In our staudy, the median values of the UIC in pregnant women indicate optimal iodine intakes during all the pregnancy with the proportions with adequate iodine intake (150–249 µg/L) of 27, 36 and 32% during the pregancy and 76%, 78% and 80% respectively of pregnant women consumed sufficiently iodized salt. A median of 150–249 µg/L is recommended as an indication of sufficient iodine intake during pregnancy [9]. Several study reporeted a decline in UIC in pregnancy [13–15].
In our study, 23, 15 and 24% of PW had UIC values under 150 µg/L while 41, 43 and 40% had more than adequate iodine intake respectively for the three trimesters.
This decrease may indicate that iodine storage has been depleted as a result of renal excretion, nutritional insufficiency, or consumption by the maternal-fetal or to meet the increase in thyroid hormone requirement induced by pregnancy [16, 17]. The decrease in iodine concentration under 150 µg/L, may be explained by the difference in salt quality and ptassium iodine content consumed by pregnant women and that potassium iodine content in table salt, presents differences between the samples analysed additionally, due to the population's fish-eating habits and considering that Algeria's coastal sand rural areas are relatively proximity to the sea [16] and because iodine status has been irregularly monitored.
Beside UIC, that 90% of ingested iodine is excreted in the urine, a various others indicators which are used in monitoring and evaluating IDD control programmes, such as thyroid volume, hormone (TSH, T4) and thyroglobulin (Tg) [4, 5]. According to Glinoer [18] and Zimmermann [19], there is an increase in renal iodine excretion during the early stages of pregnancy due to the higher iodine needs, which as shown in our study results to an increase in maternal T4 production to ensure a transfer of thyroid hormones to the fetus and maintain a state of maternal euthyroidism, during which the fetal thyroid gland is not yet functional.
Level of FT4 decrease between the first and second trimester. A similar decrease has been reported by other studies [20, 21]. In order to maintain adequate maternal levels of free T4 and T3, the production of thyroids hormones increases by about 50% during pregnancy. The decrease in circulating FT4 levels in pregnant women in our study could be explained by the fact that the fetal thyroid gland is not functionally mature before the 18th-20th week of pregnancy. T4 is the main thyroid hormone transferred through the placenta. On the other hand, increased estrogen concentrations during pregnancy induce an increase in hepatic synthesis and sialylation of TBG, Thus decreasing its metabolic clearance. This results in a double increase in serum TBG and total T4 and T3, resulting in a transient decrease in free serum T4 and T3 throughout pregnancy. Thus, free T4 concentrations remain normal or decrease slightly [22].
In addition, during pregnancy the activity of placental desiodinase D3 is increased to regulate the levels of fetal blood in active hormones and recycle iodine. On the other hand, hCG would have a stimulatory effect on the transfer of iodine through the placenta (cytotrophoblastic cells) from the mother to the fetal compartment, notably by a transcriptional and translational effect of the sodium-iodide carrier gene (NIS) at the placental level [23].
Insufficient iodine intake leads to a shift towards increased preferential thyroid production of T3 and reduced production of T4 in order to save iodine. This can lead to low levels of T4 and FT4, while TSH concentrations are maintained in normal values due to the persistent negative feedback of T3. This adaptation can be beneficial for the mother, however, since T4 is the main thyroid hormone that crosses the placenta, Maternal HT supply to the fetus may be compromised [24]. Several studies have described the consequences of maternal iodine deficiency and maternal thyroid dysfunction in both mother and fetus [25]. Therefore, iodine supplementation is necessary during pregnancy to provide a supply for the mother and fetus [24].
In our study, the mean serum TSH concentration of pregnant women increased gradually from the first to the third trimester, with a significant difference between (p = 0.048).
Lower serum TSH levels in the first trimester could be explained by the high level of chorionic gonadotropin (hCG) secreted by syncytiotrophoblasts cells, which stimulates the corpus luteum to produce progesterone, essential for maintaining pregnancy. hCG is structurally similar to TSH and also has thyrotropic effects, leading to an increase in the first trimester of FT4 and FT3 and a concomitant suppression of circulating TSH. It has been suggested that such a mechanism of regulation of the foetus-maternal endocrine system allows, in early pregnancy, to have adequate concentrations of thyroid hormones necessary for fetal development since its thyroid gland still does not have the ability to synthesize its own hormones thyroid [18].
Our study showed normal serum Tg levels. However, studies reporting the relationship between serum Tg levels and iodine intakes in pregnant women are rare and no international reference is available. The few published data suggest that Tg could be slightly elevated during pregnancy in iodine-deficient pregnant women due to increased thyroid activity [27].
In our study, the proportions of positive anti-TPO antibody titers were during pregnancy with high averages over the three trimesters. Autoimmune thyroid diseases usually regress during pregnancy due to pregnancy-induced immunosuppression [28, 29]. Mechanisms that trigger the development of abnormal immune response and the relationship of self-related thyroid diseases-immune with excess iodine are still poorly understood and that an increase in thyroglobulin (Tg) iodization increases its immunogenicity and promotes oxidative damage [30–32].
The study of linear regression in the presence of anti-TPO antibodies showed a significant correlation between TSH levels and positive antibody titersTPO in the first trimester of pregnancy. This result is in agreement with the fact that the presence of high titres in anti- andTPO would be a predictor of subclinical hypothyroidism in pregnant women revealed by serum levels of TSH [33].
In the second trimester, a very significant positive correlation was found between the weeks of pregnancy and UIC due to increased glomerular filtration during pregnancy [34, 35]. A very significant correlation is also observed between the levels of FT4 and thyroglobulin. This association could be a reflection of an increased activity of the maternal thyroid gland to meet the needs of the fetus whose thyroid gland is non-functional before the 20th week of pregnancy [36].
During the third trimester, the weeks of pregnancy are positively correlated with serum thyroglobulin levels. According to Glinoer et al. [37], high serum thyroglobulin concentrations reflect a change in the anatomical structure of the thyroid and would be a marker for increased thyroid volume. Thyroglobulin elevation during the third trimester of pregnancy is also observed in other studies [38, 39]. Although thyroglobulin is an indicator of iodine deficiency and excess in a population [40], these results suggest that the increase in serum Tg concentration during pregnancy is mainly caused by increased thyroid secretion due to increased thyroid activity independently of iodine deficiency [18, 41].
The analysis of our results for pregnant women in the 3rd trimester of their pregnancy showed that circulating levels of Tg are strongly correlated with anti-TPO antibody titers (p = 7.96 10− 5) due to the fact that the majority of pregnant women were in euthyroidism and positive for TPO-anti antibodies indicating an auto-thyroid diseaseimmune, probably in the process of installation, with a high predisposition to functional alterations of the gland during pregnancy or postpartum [42, 43].
Analysis of the potassium iodate content of table salt marketed in Algeria, showed that only 42% were samples analyzed respected the Algerian recommendation regarding iodine content in table salts (50.55–84.25 mg/k of salt) for the prevention of iodine deficiency disorders (TDCI) compulsory by an executive decree [44].
More than 70% of pregnant women with normal UIC, consumed sufficiently iodized salt, and less than 58% of the products marketed in Algeria does respect the recommendation of the Algerian regulations [44]. Our findings are similar to Guerras' [45] findings, which indicate that only 17,65% of the samples collected throughout the country conformed to the requirements established forth in the decree, compared to 57.35% and 11.76%, respectively, for samples with low contents (< 50.55 mg KIO3/kg) and elevated contents (> 84.25 mg KIO3/kg). Iodization in the Algiers region was found to be more adequate than in the regions of Batna, Biskra, M'sila, and Bordj Bou Arreridj, according to a comparison of iodine levels in samples obtained from these regions. This might be the result of the way salt is stored to prevent iodization, how salt is sold retail, and the sort of packaging that the salt is packaged in to influence its iodine level. It would appear that this deficiency still persists in both mountainous and coastal regions since 17%, 12% and 15% respectively of pregnant women consumed low-iodine salt..