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<i>Summary</i> <p>This is the first study to investigate bone microarchitecture in patients with syndrome of inappropriate secretion&#xa0;of thyrotropin (SITSH). Patients with SITSH had impaired bone microarchitecture compared with healthy controls, and the bone loss was associated with the degree of thyrotoxicosis.</p> Purpose <p>This study aims to evaluate bone microarchitecture through high-resolution peripheral quantitative computed tomography (HR-pQCT) in patients with syndrome of inappropriate secretion&#xa0;of thyrotropin (SITSH).</p> Methods <p>This cross-sectional study enrolled 32 patients with SITSH. All patients underwent HR-pQCT at distal radius and tibia to quantify bone geometry, volumetric bone mineral density (vBMD) and bone microarchitecture. Of the patients with SITSH, 18 were surgically confirmed to have thyrotropin-secreting pituitary adenoma (TSHoma). An additional 3 patients were clinically diagnosed with TSHoma but did not undergo surgery. The remaining patients were clinically considered to have thyroid hormone resistance, despite the absence of pathogenic variants on genetic testing. Each patient with SITSH was matched by age and gender with one patient with primary hyperthyroidism and one healthy control to analyze the effect of thyroid function on bone microarchitecture.</p> Results <p>All patients with SITSH in this study presented with elevated thyroid hormone levels and concomitant clinical symptoms of hypermetabolism. Compared with age- and gender-matched healthy controls, patients with SITSH exhibited reduced vBMD, decreased trabecular number, increased trabecular separation, and thinner cortical thickness measured by HR-pQCT. At the non-weight-bearing distal radius, their bone microstructural deficits, including low bone volume, sparse trabeculae, and thin cortex, were comparable to those seen in primary hyperthyroidism. However, at the weight-bearing distal tibia, both trabecular and cortical microarchitecture were more severely compromised in SITSH than in primary hyperthyroidism. In the subgroup analysis of TSHoma, 18 patients were diagnosed as TSHoma after surgery, and they had lower vBMD and decreased cortical thickness compared with healthy controls. While radial microarchitectural impairment in TSHoma was similar to that in primary hyperthyroidism, tibial damage was markedly more severe. Moreover, patients with higher levels of thyroid hormones showed compromised bone microarchitecture.</p> Conclusion <p>Compared with healthy controls, patients with SITSH exhibited impairment in bone microarchitecture. The degree of impairment at the non-weight-bearing distal radius was comparable to that in primary hyperthyroidism, but microarchitectural deterioration was more pronounced in SITSH at the weight-bearing distal tibia.</p>

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Bone microarchitecture assessed by HR-pQCT in syndrome of inappropriate secretion of thyrotropin with thyrotoxicosis

  • 期刊论文

  • 发表日期：

    2026年2月24日

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  • Zihan Chen,
  • He Liu,
  • Xi Wang,
  • Hanze Du,
  • Xiaofeng Chai,
  • Mei Li,
  • Xiaolan Lian,
  • Naishi Li,
  • Weibo Xia

摘要

Summary

This is the first study to investigate bone microarchitecture in patients with syndrome of inappropriate secretion of thyrotropin (SITSH). Patients with SITSH had impaired bone microarchitecture compared with healthy controls, and the bone loss was associated with the degree of thyrotoxicosis.

Purpose

This study aims to evaluate bone microarchitecture through high-resolution peripheral quantitative computed tomography (HR-pQCT) in patients with syndrome of inappropriate secretion of thyrotropin (SITSH).

Methods

This cross-sectional study enrolled 32 patients with SITSH. All patients underwent HR-pQCT at distal radius and tibia to quantify bone geometry, volumetric bone mineral density (vBMD) and bone microarchitecture. Of the patients with SITSH, 18 were surgically confirmed to have thyrotropin-secreting pituitary adenoma (TSHoma). An additional 3 patients were clinically diagnosed with TSHoma but did not undergo surgery. The remaining patients were clinically considered to have thyroid hormone resistance, despite the absence of pathogenic variants on genetic testing. Each patient with SITSH was matched by age and gender with one patient with primary hyperthyroidism and one healthy control to analyze the effect of thyroid function on bone microarchitecture.

Results

All patients with SITSH in this study presented with elevated thyroid hormone levels and concomitant clinical symptoms of hypermetabolism. Compared with age- and gender-matched healthy controls, patients with SITSH exhibited reduced vBMD, decreased trabecular number, increased trabecular separation, and thinner cortical thickness measured by HR-pQCT. At the non-weight-bearing distal radius, their bone microstructural deficits, including low bone volume, sparse trabeculae, and thin cortex, were comparable to those seen in primary hyperthyroidism. However, at the weight-bearing distal tibia, both trabecular and cortical microarchitecture were more severely compromised in SITSH than in primary hyperthyroidism. In the subgroup analysis of TSHoma, 18 patients were diagnosed as TSHoma after surgery, and they had lower vBMD and decreased cortical thickness compared with healthy controls. While radial microarchitectural impairment in TSHoma was similar to that in primary hyperthyroidism, tibial damage was markedly more severe. Moreover, patients with higher levels of thyroid hormones showed compromised bone microarchitecture.

Conclusion

Compared with healthy controls, patients with SITSH exhibited impairment in bone microarchitecture. The degree of impairment at the non-weight-bearing distal radius was comparable to that in primary hyperthyroidism, but microarchitectural deterioration was more pronounced in SITSH at the weight-bearing distal tibia.