Neutralizing and decoupling the effects of lithium medication

Abstract

Abstract Lithium-induced hypothyroidism in the neonate is a growing concern for lactating mothers. Maternal hypothyroidism in the postpartum period could lead to hypothyroidism in the infant via maternal compromised thyroid hormones (likely T4) in breast milk, and lithium in breast milk could have a direct effect on the neonatal thyroid axis. We have investigated lactating dams and pups, lithium-treated, with and without iodine supplement and control dams. We employed Enzym-linked immunosorbent assay and inductively coupled plasma mass spectrometry to assess hormone profiles and intrathyroidal iodine content. The mechanism for supplemented iodine uptake in the presence of lithium is hypothesized by change in membrane potential across the blood vessel and follicular cell(lactocyte) caused by variation in the gradient concentration of negative iodide ion, positive lithium, sodium, and potassium ions. Interestingly, lithium administered directly to pups from control mothers (average dose 900 mg/50kg/24 hours), did not affect their weight, thyroid hormones, blood urea, and intrathyroidal iodine content despite traces of lithium found in their blood and thyroid. The iodine pathway in presence of lithium content in both thyroid follicular cell and lactocyte has been regulated by gradient concentration of negative (iodide) and positive ions (lithium, potassium, and sodium). The results also demonstrate that lithium administration in lactating dams alters thyroid hormones (T4) and blood urea in both dams and pups, which could be reversed by iodine supplement. In future, supplementing iodine may be potentially useful in clinical practices to address the neonate concerns of lactating mothers and their infants either caused by prolonged lithium medication or maternal iodine deficiency.