Endocrinology Unit, Department of Clinical and Experimental Medicine, University of Catania, Garibaldi Nesima Hospital, Catania, Italy.
Endocrinol Diabetes Metab. 2023 Mar;6(2):e406. doi: 10.1002/edm2.406. Epub 2023 Feb 1.
Therapy for hypothyroid obese patients is still under definition since the thyrotropin-stimulating hormone (TSH) level is a less reliable marker of euthyroidism than nonobese patients. Indeed, TSH levels positively correlate with body mass index (BMI), and this increase may be a compensatory mechanism aimed at increasing energy expenditure in obese people. In contrast, the correlation of BMI with thyroid hormone levels is not completely clear, and conflicting results have been obtained by several studies. The L-T4 replacement dose is more variable in obese hypothyroid patients than in nonobese patients, and a recent study indicated that the L-T4 replacement dose is related to lean body mass in obese thyroidectomized patients. We aimed to study the correlations of L-T4-administered dose, thyroid hormone levels and TSH secretion with basal metabolic rate (BMR) and total calculated deiodinase activity (GD) in obese and nonobese athyreotic patients. We also looked for individualized L-T4 replacement dose set points to be used in clinical practice.
We studied retrospectively 160 athyreotic patients, 120 nonobese and 40 obese. GD was calculated by SPINA Thyr 4.2, the responsiveness of the hypothalamic/pituitary thyrotrope by Jostel's thyrotropin (TSH) index and BMR by the Mifflin-St. Jeor formula, the interplay of GD and BMR with L-T4, thyroid hormones and TSH index (TSHI) was also evaluated.
In our study, the L-T4 dose was an independent predictor of GD, and approximately 30% of athyreotic patients under L-T4 therapy had a reduced GD; FT4 levels were higher and negatively modulated by BMR in obese athyreotic patients respect to nonobese, in these patients a T4 to T3 shunt, in terms of TSHI suppression is observed suggesting a defective hypothalamic pituitary T4 to T3 conversion and a resistance to L-T4 replacement therapy.
L-t4 dose is the most important predictor of GD, BMR modulates T4 levels in obese athyreotic patients that are resistant to L-T4 replacement therapy.
由于促甲状腺激素（TSH）水平作为甲状腺功能正常的标志物，不如非肥胖患者可靠，因此治疗甲状腺功能减退症肥胖患者的方法仍有待确定。事实上，TSH 水平与体重指数（BMI）呈正相关，这种增加可能是一种旨在增加肥胖人群能量消耗的代偿机制。相反，BMI 与甲状腺激素水平的相关性并不完全清楚，并且一些研究得出了相互矛盾的结果。肥胖甲状腺功能减退症患者的 L-T4 替代剂量比非肥胖患者更具变异性，最近的一项研究表明，L-T4 替代剂量与肥胖甲状腺切除患者的瘦体重有关。我们旨在研究肥胖和非肥胖甲状腺功能减退症患者的 L-T4 给药剂量、甲状腺激素水平和 TSH 分泌与基础代谢率（BMR）和总计算脱碘酶活性（GD）的相关性。我们还寻找了可用于临床实践的个体化 L-T4 替代剂量设定点。
我们回顾性研究了 160 例甲状腺功能减退症患者，其中 120 例非肥胖，40 例肥胖。通过 SPINA Thyr 4.2 计算 GD，通过 Jostel's TSH（TSH）指数计算下丘脑/垂体促甲状腺激素的反应性，通过 Mifflin-St. Jeor 公式计算 BMR，还评估了 GD 和 BMR 与 L-T4、甲状腺激素和 TSHI 的相互作用。
在我们的研究中，L-T4 剂量是 GD 的独立预测因子，大约 30%接受 L-T4 治疗的甲状腺功能减退症患者 GD 降低；肥胖甲状腺功能减退症患者的 FT4 水平更高，BMR 负调节，与非肥胖患者相比，这些患者存在 T4 到 T3 分流，表现为 TSHI 抑制，表明下丘脑-垂体 T4 到 T3 转化缺陷和对 L-T4 替代治疗的抵抗。
L-T4 剂量是 GD 的最重要预测因子，BMR 调节肥胖甲状腺功能减退症患者的 T4 水平，这些患者对 L-T4 替代治疗有抵抗。
