Vitamin D Deficiency & Parathyroid Disease

Hyperparathyroidism is a condition in which the parathyroid glands secrete too much parathyroid hormone, or PTH. The primary function of PTH is to maintain calcium levels in the blood. To do this, PTH stimulates bone resorption, thereby increasing calcium levels in the blood. If PTH is too high symptoms of bone and joint pain may occur. The major complications of hyperparathyroidism are decreased bone mineral density and kidney stones. There are two types of hyperparathyroidism, primary and secondary and they differ in their causality and relationship to vitamin D deficiency.

Primary Hyperparathyroidism

The text, "Endocrinology: An Integrated Approach" notes that in 80 percent of cases, primary hyperparathyroidism is caused by a benign tumor and the disorder is 2.5 times more prevalent in women than in men and it increases with advancing age. In primary hyperparathyroidism, blood calcium levels are elevated because of the increase in bone resorption. The University of Texas Medical Branch reports that symptoms of primary hyperparathyroidism typically occur when blood calcium levels are elevated greater than 12 mg/dL and that only 25 percent of patients will actually develop symptoms. The website, Parathyroid.com reports that 67 percent of people with primary hyperparathyroidism have vitamin D deficiency, which is caused by the high levels of calcium.

Secondary Hyperparathyroidism

In contrast to primary hyperparathyroidism, in secondary hyperparathyroidism calcium levels are low. This low level of calcium is most often the result of kidney disease, but it may also be caused by vitamin D deficiency. The low level of calcium stimulates production of PTH, which increases bone resorption. The incidence of secondary hyperparathyroidism is related to the incidence of kidney disease and calcium and vitamin D deficiency. According to an article in the journal "Kidney International," 33 percent of men and women with severe vitamin D deficiency and 16 percent of those with moderate vitamin D deficiency also had secondary hyperparathyroidism.

Vitamin D

Vitamins D2 and D3 are precursors to the active hormone, calcitriol. Vitamins D2 and D3 can be obtained from dietary sources and vitamin D3 is also made in the skin from a cholesterol derivative. Skin synthesis of vitamin D3 requires ultraviolet sunlight. Vitamins D2 and D3 are biologically inactive. Activation requires a two-step conversion of vitamins D2 and D3 to calcitriol that takes place in the liver and the kidney. The primary function of the activated hormone of vitamins D2 and D3 is to increase the intestinal absorption of dietary calcium. Calcitriol has several other functions including regulating bone homeostasis, stimulating immune system function and controlling cell growth.

PTH Regulation

The release of PTH from the parathyroid glands is controlled directly by the level of calcium in the blood. High levels of calcium will turn off the release of PTH; however in a person with primary hyperparathyroidism the high levels of calcium do not fully suppress the release of PTH. In a person who has secondary hyperparathyroidism the low circulating levels of calcium stimulate the production of PTH leading to its elevation in the blood.

Vitamin D Regulation

PTH partly controls the synthesis of calcitriol by increasing the enzyme in the kidney that performs the last step in converting vitamin D3 to calcitriol. So in effect, high levels of PTH should increase levels of vitamin D hormone synthesis; however calcium turns off the enzyme that synthesizes calcitriol. Therefore in patients with primary hyperparathyroidism the high calcium levels turn off the production of calcitriol, indirectly causing vitamin D deficiency. In a person who has secondary hyperparathyroidism and has vitamin D deficiency the high levels of PTH cannot turn on synthesis of calcitriol because there is an inadequate level of vitamin D in the body.