Scholarlink

<p>We commend Chengming Li et al. for examining the link between sarcopenia and residual back pain after PKP. However, their retrospective single‑center study (<i>N</i> = 231) has notable limitations. Sarcopenia was diagnosed solely via SMI at T12 on CT, without functional measures (e.g., grip strength, gait speed), and T12 is not a standard spinal muscle evaluation level, risking diagnostic bias. Pain was assessed only by VAS, lacking detail on characteristics or frequency, hindering mechanistic insight. Causal inference is weak due to unaddressed reverse causality—pre‑operative pain may cause disuse atrophy—and uncontrolled confounders like protein intake, vitamin D, and medications. Methodological transparency is insufficient: missing data handling among 472 initial patients was unspecified, and surgical details (team, experience, cement distribution) were omitted, affecting reproducibility. Finally, proposed mechanisms (biomechanical imbalance, chronic inflammation) rely solely on cited literature without direct validation from study data, such as inflammatory markers or spinal stability assessments.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Letter to the editor regarding “association between sarcopenia on residual back pain after percutaneous kyphoplasty for osteoporotic vertebral compression fractures”

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年3月24日

查看全文
  • Dingchang He,
  • Lin Wei,
  • Xin Liu,
  • Xiaochun Fan

摘要

We commend Chengming Li et al. for examining the link between sarcopenia and residual back pain after PKP. However, their retrospective single‑center study (N = 231) has notable limitations. Sarcopenia was diagnosed solely via SMI at T12 on CT, without functional measures (e.g., grip strength, gait speed), and T12 is not a standard spinal muscle evaluation level, risking diagnostic bias. Pain was assessed only by VAS, lacking detail on characteristics or frequency, hindering mechanistic insight. Causal inference is weak due to unaddressed reverse causality—pre‑operative pain may cause disuse atrophy—and uncontrolled confounders like protein intake, vitamin D, and medications. Methodological transparency is insufficient: missing data handling among 472 initial patients was unspecified, and surgical details (team, experience, cement distribution) were omitted, affecting reproducibility. Finally, proposed mechanisms (biomechanical imbalance, chronic inflammation) rely solely on cited literature without direct validation from study data, such as inflammatory markers or spinal stability assessments.