Ladenson P W, Goldenheim P D, Ridgway E C
J Clin Endocrinol Metab. 1983 Jun;56(6):1252-9. doi: 10.1210/jcem-56-6-1252.
Acute cardiovascular, renal, pulmonary, metabolic, and pituitary responses to therapy of hypothyroidism with 25 micrograms iv T3 (group I G-I, n = 11) or 50 micrograms iv T3 (group II, G-II, n = 10)/day for 1 week have been studied. Serum T3 levels were acutely normalized in both groups with the mean basal serum T3 levels (X +/- SE) after 7 days, 98 +/- 10 micrograms/dl and 229 +/- 19 ng/dl, respectively. Myocardial performance, noninvasively assessed by the pulse wave arrival time (QKd) and the phonocardiographic systolic time interval ratio was significantly altered after 1 day of therapy (QKd for G-I = -10 +/- 4 msec, P less than 0.05; and for G-II = -18 +/- 14 msec, P less than 0.01). After 7 treatment days, both the mean QKd (203 +/- 7 msec, P less than 0.001) and phonocardiographic systolic time interval ratio (0.41 +/- 0.02, P less than 0.01) were within the normal range in G-II. Abnormal pretreatment renal excretion of an oral water load (G-I, 65 +/- 6%; and G-II, 57 +/- 6%) was also reversed after 1 week (G-I, 84 +/- 5%, P less than 0.05; and G-II, 89 +/- 5%, P less than 0.01). Patients with blunted hypercapnic (n = 6) and hypoxic (n = 4) ventilatory drives were improved in both groups after 6 days. The mean basal metabolic rate, serum cholesterol, and serum creatine phosphokinase were altered by the week of therapy in a dose-response manner, and were in the normal range in G-II. Pituitary TSH secretion was promptly suppressed in both groups. Two hours after the first T3 dose, the mean serum TSH for G-I and G-II decreased to 85% (P less than 0.02) and 70% (P less than 0.001) of their respective pretreatment values. After 7 days of therapy, the mean basal TSH levels had declined to 75% (P less than 0.001) and 5% (P less than 0.001%) of pretreatment, respectively. In comparison with previous observations of responses to 100 micrograms/day iv T4 for 1 week, the 25 micrograms dose T3 was equivalent in terms of changes in basal serum T3 and peripheral (nonpituitary) tissue responses, but less effective than T4 in lowering serum TSH. Based on these parameters, 50 micrograms/day iv T3 was the most effective of the three regimens within this time frame. The implications of these observations in the clinical management of severe complicated myxedema are discussed.
研究了急性心血管、肾脏、肺部、代谢及垂体对甲状腺功能减退症患者采用每日静脉注射25微克三碘甲状腺原氨酸（I组，G-I，n = 11）或50微克三碘甲状腺原氨酸（II组，G-II，n = 10）治疗1周的反应。两组患者的血清三碘甲状腺原氨酸水平均迅速恢复正常，7天后平均基础血清三碘甲状腺原氨酸水平（X±SE）分别为98±10微克/分升和229±19纳克/分升。治疗1天后，通过脉搏波到达时间（QKd）和心音图收缩时间间期比值进行无创评估的心肌功能发生了显著改变（I组QKd=-10±4毫秒，P<0.05；II组QKd=-18±14毫秒，P<0.01）。治疗7天后，II组的平均QKd（203±7毫秒，P<0.001）和心音图收缩时间间期比值（0.41±0.02，P<0.01）均在正常范围内。口服水负荷试验前异常的肾脏排泄情况（I组，65±6%；II组，57±6%）在1周后也得到了改善（I组，84±5%，P<0.05；II组，89±5%，P<0.01）。两组中高碳酸血症通气驱动减弱（n = 6）和低氧通气驱动减弱（n = 4）的患者在6天后均有改善。平均基础代谢率、血清胆固醇和血清肌酸磷酸激酶在治疗1周后呈剂量反应性改变，II组均在正常范围内。两组患者垂体促甲状腺激素分泌均迅速受到抑制。首次注射三碘甲状腺原氨酸后2小时，I组和II组的平均血清促甲状腺激素分别降至各自治疗前值的85%（P<0.02）和70%（P<0.001）。治疗7天后，平均基础促甲状腺激素水平分别降至治疗前的75%（P<0.001）和5%（P<0.001%）。与之前观察到的每日静脉注射100微克甲状腺素治疗1周的反应相比，25微克剂量的三碘甲状腺原氨酸在基础血清三碘甲状腺原氨酸变化和外周（非垂体）组织反应方面相当，但在降低血清促甲状腺激素方面不如甲状腺素有效。基于这些参数，在这个时间框架内，每日静脉注射50微克三碘甲状腺原氨酸是三种治疗方案中最有效的。讨论了这些观察结果对重度复杂黏液性水肿临床管理的意义。
