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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