PLASMA CONCENTRATION CHANGE OF VIP, Β-EP, ENK, AND PGE2 IN CLASSICAL TRIGEMINAL NEURALGIA PATIENTS AFTER BTX-A TREATMENT

Yuan Chen, YongYue Wang, Yajun Lian*, haifeng Zhang, nanChang Xie

The First Affiliated Hospital of Zhengzhou University, Νo. 1 Jianshe East Road Zhengzhou

 Objective: It is to investigate the clinical effect of serum CEA, CA153, CYFRA21-1, CA125, NSE, and CA199 in the application of Myrian imaginObjective: This research aims to investigate vasoactive intestinal peptide (VIP), beta-endorphin (β-EP), encephalin (ENK) and prostaglandin E2 (PGE2) levels in relation to classical trigeminal neuralgia (TN). This research also examines the influence of Botulinum Toxin Type A (BTX-A) on the concentration of VIP, β-EP, ENK and PGE2 in plasma.

Methods: Patients were recruited from outpatients and inpatients attending the neurology department of the First Affiliated Hos- pital of Zhengzhou University, from October 2014 to March 2015. Twenty-eight TN patients were assigned to receive treatment with BTX-A. Fasting venous blood was sampled from the elbow, before and after treatment with BTX-A, serving as Group A and Group B re- spectively. Thirty-four healthy individuals were recruited from the physical examination department to act as a control (Group C). VIP, β-EP, ENK and PGE2 levels were measured by enzyme linked immunosorbent assay (ELISA). Statistical data was analysed using SPSS.

Results: (1) When compared with Group B and Group C, the concentration of VIP in plasma was significantly increased in Group A, with no significant difference in the level of plasma VIP found between Group B and Group C. (2) Mean plasma β-EP levels decreased in TN patients both before and after BTX-A therapy when compared to a control. Mean β-EP plasma levels in Group B was found to be higher than that of Group A. A negative linear correlation was found between the levels of plasma β-EP and VAS before treatment, with an increase of β-EP level following treatment correlating with a reduction in VAS. (3) No significant difference in plas- ma levels of ENK and PGE2 was found between any of the groups.

Conclusions: VIP overexpression and insufficient β-EP expression may be related to the pathogenesis of TN. BTX-A inhibited the synthesis and release of VIP and facilitated the synthesis and release of β-EP, alleviating pain in a dose-independent way. BTX-A had no effect on plasma PGE2 and ENK levels. β-EP is a crucial analgesic involved in the pathogenesis of TN, directly affecting the intensity of symptoms.