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home:diseases:hyperparathyroidism [02.18.2019] – [Secondary hyperparathyroidism] sallieqhome:diseases:hyperparathyroidism [09.14.2022] (current) – external edit 127.0.0.1
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-Joyce Waterhouse, Ph.D. has [[http://synergyhn.com/lesions/|described in detail]] a number of flaws in studies that use the relationship between low 25D and secondary hyperparathyroidism in order to estimate an optimal level of 25D. One problem is that they usually fail to ensure that subjects are consuming adequate calcium before assessing the relationship between 25-D and PTH. +Joyce Waterhouse, Ph.D. has [[https://synergyhn.com/lesions/|described in detail]] a number of flaws in studies that use the relationship between low 25D and secondary hyperparathyroidism in order to estimate an optimal level of 25D. One problem is that they usually fail to ensure that subjects are consuming adequate calcium before assessing the relationship between 25-D and PTH. 
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-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.(({{pubmed>long:16960175}})) 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.(({{pubmed>long:17854393}}))+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.(({{pmid>long:16960175}})) 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.(({{pmid>long:17854393}}))
  
 ==== vitamin D ==== ==== vitamin D ====
  
  
-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.” (({{pubmed>long:16369900}})) 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.(({{pubmed>long:6611345}}))+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.” (({{pmid>long:16369900}}))  
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 +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.(({{pmid>long:6611345}}))
  
 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 inflammation caused by the Th1 pathogens. 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 inflammation caused by the Th1 pathogens.
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-<note>Dear MPKB Reader: You have arrived at one of the articles that has not yet completed the development and review process in the knowledge base. Some of the content here may be helpful, but please know that this page is not complete. There are about 400 articles in the KB, and this is one we are still working on. Thanks for your patience.</note> 
  
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home/diseases/hyperparathyroidism.1550524403.txt.gz · Last modified: 02.18.2019 by sallieq
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