Receptor activator of nuclear factor κB ligand and osteoprotegerin in men with thyroid cancer

Background  Suppressive thyroid hormone therapy is generally a lifelong treatment for patients with differentiated thyroid cancer (DTC). However, long-standing thyrotropin (TSH) suppression is a risk factor for osteoporosis. Osteoprotegerin (OPG) and receptor activator of nuclear factor κB ligand (RANKL) are central regulators of bone turnover. The aim was to analyze the effects of a suppressive thyroid hormone therapy in males with DTC on the OPG/RANKL system and on bone metabolism. Patients and methods  The OPG and soluble RANKL (sRANKL) were determined in 40 men (mean age, 53·2 years) with DTC on suppressive thyroid hormone therapy (TSH; 0·053 ± 0·037 mU L−1, duration 5·7 ± 4·4 years) and 120 healthy controls matched for age. The markers of bone metabolism were C-terminal telopeptide of type I collagen in serum (sCTx) and osteocalcin (OC). Results  The control group had OPG values (mean ± SD) of 1·9 ± 1·0 pmol L−1 and sRANKL values of 0·40 ± 0·62 pmol L−1. In patients with DTC, results for OPG were 3·03 ± 1·04 pmol L−1 (P < 0·05) and for sRANKL were 0·13 ± 0·16 pmol L−1 (P < 0·05). The control group presented values for sCTx of 2669 ± 1132 pmol L−1 and for OC of 17·89 ± 6·5 ng mL−1. Patients with DTC on suppressive thyroid hormone therapy had increased sCTx values of 3810 ± 2020 pmol L−1 (P = 0·03) but comparable OC values of 19·21 ± 7·67 ng mL−1 (NS). Conclusion  Suppressive thyroid hormone therapy in men with DTC increased bone degradation and induced significant changes in the OPG/RANKL system. These changes include, besides the risk of osteoporosis, possible negative effects on the vascular function and an increased risk of cardiovascular disease.