Kaiserman I, Avni M, Sack J
Pediatric Endocrinology Unit, Chaim Sheba Medical Center, Tel-Hashomer, Israel.
Horm Res. 1995;44(5):229-37. doi: 10.1159/000184631.
Thyroxine intoxication is a benign, nonfatal condition, relatively common in the pediatric age group. We present here a detailed laboratory follow-up of all thyroidal hormones in 2 healthy girls who inadvertently ingested 2,500 micrograms of L-thyroxine. The two girls were hospitalized and treated with ipecac, gastric lavage, propranolol, prednisone, cholestyramin and propyl-thiouracil. All physical signs were normal and no symptoms were reported. All thyroidal hormones were measured 12 times from 2 h to 20 days after the ingestion. For T4, T3, rT3 and thyroglobulin (Tg) a one-compartment kinetic model was formulated and fitted to the empirical data. The kinetic data constants of production and elimination were calculated, as well as the metabolic clearance rate. All laboratory values were similar in both girls. T4 serum levels were already high 2 h after the intoxication and returned to normal values only after 13 days. Fitting the T4 serum levels with a one-compartment model resulted in absorption and degradation constants similar to those in normal adult subjects. Thyroid-stimulating hormone (TSH) levels decreased reaching their lowest concentration 14 h after the intoxication. They remained low till the 4th day, after which they rose gradually. Twenty days after the intoxication, TSH levels were still below their initial values. T3 reached its peak levels 11 h after the ingestion and decreased to normal values after 3 days. Both T3 production constants and T3 degradation constants were significantly increased. rT3 reached its peak level on the 2nd day after the intoxication and decreased to normal values on the 4th day. Its production and degradation constants were somewhat below normal levels. The T3/rT3 ratio decreased from a normal level of around 3 to as low as 1 and rose again after 13 days to extremely high levels (as high as 8). Tg serum levels dropped continuously with a half-life of 1-5 days and started rising again after 2-13 days. In conclusion, T4 intoxication in the child is combated primarily by a significant increase in T3 production and degradation, while meticulously maintaining relatively low T3 levels.
甲状腺素中毒是一种良性、非致命性疾病,在儿童年龄组中相对常见。我们在此展示了对2名意外摄入2500微克左甲状腺素的健康女孩所有甲状腺激素进行的详细实验室跟踪情况。这两名女孩住院并接受了吐根糖浆、洗胃、普萘洛尔、泼尼松、消胆胺和丙硫氧嘧啶治疗。所有体征均正常,未报告任何症状。在摄入后2小时至20天内对所有甲状腺激素进行了12次测量。对于T4、T3、反T3(rT3)和甲状腺球蛋白(Tg),建立了单室动力学模型并拟合经验数据。计算了生成和消除的动力学数据常数以及代谢清除率。两名女孩的所有实验室值均相似。中毒后2小时T4血清水平就已升高,仅在13天后才恢复到正常值。用单室模型拟合T4血清水平得到的吸收和降解常数与正常成年受试者相似。促甲状腺激素(TSH)水平在中毒后14小时下降至最低浓度。在第4天之前一直保持较低水平,之后逐渐上升。中毒20天后,TSH水平仍低于初始值。T3在摄入后11小时达到峰值水平,3天后降至正常值。T3的生成常数和降解常数均显著增加。rT3在中毒后第2天达到峰值水平,第4天降至正常值。其生成和降解常数略低于正常水平。T3/rT3比值从正常水平约3降至低至1,并在13天后再次上升至极高水平(高达8)。Tg血清水平持续下降,半衰期为1 - 5天,并在2 - 13天后再次开始上升。总之,儿童T4中毒主要通过T3生成和降解的显著增加来对抗,同时精心维持相对较低的T3水平。