Primary Hyperparathyroidism (PHPT) and Hypoparathyroidism (hypoPT) in Pregnancy and Lactation
Author: Boyanov, Mihail A.
Abstract:
During pregnancy the concentration of 1,25(OH)2 vitamin D increases and the calcium needed by the fetus comes mainly from the gastrointestinal tract. Towards the end of pregnancy, the secretion of PTH-related protein (PTHrP) increases, which ensures the extraction of calcium from the mother’s bones during lactation. This leads to a physiological suppression of PTH in the first half of pregnancy. PTHrP also binds to the PTH type 1 receptor and further complicates the homeostasis. Pregnancy is characterized by an increased production of PTH-related peptide, PTHrP, which would ensure calcium resorbtion from the maternal bone and would decrease urine calcium excretion. PTH is physiologically suppressed in pregnancy. PTHrP binds to the PTH type 1 receptor and affects the calcium homeostasis. During the first trimester PTH can fall by up to 70% and it starts slowly rising to reach the reference midpoint in the third trimester. Diagnosing primary hyperparathyroidism during pregnancy can therefore be quite challenging (high PTH is blunted). If untreated, the maternal hypercalcemia activates the calcium-sensing receptor and causes
functional hypoparathyroidism in the fetus. The risk for neonatal tetany is as high as 15%, and for stillbirth – up to 2%. Other complications include abortion, low birth weight and supravalvular aortic stenosis in the newborn. The hypocalcemia in hypoparathyroidism (especially if acute) can lead to abortion, pre-term delivery and neonatal death. Chronic maternal hypocalcemia is associated with fetal hyperparathyroidism with skeletal abnormalities, fractures and parathyroid hyperplasia. On the contrary, if the mother is over-replaced with calcium, this can induce severe neonatal hypocalcemia. We present a clinical review on the topic of diseases of the parathyroids during pregnancy and lactation with a focus on clinical follow-up and optimal management.
