Comparison of Surgical Outcome Between Diabetic Versus Nondiabetic Patients After Lumbar Fusion.

BACKGROUND: The prevalence of diabetes mellitus (DM) is increasing worldwide. Thereby, an increasing rate of patients with DM are subjecting to spine surgery. Reviewing the literature, a higher rate of surgery-related complications is reported in DM patients. There is no prospective study comparing the outcomes of lumbar fusion surgery in patients with and without DM. We aimed to investigate whether DM is associated with worse patient-reported outcomes, lower fusion rate, and higher complication rate in subjects undergoing spinal lumbar fusion surgery. METHODS: Forty-eight subjects with DM (DM group) and 48 controls (control group) were recruited. Data regarding age, duration of diabetes, comorbidities, fasting blood sugar, HbA1c, insulin dependence, duration of operation and the volume of bleeding, and the number of infused packed cell were recorded for all patients. Pain and functional status of the patients using the visual analogue scale (VAS) and Oswestry Disability Index (ODI) were measured before operation and 2 weeks, 6 months, and 1 year after lumbar spinal fusion surgery. Using lumbar computed tomography scan and anteroposterior and lateral x-ray 1 year after the surgery, fusion was assessed. RESULTS: Fusion rate after 1 year was 78% in the control group and 53% in the DM group (P = .02). Patients with DM had higher VAS scores comparing to controls 1 year after the operation, but the difference was not significant (P = .07). However, comparing the functional status of the subjects, significantly higher ODI scores were found among DM patients comparing to controls (P = .002). CONCLUSION: Rate of fusion among diabetic patients who undergo lumbar spinal fusion surgery is lower than healthy controls. Spine surgeons should consider this to provide the best possible facilities during the surgery to increase the fusion rate in these patients.

Serum IL-10 involved in morphine tolerance development during adjuvant-induced arthritis

Opioid receptors play an important role in modulation of hyperalgesia in inflamed tissues, but chronic morphine application induces such side effects as tolerance. There is near communications between cytokines and mu opioid receptor expression. This study was aimed to assess the role of serum IL-10 in morphine tolerance development during adjuvant-induced arthritis. Adjuvant arthritis (AA) was induced on day 0 by single injection of Complete Freund’s Adjuvant (CFA) into the rats’ hindpaw. Hyperalgesia, edema, and spinal mu opioid receptor (mOR) variations were assessed on 0, 7, 14, and 21 days of the study. For assessment of the morphine tolerance development, morphine effective dose (4 mg/kg) was administered from the 14th day after CFA injection and continued until the morphine post-dose paw withdrawal latency (PWL); it did not significantly differ from the baseline. For assessment of the effects of IL-10 on tolerance induction, a neutralizing dose (ND50) of anti-IL-10 was administered daily during different stages of the study. AA induction in the right hindpaw of rats resulted in unilateral inflammation and hyperalgesia within 21 days of the study. Anti-IL-10 antibody administration in the AA rats induced marked elevation of hyperalgesia compared to the AA control group. Our data also indicated that morphine effective anti-hyperalgesic dose significantly decreased in the AA rats compared to the control group, which this symptom was aligned with spinal mu opioid receptor (mOR) expression increase during AA. Moreover, there was a significant difference in morphine tolerance induction between the AA and control rats, and our results also demonstrated that IL-10 played an important role in tolerance-induction process. It can be concluded that morphine tolerance slowly progressed when administered morphine effective dose was reduced during AA chronic inflammation. On the other hand, it seems that increased level of serum IL-10 may affect morphine tolerance development during inflammation

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Serum IL-10 involved in morphine tolerance development during adjuvant-induced arthritis.

Opioid receptors play an important role in modulation of hyperalgesia in inflamed tissues, but chronic morphine application induces such side effects as tolerance. There is near communications between cytokines and mu opioid receptor expression. This study was aimed to assess the role of serum IL-10 in morphine tolerance development during adjuvant-induced arthritis. Adjuvant arthritis (AA) was induced on day 0 by single injection of Complete Freund's Adjuvant (CFA) into the rats' hindpaw. Hyperalgesia, edema, and spinal mu opioid receptor (mOR) variations were assessed on 0, 7, 14, and 21 days of the study. For assessment of the morphine tolerance development, morphine effective dose (4 mg/kg) was administered from the 14th day after CFA injection and continued until the morphine post-dose paw withdrawal latency (PWL); it did not significantly differ from the baseline. For assessment of the effects of IL-10 on tolerance induction, a neutralizing dose (ND50) of anti-IL-10 was administered daily during different stages of the study. AA induction in the right hindpaw of rats resulted in unilateral inflammation and hyperalgesia within 21 days of the study. Anti-IL-10 antibody administration in the AA rats induced marked elevation of hyperalgesia compared to the AA control group. Our data also indicated that morphine effective anti-hyperalgesic dose significantly decreased in the AA rats compared to the control group, which this symptom was aligned with spinal mu opioid receptor (mOR) expression increase during AA. Moreover, there was a significant difference in morphine tolerance induction between the AA and control rats, and our results also demonstrated that IL-10 played an important role in tolerance-induction process. It can be concluded that morphine tolerance slowly progressed when administered morphine effective dose was reduced during AA chronic inflammation. On the other hand, it seems that increased level of serum IL-10 may affect morphine tolerance development during inflammation.