Tajtáková M, Langer P, Gonsorcíková V, Hancinová D
First Clinic of Internal Medicine, Faculty of Medicine, P J Safárik University, Kosice, Slovakia.
Eur J Endocrinol. 1998 Jun;138(6):674-80. doi: 10.1530/eje.0.1380674.
To evaluate whether small iodine supplements decrease the incidence of adolescent thyroid hypertrophy in an iodine-sufficient population or whether such thyroid enlargement should be considered an inevitable physiological phenomenon.
Beginning in September 1991 (after an initial examination in September 1990), 54 11-year-old children in Bardejov, Slovakia were given small iodine supplements (Thyrojod depot tablets containing 1530 microg iodide) every 2 weeks for 2 years followed by once weekly for 2 years. A second group of 63 children served as controls. In June 1995, there were still 52 treated and 60 control children in the study and these were examined; 44 treated and 48 control children remained in the study until June 1997.
In 1990, 1993, 1995, 1996 and 1997 the thyroid volume (ThV) was measured by ultrasound. Serum levels of TSH, thyroglobulin, total and free thyroxine and tri-iodothyronine and anti-thyroid peroxidase (anti-TPO), anti-thyroglobulin (anti-TG) and anti-TSH receptor (TSR) antibodies were estimated in 1990 and 1994, while only TSH, and anti-TPO and anti-TSR antibodies were measured in 1997.
There was no difference between the groups at any interval in the serum levels of the hormones measured. Marginally increased TSH was found in two treated and two control children. Anti-TSR antibodies were negative in all children, while anti-TPO and anti-TG antibodies were found in one treated and four control children. At the age of 10 years (1990), 84% of all ThVs were less than 4 ml, indicating a previous life-long sufficient iodine intake. After the treatment was completed (June 1995), a significant difference in ThV (P < 0.04) was found between the whole treated (5.78 +/- 0.19 ml) and the whole control group (6.56 +/- 0.30 ml). However, there was already a marked difference in the 75th percentile (6.4 ml in treated vs 8.5 ml in controls) due to more rapid thyroid growth in certain children of the control group (ThV > 7.0 ml in 6/52 treated children vs 24/60 controls; P < 0.01). Since such differences were much higher in 1997, the children in each group whose ThV was in the range of the upper 25% in 1997 were retrospectively evaluated as arbitrary separate subgroups in all the time intervals and compared with the remaining 75% of children who showed moderate thyroid growth rate. Two years after the termination of treatment (June 1997), excessive thyroid growth continued in the upper quarter of 12 controls with the highest ThV (13.60 +/- 0.40 ml or 7.60 +/- 0.29 ml/m2; 12/12 with ThV > 11.0 ml), and a similar subgroup now also appeared in 11 previously treated children (10.79 +/- 0.51 ml or 6.19 +/- 0.30 ml/m2; 5/11 with ThV > 11.0 ml). At the same time, ThV in the remaining 75% of both control (8.12 +/- 0.38 ml or 4.82 +/- 0.17 ml/m2; 3/36 with ThV > 11.0 ml) and treated (7.20 +/- 0.30 ml or 4.39 +/- 0.17 ml/m2; 0/33 with ThV > 11.0 ml) children was significantly less (P < 0.01 to P < 0.001) than that in the appropriate rapidly growing subgroups. During the whole observation period (1990-1997), no difference was found between treated and control subgroups with moderate thyroid growth.
Since iodine intake in Slovakia has been adequate for decades and sporadic iodine deficiency is highly unlikely, the observed excessive thyroid growth in certain adolescents may result from causes other than simple iodine deficiency (e.g. hereditary), which are nevertheless ameliorated by small iodine supplements. The question remains whether such a subgroup with rapidly growing thyroids should be included in the range of normal thyroid volumes in adolescents.
评估在碘充足人群中补充少量碘是否能降低青少年甲状腺肿大的发生率,或者这种甲状腺肿大是否应被视为一种不可避免的生理现象。
从1991年9月开始(在1990年9月进行初次检查之后),斯洛伐克巴尔代约夫的54名11岁儿童每2周补充一次少量碘(含1530微克碘化物的甲状腺碘长效片),持续2年,之后每周补充一次,再持续2年。另一组63名儿童作为对照。1995年6月,研究中仍有52名接受治疗的儿童和60名对照儿童,并对他们进行了检查;44名接受治疗的儿童和48名对照儿童一直参与研究直至1997年6月。
在1990年、1993年、1995年、1996年和1997年,通过超声测量甲状腺体积(ThV)。在1990年和1994年测定血清促甲状腺激素(TSH)、甲状腺球蛋白、总甲状腺素和游离甲状腺素、三碘甲状腺原氨酸以及抗甲状腺过氧化物酶(抗-TPO)、抗甲状腺球蛋白(抗-TG)和抗促甲状腺激素受体(TSR)抗体的水平,而在1997年仅测量TSH、抗-TPO和抗-TSR抗体。
在各个时间间隔,所测激素的血清水平在两组之间均无差异。在两名接受治疗的儿童和两名对照儿童中发现TSH略有升高。所有儿童的抗-TSR抗体均为阴性,而在一名接受治疗的儿童和四名对照儿童中发现了抗-TPO和抗-TG抗体。在10岁时(1990年),所有甲状腺体积中有84%小于4毫升,表明此前终生碘摄入充足。治疗结束后(1995年6月),整个接受治疗组(5.78±0.19毫升)和整个对照组(6.56±0.30毫升)的甲状腺体积存在显著差异(P<0.04)。然而,由于对照组中某些儿童甲状腺生长更快(接受治疗的儿童中有6/52甲状腺体积>7.0毫升,而对照组中有24/60;P<0.01),第75百分位数已有明显差异(接受治疗组为6.4毫升,对照组为8.5毫升)。由于1997年这种差异更大,对每组中甲状腺体积在1997年处于上25%范围的儿童在所有时间间隔均作为任意单独亚组进行回顾性评估,并与其余甲状腺生长速度适中的75%儿童进行比较。治疗终止两年后(1997年6月),甲状腺体积最大的12名对照儿童中的上四分位甲状腺过度生长仍在继续(13.60±0.40毫升或7.60±0.29毫升/平方米;12/12甲状腺体积>11.0毫升),并且在11名先前接受治疗的儿童中现在也出现了类似亚组(10.79±0.51毫升或6.19±0.30毫升/平方米;5/11甲状腺体积>11.0毫升)。与此同时,对照组和接受治疗组其余75%儿童的甲状腺体积(对照组为8.12±0.38毫升或4.82±0.17毫升/平方米;3/36甲状腺体积>11.0毫升;接受治疗组为7.20±0.30毫升或4.39±0.17毫升/平方米;0/33甲状腺体积>11.0毫升)明显小于(P<0.01至P<0.001)相应的快速生长亚组。在整个观察期(1990 - 1997年),甲状腺生长速度适中的治疗亚组和对照亚组之间未发现差异。
由于斯洛伐克数十年来碘摄入充足,散发性碘缺乏极不可能,因此在某些青少年中观察到的甲状腺过度生长可能由单纯碘缺乏以外的原因(如遗传)导致,不过补充少量碘可使其得到改善。问题仍然是,这样一个甲状腺快速生长的亚组是否应被纳入青少年正常甲状腺体积范围。