Decreased Parathyroid Hormone, Activated Vitamin D and Serum Calcium

Parathyroid hormone (PTH) is responsible for calcium release from the bone and activation of vitamin D in the kidney. Activated vitamin D, called D1/25, in turn stimulates GI track for proper calcium absorption. Reduced quantity or quality of PTH can lead to hypocalcemia.

This original retrospective study from University of Maryland shows that supplementation with pre-hormone vitamin D2 (high dose) protects the patient from hypocalcemia more than activated-hormone Calcitriol, without causing hypercalcemia, renal injury or kidney stones.

It is important to note that study subjects must have had partial PTH deficiency in order to respond to D2 better than Calcitriol; or perhaps, D2 is converted to D1/25 via other non-PTH-dependent pathways.


Hypocalcemia ~ low calcium in the blood

Hypercalcemia ~ high calcium in the blood

Skin or Diet: Pre-hormone Vitamin D ~ D2 ~ Ergocalciferol ~ D3 ~ Cholecalciferol

Liver: Intermediate pre-hormone ~ storage pre-hormone ~ D25

Kidney: Activated Vitamin D ~ D1/25 ~ Calcitriol


Also see:

Vitamin D alternative in severe GI malabsorption

J  C  E  M

Retrospective Study

May 2017


Options for chronic treatment of hypoparathyroidism include calcitriol, recombinant human parathyroid hormone, and high-dose vitamin D (D2). D2 is used in a minority of patients because of fear of prolonged hypercalcemia and renal toxicity. There is a paucity of recent data about D2 use in hypoparathyroidism.


Compare renal function, hypercalcemia, and hypocalcemia in patients with hypoparathyroidism treated chronically with either D2 (D2 group) or calcitriol


A retrospective study of patients with hypoparathyroidism treated at the University of Maryland Hospital. Participants were identified by a billing record search with diagnosis confirmed by chart review. Thirty patients were identified; 16 were treated chronically with D2, 14 with calcitriol. Data were extracted from medical records.


Serum creatinine and calcium, hospitalizations, and emergency department (ED) visits for hypercalcemia and hypocalcemia.


D2 and calcitriol groups were similar in age (58.9 vs. 50.9 years, P = 0.28), sex, and treatment duration (17.8 vs 8.5 years, P = 0.076).

Hospitalization or ED visits for hypocalcemia occurred in none of the D2 group vs. four of 14 in the calcitriol group (P = 0.03); three in the calcitriol group had multiple ED visits.

There were no differences between D2 and calcitriol groups in hospitalizations or ED visits for hypercalcemia, serum creatinine or calcium, or kidney stones.


We found less morbidity from hypocalcemia in hypoparathyroid patients treated chronically with D2 compared with calcitriol and found no difference in renal function or morbidity from hypercalcemia. Treatment with D2 should be considered in patients with hypoparathyroidism, particularly in those who experience recurrent hypocalcemia.