Does thyroid function disorder play a vital role in the pathogenesis of neonatal cholestasis?

Neonatal cholestasis is a syndrome characterized by decreased bile flow in infants and has several underlying causes, including genetic and metabolic diseases. Thyroid dysfunction may contribute to the pathophysiology of cholestasis, although it is not often acknowledged as a major cause. Further research into this possible connection is necessary because studies have linked thyroid conditions, including hyperthyroidism and euthyroid sick syndrome, to liver damage in newborns. This study aimed to evaluate the thyroid function in infants with neonatal cholestasis and determine whether it has a role in the diagnosis of other causes of neonatal cholestasis.

The study included 100 infants with neonatal cholestasis of different causes (50 infants with biliary atresia [BA] and 50 infants with other causes of neonatal cholestasis other than BA) attending the National Liver Institute, Menoufia University, between July 2024 and January 2025. The infants were evaluated for serum free triiodothyronine (T3), free tetraiodothyronine (T4), and thyroid-stimulating hormone (TSH).

T3 was significantly higher in the non-BA group (3.97 ±0.45) than the BA group (p < 0.0001), while T4 and TSH did not significantly differ among the studied patients (p ≥ 0.05).

The results demonstrated significant differences in T3 levels, with higher levels observed in the non-BA group, while T4 and TSH showed no significant differences between the two groups. These findings suggest that thyroid dysfunction may be associated with neonatal cholestasis, particularly in conditions other than BA.