Effect of perinatal asphyxia on level of thyroid hormones in term neonates

Abstract

INTRODUCTIONPerinatal asphyxia is the one of major public health problem in the world. It is the major cause of morbidity and mortality. It accompanies one of the three most common causes of death along with prematurity and bacterial infections.1 It causes decreased perfusion to the tissues causes diving seal reflex which causes shunting of blood away from lung, kidney, GIT, skin to brain, adrenals and heart.2 Cellular dysfunction occurs as a result of diminished oxidative phosphorylation and ATP production. Impaired oxidative phosphorylation can occur during the primary hypoxic ischemic insults as well as during a secondary energy failure that usually occurs approximately 6 to 24 hours after the initiating insult.Cell death can be either immediate or delayed, and either necrotic or apoptotic.In hypoxic adults and older children effect of hypoxia on thyroid metabolism has been studied. [3][4][5][6][7][8]24 Effect of hypoxia on thyroid indices in term new-born have also been evaluated with conflicting results. [8][9][10] For the development of central nervous system thyroid hormone plays a pivotal role. In non-thyroidal illnesses low level of thyroid hormones are associated with poor prognosis. The present study was conducted to evaluate the effect of perinatal asphyxia on level of thyroid hormones by comparing thyroid profile in cord blood and venous blood at 18-24 hour after birth in new-borns with and without asphyxia. ABSTRACT Background:To evaluate how perinatal asphyxia alters the thyroid function in term newborn by comparing cord blood and 18-24 hours venous blood in between newborns with and without asphyxia. Methods: A prospective case-control study was carried out at Tertiary care pediatric center in central India. 60 Full term newborn with perinatal asphyxia requiring bag and mask ventilation for ≥1 minute or APGAR at 1 and 5 minute ≤7 or required intubation for resuscitation as cases and control -60 normal term newborn with APGAR ≥7 at 1 and 5 minute were selected. Cord blood and 18 to 24 hour after birth venous blood were collected in both groups and compared for level of thyroid hormones (T3, T4, TSH) via radioimmunoassay. Results: There was no significant difference observed in cord blood thyroid hormones (P>0.05). But a significant lower level of thyroid hormones observed in asphyxiated group as compared to control group in venous sample 18-24 hours after birth [mean± standard deviation; T3 case=68.87 ± 21.08, T3 control=79.93 ± 20.52, P=0.004; T4 case 6.48 ± 2.41, T4 control=8.89 ± 1.46, P<0.001; TSH case=4.33 ± 4.36; TSH control=8.45 ± 1.70, P<0.001]. Conclusions: Perinatal asphyxia depresses the TSH level which further leads to decrease in T3 and T4 suggestive of central hypothyroidism.

Hypothyroxinemia in sick term neonates and its risk factors in an extramural neonatal intensive care unit: a prospective cohort study

“…Similar results were found by other authors as well ( 23 ). In some studies, the cord blood levels of TSH, T3, T4, and FT4 in asphyxiated babies did not differ from those in normal babies, but the levels done at 18–24 hours of birth showed significantly lower values ( 19 , 24 , 25 ). This suggests a central hypothyroidism secondary to asphyxia.…”

Study of Impact of Birth Asphyxia on Thyroid Hormone in Newborn.

“…Reduced T3 and T4 concentrations are likely a result of decreasing TSH levels. [19,29] Hypoxia-induced modification of the thyroid hormone pathway is another probable cause. Moshang Jr T. et al in his study had found elevated rT3 levels among individuals with acute hypoxia.…”