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Results for “Maternal thyroid status”

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PubMed2026

Perinatal depression, maternal thyroid status and fetus/infant health and development: A systematic review.

BACKGROUND: Thyroid hormones are known to influence both maternal depression and child developmental outcomes, while maternal depression independently affects child outcomes. The potential interaction between thyroid dysfunction and depression in shaping child development remains insufficiently explored. The present study addresses such interplay. METHODS: Following PRISMA 2020 and JBI guidelines, three databases were searched through December 2025 for primary studies on maternal thyroid status, perinatal depression, and child development. Risk of bias (RoB) was assessed using validated tools. Due to clinical and methodological heterogeneity, data were synthesized narratively following SWiM guidelines. RESULTS: Eleven studies were included. Beyond independent risks for preterm birth and behavioral problems, limited evidence supports a synergistic model, while most studies likely reflect the simple co-occurrence of risks. Maternal thyroid peroxidase antibodies (TPO-Ab) were associated with child externalizing problems exclusively in the presence of clinical depression. High depressive symptoms also attenuated the cognitive benefits of prenatal iodine supplementation. Thyroid status appears to function as a risk moderator rather than a mediator. However, 50% of observational studies presented high RoB, primarily due to participant attrition. CONCLUSION: Findings are still scarce to support a synergistic risk model where specific maternal thyroid parameters (i.e. thyroid autoimmunity and iodine status) may moderate the impact of depressive symptoms on child development. Despite the high RoB in half of the studies, results highlight the need for integrated screening protocols. Simultaneously assessing mental health and thyroid status may optimize risk stratification for high-risk mother-infant dyads.

Female↗

PubMed1978

Fetal hypothyroidism and maternal thyroid status in severe endemic goiter.

The relationship between maternal thyroid function and newborn thyroid function was studied in a region of very severe endemic goiter (Ubangi, Republic of Zaïre). T4, T3, and TSH concentrations were measured in the sera of 56 mothers (at the time of delivery) and 60 newborns (in the cord). The results obtained in these groups (untreated) were compared with those obtained in two control groups, comprising 53 mothers whose iodine deficiency had been corrected by the injection of iodized oil and 68 neonates born to such mothers. The results show that the mean (+/- SEM) T4 serum concentration (micrograms per dl) was 11.5 +/- 0.7 in the untreated mothers compared with 15.7 +/- 0.7 in the treated mothers (P less than 0.001), and 9.4 +/- 0.8 in the untreated newborns compared with 12.4 +/- 0.5 in the newborns of treated mothers (P less than 0.01). The values observed for the mean T3 serum concentrations (nanograms per dl) in the same groups were 171 +/- 10 and 154 +/- 9 (mothers; P greater than 0.05) and 68 +/- 6 and 55 +/- 6 (newborns; P greater than 0.05); the mean TSH serum concentrations (microunits per ml) were 8.7 (7.6 - 9.9) and 5.4 (4.9 - 5.9; mothers; P less than 0.001) and 19.6 (16.6 - 23.2) and 6.4 (5.8 - 7.0; newborns; P less than 0.001). The proportion of untreated newborns, i.e. 40%, with individual TSH values deviating by more than 2 SDS above the mean of the treated newborns is much greater than the corresponding proportion, i.e. 15%, of untreated mothers in relation to the treated ones. In 6 out of 34 untreated newborns, definite biochemical signs of congenital hypothyroidism were observed. Correlation coefficients were calculated between the untreated subjects. A positive correlation coefficient of 0.80 (P less than 0.001) was observed between the serum T4 concentrations of the mothers and those of the newborns, and one of 0.61 (P less than 0.001) was observed between their respective serum TSH values. Significant inverse correlations were observed between maternal serum T4 and cord serum TSH (-0.79; P less than 0.001) and between cord T4 concentrations and maternal TSH concentrations (-0.57; P less than 0.01). No definite trend is observed between the variations of serum T3 on one hand, and those of serum T4 or serum TSH on the other hand. Out of 51 mothers in whom serum T4 was determined, 11 showed values below 8 micrograms /dl; the newborns of those mothers showed very low serum T4 values (5.5 +/- 1.6 micrograms/100 ml) and extremely high serum TSH levels [144 (98-210) microU/ml]. It is concluded that, contrary to the situation observed in physiological conditions, maternal thyroid function in regions of severe endemic goiter is a good indicator of newborn thyroid function. The reasons for this probably lie in the influence of environmental factors acting simultaneously on the mother and the fetus.

Congenital Hypothyroidism↗

PubMed1978

Teratogenicity of ethylenethiourea and thyroid function in the rat.

Ethylenethiourea (ETU) was given by gavage at a dose of 40 mg/kg/day from Days 7 through 15 of gestation to hypothyroid and euthyroid rats, and to rats given exogenous thyroxine, to determine whether ETU teratogenicity occurs through alteration of maternal thyroid function. At sacrifice on Day 20 of gestation 84-100% of the fetuses in all groups given ETU were malformed regardless of the thyroid status of the dams. Ten percent of the fetuses of dams thyroparathyroidectomized at 75 days of age that were not given ETU were malformed; no malformations were noted among the fetuses of the other groups not given ETU. Hence, ETU was found to induce teratogenicity in rats but not through alteration of maternal thyroid status. In addition, it was determined that ETU lowered serum thyroxine concentration, that hypothyroidism itself increased the background level of malformations in the rat, and that hypothyroidism qualitatively and quantitatively increased the incidence of specific malformations after ETU administration.

Animals↗

PubMed1978

Effect of maternal hypothyroidism and triiodothyronine on the fetus and newborn in rats.

Of 36 adult female rats studied 19 were radiothyroidectomized; 3 weeks later all rats were bred. Radiothyroidectomized rats were divided into Groups I-III. Group I was untreated. Maternal weight gain was not noted until day 9 and was steady thereafter. Group III rats were treated with triiodothyronine up to the first day of pregnancy, but were hypothyroid during gestation (elevated TSH and low T3). Group II rats were treated with T3 up to the day of delivery. The pregnancy, its outcome, and TSH and T3 levels were similar to the normal controls (Group VI). Pregnancy, its outcome, and TSH and T3 levels were not different from controls when T3 was given to normal rats up to day 1 of pregnancy (Group IV). T3 concentrations were elevated in the normal rats which were given T3 continuously up to the day of delivery (Group V). However, the animals did not appear to be thyrotoxic and TSH was not suppressed. The size of the litters of Group I mothers was significantly less than in other groups and this difference may be attributed to an increased tendency to resorb implanted fetuses in untreated hypothyroid mothers. However, activity, day of eye opening weight gain, and TSH and T3 levels of the pups of all the groups were similar up to age 21 days. The data indicate the independence of the fetal pituitary-thyroid axis from maternal thyroidal status in rats.

Animals↗

PubMedDate not supplied

Development of sucrase activity: effect of maternal hormonal status and fetal programming of jejuno-ileal differences.

The first part of the paper deals with the effect of changes in the mother's hormonal status on the development of the small intestine of her offspring. Administration of cortisone or triiodothyronine (T3) to pregnant rats evokes a precocious appearance of sucrase activity in the fetal small intestine. Administered to lactating rats, T3 evokes a precocious increase in sucrase activity in sucklings and leads to increased T3 levels and decreased TSH levels in the mother's milk and in sera of mothers and sucklings. These experiments show that (a) sucrase activity can be induced in the fetal period; (b) changes in the mother's hormonal balance during the fetal and suckling period can influence the development of the small intestine; and (c) levels of thyroid hormones in milk can be altered experimentally. The second part deals with jejuno-ileal gradients in villus size and sucrase activity. Both gradients appear in fetal jejunal and ileal implants developing in adult hosts. Our experiments indicate that (a) the gradients are already 'programmed' during the fetal period; and (b) direct contact with food, and proximity of the jejunum to the flow of digesta from the stomach, are not decisive for expression of the jejuno-ileal gradients, but may play a 'tuning' role.

Acetylglucosaminidase↗

PubMed1979

Iodization and thyroid status in relation to stillbirths and congenital anomalies.

Thyroid status is known to have an important bearing on the ability of a woman to conceive, and to bring a normal infant to term. Thyroid status has changed in a number of previously iodine deficient countries as a result of recent iodization programmes. In this study, examination has been made of changes in the rates of two pregnancy outcomes in Tasmania, a State of Australia, namely, stillbirth and infant death due to congenital anomalies. Tasmania began iodine supplementation in 1950. Stillbirth rates declined more rapidly than in Australia as a whole, but show a peak associated with the peak of iodine-induced thyrotoxicosis in 1966. Congenital anomalies causing death show an initial rise in the early 1950s. It is suggested that this is due to persistence of iodine deficiency in the foetus after maternal iodine status improved sufficiently to allow term delivery of a live infant. The later fall coincides with the reaching of reproductive age by the first cohort of Tasmanian women who had been iodine sufficient since childhood, who would therefore not deprive their own foetus of iodine. Examination of trends in New Zealand, Switzerland and Finland, which have each introduced iodization programmes, confirms the largely beneficial effect of iodine supplementation on the rate of infant death due to congenital anomalies.

Adolescent↗