Changes in calciotrophic hormones and biochemical markers of bone turnover in normal human pregnancy

Abstract

Gallacher SJ, Fraser WD, Owens OJ, Dryburgh FJ, Logue FC, Jenkins A, Kennedy J, Boyle IT. Changes in calciotrophic hormones and biochemical markers of bone turnover in normal human pregnancy. Eur J Endocrinol 1994;131:369–74. ISSN 0804–4643 Plasma concentrations of parathyroid hormone-related protein (PTHrP), parathyroid hormone, alkaline phosphatase, osteocalcin and albumin-adjusted calcium were measured along with nephrogenous cyclic adenosine monophosphate (NcAMP) in 10 normal women longitudinally through pregnancy. In addition, an assessment of bone resorption was made in these same subjects by the measurement in true fasting urine specimens of the calcium/creatinine ratio (Ca/Cr), hydroxyproline/ creatinine ratio (HP/Cr), pyridinoline/creatinine ratio (Pyr/Cr) and deoxypyridinoline/creatinine ratio (Dpyr/Cr). The PTHrP level rose through pregnancy from (mean±sem) 0.8 ± 0.2 pmol/l in the first trimester to 2.7 ± 0.2 pmol/l 6 weeks postpartum (p < 0.0001). Serum alkaline phosphatase rose from 94 ± 8 U/l (first trimester) to 347 ± 25 U/l at term (p < 0.0001). A significant positive correlation was evident between PTHrP and alkaline phosphatase up to term (r = 0.44, p < 0.005). Parathyroid hormone concentrations remained unchanged during pregnancy but rose significantly postpartum from 1.8 ± 0.2 pmol/l (first trimester) to 3.1 ± 0.5 pmol/l (p < 0.0001). Similarly, osteocalcin, a marker of bone formative activity, remained unchanged through pregnancy but rose significantly at 6 weeks after delivery to 0.38 ± 0.05 nmol/l from 0.19 ± 0.03 nmol/l (first trimester) (p = 0.019). No significant change was noted in serum-adjusted calcium or NcAMP, either through pregnancy or at the postpartum assessment. Fasting urinary Ca/Cr fell through pregnancy from 0.70 ± 0.11 (first trimester) to a nadir of 0.19 ± 0.04 6 weeks postpartum (p = 0.007). Fasting urinary HP/Cr rose from 0.026 ± 0.003 (first trimester) to a peak of 0.049 ± 0.012 (third trimester), thereafter falling to 0.024 ± 0.002 6 weeks after delivery. Fasting urinary Pyr/Cr rose from 30.5 ± 1.7 (first trimester) to a peak of 58.3 ± 6.6 (term) (p = 0.009); Dpyr/Cr also increased through pregnancy from 9.9 ± 1.3 (first trimester) to 16.1 ± 1.7 (term) (p = 0.01). Previous studies have suggested that the placenta (during pregnancy) and breast milk (postpartum) are the main sources of PTHrP in pregnancy. This study illustrates that changes in plasma concentrations of PTHrP also can be demonstrated— although whether or not circulating PTHrP has a specific endocrine function is not clear. SJ Gallacher, University Department of Medicine, Queen Elizabeth Building, Glasgow Royal Infirmary, 10 Alexandra Parade, Glasgow G31 2ER, UK