Postherpetic neuralgia (PHN), as the most challenging complication of herpes zoster, is closely associated with intense and persistent inflammatory responses triggered by viral reactivation. Scientific evidence clearly demonstrates that the reactivation of varicella-zoster virus (VZV) in sensory ganglia not only causes skin lesions but, more critically, initiates a severe inflammatory storm that spreads to the peripheral and even central nervous systems. The key players in this inflammation-pro-inflammatory cytokines and immune cells-exhibit detectable changes in their activity and concentration in the blood, providing a crucial window for identifying predictive and diagnostic laboratory markers for PHN. Studies reveal that PHN patients commonly exhibit significant inflammatory imbalances in their blood: levels of key pro-inflammatory cytokines such as interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-A), interleukin-1 beta (IL-1B), and interleukin-17 (IL-17) are markedly and persistently elevated. These cytokines not only directly act on damaged nerves, increasing their excitability and inducing ectopic discharges, but also drive peripheral and central sensitization, amplifying pain signals. Concurrently, impaired immune regulation is evidenced by reduced numbers or functionality of regulatory T cells (Tregs) in the blood, while pro-inflammatory T helper 17 cells (Th17) are relatively increased, leading to an imbalanced Th17/Treg ratio that further exacerbates the inflammatory environment. Additionally, nonspecific systemic inflammatory markers such as C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR) are often elevated during the acute phase or in patients with persistent pain and correlate with pain intensity. Beyond cytokines and immune cell profiles, pain-related neuropeptides like substance P (SP) and calcitonin gene-related peptide (CGRP) are also abnormally elevated in the serum of PHN patients, directly participating in the transmission
