Numan DEMİRALP, Sema Tuncer UZUN, Gülçin BÜYÜKBEZİRCİ, Sevgi KELEŞ, Şule ARICAN, Resul YILMAZ, Ruhiye REİSLİ, İsmail REİSLİ
Journal of Surgery and Medicine - 2026;10(6):0-0
Background/Aim: Neuropathic pain is a complex condition with an incompletely understood pathogenesis, and immunologic mechanisms are increasingly recognized as important contributors. This study aimed to evaluate the association between immunologic marker levels and the development of postherpetic neuralgia in patients with acute herpes zoster, with a particular focus on the impact of diabetes mellitus. Methods: In this prospective observational study, 20 patients with acute herpes zoster and a Douleur Neuropathique 4 score of 4 or higher were enrolled. Patients were categorized into two groups: those with diabetes mellitus (Group I, n = 10) and those without diabetes mellitus (Group II, n = 10). Routine laboratory parameters, including hemogram, C -reactive protein, erythrocyte sedimentation rate, fasting blood glucose, and hemoglobin A1c, were recorded. Immunologic markers, including CD3+, CD4+, CD8+, FOXP3+ regulatory T cells, natural killer cell subsets (regulatory, defective, cytotoxic, CD56 bright, and CD56 dim), and NK CD57, were analyzed at baseline and at month 3. Results: NK defective subset levels were lower in Group I than in Group II at baseline and at month 3 ( P = 0.028 and P = 0.037, respectively). During follow -up, significant reductions in CD3+, CD4+, and CD8+ levels were observed in Group I ( P = 0.013, P = 0.017, and P = 0.041, respectively), whereas significant decreases in NK defective and NK regulatory subsets were identified in Group II ( P = 0.037 and P = 0.047, respectively). At the 3 -month assessment, all patients met the study definition of postherpetic neuralgia. Conclusion: Diabetes mellitus was associated with alterations in natural killer cell subpopulations, suggesting impaired innate immune function in patients with acute herpes zoster. However, within the limitations of this small cohort, diabetes mellitus did not appear to independently increase the risk of postherpetic neuralgia. Larger , well -designed studies are needed to clarify the predictive role of immunologic markers in chronic neuropathic pain outcomes.
