Résumé:
Thyroid hormones are essential for the normal development of the fetus. During pregnancy, fetal growth depends on the transfer of maternal thyroid hormones and optimal thyroid hormone availability is ensured by stimulation of the maternal thyroid by human chorionic gonadotropin (hCG).
Thyroid dysfunction such as hypothyroidism, hyperthyroidism, and thyroid nodules may develop during pregnancy, resulting in abortion, placental abruption, pre-eclampsia, preterm delivery, and reduced intellectual function in offspring.
The objective of our study is based on the evaluation of thyroid disturbances in a population of 216 pregnant women by the enzymatic determination of thyroid parameters namely: TSH; FT3 and FT4 and the anti-TPO antibody.
Hypothyroidism during pregnancy is defined by high rates of TSH greater than the reference range of the population and specific to the quarter and low rates of free T4.
Untreated hypothyroidism during pregnancy has been consistently associated with an increased risk of adverse pregnancy complications as well as adverse effects on fetal neurocognitive development.
The apparent hyperthyroidism during pregnancy is characterized by a decrease in TSH and an increase in free T4 levels. Under these thyroid disturbances, women may have significant vomiting, lose weight, feel tired. This disturbance, if it persists, can cause a baby's growth retardation or prematurity and increase the risk of maternal toxemia in the mother.
The anti-TPO status may reflect thyroid autoimmunity. The positivity of the anti-TPO antibody is linked to numerous undesirable results such as miscarriage, premature delivery and low birth weight.
