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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 | | | |
| | | | | |
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| | | | | |
| |- | | |- |
| |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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| =Symptoms=
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| *Clinical symptoms depends on two features:<ref name="pmid28138323">{{cite journal |vauthors=Abate EG, Clarke BL |title=Review of Hypoparathyroidism |journal=Front Endocrinol (Lausanne) |volume=7 |issue= |pages=172 |year=2016 |pmid=28138323 |pmc=5237638 |doi=10.3389/fendo.2016.00172 |url=}}</ref>
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| **Acuteness of hypocalcemia
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| **The absolute level of serum calcium
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| *Patients presents dramatically and tends to have more symptoms if there is an acute drop in serum calcium compared to patients with chronic hypocalcemia.<ref name="pmid8325292">{{cite journal |vauthors=Tohme JF, Bilezikian JP |title=Hypocalcemic emergencies |journal=Endocrinol. Metab. Clin. North Am. |volume=22 |issue=2 |pages=363–75 |year=1993 |pmid=8325292 |doi= |url=}}</ref>
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| ===Common symptoms===
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| Common symptoms of hypoparathyroidism include:<ref name="pmid28138323">{{cite journal |vauthors=Abate EG, Clarke BL |title=Review of Hypoparathyroidism |journal=Front Endocrinol (Lausanne) |volume=7 |issue= |pages=172 |year=2016 |pmid=28138323 |pmc=5237638 |doi=10.3389/fendo.2016.00172 |url=}}</ref><ref name="pmid18535072">{{cite journal |vauthors=Cooper MS, Gittoes NJ |title=Diagnosis and management of hypocalcaemia |journal=BMJ |volume=336 |issue=7656 |pages=1298–302 |year=2008 |pmid=18535072 |pmc=2413335 |doi=10.1136/bmj.39582.589433.BE |url=}}</ref>
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| *Tetany (hallmark of acute hypocalcemia)
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| *Paresthesia in fingertips, toes, perioral area
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| *Carpopedal spasms
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| *Circumoral numbness
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| *Abdominal pain
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| *Biliary colic
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| *Dysphoria
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| *Fatigue
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| *Muscle cramps
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| *Myoclonic jerks
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| *New onset seizure due to hypocalcemia or worsening of seizures
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| *Painful menstruation
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|
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| ===Less common synptoms===
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| Less common symptoms of hypoparathyroidism include:<ref name="pmid28138323">{{cite journal |vauthors=Abate EG, Clarke BL |title=Review of Hypoparathyroidism |journal=Front Endocrinol (Lausanne) |volume=7 |issue= |pages=172 |year=2016 |pmid=28138323 |pmc=5237638 |doi=10.3389/fendo.2016.00172 |url=}}</ref><ref name="pmid18535072">{{cite journal |vauthors=Cooper MS, Gittoes NJ |title=Diagnosis and management of hypocalcaemia |journal=BMJ |volume=336 |issue=7656 |pages=1298–302 |year=2008 |pmid=18535072 |pmc=2413335 |doi=10.1136/bmj.39582.589433.BE |url=}}</ref>
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| *Cognitive impairment
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| *Decreased concentration
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| *Hoarseness (due to laryngospasm)
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| *Neuromuscular irritability
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| *Palpitations due cardiac dysarrhythmias
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| *Personality disturbances and/or mood changes
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| *Symptoms of acute cardiomyopathy
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| *Wheezing and dyspnea (due to bronchospasm)
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| *Electrocardiographic changes that mimic myocardial infarction, or congestive heart failure (decreased cardiac contractility is related to low serum calcium and possibly parathyroid hormone deficiency, as there are PTH receptors in cardiac myocytes).<ref name="pmid24919035">{{cite journal |vauthors=Kimura S, Yoshioka K |title=Parathyroid hormone and parathyroid hormone type-1 receptor accelerate myocyte differentiation |journal=Sci Rep |volume=4 |issue= |pages=5066 |year=2014 |pmid=24919035 |pmc=4052750 |doi=10.1038/srep05066 |url=}}</ref>
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| *Cardiac manifestations
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| **prolonged QT interval and T-wave alternans, , and congestive heart failure due to decreased cardiac contractility related to low serum calcium and possibly PTH deficiency, as there are PTH receptors in cardiac myocytes.
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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}} |