The importance of reverse triiodothyronine in hypothyroid children on replacement treatment.

Reverse triiodothyronine (rT3), triiodothyronine (T3), thyroxine (T4), and thyroid stimulating hormone (TSH) values were measured by radioimmunoassay in 40 children with congenital hypothyroidism who were being given levothyroxine (0.05-0.35 mg/day) and in 14 normal controls. In 15 of the children with hypothyroidism the treatment, judged by serum T4 and TSH values and thyrotrophin releasing hormone (TRH) test, seemed to be adequate and their mean rT3 value and rT3:T4 ratio were comparable with the controls. The remaining 25 children had a raised serum T4 and a low TSH value. Only 4 (16%) of these children had an abnormally high T3 concentration but the rT3 value was raised in 23 (92%) and their mean rT3 value and rT3:T4 ratio were significantly higher than in the control children. Less than 20% of this ''overtreated'' group, however, had clinical hyperthyroidism. We suggest that in patients on T4 replacement treatment the peripheral thyroid homeostatic mechanisms produce larger amounts of rT3, thereby preventing high T3 values where serum T4 values are raised. This may explain why the ''overtreated'' children showed no clinical evidence of hyperthyroidism. These findings emphasise the protective and selective role of peripheral monodeiodination.     

Effects of anticonvulsant drugs on thyroid hormones in epileptic children.

Serum total and free thyroid hormones, reverse T3 (rT3), thyroxin binding globulin (TBG) and thyroid stimulating hormone (TSH) concentrations were measured in 35 epileptic patients receiving anticonvulsants (phenobarbitone, phenytoin). There was a significant reduction found in total thyroxine (TT4), free thyroxine (FT4), total triiodothyronine (TT3), free triiodothyronine (FT3) and rT3 in the group treated with, phenytoin. The thyroid hormone levels were within normal limits in the group receiving phenobarbitone.     

Pseudohypoparathyroidism with hypothyroidism (author's transl)

This is a report about three children suffering from pseudo-hypoparathyroidism type I and moderate primary hypothyroidism. The thyroid dysfunction was characterised by slightly low plasma thyroxine and high basal TSH showing an increased response to TRH. T3 and rT3 were within normal limits, the size of the thyroid glands and also bone age were normal. The plasma concentrations of T4 and TSH and the response of TSH to TRH were no different during hypocalcemia from those obtained in normocalcemia during vitamin D treatment. Thyroxine treatment could normalize T4 and TSH. Moderate hypothyroidism is frequently present in pseudohypoparathyroidism. It has to be assumed that the same genetical defect of the second messenger, already proved to exist in the kidneys of patients with pseudohypoparathyroidism may also exist in the thyroid gland.     

Longitudinal study on thyroid function in patients with thalassemia major

Primary hypothyroidism is one of the most frequent complications observed in patients suffering from thalassemia. We investigated thyroid function in a group of patients attending the Pediatric Department of Cardarelli Hospital in order to determine in how many patients thyroid function worsened during a 12 year-period of follow up. PATIENTS AND MEASUREMENTS: Fifty patients with beta-thalassemia major (27 females and 23 males), mean age 25.7+/-1.4 years, were re-evaluated according to the criteria of Faglia et al. Thyroid dysfunction was defined as follows: overt hypothyroidism (low FT4 and increased TSH levels >10 microU/ml); compensated hypothyroidism (normal FT4, TSH 5-10 microU/ml, and abnormal TRH test); subclinical hypothyroidism (normal FT4, basal TSH 0-5 microU/ml, abnormal TRH test). Correlation with hematological, biochemical and growth parameters was evaluated. RESULTS: Ten out of 50 patients evaluated in a previous study had moved to other centers, and four patients had died from cardiac problems. Thus, 36 patients completed a 12 year-period of follow-up. In 25% of the patients the degree of thyroid dysfunction worsened with different degrees of severity. The prevalence of overt hypothyroidism had risen to 13.9% from 8.4%. No cases of secondary hypothyroidism were observed, and anti-thyroglobulin and anti-thyroperoxidase (TPO) antibody titers were negative in all patients. Five (28%) out of 17 patients with normal thyroid function previously (one female, four male) showed an exaggerated TSH response to a TRH test, with normal serum levels of FT4, and they were classified as having subclinical hypothyroidism; while another patient died of cardiac complications. Four out of twelve patients with previous subclinical hypothyroidism showed worsening with a different degree of severity: two females changed to compensated hypothyroidism, and two males to overt hypothyroidism. Furthermore, two out of six patients with compensated hypothyroidism and one out of four patients with overt hypothyroidism died of cardiac failure. In all patients there was no correlation between serum ferritin levels, blood transfusion, pretransfusion Hb levels and worsening of thyroid function. Echographic data showed features of dishomogeneity of the parenchyma with different degrees of severity in accordance with the criteria of Sostre and Reyes. The highest score was observed in all patients with overt and compensated hypothyroidism. CONCLUSIONS: A slow worsening of thyroid function was observed in 25% of the studied patients and only two of them developed overt hypothyroidism. The echographic pattern seems to be strongly predictive of thyroid dysfunction.     

Short-term hyperthyroidism followed by transient pituitary hypothyroidism in a very low birth weight infant born to a mother with uncontrolled Graves' disease

Transient hypothyroxinemia in infants born to mothers with poorly controlled Graves' disease was first reported in 1988. We report that short-term hyperthyroidism followed by hypothyroidism with low basal thyroid-stimulating hormone (TSH) levels developed in a very low birth weight infant born at 27 weeks of gestation to a noncompliant mother with thyrotoxicosis attributable to Graves' disease. We performed serial thyrotropin-releasing hormone (TRH) tests in this infant and demonstrated that TSH unresponsiveness to TRH disappeared at 6.5 months of age. The maternal thyroid function was free triiodothyronine (FT(3)), 21.1 pg/mL; free thyroxine (FT(4)), 8.1 ng/dL; TSH, <0.03 microU/mL; thyroid-stimulating hormone receptor antibody, 52% (normal: <15%); thyroid-stimulating antibody, 294% (normal: <180%); and thyroid-stimulation blocking antibody, 9% (normal: <25%) on the day of delivery. A nonstress test revealed fetal tachycardia >200 beats per minute, and a male infant weighing 1152 g was born by emergency cesarean section. Thyroid-stimulating hormone receptor antibody was 16% and thyroid-stimulating antibody was 370% in the cord blood. We administered 10 mg/kg per day of oral propylthiouracil from day 1. Tachycardia along with elevated FT(4) and FT(3) levels in the infant decreased from 200/minute to 170/minute, 4.7 ng/dL to 2.9 ng/dL, 7.0 pg/mL to 4.8 pg/mL, respectively, in the first 33 hours. At 5 days, FT(4) and FT(3) were 1.1 ng/dL and 2.9 pg/mL, respectively, and we stopped propylthiouracil administration. Although FT(4) decreased to 0.4 ng/dL, TSH was quite low and did not respond to intravenous TRH by 14 days of age. We began daily levothyroxine 5-micro/kg supplementation. The responsiveness of TSH to TRH did not become significant until 4 months old and normalized at 6.5 months old. At this time, levothyroxine was stopped. We conclude that placental transfer of thyroid hormones may cause hyperthyroidism in the fetal and early neonatal periods and lead to transient pituitary hypothyroidism in an infant born to a mother with uncontrolled Graves' disease.     

Changes in thyroid function after bone marrow transplant in young patients

BACKGROUND: Changes in thyroid function among young patients who received bone marrow transplantation (BMT) were evaluated. METHODS: The study included 91 patients (50 males) who underwent BMT from 1985 to 1995 at the age of 0.6-21 years. Sixty patients had neoplastic disease such as leukemia or lymphoma, and the remainder had non-neoplastic diseases. Preconditioning regimen for BMT included 12 Gy of fractionated-total body irradiation (TBI) for patients with neoplastic disease and 3-8 Gy of irradiation for the remaining patients, in addition to chemotherapy. Evaluation of thyroid function was performed by serial assessment of basal serum FT4, FT3, TSH concentrations as well as by TRH test. RESULTS: No patient had overt hypothyroidism or elevated basal TSH concentrations (>10 mU/L). However, 6 (7%) of patients experienced exaggerated peak TSH response to TRH stimulation several years after BMT. In 33 patients whose thyroid status was evaluated before, within 3 months, and 1 year after BMT, serum FT3 concentrations as well as peak TSH response to TRH stimulation significantly decreased immediately after BMT (<3 months) and normalized within 1 year. However, serum FT4 concentrations did not change significantly. One patient developed primary hypothyroidism and another developed follicular adenoma of the thyroid 5 and 12 years after BMT, respectively. CONCLUSION: Short-term changes in thyroid function after BMT can indicate euthyroid sick syndrome rather than tertiary hypothyroidism. It must be noted that overt hypothyroidism may occur several years after BMT, hence long-term follow-up of thyroid function is warranted.     

Thyroid function in healthy premature infants.

Thyroid function was studied in healthy premature and term infants between 12 hours and 3 months of age. T4 and FT4I followed parallel courses in both groups; during the first 45 days, however, the values were significantly lower in premature infants under 34 weeks' EGA than in term infants (P less than 0.001). The post-delivery peak in TSH concentration (mean +/- SD) was 71.8 +/- 19.2 microunits/ml in the premature infants. In five premature infants, injection of TRH elicited a TSH increment of 29.4 +/- 20.7 microunits/ml at 30 minutes. T3 concentration was not significantly different in premature and term infants.     

苯巴比妥、苯妥英、卡马西平对癫痫患儿甲状腺激素的影响

观察常用抗癫痫药物对癫痫患儿血清甲状腺激素的影响。对无甲状腺功能减退临床表现的癫痫患儿(各组均20例)共80例,应用RIA法测定血清TT4、TT3、FT4、FT3、rT3、TSH浓度。结果未经治疗癫痫患儿所有激素水平与正常对照组比较无显著差异,苯巴比妥组FT4值低于正常对照组(P<0.01),卡马西平组TT4、FT4值也明显降低(P<0.01),苯妥英组TT4、FT4、FT3值均显著降低(P<0.01),所有各组rT3、TSH无改变。资料表明,抗癫痫药物对甲状腺激素影响强度依次为苯妥英钠、卡马西平、苯巴比妥。     

Euthyroid sick syndrome in children with acute viral hepatitis A.

According to the clinical findings, the activity of serum asparate aminotransferase (EC 2.6.1.1), alanine aminotransferase (EC 2.6.1.2) and the level of total bilirubin, 45 children with acute viral hepatitis A were divided into two groups: with mild and moderately severe degree of disease. By determining the products of the peripheral thyroxine metabolism-T3 and rT3, as well as the other thyroid parameters (T4, FT4, TSH and TBG) we have found significantly lower T3 level and significantly higher T4 and TBG levels in both groups of patients in comparison with control group. At the same time, the level of biologically less active rT3 was increased in patients with moderately severe form of disease, while no differences were found in the values of TSH between the ill and control patients. TRH induced TSH release was normal in all patients. The results of this study point to the development of euthyroid sick syndrome or low T3 syndrome in children with viral hepatitis A.     

Thyroid hormone concentrations in preterm infants born to pre-eclamptic women with placental insufficiency

The aim of this study was to compare thyroid function in preterm infants born to women with placental insufficiency (n = 15) and those born to women without placental insufficiency (n = 13). Gestational ages ranged between 28 and 33 weeks. Concentrations of free thyroxine (FT4), thyrotropin (TSH), triiodothyronine (T3) and reverse T3 (rT3) were measured by radioimmmunoassays in cord blood and on d 1, 3, 5, 7, 14 and 21. Infants born to the women with placental insufficiency had significantly lower mean FT4 (p = 0.001), TSH (p = 0.002) and rT3 values (p = 0.025) in cord blood, and higher rT3 values on d 5 (p = 0.019) and d 7 (p = 0.025). The following conclusions were reached: (i) preterm infants born to pre-eclamptic women with placental insufficiency have intact hypothalamic-pituitary-thyroid axes; (ii) compared to preterm infants born to healthy women, preterm infants born to pre-eclamptic women with placental insufficiency have lower FT4 and TSH concentrations before birth and (iii) elevated rT3 concentrations after birth, suggesting a temporarily impaired hepatic type 1 deiodination process.     

Reverse triiodothyronine, thyroid hormone, and thyrotrophin concentrations in placental cord blood.

Reverse triiodothyronine (rT3), triiodothyronine (T3), thyroxine (T4), thyroxine binding globulin (TBG), and thyrotrophin (TSH) were measured in sera from placental cord blood in an unselected series of 272 deliveries. In this series the concentrations of rT3 (mean 3.33 nmol/l, 95% confidence limits 1.6--7.0 nmol/l), were log normally distributed and did not overlap the adult normal range (0.11--0.44 nmol/l). There were no correlations between the cord blood concentrations of rT3, T3, T4, and TSH. The cord serum rT3 concentration was not influenced by maturity, birth-weight, or neonatal risk factors, whereas these factors did affect the concentrations of T3, T4, AND TBG. There is no arteriovenous rT3 concentration difference across the placenta, therefore the cord rT3 reflects the systemic rT3 concentration in the baby at birth. As rT3 in the neonate largely, if not entirely, derives from thyroxine from the fetal thyroid, measurement of the cord rT3 concentration may be a good immediate screening test for neonatal hypothyroidism.     

Thyroid-stimulating hormone, prolactin, and growth hormone response to thyrotropin-releasing hormone in treated children with congenital hypothyroidism

The purpose of the present study was to assess thyroid-stimulating hormone (TSH), prolactin, and growth hormone responses to TRH stimulation in 12 congenitally hypothyroid children adequately treated with L-thyroxine from the first weeks of life. Although clinically euthyroid, six of these children were found to have abnormally high basal serum TSH concentrations despite clinical euthyroidism. Serum triiodothyroxine and L-thyroxine concentrations were normal and did not differ whether the children had elevated or normal basal serum TSH. All six of the children with high basal TSH had an exaggerated TSH response to TRH and 4 of them also had an augmented prolactin response to TRH. The children with normal basal TSH concentrations had normal TSH and prolactin responses to TRH. An abnormal ("paradoxical") elevation of growth hormone concentration in response to TRH was found in four of seven children in a separate group of patients who had prolonged, untreated primary hypothyroidism, but such responses were not found in any of the adequately treated children. These findings suggest the following conclusions: 1) the phenomenon of high serum concentrations of TSH in conjunction with normal L-thyroxine and triiodothyronine levels (and clinical euthyroidism), is prevalent in congenital hypothyroid patients. 2) These patients have an exaggerated response of their pituitary thyrotroph and lactotroph cells to TRH, presumably caused by selective and relative resistance of these cells to the inhibitory effects of thyroid hormones. 3) Congenital hypothyroidism is not associated with abnormal somatotroph cell responses to TRH.     

Disorders of thyroid gland function--hypothyroidism in childhood. An ambulatory follow-up study

42 children with different kinds of hypothyroidism, who had been treated with thyroid hormones during several years, were thoroughly follow-up examined in 1988. Apart from few exceptions, patients in therapy attained standard data in length. Concerning skeleton maturation, clear differences between boys and girls were found. While male patients, with one exception, showed a retardation of bone-age, in females both, retardation and acceleration of bone-development were found. Serum concentration of FT4 and FT3 were chosen as hormonal parameter, and TSH was taken basal and after stimulation with TRH. Normal FT4 levels were found in 29 patients. In 5 children FT4 was significantly lower, in 8 cases an elevation of this serum-parameter was observed. Measurement of serum FT3 in 27 patients showed normal levels in 18 children. In 4 cases low and in 5 elevated FT4 levels were found. 29 patients had basal TSH concentrations within normal range, in 13 the estimated levels were elevated. TRH-stimulation carried out on 40 children showed normal serum TSH response for 13 of them. In 14 children an exaggerated TSH response to TRH occur, in 13 TSH still remain low after stimulation with TRH. Serum-GOT, -GPT, -Gamma GT and -CK were determined as encymic parameters. In 5 patients a typical hypothyroidism-associated GOT- and CK-elevation was found. 3 children showed an isolated rise of GOT-, 8 an isolated CK-elevation.     

Investigation of the relationship between low Apgar scores and early neonatal thyroid function

BACKGROUND: The aim of the present study was to assess the effects of low Apgar scores on perinatal thyroid function. METHODS: Forty full-term infants delivered by the normal spontaneous vaginal route were enrolled into the study. All babies had 1 and 5 min Apgar scores below 4. The control group consisted of 26 full-term healthy neonates. Cord blood and serum tri-iodothyronine (T3), thyroxine (T4), reverse tri-iodothyronine (rT3), free thyroxine (FT4), thyroid-stimulating hormone (TSH) and thyroid-binding globulin (TBG) determinations were performed by an enzyme immunoassay method. RESULTS: The mean values of FT4 and T4 observed in the cord blood of the study group were significantly lower compared with matched controls, whereas the mean TSH values were significantly higher. There were no differences in concentrations of T3, rT3 and TBG between the two groups. CONCLUSIONS: These results demonstrate the existence of transient hypothyroidism at birth in babies with Apgar scores below 4 delivered by the spontaneous vaginal route.     

Increased plasma thyroid stimulating hormone in treated congenital hypothyroidism: relation to severity of hypothyroidism, plasma thyroid hormone status, and daily dose of thyroxine

Plasma thyroid stimulating hormone (TSH) concentrations obtained during the first four years of treatment in 418 children with congenital hypothyroidism, identified by neonatal screening, were examined in relation to paired measurements of plasma thyroxine (n = 1945), free thyroxine (n = 836), triiodothyronine (n = 480), and free triiodothyronine (n = 231), and estimated daily dose of thyroxine at the time of blood sampling. Overall, plasma TSH was above 7 mU/l in 1280 out of 2960 samples (43%); the percentage was not related to severity of hypothyroidism at diagnosis. Mean values for thyroxine and free thyroxine, and to a lesser extent free triiodothyronine, were consistently lower in samples with TSH concentrations over 7 mU/l and this was the case in patients with either severe or less severe hypothyroidism. Raised TSH concentrations were also associated with lower mean doses of thyroxine (micrograms/kg/day) but here the mean doses of thyroxine in children with severe hypothyroidism were higher than in the children with less severe hypothyroidism. The mean dose of thyroxine associated with low/normal TSH values was highest in the first 6 months and fell progressively. Thyroxine dose was significantly related to thyroxine and free thyroxine concentrations but not to triiodothyronine and free triiodothyronine and the latter appeared to be of limited value as measures of plasma thyroid hormone status during treatment.     

Increased plasma thyroid stimulating hormone in treated congenital hypothyroidism: relation to severity of hypothyroidism, plasma thyroid hormone status, and daily dose of thyroxine.

Plasma thyroid stimulating hormone (TSH) concentrations obtained during the first four years of treatment in 418 children with congenital hypothyroidism, identified by neonatal screening, were examined in relation to paired measurements of plasma thyroxine (n = 1945), free thyroxine (n = 836), triiodothyronine (n = 480), and free triiodothyronine (n = 231), and estimated daily dose of thyroxine at the time of blood sampling. Overall, plasma TSH was above 7 mU/l in 1280 out of 2960 samples (43%); the percentage was not related to severity of hypothyroidism at diagnosis. Mean values for thyroxine and free thyroxine, and to a lesser extent free triiodothyronine, were consistently lower in samples with TSH concentrations over 7 mU/l and this was the case in patients with either severe or less severe hypothyroidism. Raised TSH concentrations were also associated with lower mean doses of thyroxine (micrograms/kg/day) but here the mean doses of thyroxine in children with severe hypothyroidism were higher than in the children with less severe hypothyroidism. The mean dose of thyroxine associated with low/normal TSH values was highest in the first 6 months and fell progressively. Thyroxine dose was significantly related to thyroxine and free thyroxine concentrations but not to triiodothyronine and free triiodothyronine and the latter appeared to be of limited value as measures of plasma thyroid hormone status during treatment.     

南京地区1998-2009年新生儿先天性甲状腺功能减低症筛查及治疗随访结果分析

目的 总结并分析1998年1月- 2009年12月南京地区新生儿先天性甲状腺功能减低症(CH)的筛查结果.方法 采集出生72 h新生儿442 454例的足跟血滴于滤纸上,采用时间分辨免疫法测定滤纸血斑促甲状腺激素(TSH),阳性者召回进一步测定静脉血TSH、三碘甲状腺原氨酸(T3)、四碘甲状腺原氨酸(T4)、游离T3(FT3)、游离T4(FT4)以明确诊断.确诊者立即开始予左旋甲状腺素片(4.3～12.0μg·kg-1·d-1)替代治疗,定期监测其甲状腺功能,测量其身高、体质量,其中68例患儿子智力测试,以评估疗效.结果 12 a共筛查442 454人,确诊CH 183例,发病率为0.41‰,对117例进行随访.初始治疗时间的中位数为18 d(7～67d),初始左旋甲状腺素的平均剂量为7.35 μg·kg-1·d-1.CH患儿的身高、体质量结果基本达到正常参照标准.盖泽尔婴幼儿发展量表(GESELL)测试结果显示1例智能发育落后,8例智能发育迟缓.T4、FT4的治疗前水平与患儿的GESELL测试总分、适应性及精细运动均呈正相关(Pa＜0.05).结论 经筛查确诊的CH患儿,应尽可能早地进行激素替代治疗,可有效改善其预后.因此新生儿筛查及随访治疗工作值得推广和完善.     

Thyroid hormone levels and their relationship to survival in children with bacterial sepsis and septic shock

OBJECTIVES: Reported studies have showed alternations of thyroid hormones in critical illness mostly in adults and some in children. In this study, we aimed to measure thyroid hormone levels in children with sepsis and septic shock and investigate the relationship of these hormones with clinical state and survival. PATIENTS AND METHODS: Thyroid hormone levels of children with sepsis and septic shock, and age- and sex-matched controls were measured. RESULTS: There were 51 children in sepsis (group S), 21 children in septic shock (group SS) and 30 in the control (group C) group. Total triiodothyronine (TT3) levels were (nmol/l): 0.91 +/- 0.22, 0.64 +/- 0.23, 2.11 +/- 0.59; free triiodothyronine (FT3) (pmol/l): 0.027 +/- 0.006, 0.018 +/- 0.007, 0.049 +/- 0.010; total thyroxine (TT4) (nmol/l): 100.62 +/- 21.93, 65.79 +/- 19.35, 109.65 +/- 19.35; free thyroxine (FT4) (pmol/l): 18.06 +/- 3.87, 10.32 +/- 1.29, 19.35 +/- 3.87; and thyroid stimulating hormone (TSH) (mIU/ml): 5.0 +/- 2.0, 4.8 +/- 2.4, 5.2 +/- 3.0, in children with sepsis, septic shock, and controls, respectively. The TT3, FT3, TT4, and FT4 levels of group SS were significantly lower than those of groups S and C. The TT3 and FT3 levels of group S were lower than in group C, but there was no significant difference between TT4, and FT4 levels of groups S and C. TSH levels were slightly decreased in both sepsis and septic shock, but the difference was not significant. Eleven (21.6%) children with sepsis and 15 (71.4%) children with septic shock died (p < 0.001). The levels of TT3, FT3, TT4 and FT4 were markedly lower in non-survivors of groups S and SS compared to survivors (p < 0.001). CONCLUSIONS: These changes in the hypothalamo-pituitary-thyroidal axis may suggest a possible prognostic value of thyroid hormone levels in children with sepsis and septic shock. To the best of our knowledge, this report is the first study to compare thyroid hormone levels in a large number of patients with sepsis and septic shock with those in healthy controls in childhood.     

Thyroid function in premature infants of different gestational age during the first month of life (author's transl)

To assess the function of the thyroid gland in premature infants of different gestational ages during the first month of life we determined simultaneously TSH, T4, T3, and rT3 serum concentrations in 116 preterm infants (gestational ages 31st to 38th week) during each of the first 30 days of life. The serum concentrations of TSH, T3, and rT3 changed significantly during this period. The TSH and rT3 values were highly increased on the first day and decreased thereafter. The T3 values, however, increased significantly during this period. During the first month of life the T4 values remained roughly unchanged independent of the age of the children. There was no significant influence on serum concentrations of thyroid hormones by gestational age. The 65 preterm infants with adaptational disorders showed no difference in their patterns of TSH and thyroid gland activity during the first month of life compared with 51 healthy premature infants. From the 4th to the 6h day of life -- a recommended period for the screening of congenital hypothyroidism -- the differences of TSH values measured were insignificant (16-18 muU/ml). The T4 values on these days remained all above 6.8 microgram/dl.     

亚临床甲状腺功能减退症对患儿骨龄和身高的影响

目的 观察亚临床甲状腺功能减退症(甲减)对儿童骨龄(BA)、身高及甲状腺激素水平的影响.方法 选取30例亚临床甲减患儿为亚临床甲减组,30例体检健康儿童为健康对照组.对每位研究对象采用同一磅秤标准,测量其身高、体质量.采用Greulich-Pyle图谱法对各组儿童左手腕指关节正位片进行BA水平的评定;采用罗氏化学发光免疫分析仪E170检测各组儿童促甲状腺激素(TSH)、游离三碘甲腺原氨酸(FT3)、游离甲状腺素(FT4)水平.采用SPSS 17.0软件比较2组儿童BA、身高、TSH、FT3及FT4的差异;BA与身高、TSH、FT3及FT4间进行Pearson相关分析.结果 亚临床甲减组儿童的BA[(8.17±2.29)岁]、身高[(131.47±13.41) cm]水平均落后于健康对照组[(10.08±2.75)岁、(141.05±15.12) cm](t=2.92、2.60,Pa<0.05);TSH水平[(5.93±1.77) mIU·L-1]显著高于健康对照组[(2.66±1.28) mIU·L-1](t=8.17,P<0.001).亚临床甲减组儿童的BA与身高呈显著正相关(r=0.940,P<0.01);BA与TSH呈显著负相关(r=-0.450,P<0.05).亚临床甲减组FT3[(5.43±1.37) pmol·L-1]、FT4[(17.29±2.03) pmol·L-1]与健康对照组[(5.83±1.11) pmol·L-1、(17.22±1.96) pmol·L-1 ]比较差异均无统计学意义(t=1.24、0.14,Pa>0.05).结论 儿童亚临床甲减可引起BA、身高的落后,需要用药物进行干预治疗.