Postoperative Changes in Hematological, Biochemical, and Redox Status Parameters in Spinal Osteoarthritis Patients Undergoing Spinal Decompression and Stabilization Surgery

脊柱骨关节炎患者接受脊柱减压和稳定手术后血液学、生化和氧化还原状态参数的术后变化

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Abstract

Background/Objectives: Spinal osteoarthritis (sOA) is a degenerative condition marked by pain, inflammation, and restricted mobility. While surgical interventions such as spinal decompression and stabilization are common, their impact on redox status and inflammatory markers remains underexplored. This study aimed to assess the effects of surgery on clinical, hematological, biochemical, and redox parameters in patients with sOA. Methods: A total of 25 patients diagnosed with sOA underwent spinal decompression and stabilization surgery. Preoperative and postoperative assessments included hematological and biochemical analyses, redox status evaluation (TAS, TOS, GSH, AOPP, SOD), and inflammatory markers such as IL-6. Disease severity was graded using the Kellgren-Lawrence (K-L) system. Results: Postoperatively, there was a significant decrease in neutrophil count (p = 0.014) and AOPP levels (p < 0.001), with a corresponding increase in lymphocyte count (p = 0.016), erythrocyte count (p = 0.036), and IL-6 levels (p = 0.008). TAS levels decreased (p = 0.006), while enzymatic antioxidants, such as SOD increased (p = 0.031). Erythrocyte GSH remained low, with a non-significant postoperative decrease. Patients with higher K-L grades exhibited greater redox imbalance, with reduced preoperative GSH and elevated postoperative superoxide anion, TOS, and SOD levels. More severe cases also showed decreased postoperative erythrocyte, hemoglobin, and PTH levels, and increased TAS and AOPP levels. Factorial analysis highlighted clusters associated with oxidative stress, inflammation, and clinical performance. Conclusions: The results underscore the complex relationship between inflammation, oxidative stress, and recovery in sOA. These findings suggest the importance of targeted postoperative strategies to support redox homeostasis and modulate inflammation in sOA patients.

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