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Resumen

Estas son las conclusiones obtenidas en un estudio publicado en la revista “Journal of Clinical Endocrinology & Metabolism" , llevado a cabo por investigadores italianos.

Es por esta razón que los investigadores italianos recomiendan el cribado de rutina de la función tiroidea en mujeres embarazadas dados los resultados de su estudio. Realizaron el seguimiento de los hijos de 16 mujeres de Sicilia, durante 10 años, donde el déficit de yodo es frecuente, comparándolos con niños de otra región. El THDA se diagnosticó en 11 de los 16 niños del área donde existía deficiencia de yodo, frente a ninguno en la región donde no se registraba tal deficiencia.

Los autores sugieren que el THDA y un menor coeficiente intelectual relacionado con el anterior pueden ser resultado de hipotiroxinemia de las madres en la primera mitad del embarazo.

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Abstract

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 T3 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 T3 available to the developing fetal brain.