Sunday, November 25, 2018

When one has hypocalcemia as a result of vitamin D Deficiency, how does the parathyroid gland work at homeostasis?




When one has hypocalcemia as a result of vitamin D Deficiency, how does the parathyroid gland work at homeostasis?

Calcium levels are closely controlled in the human body to prevent hyperactivity of nerve and muscle cells when Calcium concentrations too low (less than 8.5 mg/dL), and to prevent slowed function of cells when too high (more than 10.5 mg/dL) (1). Low levels of serum calcium stimulate the parathyroid gland to release Parathyroid Hormone (PTH) which acts to raise serum calcium levels in 3 ways:  increased renal resorption of Calcium (preventing loss), bone resorption of Calcium, and increased absorption in intestinal tract (1,2). PTH elevations in blood cause vitamin D (in the serum storage form 25-OH D) to be taken up in the proximal tubule cells of the kidney where it is hydroxylated (by enzyme 1-hydroxylase) into the active form of Vitamin D called calcitrol (or 1,25-(OH)2 (1). This active form of vitamin D, calcitrol, can perform work in kidneys (preventing calcium loss in urine), or be released by kidney and taken up in peripheral tissues such as bone (where it influences osteoclasts to increase serum calcium levels) and the intestines where it functions to allow more calcium to be absorbed from diet (1).  Once the serum calcium levels return to normal range, the PTH levels fall and less calcitriol is produced (1). Calcitrol in serum has a half-life of only 2-6 hours (compared with storage form 25-OH D which has half-life of 2-3 weeks) so levels fall quickly (1). Note that since PTH converts 25 (OH)D to 1,25- (OH)2, vitamin D deficiency may be missed by measuring 1,25-(OH)2 levels (2).

When Vitamin D status is insufficient, as measure by serum 25(OH)D, this may be from lack of sunlight, insufficient 7-dehydrocholesterol in skin, renal 1-hydraoxulase in kidneys, and decreased intestinal absorption (1).  Deficiency of vitamin D is associated with reduced Calcium absorption from intestines, and low serum calcium (total and ionized) (2). Low serum calcium is associated with secondary hyperpararthyroidism, especially when 25(OH)D levels are less than 15 nm/mL (2). PTH homeostasis occurs as serum calcium is maintained as PTH induces bone turnover releasing calcium into blood stream (2). Along with rising serum calcium, higher levels of Alkaline Phosphatase, lower levels of urinary Calcium and increased levels of urinary Phosphate is seen (2). Loss of phosphate in urine results in in hypophosphatemia (2). The bone turnover of calcium and reduced levels of serum phosphate result in decreased bone mineralization and in chronic state osteomalacia. To prevent problems with bone mineralization, supplement with vitamin D is essential. Treatment of deficiency can be with supplements given as 50,000 IU once a week for 8-12 weeks (goal 25-OH D in serum is 30 ng/mL) or 1-2,000 IU daily for 2-3 months.

1/ Gropper et al. Advanced Nutrition in Human Metabolism. 7th Ed. Cengage. 2018.
2/ Bringhurst F, Demay MB, Kronenberg HM. Bone and Mineral Metabolism in Health and Disease. In: Jameson J, Fauci AS, Kasper DL, Hauser SL, Longo DL, Loscalzo J. eds. Harrison's Principles of Internal Medicine, 20e New York, NY: McGraw-Hill`

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