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<p>We commend Seong et al. for exploring associations between COVID-19 and osteonecrosis of the femoral head (ONFH). However, their retrospective single-center study (<i>N</i> = 84) has critical limitations. The exclusion of patients with chronic comorbidities and highly imbalanced group sizes (e.g., DEX + MPS:12 vs. DEX:66) risk bias and reduced generalizability. Steroid dose equivalence (1&#xa0;mg MPS = 0.1875&#xa0;mg DEX) lacks authoritative validation, potentially underestimating MPS’s osteotoxicity. Higher cumulative doses in the DEX + MPS group (380&#xa0;mg vs. 125&#xa0;mg DEX) were attributed to “pharmacological synergy” without mechanistic evidence, contrasting findings that ONFH risk correlates with total dose, not drug type. Confounding factors, including greater pulmonary involvement (59.2% vs. 36.3%) and prolonged hospitalization in the DEX + MPS group, were inadequately controlled, possibly conflating disease severity with steroid effects. Conclusions oversimplify ONFH etiology by emphasizing steroid doses alone, neglecting viral-induced vascular injury and suboptimal imaging methods (X-ray/CT/MRI mix) that may miss subclinical lesions. Proposed “cautious steroid use” lacks clear thresholds, as the maximum dose (446&#xa0;mg DEX-equivalent) was far below established risk levels (&gt; 3,000&#xa0;mg prednisone-equivalent) (1). These limitations warrant cautious interpretation of the findings.</p>

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Letter to the editor regarding “osteonecrosis of the femoral head in post-COVID-19 patients: a retrospective comparative study”

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年6月5日

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  • Xin Liu,
  • Yunzhuan Luo,
  • Dingchang He,
  • Zujian Xu

摘要

We commend Seong et al. for exploring associations between COVID-19 and osteonecrosis of the femoral head (ONFH). However, their retrospective single-center study (N = 84) has critical limitations. The exclusion of patients with chronic comorbidities and highly imbalanced group sizes (e.g., DEX + MPS:12 vs. DEX:66) risk bias and reduced generalizability. Steroid dose equivalence (1 mg MPS = 0.1875 mg DEX) lacks authoritative validation, potentially underestimating MPS’s osteotoxicity. Higher cumulative doses in the DEX + MPS group (380 mg vs. 125 mg DEX) were attributed to “pharmacological synergy” without mechanistic evidence, contrasting findings that ONFH risk correlates with total dose, not drug type. Confounding factors, including greater pulmonary involvement (59.2% vs. 36.3%) and prolonged hospitalization in the DEX + MPS group, were inadequately controlled, possibly conflating disease severity with steroid effects. Conclusions oversimplify ONFH etiology by emphasizing steroid doses alone, neglecting viral-induced vascular injury and suboptimal imaging methods (X-ray/CT/MRI mix) that may miss subclinical lesions. Proposed “cautious steroid use” lacks clear thresholds, as the maximum dose (446 mg DEX-equivalent) was far below established risk levels (> 3,000 mg prednisone-equivalent) (1). These limitations warrant cautious interpretation of the findings.