 mU/L had significantly higher body mass index, higher low density lipoprotein (LDL)-cholesterol levels, and lower lipoprotein(a) levels. No differences in triglycerides, apolipoprotein A1 (ApoA1), apolipoprotein B (ApoB), adiponectin, or resistin levels were observed between groups. In the overall cohort, adiponectin levels were positively correlated with high density lipoprotein (HDL)-cholesterol and lipoprotein(a), whereas resistin was positively correlated with hs-CRP and triglyceride levels. Hs-CRP levels were positively correlated with anti-thyroglobulin antibody titers, and homocysteine levels were negatively correlated with FT3. In the subgroup with TSH >2.5 mU/L, FT4 was positively correlated with ApoA1 and HDL-cholesterol and negatively correlated with lipoprotein(a), while resistin was positively correlated with TSH. In patients with TSH ≤2.5 mU/L, adiponectin levels were negatively correlated with TSH.

Our study highlights a complex interrelationship between cardiovascular risk factors in patients with AIT. Patients with AIT and TSH >2.5 mU/L may have a more atherogenic lipid profile.