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| __NOTOC____NOTOC__
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| {{Hyperparathyroidism}}
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| {{CMG}}; {{AE}} {{Anmol}} | | {{CMG}}; {{AE}} {{Anmol}} |
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| == Classification == | | ==Tables== |
| {| class="wikitable" | | {| class="wikitable" |
| ! colspan="4" |Classification of hyperparathyridism | | |+ |
| | !Diagnosis |
| | !Lab findings |
| | ! |
| | ! |
| |- | | |- |
| |Features
| | ! |
| |'''Primary hyperparathyroidism'''
| | ! |
| |'''Secondary hyperparathyroidism'''
| | ! |
| |'''Tertiary hyperparathyroidism'''
| | ! |
| |- | | |- |
| |Pathology | | | |
| |Hyperfunction of parathyroid cells due to hyperplasia, adenoma or carcinoma. | | | |
| |Physiological stimulation of parathyroid in response to hypocalcaemia. | | | |
| |Following long term physiological stimulation leading to hyperplasia. | | | |
| |- | | |- |
| |Cause | | | |
| | | | | |
| | | | | |
| | | | | |
| |- | | |- |
| |Associations | | | |
| |May be associated with multiple endocrine neoplasia. | | | |
| |Usually due to chronic renal failure or other causes of Vitamin D deficiency. | | | |
| |Seen in chronic renal failure. | | | |
| |-
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| |Serum calcium
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| |High
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| |Low/Normal
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| |High
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| |-
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| |Serum phosphate
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| |Low/Normal
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| |High
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| |High
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| |-
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| |Management
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| |Usually surgery if symptomatic. Cincacalcet can be considered in those not fit for surgery.
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| |Treatment of underlying cause.
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| |Usually cinacalcet or surgery in those that don't respond.
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| |} | | |} |
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| =Differential Diagnosis=
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| {|
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| ! colspan="8" style="background: #4479BA; text-align: center;" |{{fontcolor|#FFF|Differential diagnosis of hyperparathyroidism on the basis of hypocalcemia}}
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| |-
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| | colspan="2" rowspan="2" style="background: #7d7d7d; text-align: center;" |{{fontcolor|#FFF|'''Disorders'''}}
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| | rowspan="2" style="background: #7d7d7d; text-align: center;" |{{fontcolor|#FFF|'''Mechanism of hypocalcemia'''}}
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| ! colspan="4" style="background: #7d7d7d; text-align: center;" |{{fontcolor|#FFF|Laboratory findings}}
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| |-
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| |style="background: #7d7d7d; text-align: center;" |{{fontcolor|#FFF|Serum PTH}}
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| |style="background: #7d7d7d; text-align: center;" |{{fontcolor|#FFF|Serum Calcium}}
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| |style="background: #7d7d7d; text-align: center;" |{{fontcolor|#FFF|Serum Phosphate}}
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| |style="background: #7d7d7d; text-align: center;" |{{fontcolor|#FFF|Other findings}}
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| |-
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| | colspan="2" style="padding: 5px 5px; background: #DCDCDC;" align="center" |'''Hypoparathyroidism'''
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| | style="padding: 5px 5px; background: #F5F5F5;" |
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| *There is deficiency of parathyroid hormone in hypoparathyroidism.
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| *Deficiency of parathyroid hormone causes body to decrease:
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| **Reabsorption of calcium from bone.
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| **Excretion of phosphate.
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| **Reabsorbtion of calcium from distal tubules.
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| **Vitamin D mediated absorption of calcium from intestine.
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| | style="padding: 5px 5px; background: #F5F5F5;" align="center" |'''↓'''
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| | style="padding: 5px 5px; background: #F5F5F5;" align="center" |'''↓'''
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| | style="padding: 5px 5px; background: #F5F5F5;" align="center" |'''↑'''
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| | style="padding: 5px 5px; background: #F5F5F5;" |
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| *'''↓''' 1,25 Dihydroxy vitamin D
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| *Normal urinary cAMP
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| *Normal urinary phosphate
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| |-
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| | rowspan="5" style="padding: 5px 5px; background: #DCDCDC;" align="center" |'''Pseudohypoparathyroidism''' <ref name="pmid23076042">{{cite journal |vauthors=Levine MA |title=An update on the clinical and molecular characteristics of pseudohypoparathyroidism |journal=Curr Opin Endocrinol Diabetes Obes |volume=19 |issue=6 |pages=443–51 |year=2012 |pmid=23076042 |pmc=3679535 |doi=10.1097/MED.0b013e32835a255c |url=}}</ref><ref name="pmid21816789">{{cite journal |vauthors=Mantovani G |title=Clinical review: Pseudohypoparathyroidism: diagnosis and treatment |journal=J. Clin. Endocrinol. Metab. |volume=96 |issue=10 |pages=3020–30 |year=2011 |pmid=21816789 |doi=10.1210/jc.2011-1048 |url=}}</ref><ref name="pmid25891861">{{cite journal |vauthors=Lee S, Mannstadt M, Guo J, Kim SM, Yi HS, Khatri A, Dean T, Okazaki M, Gardella TJ, Jüppner H |title=A Homozygous [Cys25]PTH(1-84) Mutation That Impairs PTH/PTHrP Receptor Activation Defines a Novel Form of Hypoparathyroidism |journal=J. Bone Miner. Res. |volume=30 |issue=10 |pages=1803–13 |year=2015 |pmid=25891861 |pmc=4580526 |doi=10.1002/jbmr.2532 |url=}}</ref>
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| | style="padding: 5px 5px; background: #DCDCDC;" align="center" |'''Type 1a'''
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| | style="padding: 5px 5px; background: #F5F5F5;" |
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| *[[Genetic defect]] causing end organ resistance to the action of [[parathyroid hormone]] (PTH).
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| *[[Heterozygous]] ''[[GNAS1|GNAS]]'' inactivating mutations that reduce expression or function of Gα<sub>s</sub>
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| | style="padding: 5px 5px; background: #F5F5F5;" align="center" |'''↑'''
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| | style="padding: 5px 5px; background: #F5F5F5;" align="center" |'''↓'''
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| | style="padding: 5px 5px; background: #F5F5F5;" align="center" |'''↑'''
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| | style="padding: 5px 5px; background: #F5F5F5;" |
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| * '''↓''' 1,25 Dihydroxy vitamin D
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| * '''↓''' Urinary cAMP
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| * '''↓''' Urinary phosphate
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| |-
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| | style="padding: 5px 5px; background: #DCDCDC;" align="center" |'''Type 1b'''
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| | style="padding: 5px 5px; background: #F5F5F5;" |
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| *[[Genetic defect]] causing end organ resistance to the action of [[parathyroid hormone]] (PTH).
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| *[[Familial]]- [[heterozygous]] deletions in ''[[STX16|STX]]16'', NESP55, and/or AS exons or loss of [[methylation]] at ''[[GNAS1|GNAS]]''
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| | style="padding: 5px 5px; background: #F5F5F5;" align="center" |'''↑'''
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| | style="padding: 5px 5px; background: #F5F5F5;" align="center" |'''↓'''
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| | style="padding: 5px 5px; background: #F5F5F5;" align="center" |'''↑'''
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| | style="padding: 5px 5px; background: #F5F5F5;" |
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| * '''↓''' 1,25 Dihydroxy vitamin D
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| * '''↓''' Urinary cAMP
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| * ↓ Urinary phosphate
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| |-
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| | style="padding: 5px 5px; background: #DCDCDC;" align="center" |'''Type 1c'''
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| | style="padding: 5px 5px; background: #F5F5F5;" |
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| *[[Genetic defect]] causing end organ resistance to the action of [[parathyroid hormone]] (PTH).
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| *[[Heterozygous]] ''[[GNAS1|GNAS]]'' inactivating mutations that reduce expression or function of Gα<sub>s</sub>
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| | style="padding: 5px 5px; background: #F5F5F5;" align="center" |'''↑'''
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| | style="padding: 5px 5px; background: #F5F5F5;" align="center" |'''↓'''
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| | style="padding: 5px 5px; background: #F5F5F5;" align="center" |'''↑'''
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| | style="padding: 5px 5px; background: #F5F5F5;" |
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| * '''↓''' 1,25 Dihydroxy vitamin D
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| * '''↓''' Urinary cAMP
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| * '''↓''' Urinary phosphate
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| |-
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| | style="padding: 5px 5px; background: #DCDCDC;" align="center" |Type 2
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| | style="padding: 5px 5px; background: #F5F5F5;" |
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| *[[Genetic defect]] causing end organ resistance to the action of [[parathyroid hormone]] (PTH).
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| | style="padding: 5px 5px; background: #F5F5F5;" align="center" |'''↑'''
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| | style="padding: 5px 5px; background: #F5F5F5;" align="center" |'''↓'''
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| | style="padding: 5px 5px; background: #F5F5F5;" align="center" |'''↑'''
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| | style="padding: 5px 5px; background: #F5F5F5;" |
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| * '''↓''' 1,25 Dihydroxy vitamin D
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| * Normal urinary cAMP
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| * '''↓''' Urinary phosphate
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| |-
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| | style="padding: 5px 5px; background: #DCDCDC;" align="center" |'''Pseudopseudohypoparathyroidism'''
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| | style="padding: 5px 5px; background: #F5F5F5;" |
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| *[[Genetic defect]] causing end organ resistance to the action of [[parathyroid hormone]] (PTH).
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| *Combination of inactivating mutations of ''[[GNAS1]]'' and [[Albright's hereditary osteodystrophy|Albright's osteodystrophy]]
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| | style="padding: 5px 5px; background: #F5F5F5;" align="center" |Normal
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| | style="padding: 5px 5px; background: #F5F5F5;" align="center" |Normal
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| | style="padding: 5px 5px; background: #F5F5F5;" align="center" |Normal
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| | style="padding: 5px 5px; background: #F5F5F5;" | --
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| |-
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| | colspan="2" style="padding: 5px 5px; background: #DCDCDC;" align="center" |'''Hypomagnesemia'''<ref name="pmid26069819">{{cite journal |vauthors=Jahnen-Dechent W, Ketteler M |title=Magnesium basics |journal=Clin Kidney J |volume=5 |issue=Suppl 1 |pages=i3–i14 |year=2012 |pmid=26069819 |pmc=4455825 |doi=10.1093/ndtplus/sfr163 |url=}}</ref><ref name="pmid227929">{{cite journal |vauthors=Freitag JJ, Martin KJ, Conrades MB, Bellorin-Font E, Teitelbaum S, Klahr S, Slatopolsky E |title=Evidence for skeletal resistance to parathyroid hormone in magnesium deficiency. Studies in isolated perfused bone |journal=J. Clin. Invest. |volume=64 |issue=5 |pages=1238–44 |year=1979 |pmid=227929 |pmc=371269 |doi=10.1172/JCI109578 |url=}}</ref>
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| | style="padding: 5px 5px; background: #F5F5F5;" |
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| *Decreased parathyroid hormone (PTH) secretion
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| *Skeletal resistance to PTH
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| | style="padding: 5px 5px; background: #F5F5F5;" align="center" |Inappropriately '''↓'''
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| | style="padding: 5px 5px; background: #F5F5F5;" align="center" |Normal/'''↓'''
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| | style="padding: 5px 5px; background: #F5F5F5;" align="center" | --
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| | style="padding: 5px 5px; background: #F5F5F5;" |
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| * '''↓''' serum magnesium
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| * '''↓'''/Normal serum potassium
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| |-
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| | colspan="2" style="padding: 5px 5px; background: #DCDCDC;" align="center" |'''Hypoalbuminemia'''
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| | style="padding: 5px 5px; background: #F5F5F5;" |
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| *Majority of calcium in blood is bound to albumin. So when there is a decrease in concentration of albumin due to any condition, there is a relative hypocalcemia as well.
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| | style="padding: 5px 5px; background: #F5F5F5;" align="center" | --
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| | style="padding: 5px 5px; background: #F5F5F5;" align="center" |'''↓'''
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| | style="padding: 5px 5px; background: #F5F5F5;" align="center" | --
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| | style="padding: 5px 5px; background: #F5F5F5;" |
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| * '''↓''' serum albumin
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| *Normal albumin-corrected serum total calcium
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| *Normal ionised calcium
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| |-
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| | colspan="2" style="padding: 5px 5px; background: #DCDCDC;" align="center" |'''Hypovitaminosis D'''
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| | style="padding: 5px 5px; background: #F5F5F5;" |
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| *Decrease in vitamin D meediated calcium absorption from gut.
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| | style="padding: 5px 5px; background: #F5F5F5;" align="center" |'''↑'''
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| | style="padding: 5px 5px; background: #F5F5F5;" align="center" |'''↓'''
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| | style="padding: 5px 5px; background: #F5F5F5;" align="center" |'''↓'''/Low-normal
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| | style="padding: 5px 5px; background: #F5F5F5;" |
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| * '''↓''' 25 Hydroxy vitamin D
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| |-
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| | colspan="2" style="padding: 5px 5px; background: #DCDCDC;" align="center" |'''Chronic kidney disease'''
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| | style="padding: 5px 5px; background: #F5F5F5;" |
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| *[[Chronic renal failure]] leads to high serum [[inorganic phosphate]] and low serum [[calcium]] and deficiency of active form of [[vitamin D]] ([[1,25-dihydroxy vitamin D]]/[[calcitriol]])
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| | style="padding: 5px 5px; background: #F5F5F5;" align="center" |'''↑'''
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| | style="padding: 5px 5px; background: #F5F5F5;" align="center" |'''↓'''/Normal
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| | style="padding: 5px 5px; background: #F5F5F5;" align="center" |'''↑'''
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| | style="padding: 5px 5px; background: #F5F5F5;" |
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| * '''↓''' Glomerular flitration rate
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| |}
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| ==References== | | ==References== |
| | {{reflist|2}} |