氟西汀治疗持续的躯体形式的疼痛障碍的疗效及其作用机制

目的：研究氟西汀对持续的躯体形式的疼痛障碍（以下简称持续疼痛障碍）的疗效及其与5－羟色胺（5－HT）2A受体基因多态性的关系。方法：用氟西汀（20mg/d)治疗62例持续疼痛障碍患者（病例组），共6周，应用疼痛量表（MOSPM）及汉密尔顿抑郁量表（HAMD；17项）于治疗前及治疗后第2，4，6周末进行评定，采用聚合酶链反应－限制性片段长度多态技术，测定5－HT2A受体基因多态性，并与正常人对照，结果：（1）MOSPM及HAMD评定；氟西汀治疗的有效率均瞎长而增加，在治疗第6周末分别达到76％和79％，（2）经Z检验，有效组中C／C基因型15个（38％）和C等位基因频率45个（58％）] 无效组分别为1个（8％）和6个（25％）]，无效组中T／T基因型7个（58％）]和T等位基因频率18个（75％）]高于有效组分别为9个（23％和33个（42％）]，差异均有显著性（P＜0．05，而T／C基因型频率两组的差异无显著性分别为15个（38％）和4个（33％）]，结论：氟西汀可缓解该类患者的疼痛及抑郁症状，其镇痛疗效可能与5－HT2A受体基因T102C多态性有关。

Efficacy of fluoxetine and its mechanism for patients with persist somatoform pain disorder

Objective To study the efficacy of fluoxetine for the patients with persist somatoform pain disorder and the relationship between the efficacy of fluoxetine and serotonin 2A (5 HT 2A ) receptor gene T102C polymorphism Methods Sixty two patients who met with ICD 10 criteria for persist somatoform pain disorder (F45 4) were treated with fluoxetine (20 mg/day) for 6 weeks The Medical Outcome Study Pain Measures (MOSPM) and Hamilton Depression Scale (HAMD) 17 items were used to assess the therapeutic efficacy According to the efficacy rate of MOSPM, the patients were divided into responder or non responder group Fifty one patients were examined the genotypes and allele frequencies of 5 HT 2A receptor gene T102C polymorphism with polymerase chain reaction restriction fragment length polymorphism (PCR RFLP) Results The efficacy rate of fluoxetine on the score of MOSPM were 19%, 48% and 76% at the 2 nd, 4 th and 6 th weekend respectively, and the effect rate of antidepressant were 24%, 56% and 79% according to HAMD score There were significant difference of T/T, C/C genotypes and T,C alleles between the responder group and non responder group( Z =3 165, 3 822, 3 125, 3 125, respectively), but no difference were found in T/C genotype( Z =0 463) Conclusion Fluoxetine can alleviate the pain and depressive symptoms of the patients with persist somatoform pain disorder, and there may be some relation between the analgesic efficacy of fluoxetine and 5 HT 2A receptor gene T102C polymorphism