Markers of Bone Mineral Metabolism in Thyroid Disorders

Abstract

Abstract Background and Aim: Thyroid hormones are essential for normal skeletal development and bone metabolism. Despite various studies, the effect of thyroid hormone on bone metabolism has not been clearly understood. We studied the bone formation markers (procollagen type 1 N-propeptide [P1NP] and osteocalcin [OC]) and bone resorption markers (C-terminal cross-linking telopeptide of type 1 collagen [CTX] and tartrate-resistant acid phosphatase [TRAP]) in patients with thyroid disorders and the effect of treatment on them. Furthermore, a study correlating these markers with thyroid-stimulating hormone (TSH) levels was done. Materials and Methods: This cross-sectional study recruited 60 cases (40 – hypothyroid and 20 – hyperthyroid) and 20 controls based on inclusion and exclusion criteria. To evaluate the effect of treatment, cases were further subdivided based on the duration of treatment received into 0-month (newly diagnosed), 1–6-month, and >6-month treatment subgroups. Both the cases and control underwent a thorough history, clinical examination, and detailed investigation based on a predesigned proforma. Results: In hyperthyroidism with 0-month treatment subgroup, both formation (OC, P1NP) and resorption (CTX) markers were significantly increased compared to control (P < 0.05), which became insignificant on treatment (1–6 months) with antithyroid medication despite low TSH value. Contrarily, in hypothyroidism, a statistically significant (P < 0.05) lower mean value of markers (OC, P1NP, and CTX) was observed only in the subgroup with levothyroxine supplementation. In hyperthyroidism, both the formation (OC and P1NP) and resorption markers (CTX and TRAP) showed a strong negative (P < 0.001) correlation with TSH, the strength of correlation decreased, and became insignificant on treatment. In hypothyroidism, only P1NP and CTX showed an overall significant positive (P < 0.05) correlation with TSH. Conclusion: Hyperthyroidism has high bone turnover markers, which showed early reversibility of markers on treatment with antithyroid medication despite low TSH, whereas in hypothyroidism, significantly lower mean value of markers is seen only in the subgroup with levothyroxine supplementation, probably owing to the suppressive effect of TSH. P1NP and CTX showed high sensitivity in both hypothyroidism and hyperthyroidism. The pattern of correlation between TSH and bone metabolism markers in hyperthyroidism suggests a direct negative effect of TSH on bone turnover, whereas in hypothyroidism, it either suggests TSH showing a positive correlation at a very high level which becomes negative as the TSH value decreases or TSH is not a dominant hormone regulating bone metabolism in hypothyroidism.