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Secondary hyperparathyroidism

Low calcium in the bloodstream can lead to a condition called secondary hyperparathyroidism. The condition alters the level of parathyroid hormone in the body, which can result in bone loss. In the long run, the best way to reverse bone loss is to bring the level of 1,25D in the body back into a range where minerals will no longer be leached from the bones and the level of inflammatory cytokinesAny of various protein molecules secreted by cells of the immune system that serve to regulate the immune system. can return to normal. In the meantime, getting the RDA of calcium from foods and supplements without vitamin D can be helpful.

In patients with the disease, the kidneys try to compensate for the low level of calcium by increasing the conversion of 25-DThe vitamin D metabolite widely (and erroneously) considered best indicator of vitamin D "deficiency." Inactivates the Vitamin D Nuclear Receptor. Produced by hydroxylation of vitamin D3 in the liver. to 1,25-DPrimary biologically active vitamin D hormone. Activates the vitamin D nuclear receptor. Produced by hydroxylation of 25-D. Also known as 1,25-dihydroxycholecalciferol, 1,25-hydroxyvitamin D and calcitirol.. Because the illness involves the vitamins D, many doctors mistakenly think that supplementation with the steroid might help the problem. However, the truth is that this condition is best corrected by bringing the level of calcium intake back into range.

When researchers at Winthrop University Hospital made sure that subjects consumed adequate calcium, they found that only a small percentage of patients with low 25-D actually had elevated levels of PTH, and that just 16 ng/ml of 25-D is usually enough to keep PTH in the correct range.1) This was confirmed by a recent study which found that PTH levels frequently remain normal even in patients with very low 25-D. The bone density of the elderly subjects in the study also remained the same as subjects taking higher levels of 25-D as long as their PTH remained normal.2)

In reality, 25-D may account for only a very small percentage of variation in PTH levels, especially when subjects are taking adequate calcium. Several studies have shown that low magnesium, increasing age, or elevated serum phosphate and creatinine due to kidney disease also greatly contribute to the level of PTH, causing researchers at the University Hospital of New Norway to conclude that elevated PTH “is therefore probably a result of a combination of factors.” 3) It’s not surprising then, that several studies have noted that giving vitamin D to patients with low levels of 25-D often does nothing to bring PTH back to normal levels.4)

In the end, it is perfectly possible that when calcium intake is adequate, most of what remains of the association between low 25-D and elevated PTH is simply part of the pathogenesis of chronic disease and osteoporosis. Just as the low 25-D seen in patients with chronic disease is the result rather than the cause of the disease process, elevated PTH in patients with low 25-D may simply be an indicator of inflammationThe complex biological response of vascular tissues to harmful stimuli such as pathogens or damaged cells. It is a protective attempt by the organism to remove the injurious stimuli as well as initiate the healing process for the tissue. caused by the Th1 pathogensThe community of bacterial pathogens which cause chronic inflammatory disease - one which almost certainly includes multiple species and bacterial forms..

From Medscape Medical News AACE 2009: Vitamin D Deficiency May Help Patients With Primary Hyperparathyroidism Samuel I. Beard, Jr. May 20, 2009 (Houston, Texas) — Patients with primary hyperparathyroidism (PHPT) and vitamin D deficiency showed less loss of bone mineral density (BMD) than previously expected, according to a study presented here at the American Association of Clinical Endocrinologists 18th Annual Meeting and Clinical Congress.

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References

1)
Optimal vitamin D status and serum parathyroid hormone concentrations in African American women.
Aloia JF, Talwar SA, Pollack S, Feuerman M, Yeh JK
Am J Clin Nutr84p602-9(2006 Sep)
2)
Hypovitaminosis D and parathyroid hormone response in the elderly: effects on bone turnover and mortality.
Chen JS, Sambrook PN, March L, Cameron ID, Cumming RG, Simpson JM, Seibel MJ
Clin Endocrinol (Oxf)68p290-8(2008 Feb)
3)
Causes of secondary hyperparathyroidism in a healthy population: the Tromsø study.
Saleh F, Jorde R, Sundsfjord J, Haug E, Figenschau Y
J Bone Miner Metab24p58-64(2006)
4)
Persistence of parathyroid hypersecretion after vitamin D treatment in Asian vegetarians.
Dandona P, Mohiuddin J, Weerakoon JW, Freedman DB, Fonseca V, Healey T
J Clin Endocrinol Metab59p535-7(1984 Sep)
home/diseases/hyperparathyroidism.txt · Last modified: 10.17.2018 by sallieq
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