Grussendorf M
Abteilung für Innere Medizin, Universitätsklinikum, Ulm.
Med Klin (Munich). 1996 Aug 15;91(8):489-93.
In terms of the pathomechanism, TSH and intrathyroid iodine deficiency are the interconnecting elements between alimentary iodine deficiency and the growth and genesis of goiter. L-Thyroxine treatment for suppression of hypophyseal TSH production and supplementary iodide have a synergistic effect in reducing the size of goiter. An individual adaptation of the L-Thyroxine dose is necessary for optimal TSH suppression. Excessive suppression of the TSH level prevents uptake of iodine by the thyroid and thus compensation of the intrathyroid iodine deficiency. Combination therapy of an individually adjusted amount of L-Thyroxine with a small, mostly constant amount of iodine is a recognized concept of goiter therapy today. Administration of a combination preparation with an individually adjustable dose of L-Thyroxine and 150 micrograms iodine complies with these recommendations and improves compliance since only one tablet is required.
In the present study, the thyroid iodine supply, efficacy and tolerance of such a combination preparation was tested for the first time in 49 patients with euthyroid iodine deficiency goiter (group A). 45 patients receiving an individual L-Thyroxine therapy served as controls (group B).
Supplementation of individually dosable L-Thyroxine with 150 micrograms iodide leads to a markedly raised iodine excretion in the urine (p < 0.005). This is an indirect indication of an improved thyroid iodine supply. Patients of group A showed a greater reduction of the thyroid volume (18.5% as compared to 16.8%, p = n. s.) and a more persistent TSH suppression (lowering by 39% [group A] as compared to a rise of 17% [group B]) in relation to the initial value (p < 0.004). This is attributable to the improved supply of iodine.
The combination therapy tested was tolerated just as well as the mono-L-Thyroxine treatment with better efficacy.
就发病机制而言,促甲状腺激素(TSH)和甲状腺内碘缺乏是膳食碘缺乏与甲状腺肿生长和发生之间的相互关联因素。左甲状腺素治疗抑制垂体TSH分泌以及补充碘化物在缩小甲状腺肿大小方面具有协同作用。为实现最佳TSH抑制,需要对左甲状腺素剂量进行个体化调整。过度抑制TSH水平会阻止甲状腺摄取碘,从而无法补偿甲状腺内碘缺乏。将个体化调整剂量的左甲状腺素与少量(大多恒定)碘联合治疗是当今公认的甲状腺肿治疗理念。给予一种具有个体化可调节剂量左甲状腺素和150微克碘的复方制剂符合这些建议,并且由于只需服用一片药,从而提高了依从性。
在本研究中,首次在49例甲状腺功能正常的碘缺乏性甲状腺肿患者(A组)中测试了这种复方制剂的甲状腺碘供应、疗效和耐受性。45例接受个体化左甲状腺素治疗的患者作为对照(B组)。
补充个体化可调节剂量的左甲状腺素与150微克碘化物导致尿碘排泄显著增加(p < 0.005)。这是甲状腺碘供应改善的间接指标。与初始值相比,A组患者的甲状腺体积缩小幅度更大(分别为18.5%和16.8%,p = 无显著差异),TSH抑制更持久(A组降低39%,而B组升高17%)(p < 0.004)。这归因于碘供应的改善。
所测试的联合治疗与单一左甲状腺素治疗耐受性相当,但疗效更好。