Attention deficit and hyperactivity disorders in the offspring of mothers exposed to mild-moderate iodine deficiency:: A possible novel iodine deficiency disorder in developed countries

被引:303
作者
Vermiglio, F
Lo Presti, VP
Moleti, M
Sidoti, M
Tortorella, G
Scaffidi, G
Castagna, MG
Mattina, F
Violi, MA
Crisà, A
Artemisia, A
Trimarchi, F
机构
[1] Univ Messina, Dipartimento Clin Sperimentale Med & Farmacol, Sez Endocrinol, I-98125 Messina, Italy
[2] Univ Messina, Dipartimento Sci Pediat, Sez Neuropsichiatria Infantile, I-98125 Messina, Italy
[3] Univ Messina, Dipartimento Diagnost Lab, Serv Biochim Clin, I-98125 Messina, Italy
关键词
D O I
10.1210/jc.2004-0571
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Over a period of almost 10 yr, we carried out a prospective study of the neuropsychological development of the offspring of 16 women from a moderately iodine-deficient area ( area A) and of 11 control women from a marginally iodine-sufficient area ( area B) whose thyroid function had been monitored during early gestation. Attention deficit and hyperactivity disorder (ADHD) was diagnosed in 11 of 16 area A children (68.7%) but in none from area B. Total intelligence quotient score was lower in area A than in area B children (92.1 +/- 7.8 vs. 110 +/- 10) and in ADHD children when compared with both non-ADHD children from the same area and control children (88.0 +/- 6.9 vs. 99.0 +/- 2.0 and 110 +/- 10, respectively). Seven of 11 ADHD children (63.6%) were born to the seven of eight area A mothers who became hypothyroxinemic at early gestation, whereas only one of five non-ADHD children was born to a woman who was hypothyroxinemic at 20 wk of gestation. So far, a similar prevalence of ADHD has been reported only in children with generalized resistance to thyroid hormones. This might suggest a common ADHD pathogenetic mechanism consisting either of reduced sensitivity of the nuclear receptors to thyroid hormone ( generalized resistance to thyroid hormones) or reduced availability of intracellular T(3) for nuclear receptor binding. The latter would be the ultimate consequence of maternal hypothyroxinemia ( due to iodine deficiency), resulting in a critical reduction of the source of the intracellular T(3) available to the developing fetal brain.
引用
收藏
页码:6054 / 6060
页数:7
相关论文
共 34 条
[1]  
[Anonymous], 2000, Diagnostic and Statistical Manual of Mental Disorders
[2]  
Barkley RA, 1997, J DEV BEHAV PEDIATR, V18, P271
[3]  
BERT CLT, 1979, DEV MED, V71
[4]   CONGENITAL HYPOTHYROIDISM, AS STUDIED IN RATS - CRUCIAL ROLE OF MATERNAL THYROXINE BUT NOT OF 3,5,3'-TRIIODOTHYRONINE IN THE PROTECTION OF THE FETAL BRAIN [J].
CALVO, R ;
OBREGON, MJ ;
DEONA, CR ;
DELREY, FE ;
DEESCOBAR, GM .
JOURNAL OF CLINICAL INVESTIGATION, 1990, 86 (03) :889-899
[5]   Fetal tissues are exposed to biologically relevant free thyroxine concentrations during early phases of development [J].
Calvo, RM ;
Jauniaux, E ;
Gulbis, B ;
Asunción, M ;
Gervy, C ;
Contempré, B ;
de Escobar, GM .
JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 2002, 87 (04) :1768-1777
[6]  
Castellanos FX, 1996, ARCH GEN PSYCHIAT, V53, P607
[7]   Is neuropsychological development related to maternal hypothyroidism or to maternal hypothyroxinemia? [J].
de Escobar, GM ;
Obregón, MJ ;
del Rey, FE .
JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 2000, 85 (11) :3975-3987
[8]   CONTRIBUTION OF MATERNAL THYROXINE TO FETAL THYROXINE POOLS IN NORMAL RATS NEAR TERM [J].
DEESCOBAR, GM ;
CALVO, R ;
OBREGON, MJ ;
DELREY, FE .
ENDOCRINOLOGY, 1990, 126 (05) :2765-2767
[9]   EFFECTS OF MATERNAL HYPOTHYROIDISM ON THE WEIGHT AND THYROID-HORMONE CONTENT OF RAT EMBRYONIC-TISSUES, BEFORE AND AFTER ONSET OF FETAL THYROID-FUNCTION [J].
DEESCOBAR, GM ;
PASTOR, R ;
OBREGON, MJ ;
DELREY, FE .
ENDOCRINOLOGY, 1985, 117 (05) :1890-1900
[10]   COMPARISON OF MATERNAL TO FETAL TRANSFER OF 3,5,3'-TRIIODOTHYRONINE VERSUS THYROXINE IN RATS, AS ASSESSED FROM 3,5,3'-TRIIODOTHYRONINE LEVELS IN FETAL TISSUES [J].
DEESCOBAR, GM ;
OBREGON, MJ ;
DEONA, CR ;
DELREY, FE .
ACTA ENDOCRINOLOGICA, 1989, 120 (01) :20-30