The Placenta as a Parathyroid: Pregnancy-Induced Normalization of Refractory Postsurgical Hypoparathyroidism
https://doi.org/10.15605/jafes.041.S1
- Author:
Dinehs Rao
1
;
Siti Sanaa Wan Azman
1
;
Dorothy Maria Anthony Bernard
1
;
Foo Siew Hui
1
Author Information
1. Endocrine Unit, Medical Department, Hospital Selayang
- Publication Type:Journal Article
- MeSH:
Female;
Pregnancy;
Hypoparathyroidism;
Placenta
- From:
Journal of the ASEAN Federation of Endocrine Societies
2026;41(S1):78-79
- CountryPhilippines
- Language:English
-
Abstract:
Introduction:Permanent hypoparathyroidism is a recognized complication of total thyroidectomy, with an estimated incidence
of 10.47%. Standard treatment involves supplementation
with calcium and activated vitamin D. However, some
patients remain refractory to conventional therapy and fail
to achieve normocalcemia. During pregnancy, significant
physiological changes occur in calcium-regulating
hormones. Notably, the placenta increases the production
of parathyroid hormone-related peptide (PTHrP), which
acts as a calcitropic hormone, mimicking the effects of
parathyroid hormone.
Case:A 38-year-old female with a history of total thyroidectomy
14 years ago for follicular thyroid carcinoma presented
with permanent hypoparathyroidism. Her condition
was refractory to high-dose replacement therapy, which
included calcium carbonate 3 g BD, alfacalcidol 4 mcg ON,
calcitriol 1 mcg BD, and cholecalciferol 100,000 IU OD.
Despite compliance, her serum calcium levels fluctuated
between 1.7 and 1.93 mmol/L, necessitating intermittent
intravenous calcium infusions. Laboratory investigations
showed a phosphate level of 1.63 mmol/L and 24-hour
urine calcium of 4.81 mmol/L. Her thyroid function
remained stable on levothyroxine 150 mcg daily (T4:
12.0 pmol/L; thyroid-stimulating hormone: 2.93 mIU/L).
While off-label use of teriparatide was being considered,
she became pregnant. As the pregnancy progressed, her
calcium levels stabilized. Calcitriol was discontinued at 26
weeks’ gestation when her calcium reached 2.5 mmol/L.
By 30 weeks, the alfacalcidol dose was reduced to 3.5
mcg daily, with cholecalciferol dosing reduced to 50,000
IU OD. Her corrected calcium levels remained between 2.4 and 2.6 mmol/L until delivery. Similar reduction in
supplementation requirements was noted during her
previous pregnancy.
Conclusion:Elevated PTHrP during pregnancy likely contributed to
improved calcium homeostasis by increasing maternal
bone resorption and enhancing placental calcium transfer.
This case underscores the necessity of individualized,
dynamic adjustments to calcium and vitamin D therapy
based on rigorous biochemical monitoring for pregnant
patients with hypoparathyroidism.
- Full text:2026080413292544028EP_A107.pdf
