Gestational impaired glucose tolerance (GIGT)-induced suppression of fetal thyroid secretion: effect on fetal outcome. (18th June 2019)

• Record Type: Journal Article
• Authors: Shanmugam, Suganya; Dhiman, Pooja; Rajendiran, Soundravally; Nimesh, Archana; Maurya, Dilip Kumar
• Is Part Of: Journal of maternal-fetal & neonatal medicine. Volume 32:Number 12(2019)
• Page Start: 1992
• Page End: 1996
• Publication Date: 2019-06-18
• Subjects: Gestational impaired glucose tolerances -- maternal -- thyroid; Obstetrics -- Periodicals; Perinatology -- Periodicals; Infants (Newborn) -- Diseases -- Periodicals; Neonatology -- Periodicals; 618.2
• DOI: 10.1080/14767058.2017.1422716
• Languages: English
• ISSNs: 1476-7058

Abstract

Abstract: Introduction: Gestational impaired glucose tolerance (GIGT) is a milder form of gestational diabetes mellitus (GDM), which is often poorly managed. Although, GDM is known to be associated with increased incidence of thyroid dysfunction, no study has been done to study the effect of GIGT on thyroid status and its effect on fetal outcome. Here, we carried out a study to assess thyroid function and glycemic status in both maternal and cord blood of the subjects with GIGT, and to find their association with the fetal outcome. Materials and methods: Women who came to the hospital for safe confinement during 37–40th weeks of gestation were recruited in the study. Based on the 2 hours post prandial blood glucose levels with 75 grams OGTT, done at 24–28 weeks of gestation, all the subjects were stratified into two groups: (1) Cases or GIGT group – women with blood glucose levels between 120 and 140 mg/dl and (2) Controls – women with blood glucose levels of less than 120 mg/dl. Three milliliters of venous blood was collected from mothers and 3 ml of cord blood was collected during delivery. New-borns were assessed for birth weight, head circumference, abdominal circumference, thigh circumference, and crown-heel length. Glycated hemoglobin was carried out using immunoturbidimetry (DiaSys Diagnostic Systems GmbH, Holzheim, Germany) and fructosamine was estimated using dye binding method (Biosystems, Spain). Estimation of total T3 (TT3), free T3 (FT3 ), total T4 (TT4 ), free T4 (FT4 ), and TSH was done by chemiluminescence in Siemens Advia Centaur CP using competitive immunoassay. Results: Although within the normal reference range, GIGT mothers had higher concentration of free and total T4 than controls. Cord fructosamine levels were significantly higher in babies of GIGT mothers than controls, indicating the reflection of maternal hyperglycemia. There was a positive correlation between the maternal glycated hemoglobin and cord blood fructosamine in the GIGT group. Statistically significant lower levels of total T3 and T4 with high TSH levels were found in babies with GIGT mothers, indicating the suppressive effect of maternal hyperglycemia on fetal thyroid function. Birth weight, head circumference, and thigh circumference were significantly higher in babies born to mothers with GIGT, which may be a combined effect of maternal hyperglycemia and fetal thyroid suppression. Conclusions: Maternal hyperglycemia, even in milder form of GIGT may cause suppression of fetal thyroid function. Both these factors may predispose to change in fetal anthropometry, leading to a large baby. Therefore, it is recommended to evaluate maternal and cord thyroid function for timely management strategies.