Introduction: Whether subclinical hypothyroidism (SCH) is related to risk for cardiovascular disease is controversial. Inflammation and oxidation of lipoproteins play an important role in the progression and complications of atherosclerosis.
Therefore we aimed to evaluate the plasma levels of thiobarbituric acid reactive substances (TBARS) as a marker of oxidative stress, high sensitive CRP (hsCRP) and lipid profile as a risk factor for atherosclerosis in SCH before and after L-thyroxine replacement therapy, and compare to control group.
Methods: The study was performed in age- and sex-matched 26 subclinical hypothyroid patients and 27 healthy controls. Exclusion criteria were known atherosclerotic disease, diabetes, morbid obesity, familial hyperlipidemias, coagulation disorders and severe systemic diseases. The patients, who were treated with lipid lowering drugs, estrogen and asetlsalicyclic acid, were not enrolled in the study. Blood samples were obtained from patients with SCH before levothyroxine replacement, and one month after achieving a euthyroid state with levothyroxine.
Results: SCH patients had higher hsCRP levels than control group at the beginning (4.28 mg/l vs 1.88 mg/l; P=0.018). High levels of hsCRP were negatively correlated with free thyroid hormone levels (P=0.026 for FT3 and P=0.021 for FT4). After achieving euthyroid state with levothyroxine replacement, hsCRP levels decreased significantly in patients with SCH (4.28 vs 2.32; P=0.006). In our study, the L-thyroxine treatment in doses which normalize TSH secretion was not associated with significant changes in serum lipid profile (P>0.05). TBARS levels of SCH patients before and after restoration of euthyroidism were similar to control group (P>0.05).
Discussion: Our findings suggest that hsCRP values increase in patients with subclinical hypothyroidism, and may count as an additional risk factor for the development of atherosclerosis and cardiovascular disease. Normalization of thyroid state by levothyroxine replacement seems to effectively reduce serum hsCRP levels in subclinical hypothyroidism without any correlation with TBARS activity and with similar lipid levels in SCH.