Thyroid status in children with severe acute malnutrition

INTRODUCTION

Malnourished children suffer from numerous complications including vitamin deficiencies, deficiencies of minerals, and trace elements. Alterations in nutritional state, whether short term or chronic, affect internal milieu, one such change is in the physiology of the thyroid hormone, especially peripheral hormone metabolism.

Severe acute malnutrition (SAM) is a medicosocial disorder characterized by a range of pathological conditions arising from a deficiency of protein and energy and is commonly associated with infections.^[1,2] The deleterious effects of protein energy malnutrition on the thyroid function were first demonstrated in animal experiments.^[3]

The thyroid gland is the sole source of thyroxine (T4), but most of the triiodothyronine (T3) in blood is derived from the peripheral conversion of T4 by 5’-deiodinase. Both T3 and T4 in blood are associated with plasma proteins. The binding proteins normally include thyroxine-binding globulin (TBG), thyroxine-binding pre-albumin (TBPA), and albumin. In children with SAM, concentrations of all three thyroid hormone-binding proteins are extremely low; there is marked change in secretion and metabolism of thyroid hormones and in structure of thyroid gland. This result in reduction of activity of thyroid gland and hence decrease in TT3 and TT4. Several studies have been done to estimate the individual biochemical parameters in PEM. Kalk et al. in their study found that there was no significant difference between serum thyroid-stimulating hormone (TSH) concentrations in children with PEM and the controls.^[4] However, Ingenbleek in their study found changes in thyroid function and attributed them to the reduced energy and protein intake characteristic of children with malnutrition.^[5] The alteration of thyroid function is attributed to changes in iodine metabolism and decreased level of circulating proteins.

Due to paucity of literature on thyroid harmones and SAM and conflicting results specially on TT4^[4,5] levels has prompted us to do this study,on concentration of serum thyroid hormone levels in SAM children and its correlation with serum total protein and albumin levels.

MATERIALS AND METHODS

The study was carried out at Nutritional Rehabilitation Centre, department of pediatrics, KIMS, Hubli. A prospective cross-sectional study done over a period of 1 year from Dec 2018 to 2019. Ethical clearance was obtained from Institutional Ethical Committee.

RESULTS

Total of 50 children fulfilled inclusion/exclusion criteria during study period.

The demographic profile, mean thyroid function, and protein/albumin levels are shown in [Table 1]. Mean age of presentation was 18 ± 2.1 months with male-to-female ratio 0.8:1. Sixty-two percent (31 children) of our children were <12 months.

The prevalence of hypothyroidism with raised TSH was noted in 4 (8%) of children [Table 2]; however, these children did not have any overt clinical symptoms or signs suggestive of hypothyroidism.

[Table 3] shows the relationship between thyroid profile and total protein and albumin. The relation between total proteins, serum albumin, and T4 and TSH revealed no statistical significance; however, there was significance relation between low serum albumin levels and T3 with P = 0.019.

DISCUSSION

SAM is a multisystem disease and involves almost all organs of the body. In SAM, there will be decrease in the synthesis of serum proteins which have an indirect or direct effect on hormones levels in our body. Thyroid hormone plays an important role in regulation of lipid and carbohydrate metabolism and is necessary for normal growth and maturation.

We observed that low serum TT3 and TT4 levels were 22% and 28%, respectively, and elevated TSH in 08% children in our study. Turkay et al. found significant decrease in serum TT3 and TT4 in children with malnutrition with no significant increase in serum TSH concentration.^[8] In other study by Sircar et al. lower T3 levels were found among hospitalized severely malnourished children.^[9] However, Osman et al. observed no significant differences in TT3 and TT4 in malnourished and well-nourished children.^[10] The impaired thyroid functions in our children were probably due to various mineral, micronutrient (especially iodine and selenium), amino acid deficiency, and low levels of binding proteins.

We found that low T3 was significantly associated with low albumin (P < 0.01). This finding was similar to the study done by Dhanjal et al.^[11] The lowering of T3 in our children explained by the fact that lower plasma proteins consequent to dietary protein deficiency and reduced hepatic biosynthesis of these proteins. Sometimes, even vitamin deficiency usually presents in SAM and also contributes to hormone deficiency due to liver dysfunction causing decrease hepatic deiodination of T3 and T4_.^[12]

Eight percent of our children showed elevated TSH without any overt symptoms and signs of hypothyroidism. This could be probably due to exaggerated response to stimulation by thyrotropin-releasing hormone or more of impaired catabolism of TSH due to SAM.^[13] Although serum TT3 and TT4 levels were decreased with elevated TSH levels in a few of our children, still they did not appear clinically hypothyroid. This is probably an adaptive change to malnutrition, which at least enables the sick patient to conserve protein.

The limitations of our study were less sample size, and TBG, TBPA, and free T4 levels were not estimated in the present study which could have been more informative.

CONCLUSION

The impaired thyroid function and low serum T3 levels seen in SAM children were probably an adaptive change to malnutrition which enables the sick patients to conserve protein.