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| Line 43: |
Line 43: |
| |Usually cinacalcet or surgery in those that don't respond. | | |Usually cinacalcet or surgery in those that don't respond. |
| |} | | |} |
|
| |
| =Differential Diagnosis=
| |
|
| |
|
| |
| {|
| |
| ! colspan="8" style="background: #4479BA; text-align: center;" |{{fontcolor|#FFF|Differential diagnosis of hyperparathyroidism on the basis of hypocalcemia}}
| |
| |-
| |
| | colspan="2" rowspan="2" style="background: #7d7d7d; text-align: center;" |{{fontcolor|#FFF|'''Disorders'''}}
| |
| | rowspan="2" style="background: #7d7d7d; text-align: center;" |{{fontcolor|#FFF|'''Mechanism of hypocalcemia'''}}
| |
| ! colspan="4" style="background: #7d7d7d; text-align: center;" |{{fontcolor|#FFF|Laboratory findings}}
| |
| |-
| |
| |style="background: #7d7d7d; text-align: center;" |{{fontcolor|#FFF|Serum PTH}}
| |
| |style="background: #7d7d7d; text-align: center;" |{{fontcolor|#FFF|Serum Calcium}}
| |
| |style="background: #7d7d7d; text-align: center;" |{{fontcolor|#FFF|Serum Phosphate}}
| |
| |style="background: #7d7d7d; text-align: center;" |{{fontcolor|#FFF|Other findings}}
| |
| |-
| |
| | colspan="2" style="padding: 5px 5px; background: #DCDCDC;" align="center" |'''Hypoparathyroidism'''
| |
| | style="padding: 5px 5px; background: #F5F5F5;" |
| |
| *There is deficiency of parathyroid hormone in hypoparathyroidism.
| |
| *Deficiency of parathyroid hormone causes body to decrease:
| |
| **Reabsorption of calcium from bone.
| |
| **Excretion of phosphate.
| |
| **Reabsorbtion of calcium from distal tubules.
| |
| **Vitamin D mediated absorption of calcium from intestine.
| |
| | style="padding: 5px 5px; background: #F5F5F5;" align="center" |'''↓'''
| |
| | style="padding: 5px 5px; background: #F5F5F5;" align="center" |'''↓'''
| |
| | style="padding: 5px 5px; background: #F5F5F5;" align="center" |'''↑'''
| |
| | style="padding: 5px 5px; background: #F5F5F5;" |
| |
| *'''↓''' 1,25 Dihydroxy vitamin D
| |
| *Normal urinary cAMP
| |
| *Normal urinary phosphate
| |
| |-
| |
| | 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>
| |
| | style="padding: 5px 5px; background: #DCDCDC;" align="center" |'''Type 1a'''
| |
| | style="padding: 5px 5px; background: #F5F5F5;" |
| |
| *[[Genetic defect]] causing end organ resistance to the action of [[parathyroid hormone]] (PTH).
| |
| *[[Heterozygous]] ''[[GNAS1|GNAS]]'' inactivating mutations that reduce expression or function of Gα<sub>s</sub>
| |
| | style="padding: 5px 5px; background: #F5F5F5;" align="center" |'''↑'''
| |
| | style="padding: 5px 5px; background: #F5F5F5;" align="center" |'''↓'''
| |
| | style="padding: 5px 5px; background: #F5F5F5;" align="center" |'''↑'''
| |
| | style="padding: 5px 5px; background: #F5F5F5;" |
| |
| * '''↓''' 1,25 Dihydroxy vitamin D
| |
| * '''↓''' Urinary cAMP
| |
| * '''↓''' Urinary phosphate
| |
| |-
| |
| | style="padding: 5px 5px; background: #DCDCDC;" align="center" |'''Type 1b'''
| |
| | style="padding: 5px 5px; background: #F5F5F5;" |
| |
| *[[Genetic defect]] causing end organ resistance to the action of [[parathyroid hormone]] (PTH).
| |
| *[[Familial]]- [[heterozygous]] deletions in ''[[STX16|STX]]16'', NESP55, and/or AS exons or loss of [[methylation]] at ''[[GNAS1|GNAS]]''
| |
| | style="padding: 5px 5px; background: #F5F5F5;" align="center" |'''↑'''
| |
| | style="padding: 5px 5px; background: #F5F5F5;" align="center" |'''↓'''
| |
| | style="padding: 5px 5px; background: #F5F5F5;" align="center" |'''↑'''
| |
| | style="padding: 5px 5px; background: #F5F5F5;" |
| |
| * '''↓''' 1,25 Dihydroxy vitamin D
| |
| * '''↓''' Urinary cAMP
| |
| * ↓ Urinary phosphate
| |
| |-
| |
| | style="padding: 5px 5px; background: #DCDCDC;" align="center" |'''Type 1c'''
| |
| | style="padding: 5px 5px; background: #F5F5F5;" |
| |
| *[[Genetic defect]] causing end organ resistance to the action of [[parathyroid hormone]] (PTH).
| |
| *[[Heterozygous]] ''[[GNAS1|GNAS]]'' inactivating mutations that reduce expression or function of Gα<sub>s</sub>
| |
| | style="padding: 5px 5px; background: #F5F5F5;" align="center" |'''↑'''
| |
| | style="padding: 5px 5px; background: #F5F5F5;" align="center" |'''↓'''
| |
| | style="padding: 5px 5px; background: #F5F5F5;" align="center" |'''↑'''
| |
| | style="padding: 5px 5px; background: #F5F5F5;" |
| |
| * '''↓''' 1,25 Dihydroxy vitamin D
| |
| * '''↓''' Urinary cAMP
| |
| * '''↓''' Urinary phosphate
| |
| |-
| |
| | style="padding: 5px 5px; background: #DCDCDC;" align="center" |Type 2
| |
| | style="padding: 5px 5px; background: #F5F5F5;" |
| |
| *[[Genetic defect]] causing end organ resistance to the action of [[parathyroid hormone]] (PTH).
| |
| | style="padding: 5px 5px; background: #F5F5F5;" align="center" |'''↑'''
| |
| | style="padding: 5px 5px; background: #F5F5F5;" align="center" |'''↓'''
| |
| | style="padding: 5px 5px; background: #F5F5F5;" align="center" |'''↑'''
| |
| | style="padding: 5px 5px; background: #F5F5F5;" |
| |
| * '''↓''' 1,25 Dihydroxy vitamin D
| |
| * Normal urinary cAMP
| |
| * '''↓''' Urinary phosphate
| |
| |-
| |
| | style="padding: 5px 5px; background: #DCDCDC;" align="center" |'''Pseudopseudohypoparathyroidism'''
| |
| | style="padding: 5px 5px; background: #F5F5F5;" |
| |
| *[[Genetic defect]] causing end organ resistance to the action of [[parathyroid hormone]] (PTH).
| |
| *Combination of inactivating mutations of ''[[GNAS1]]'' and [[Albright's hereditary osteodystrophy|Albright's osteodystrophy]]
| |
| | style="padding: 5px 5px; background: #F5F5F5;" align="center" |Normal
| |
| | style="padding: 5px 5px; background: #F5F5F5;" align="center" |Normal
| |
| | style="padding: 5px 5px; background: #F5F5F5;" align="center" |Normal
| |
| | style="padding: 5px 5px; background: #F5F5F5;" | --
| |
| |-
| |
| | 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>
| |
| | style="padding: 5px 5px; background: #F5F5F5;" |
| |
| *Decreased parathyroid hormone (PTH) secretion
| |
| *Skeletal resistance to PTH
| |
| | style="padding: 5px 5px; background: #F5F5F5;" align="center" |Inappropriately '''↓'''
| |
| | style="padding: 5px 5px; background: #F5F5F5;" align="center" |Normal/'''↓'''
| |
| | style="padding: 5px 5px; background: #F5F5F5;" align="center" | --
| |
| | style="padding: 5px 5px; background: #F5F5F5;" |
| |
| * '''↓''' serum magnesium
| |
| * '''↓'''/Normal serum potassium
| |
| |-
| |
| | colspan="2" style="padding: 5px 5px; background: #DCDCDC;" align="center" |'''Hypoalbuminemia'''
| |
| | style="padding: 5px 5px; background: #F5F5F5;" |
| |
| *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.
| |
| | style="padding: 5px 5px; background: #F5F5F5;" align="center" | --
| |
| | style="padding: 5px 5px; background: #F5F5F5;" align="center" |'''↓'''
| |
| | style="padding: 5px 5px; background: #F5F5F5;" align="center" | --
| |
| | style="padding: 5px 5px; background: #F5F5F5;" |
| |
| * '''↓''' serum albumin
| |
| *Normal albumin-corrected serum total calcium
| |
| *Normal ionised calcium
| |
| |-
| |
| | colspan="2" style="padding: 5px 5px; background: #DCDCDC;" align="center" |'''Hypovitaminosis D'''
| |
| | style="padding: 5px 5px; background: #F5F5F5;" |
| |
| *Decrease in vitamin D meediated calcium absorption from gut.
| |
| | style="padding: 5px 5px; background: #F5F5F5;" align="center" |'''↑'''
| |
| | style="padding: 5px 5px; background: #F5F5F5;" align="center" |'''↓'''
| |
| | style="padding: 5px 5px; background: #F5F5F5;" align="center" |'''↓'''/Low-normal
| |
| | style="padding: 5px 5px; background: #F5F5F5;" |
| |
| * '''↓''' 25 Hydroxy vitamin D
| |
| |-
| |
| | colspan="2" style="padding: 5px 5px; background: #DCDCDC;" align="center" |'''Chronic kidney disease'''
| |
| | style="padding: 5px 5px; background: #F5F5F5;" |
| |
| *[[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]])
| |
| | style="padding: 5px 5px; background: #F5F5F5;" align="center" |'''↑'''
| |
| | style="padding: 5px 5px; background: #F5F5F5;" align="center" |'''↓'''/Normal
| |
| | style="padding: 5px 5px; background: #F5F5F5;" align="center" |'''↑'''
| |
| | style="padding: 5px 5px; background: #F5F5F5;" |
| |
| * '''↓''' Glomerular flitration rate
| |
| |}
| |
| ==References==
| |