Assessing The Response of Bone Mineral Metabolism and Turnover Markers To Levothyroxine in Primary Hypothyroidism

Abstract

Introduction:

Primary hypothyroidism is a common endocrine disorder with systemic effects on metabolism and skeletal health. Thyroid hormone deficiency alters calcium homeostasis, vitamin D status, and bone turnover, contributing to long-term skeletal complications.

Aim: 

To evaluate thyroid function, calcium, vitamin D, and bone-specific alkaline phosphatase (BSAP) in untreated hypothyroid patients, those on long-term levothyroxine therapy, and healthy controls.

Methods: 

A case-control study was conducted on 150 participants who were categorized into three groups: treated hypothyroidism (n=50), newly diagnosed untreated hypothyroidism (n=50), and healthy controls (n=50). Serum TSH, T3, T4, calcium, vitamin D, and Bone-specific alkaline phosphatase (BSAP) were measured using standard immunoassay and colorimetric methods. Statistical analysis was performed using ANOVA and chi-square tests.

Results:

Untreated hypothyroid patients showed significantly elevated TSH (12.8 ± 4.6 mIU/mL), reduced T3/T4, hypocalcemia (8.4 ± 0.7 mg/dL), vitamin D deficiency (15.5 ± 5.5 ng/mL), and elevated BSAP (25.0 ± 6.0 U/L) compared to treated patients (p<0.05) and controls (p 0.001). Levothyroxine therapy improved thyroid function, calcium, and vitamin D status, though BSAP remained moderately elevated compared to controls.

Conclusion: 

Untreated hypothyroidism is associated with deranged thyroid function, hypocalcemia, vitamin D deficiency, and increased bone turnover. Long-term levothyroxine therapy restores biochemical euthyroidism and improves calcium-vitamin D status but does not fully normalize bone metabolism. Early diagnosis and careful monitoring of thyroid replacement and bone health markers are essential to prevent skeletal complications.