Guasti Luigina, Marino Franca, Cosentino Marco, Cimpanelli Mariagrazia, Rasini Emanuela, Piantanida Eliana, Vanoli Paolo, De Palma Diego, Crespi Chiara, Klersy Catherine, Maroni Lorenzo, Loraschi Anna, Colombo Cristina, Simoni Cinzia, Bartalena Luigi, Lecchini Sergio, Grandi Anna M, Venco Achille
Department of Clinical Medicine, University of Insubria, Varese, Italy.
Clin J Pain. 2007 Jul-Aug;23(6):518-23. doi: 10.1097/AJP.0b013e3180735e5e.
Elevated blood pressure levels that are associated with hypalgesia and hypothyroidism have major influences on the cardiovascular system. The potential modulation of pain sensitivity by thyroid hormones is largely undetermined. Moreover, a few experimental studies show that peripheral benzodiazepine receptors (PBRs), which may be altered in hypothyroidism, seem to be related with pain perception.
Dental pain threshold and tolerance were evaluated in 19 patients followed for differentiated thyroid carcinoma (1) in severe short-term hypothyroidism (phase 1) and (2) during thyroid stimulating hormone-suppressive LT4 treatment (phase 2). PBR expression (cytofluorimetric evaluation) on peripheral blood mononuclear cells was also investigated in the 2 phases.
Pain perception differed throughout the study, the dental pain threshold was higher in phase 1 (P<0.05) whereas pain tolerance was higher but not significantly (P=0.07). Although the systolic blood pressure was higher during hypothyroidism (P<0.01), no relationship was found between blood pressure changes and pain sensitivity variations. Moreover, the multiple regression analysis showed an independent association of the clinical phase with pain sensitivity (r=-2.61, P=0.029), while accounting for systolic blood pressure. The intensity of PBRs was significantly higher in the first phase of the study (P=0.047) whereas the ratio did not significantly differ. However, no relationship was observed between pain sensitivity and PBRs.
In conclusion, in athyreotic patients, the pain sensitivity is related to the thyroid status and is independent of the increase in blood pressure induced by thyroid hormone deprivation. The PBRs do not seem to have major influence on pain sensitivity changes in hypothyroidism.
与痛觉减退和甲状腺功能减退相关的血压升高对心血管系统有重大影响。甲状腺激素对疼痛敏感性的潜在调节作用在很大程度上尚未确定。此外，一些实验研究表明，可能在甲状腺功能减退时发生改变的外周苯二氮䓬受体（PBR）似乎与疼痛感知有关。
对19例分化型甲状腺癌患者进行随访，评估其（1）严重短期甲状腺功能减退期（阶段1）和（2）促甲状腺激素抑制性左甲状腺素治疗期间（阶段2）的牙科疼痛阈值和耐受性。同时在这两个阶段研究外周血单个核细胞上的PBR表达（细胞荧光分析评估）。
在整个研究过程中疼痛感知有所不同，阶段1的牙科疼痛阈值较高（P<0.05），而疼痛耐受性较高但无显著差异（P=0.07）。虽然甲状腺功能减退期间收缩压较高（P<0.01），但未发现血压变化与疼痛敏感性变化之间存在关联。此外，多元回归分析显示临床阶段与疼痛敏感性存在独立关联（r=-2.61，P=0.029），同时考虑了收缩压。研究第一阶段PBR的强度显著较高（P=0.047），而比率无显著差异。然而，未观察到疼痛敏感性与PBR之间存在关联。
总之，在无甲状腺患者中，疼痛敏感性与甲状腺状态相关，且独立于甲状腺激素缺乏引起的血压升高。PBR似乎对甲状腺功能减退时的疼痛敏感性变化没有重大影响。
