Parathyroid disorders: Difference between revisions

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__NOTOC__
__NOTOC__
{{Parathyroid disorders}}
{{Parathyroid disorders}}
{{CMG}}; {{AE}} {{USAMA}}, {{SMP}}
{{CMG}}; {{AE}} {{Anmol}}, {{USAMA}}, {{SMP}}


{{SK}}
{{SK}} Disorders of parathyroid gland; Parathyroid gland disorders.


==Overview==
==Overview==
The parathyroid glands are small endocrine glands in the neck, usually located behind the [[thyroid]] gland, which produce [[parathyroid hormone]]. These glands were first discovered in the Indian Rhinoceros by Richard Owen in 1852. The sole function of the parathyroid glands is to maintain the body's [[calcium]] level within a very narrow range, so that the nervous and muscular systems can function properly. When blood [[calcium]] levels drop below a certain point, calcium-sensing receptors in the [[parathyroid gland]] are activated to release hormone into the blood. [[Parathyroid hormone]] (PTH, also known as parathormone) is a small protein that takes part in the control of [[calcium]] and [[phosphate]] [[homeostasis]], as well as bone physiology. [[Parathyroid hormone]] has effects antagonistic to those of [[calcitonin]]. It increases blood calcium levels by stimulating [[osteoclasts]] to break down bone and release [[calcium]]. It also increases [[gastrointestinal]] calcium absorption by activating [[vitamin D]], and promotes calcium uptake by the [[kidneys]]. Hyperparathyroidism is overactivity of the parathyroid glands resulting in excess production of [[parathyroid hormone]] (PTH). Overactivity of one or more of the parathyroid glands causes high calcium levels ([[hypercalcemia]]) and low levels of [[phosphorus]] in the blood. Hyperfunction of the parathyroid glands could be due to [[adenoma]], [[hyperplasia]] or, rarely, carcinoma of the parathyroid glands. Hyperparathyroidism may present with symptoms of [[hypercalcemia]], such as painful bones, [[kidney stones]], [[abdominal pain]], psychic moans, and [[fatigue]]. An elevated concentration of serum calcium with elevated [[parathyroid hormone]] level is diagnostic of primary hyperparathyoidism. Surgical therapy is preferred over medical therapy in primary hyperparathyroidism. Hypoparathyroidism is a disorder characterized by [[hypocalcemia]] due to insufficient secretion of PTH. Most common cause for hypoparathyroidism is post-surgical including [[thyroidectomy]], [[parathyroidectomy]], and radical [[neck dissection]]. Second most common cause for hypoparathyroidism is [[autoimmune]] including [[polyglandular autoimmune syndrome type 1]] and isolated [[autoimmune]] hypoparathyroidism. Hypoparathyroidism should be differentiated from other causes of [[hypocalcemia]]. Causes of [[hypocalcemia]] other than hypoparathyroidism include [[pseudohypoparathyroidism]], [[hypomagnesemia]], [[Vitamin D deficiency|hypovitaminosis D]], [[chronic kidney disease]], and relative [[hypocalcemia]] due to [[hypoalbuminemia]]. The hallmark of acute [[hypocalcemia]] due to [[hypoparathyroidism]] is [[tetany]]. A positive history of [[neck surgery]] and symptoms of [[hypocalcemia]] is suggestive of hypoparathyroidism. The most common symptoms of hypoparathyroidism include [[tetany]], [[paresthesia]], [[Carpopedal spasm|carpopedal spasms]], and circumoral numbness. Common symptoms of hypoparathyroidism include [[abdominal pain]], [[biliary colic]], [[fatigue]], [[muscle cramps]], [[Myoclonic jerk|myoclonic jerks]], new onset [[seizure]] due to [[hypocalcemia]] or worsening of [[Seizure|seizures]], and [[painful menstruation]]. Diagnosis of hypoparathyroidism is made by measurement of [[serum]] [[calcium]] (total and ionized), [[serum albumin]] (for correction), [[phosphate]], intact [[parathyroid hormone]] ([[PTH]]), and [[25-hydroxy vitamin D]] levels. Normal or inappropriately low serum intact [[parathyroid hormone]] ([[PTH]]) concentration in patients with subnormal [[serum albumin]] corrected total or ionized [[calcium]] concentration diagnostic of hypoparathyroidism. Pharmacologic medical therapies for hypoparathyroidism include [[Calcium supplement|calcium]] and [[Vitamin D3]] supplementation. Severe [[hypocalcemia]], a potentially life-threatening condition,  is treated as soon as possible with [[intravenous]] [[calcium]] (e.g. as [[calcium gluconate]]).
The [[parathyroid glands]] are small [[endocrine glands]] in the neck, usually located behind the [[thyroid|thyroid gland]], which produce [[parathyroid hormone]]. These glands were first discovered in the Indian Rhinoceros by Richard Owen in 1852. The sole function of the [[parathyroid glands]] is to maintain the body's [[calcium]] level within a very narrow range, so that the nervous and muscular systems can function properly. When blood [[calcium]] levels drop below a certain point, calcium-sensing receptors in the [[parathyroid gland]] are activated to release hormone into the blood. [[Parathyroid hormone]] ([[PTH]], also known as [[parathormone]]) is a small protein that takes part in the control of [[calcium]] and [[phosphate]] [[homeostasis]], as well as bone physiology. [[Parathyroid hormone]] has effects antagonistic to those of [[calcitonin]]. It increases blood calcium levels by stimulating [[osteoclasts]] to break down [[bone]] and release [[calcium]]. It also increases [[gastrointestinal]] calcium absorption by activating [[vitamin D]], and promotes calcium uptake by the [[kidneys]]. Hyperparathyroidism is overactivity of the [[parathyroid glands]] resulting in excess production of [[parathyroid hormone]] ([[PTH]]). Overactivity of one or more of the [[parathyroid glands]] causes high calcium levels ([[hypercalcemia]]) and low levels of [[phosphorus]] in the blood. Hyperfunctioning of the [[parathyroid glands]] could be due to [[adenoma]], [[hyperplasia]] or, rarely, [[carcinoma]] of the [[parathyroid glands]]. [[Hyperparathyroidism]] may present with symptoms of [[hypercalcemia]], such as painful bones, [[kidney stones]], [[abdominal pain]], psychic moans, and [[fatigue]]. An elevated concentration of [[Calcium|serum calcium]] with elevated [[parathyroid hormone]] level is diagnostic of [[Hyperparathyroidism|primary hyperparathyoidism]]. Surgical therapy is preferred over medical therapy in primary [[hyperparathyroidism]]. [[Hypoparathyroidism]] is a disorder characterized by [[hypocalcemia]] due to insufficient secretion of [[PTH]]. Most common cause for [[hypoparathyroidism]] is post-surgical including [[thyroidectomy]], [[parathyroidectomy]], and radical [[neck dissection]]. Second most common cause for [[hypoparathyroidism]] is [[autoimmune]] including [[polyglandular autoimmune syndrome type 1]] and isolated [[Hypoparathyroidism|autoimmune hypoparathyroidism]]. [[Hypoparathyroidism]] should be differentiated from other causes of [[hypocalcemia]]. Causes of [[hypocalcemia]] other than [[hypoparathyroidism]] include [[pseudohypoparathyroidism]], [[hypomagnesemia]], [[Vitamin D deficiency|hypovitaminosis D]], [[chronic kidney disease]], and relative [[hypocalcemia]] due to [[hypoalbuminemia]]. The hallmark of acute [[hypocalcemia]] due to [[hypoparathyroidism]] is [[tetany]]. A positive history of [[neck surgery]] and symptoms of [[hypocalcemia]] is suggestive of [[hypoparathyroidism]]. The most common symptoms of [[hypoparathyroidism]] include [[tetany]], [[paresthesia]], [[Carpopedal spasm|carpopedal spasms]], and circumoral [[numbness]]. Common symptoms of [[hypoparathyroidism]] include [[abdominal pain]], [[biliary colic]], [[fatigue]], [[muscle cramps]], [[Myoclonic jerk|myoclonic jerks]], new onset [[seizure]] due to [[hypocalcemia]] or worsening of [[Seizure|seizures]], and [[painful menstruation]]. Diagnosis of [[hypoparathyroidism]] is made by measurement of [[serum]] [[calcium]] (total and ionized), [[serum albumin]] (for correction), [[phosphate]], intact [[parathyroid hormone]] ([[PTH]]), and [[25-hydroxy vitamin D]] levels. Normal or inappropriately low serum intact [[parathyroid hormone]] ([[PTH]]) concentration in patients with subnormal [[serum albumin]] corrected total or ionized [[calcium]] concentration diagnostic of [[hypoparathyroidism]]. Pharmacologic medical therapies for [[hypoparathyroidism]] include [[Calcium supplement|calcium]] and [[Vitamin D3]] supplementation. Severe [[hypocalcemia]], a potentially life-threatening condition,  is treated as soon as possible with [[intravenous]] [[calcium]] (e.g. as [[calcium gluconate]]).


==Classification==
==Classification==
Parathyroid disorders may be classified as follows:<ref name="pmid21812031">{{cite journal |vauthors=Bilezikian JP, Khan A, Potts JT, Brandi ML, Clarke BL, Shoback D, Jüppner H, D'Amour P, Fox J, Rejnmark L, Mosekilde L, Rubin MR, Dempster D, Gafni R, Collins MT, Sliney J, Sanders J |title=Hypoparathyroidism in the adult: epidemiology, diagnosis, pathophysiology, target-organ involvement, treatment, and challenges for future research |journal=J. Bone Miner. Res. |volume=26 |issue=10 |pages=2317–37 |year=2011 |pmid=21812031 |pmc=3405491 |doi=10.1002/jbmr.483 |url=}}</ref><ref name="pmid11117980">{{cite journal |vauthors=Marx SJ |title=Hyperparathyroid and hypoparathyroid disorders |journal=N. Engl. J. Med. |volume=343 |issue=25 |pages=1863–75 |year=2000 |pmid=11117980 |doi=10.1056/NEJM200012213432508 |url=}}</ref>
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{{Family tree | | | | | | | E04 | | E05 | | E06 | | E07 | | |!| | E04=Post-surgical  |E05=Autoimmune |E06=Genetic defects associated |E07=Functional}}
{{Family tree | | | | | | | E04 | | E05 | | E06 | | E07 | | |!| | E04=Post-surgical  |E05=[[Autoimmune]] |E06=[[Genetic defects]] associated |E07=Functional}}
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{{Family tree | | | | | | | | | | | F01 | | | | F02 | | | | | F03| |F01=[[Pseudohypoparathyroidism]] |F02=Acrodysostosis|F03=Blomstrand chondrodysplasia}}
{{Family tree | | | | | | | | | | | F01 | | | | F02 | | | | | F03| |F01=[[Pseudohypoparathyroidism]] |F02=[[Acrodysostosis]]|F03=Blomstrand chondrodysplasia}}
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{{Family tree | | | | | | | | G01 | | | | G02 | | G03 | | | G04 | | | G01=Pseudohypoparathyroidism type 1|G02=Pseudohypoparathyroidism type 2|G03=Acrodysostosis type 1|G04=Acrodysostosis type 2}}
{{Family tree | | | | | | | | G01 | | | | G02 | | G03 | | | G04 | | | G01=[[Pseudohypoparathyroidism]] type 1|G02=[[Pseudohypoparathyroidism]] type 2|G03=[[Acrodysostosis]] type 1|G04=[[Acrodysostosis]] type 2}}
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{{Family tree | | | H01 | | | H02 | | | | H03 | | | H04 | | H01=Type 1A|H02=Type 1B|H03=Type 1C|H04=Pseudopseudohypoparathyroidism}}
{{Family tree | | | H01 | | | H02 | | | | H03 | | | H04 | | H01=Type 1A|H02=Type 1B|H03=Type 1C|H04=[[Pseudopseudohypoparathyroidism]]}}
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{{Family tree/end}}


==Diagnosis==
==Diagnosis==
{|
The diagnosis of parathyroid disorders is mainly based on serum concentration of [[parathyroid hormone]], [[calcium]], and [[phosphate]].<ref name="pmid8964825">{{cite journal |vauthors=Silverberg SJ, Bilezikian JP |title=Evaluation and management of primary hyperparathyroidism |journal=J. Clin. Endocrinol. Metab. |volume=81 |issue=6 |pages=2036–40 |year=1996 |pmid=8964825 |doi=10.1210/jcem.81.6.8964825 |url=https://watermark.silverchair.com/api/watermark?token=AQECAHi208BE49Ooan9kkhW_Ercy7Dm3ZL_9Cf3qfKAc485ysgAAAfQwggHwBgkqhkiG9w0BBwagggHhMIIB3QIBADCCAdYGCSqGSIb3DQEHATAeBglghkgBZQMEAS4wEQQMs2QB8t_zFXzSZJ4bAgEQgIIBp8fw3_iunlmFW1rMhoY9MDPeg_lHu7iYzuIrfwXHubghqdXOMvdWyttCOOgR3PHFZtE5IkmNB4hRahVQsPzHGwh5kiBmLGp9W8OQwFxrCIH0sBqjOxOiYc_yGAs0ybxF1mEh929-YxivBBC43EW1yFtSmwplSQfAWah7w6yxXbUhV8umq3pGQxqYDClp47IR7TyVeEneWZz85Z7MS80V4c-yZPG1ZPxQR-1kPk3rdji_8bAeXwJKRGScWzKPqSEQvXFWLV4sHwqgTrU53HSkURUJb8u-w4EOHMjtUATJPoGgFsZOcrf_xtPBZmcI_v5G3RO_cJDHueDwQNfRaGIO2ztcToFGmVpER4vGhqfrtr7mXHPNPyUUOa-_KWPE-qxDrUCG8kevm0tM8MButJkAmVdBxrIC4mSd8sAZb3KcfSKt9RUXFJpIiDoOut21ZFEGEU8O7vwjw4RhxridsegEUiCFWCxHftX9qUqELn90AJ2Fg1olxH9jI46KnEJPd7MNYReTvdeX5erBZmXjmP5oCT6vLYUbRLjXxyJQRl-d5N9O0vfTgZ5bbA}}</ref><ref name="pmid686009">{{cite journal |vauthors=Marx SJ, Spiegel AM, Brown EM, Koehler JO, Gardner DG, Brennan MF, Aurbach GD |title=Divalent cation metabolism. Familial hypocalciuric hypercalcemia versus typical primary hyperparathyroidism |journal=Am. J. Med. |volume=6http://www.sciencedirect.com/science/article/pii/0002934378908148?via%3Dihub5 |issue=2 |pages=235–42 |year=1978 |pmid=686009 |doi=10.1016/0002-9343(78)90814-8 |url=}}</ref><ref name="pmid18650515">{{cite journal |vauthors=Shoback D |title=Clinical practice. Hypoparathyroidism |journal=N. Engl. J. Med. |volume=359 |issue=4 |pages=391–403 |year=2008 |pmid=18650515 |doi=10.1056/NEJMcp0803050 |url=}}</ref>
 
{| class="wikitable"
! colspan="2" rowspan="2" style="background: #4479BA; text-align: center;" |{{fontcolor|#FFF|Disorder}}
! colspan="2" rowspan="2" style="background: #4479BA; text-align: center;" |{{fontcolor|#FFF|Disorder}}
! colspan="4" style="background: #4479BA; text-align: center;" |{{fontcolor|#FFF|Laboratory findings}}
! colspan="4" style="background: #4479BA; text-align: center;" |{{fontcolor|#FFF|Laboratory findings}}
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| style="background: #7d7d7d; text-align: center;" |{{fontcolor|#FFF|'''Other findings'''}}
| style="background: #7d7d7d; text-align: center;" |{{fontcolor|#FFF|'''Other findings'''}}
|-
|-
| rowspan="3" style="background: #DCDCDC; text-align: center;" | Hyperparathyroidism
! rowspan="3" style="background: #DCDCDC; text-align: center;" | Hyperparathyroidism
| style="background: #DCDCDC; text-align: center;" |Primary hyperparathyroidism
! style="background: #DCDCDC; text-align: center;" |Primary hyperparathyroidism
| style="background: #F5F5F5; text-align: center;" |'''↑'''
| style="background: #F5F5F5; text-align: center;" |'''↑'''
| style="background: #F5F5F5; text-align: center;" |'''↑'''
| style="background: #F5F5F5; text-align: center;" |'''↑'''
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*Normal/'''↑''' [[calcitriol]]
*Normal/'''↑''' [[calcitriol]]
|-
|-
| style="background: #DCDCDC; text-align: center;" |Secondary hyperparathyroidism
! style="background: #DCDCDC; text-align: center;" |Secondary hyperparathyroidism
| style="background: #F5F5F5; text-align: center;" |'''↑'''
| style="background: #F5F5F5; text-align: center;" |'''↑'''
| style="background: #F5F5F5; text-align: center;" |'''↓'''/Normal
| style="background: #F5F5F5; text-align: center;" |'''↓'''/Normal
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| style="background: #F5F5F5; text-align: center;" | --
| style="background: #F5F5F5; text-align: center;" | --
|-
|-
| style="background: #DCDCDC; text-align: center;" |Tertiary hyperparathyroidism
! style="background: #DCDCDC; text-align: center;" |Tertiary hyperparathyroidism
| style="background: #F5F5F5; text-align: center;" |'''↑'''
| style="background: #F5F5F5; text-align: center;" |'''↑'''
| style="background: #F5F5F5; text-align: center;" |'''↑'''
| style="background: #F5F5F5; text-align: center;" |'''↑'''
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| style="background: #F5F5F5; text-align: center;" | --
| style="background: #F5F5F5; text-align: center;" | --
|-
|-
| colspan="2" style="background: #DCDCDC; text-align: center;" |Familial hypocalciuric hypercalcemia
! colspan="2" style="background: #DCDCDC; text-align: center;" |Familial hypocalciuric hypercalcemia
| style="background: #F5F5F5; text-align: center;" |Normal/'''↑'''
| style="background: #F5F5F5; text-align: center;" |Normal/'''↑'''
| style="background: #F5F5F5; text-align: center;" |Normal/'''↑'''
| style="background: #F5F5F5; text-align: center;" |Normal/'''↑'''
| style="background: #F5F5F5; text-align: center;" | --
| style="background: #F5F5F5; text-align: center;" | --
| style="background: #F5F5F5;" |
| style="background: #F5F5F5;" |
* '''↓''' Urinary calcium/creatinine clearance ratio
* '''↓''' Urinary calcium/[[creatinine]] clearance ratio
|-
|-
| colspan="2" style="background: #DCDCDC; text-align: center;" |Hypoparathyroidism
! colspan="2" style="background: #DCDCDC; text-align: center;" |Hypoparathyroidism
| style="background: #F5F5F5; text-align: center;" |'''↓'''
| style="background: #F5F5F5; text-align: center;" |'''↓'''
| style="background: #F5F5F5; text-align: center;" |'''↓'''
| style="background: #F5F5F5; text-align: center;" |'''↓'''
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*Normal [[urinary]] [[phosphate]]
*Normal [[urinary]] [[phosphate]]
|-
|-
| rowspan="5" style="background: #DCDCDC; text-align: center;" |Pseudohypoparathyroidism
! rowspan="5" style="background: #DCDCDC; text-align: center;" |Pseudohypoparathyroidism
| style="background: #DCDCDC; text-align: center;" | Type 1A
! style="background: #DCDCDC; text-align: center;" | Type 1A
| style="background: #F5F5F5; text-align: center;" |'''↑'''
| style="background: #F5F5F5; text-align: center;" |'''↑'''
| style="background: #F5F5F5; text-align: center;" |'''↓'''
| style="background: #F5F5F5; text-align: center;" |'''↓'''
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*'''↓''' [[Urinary System|Urinary]] [[phosphate]]
*'''↓''' [[Urinary System|Urinary]] [[phosphate]]
|-
|-
| style="background: #DCDCDC; text-align: center;" | Type 1B
! style="background: #DCDCDC; text-align: center;" | Type 1B
| style="background: #F5F5F5; text-align: center;" |'''↑'''
| style="background: #F5F5F5; text-align: center;" |'''↑'''
| style="background: #F5F5F5; text-align: center;" |'''↓'''
| style="background: #F5F5F5; text-align: center;" |'''↓'''
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*'''↓''' [[Urinary System|Urinary]] [[phosphate]]
*'''↓''' [[Urinary System|Urinary]] [[phosphate]]
|-
|-
| style="background: #DCDCDC; text-align: center;" | Type 1C
! style="background: #DCDCDC; text-align: center;" | Type 1C
| style="background: #F5F5F5; text-align: center;" |'''↑'''
| style="background: #F5F5F5; text-align: center;" |'''↑'''
| style="background: #F5F5F5; text-align: center;" |'''↓'''
| style="background: #F5F5F5; text-align: center;" |'''↓'''
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*'''↓''' [[Urinary System|Urinary]] [[phosphate]]
*'''↓''' [[Urinary System|Urinary]] [[phosphate]]
|-
|-
| style="background: #DCDCDC; text-align: center;" | Pseudopseudohypoparathyroidism
! style="background: #DCDCDC; text-align: center;" | Pseudopseudohypoparathyroidism
| style="background: #F5F5F5; text-align: center;" |Normal
| style="background: #F5F5F5; text-align: center;" |Normal
| style="background: #F5F5F5; text-align: center;" |Normal
| style="background: #F5F5F5; text-align: center;" |Normal
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| style="background: #F5F5F5; text-align: center;" | --
| style="background: #F5F5F5; text-align: center;" | --
|-
|-
| style="background: #DCDCDC; text-align: center;" | Type 2
! style="background: #DCDCDC; text-align: center;" | Type 2
| style="background: #F5F5F5; text-align: center;" |'''↑'''
| style="background: #F5F5F5; text-align: center;" |'''↑'''
| style="background: #F5F5F5; text-align: center;" |'''↓'''
| style="background: #F5F5F5; text-align: center;" |'''↓'''
| style="background: #F5F5F5; text-align: center;" |'''↑'''
| style="background: #F5F5F5; text-align: center;" |'''↑'''
| style="background: #F5F5F5;|
| style="background: #F5F5F5;" |
*'''↓''' [[1,25-dihydroxy vitamin D|1,25 Dihydroxy vitamin D]]
*'''↓''' [[1,25-dihydroxy vitamin D|1,25 Dihydroxy vitamin D]]
*Normal [[urinary]] [[cAMP]]
*Normal [[urinary]] [[cAMP]]
*'''↓''' [[Urinary]] [[phosphate]]
*'''↓''' [[Urinary]] [[phosphate]]
|-
|-
| rowspan="2" style="background: #DCDCDC; text-align: center;" |Acrodysostosis
! rowspan="2" style="background: #DCDCDC; text-align: center;" |Acrodysostosis
| style="background: #DCDCDC; text-align: center;" |Acrodysostosis type 1
! style="background: #DCDCDC; text-align: center;" |Acrodysostosis type 1
| style="background: #F5F5F5; text-align: center;" |'''↑'''
| style="background: #F5F5F5; text-align: center;" |'''↑'''
| style="background: #F5F5F5; text-align: center;" |'''↓'''
| style="background: #F5F5F5; text-align: center;" |'''↓'''
Line 131: Line 133:
*Multiple hormone resistance
*Multiple hormone resistance
|-
|-
| style="background: #DCDCDC; text-align: center;" |Acrodysostosis type 2
! style="background: #DCDCDC; text-align: center;" |Acrodysostosis type 2
| style="background: #F5F5F5; text-align: center;" |'''↑'''
| style="background: #F5F5F5; text-align: center;" |'''↑'''
| style="background: #F5F5F5; text-align: center;" |'''↓'''
| style="background: #F5F5F5; text-align: center;" |'''↓'''
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*Multiple hormone resistance
*Multiple hormone resistance
|-
|-
| colspan="2" style="background: #DCDCDC; text-align: center;" |Blomstrand chondrodysplasia
! colspan="2" style="background: #DCDCDC; text-align: center;" |Blomstrand chondrodysplasia
| style="background: #F5F5F5; text-align: center;" |'''↑'''
| style="background: #F5F5F5; text-align: center;" |'''↑'''
| style="background: #F5F5F5; text-align: center;" |'''↓'''
| style="background: #F5F5F5; text-align: center;" |'''↓'''
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==Differentiating Parathyroid Disorders==
==Differentiating Parathyroid Disorders==
* The main presenting features of parathyroid disorders are related to calcium secretion. Accordingly, differentiating parathyroid disorders from other diseases is mainly dependent to changes in calcium level. Following algorithms are designed to differentiate diseases according to [[hypercalcemia]] and [[hypocalcemia]].
* The main presenting features of [[parathyroid]] disorders are related to [[calcium]] secretion. Accordingly, differentiating [[parathyroid]] disorders from other diseases is mainly dependent to changes in calcium level. Following algorithms are designed to differentiate diseases according to [[hypercalcemia]] and [[hypocalcemia]].<ref name="pmid21812031">{{cite journal |vauthors=Bilezikian JP, Khan A, Potts JT, Brandi ML, Clarke BL, Shoback D, Jüppner H, D'Amour P, Fox J, Rejnmark L, Mosekilde L, Rubin MR, Dempster D, Gafni R, Collins MT, Sliney J, Sanders J |title=Hypoparathyroidism in the adult: epidemiology, diagnosis, pathophysiology, target-organ involvement, treatment, and challenges for future research |journal=J. Bone Miner. Res. |volume=26 |issue=10 |pages=2317–37 |year=2011 |pmid=21812031 |pmc=3405491 |doi=10.1002/jbmr.483 |url=}}</ref><ref name="pmid8964825">{{cite journal |vauthors=Silverberg SJ, Bilezikian JP |title=Evaluation and management of primary hyperparathyroidism |journal=J. Clin. Endocrinol. Metab. |volume=81 |issue=6 |pages=2036–40 |year=1996 |pmid=8964825 |doi=10.1210/jcem.81.6.8964825 |url=https://watermark.silverchair.com/api/watermark?token=AQECAHi208BE49Ooan9kkhW_Ercy7Dm3ZL_9Cf3qfKAc485ysgAAAfQwggHwBgkqhkiG9w0BBwagggHhMIIB3QIBADCCAdYGCSqGSIb3DQEHATAeBglghkgBZQMEAS4wEQQMs2QB8t_zFXzSZJ4bAgEQgIIBp8fw3_iunlmFW1rMhoY9MDPeg_lHu7iYzuIrfwXHubghqdXOMvdWyttCOOgR3PHFZtE5IkmNB4hRahVQsPzHGwh5kiBmLGp9W8OQwFxrCIH0sBqjOxOiYc_yGAs0ybxF1mEh929-YxivBBC43EW1yFtSmwplSQfAWah7w6yxXbUhV8umq3pGQxqYDClp47IR7TyVeEneWZz85Z7MS80V4c-yZPG1ZPxQR-1kPk3rdji_8bAeXwJKRGScWzKPqSEQvXFWLV4sHwqgTrU53HSkURUJb8u-w4EOHMjtUATJPoGgFsZOcrf_xtPBZmcI_v5G3RO_cJDHueDwQNfRaGIO2ztcToFGmVpER4vGhqfrtr7mXHPNPyUUOa-_KWPE-qxDrUCG8kevm0tM8MButJkAmVdBxrIC4mSd8sAZb3KcfSKt9RUXFJpIiDoOut21ZFEGEU8O7vwjw4RhxridsegEUiCFWCxHftX9qUqELn90AJ2Fg1olxH9jI46KnEJPd7MNYReTvdeX5erBZmXjmP5oCT6vLYUbRLjXxyJQRl-d5N9O0vfTgZ5bbA}}</ref><ref name="pmid686009">{{cite journal |vauthors=Marx SJ, Spiegel AM, Brown EM, Koehler JO, Gardner DG, Brennan MF, Aurbach GD |title=Divalent cation metabolism. Familial hypocalciuric hypercalcemia versus typical primary hyperparathyroidism |journal=Am. J. Med. |volume=6http://www.sciencedirect.com/science/article/pii/0002934378908148?via%3Dihub5 |issue=2 |pages=235–42 |year=1978 |pmid=686009 |doi=10.1016/0002-9343(78)90814-8 |url=}}</ref><ref name="pmid18650515">{{cite journal |vauthors=Shoback D |title=Clinical practice. Hypoparathyroidism |journal=N. Engl. J. Med. |volume=359 |issue=4 |pages=391–403 |year=2008 |pmid=18650515 |doi=10.1056/NEJMcp0803050 |url=}}</ref><ref name="pmid11134112">{{cite journal |vauthors=Yamamoto M, Akatsu T, Nagase T, Ogata E |title=Comparison of hypocalcemic hypercalciuria between patients with idiopathic hypoparathyroidism and those with gain-of-function mutations in the calcium-sensing receptor: is it possible to differentiate the two disorders? |journal=J. Clin. Endocrinol. Metab. |volume=85 |issue=12 |pages=4583–91 |year=2000 |pmid=11134112 |doi=10.1210/jcem.85.12.7035 |url=}}</ref><ref name="pmid7356229">{{cite journal |vauthors=Marx SJ, Stock JL, Attie MF, Downs RW, Gardner DG, Brown EM, Spiegel AM, Doppman JL, Brennan MF |title=Familial hypocalciuric hypercalcemia: recognition among patients referred after unsuccessful parathyroid exploration |journal=Ann. Intern. Med. |volume=92 |issue=3 |pages=351–6 |year=1980 |pmid=7356229 |doi= |url=}}</ref><ref name="pmid26713296">{{cite journal |vauthors=Mirrakhimov AE |title=Hypercalcemia of Malignancy: An Update on Pathogenesis and Management |journal=N Am J Med Sci |volume=7 |issue=11 |pages=483–93 |year=2015 |pmid=26713296 |pmc=4683803 |doi=10.4103/1947-2714.170600 |url=}}</ref><ref name="pmid1346019">{{cite journal |vauthors=Ratcliffe WA, Hutchesson AC, Bundred NJ, Ratcliffe JG |title=Role of assays for parathyroid-hormone-related protein in investigation of hypercalcaemia |journal=Lancet |volume=339 |issue=8786 |pages=164–7 |year=1992 |pmid=1346019 |doi=10.1016/0140-6736(92)90220-W |url=}}</ref><ref name="pmid7962324">{{cite journal |vauthors=Ikeda K, Ohno H, Hane M, Yokoi H, Okada M, Honma T, Yamada A, Tatsumi Y, Tanaka T, Saitoh T |title=Development of a sensitive two-site immunoradiometric assay for parathyroid hormone-related peptide: evidence for elevated levels in plasma from patients with adult T-cell leukemia/lymphoma and B-cell lymphoma |journal=J. Clin. Endocrinol. Metab. |volume=79 |issue=5 |pages=1322–7 |year=1994 |pmid=7962324 |doi=10.1210/jcem.79.5.7962324 |url=}}</ref><ref name="pmid12679445">{{cite journal |vauthors=Horwitz MJ, Tedesco MB, Sereika SM, Hollis BW, Garcia-Ocaña A, Stewart AF |title=Direct comparison of sustained infusion of human parathyroid hormone-related protein-(1-36) [hPTHrP-(1-36)] versus hPTH-(1-34) on serum calcium, plasma 1,25-dihydroxyvitamin D concentrations, and fractional calcium excretion in healthy human volunteers |journal=J. Clin. Endocrinol. Metab. |volume=88 |issue=4 |pages=1603–9 |year=2003 |pmid=12679445 |doi=10.1210/jc.2002-020773 |url=}}</ref><ref name="pmid2918061">{{cite journal |vauthors=Mallette LE, Khouri K, Zengotita H, Hollis BW, Malini S |title=Lithium treatment increases intact and midregion parathyroid hormone and parathyroid volume |journal=J. Clin. Endocrinol. Metab. |volume=68 |issue=3 |pages=654–60 |year=1989 |pmid=2918061 |doi=10.1210/jcem-68-3-654 |url=}}</ref><ref name="pmid1313547">{{cite journal |vauthors=Jacobus CH, Holick MF, Shao Q, Chen TC, Holm IA, Kolodny JM, Fuleihan GE, Seely EW |title=Hypervitaminosis D associated with drinking milk |journal=N. Engl. J. Med. |volume=326 |issue=18 |pages=1173–7 |year=1992 |pmid=1313547 |doi=10.1056/NEJM199204303261801 |url=}}</ref><ref name="pmid8120527">{{cite journal |vauthors=Hoeck HC, Laurberg G, Laurberg P |title=Hypercalcaemic crisis after excessive topical use of a vitamin D derivative |journal=J. Intern. Med. |volume=235 |issue=3 |pages=281–2 |year=1994 |pmid=8120527 |doi= |url=}}</ref><ref name="pmid9215298">{{cite journal |vauthors=Dusso AS, Kamimura S, Gallieni M, Zhong M, Negrea L, Shapiro S, Slatopolsky E |title=gamma-Interferon-induced resistance to 1,25-(OH)2 D3 in human monocytes and macrophages: a mechanism for the hypercalcemia of various granulomatoses |journal=J. Clin. Endocrinol. Metab. |volume=82 |issue=7 |pages=2222–32 |year=1997 |pmid=9215298 |doi=10.1210/jcem.82.7.4074 |url=}}</ref><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><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><ref name="pmid10401014">{{cite journal |vauthors=Navarro JF, Mora C, Jiménez A, Torres A, Macía M, García J |title=Relationship between serum magnesium and parathyroid hormone levels in hemodialysis patients |journal=Am. J. Kidney Dis. |volume=34 |issue=1 |pages=43–8 |year=1999 |pmid=10401014 |doi=10.1053/AJKD03400043 |url=}}</ref><ref name="pmid26131288">{{cite journal |vauthors=Li K, Xu Y |title=Citrate metabolism in blood transfusions and its relationship due to metabolic alkalosis and respiratory acidosis |journal=Int J Clin Exp Med |volume=8 |issue=4 |pages=6578–84 |year=2015 |pmid=26131288 |pmc=4483798 |doi= |url=}}</ref><ref name="pmid3592447">{{cite journal |vauthors=Zaloga GP, Chernow B |title=The multifactorial basis for hypocalcemia during sepsis. Studies of the parathyroid hormone-vitamin D axis |journal=Ann. Intern. Med. |volume=107 |issue=1 |pages=36–41 |year=1987 |pmid=3592447 |doi= |url=}}</ref><ref name="pmid1147452">{{cite journal |vauthors=Weir GC, Lesser PB, Drop LJ, Fischer JE, Warshaw AL |title=The hypocalcemia of acute pancreatitis |journal=Ann. Intern. Med. |volume=83 |issue=2 |pages=185–9 |year=1975 |pmid=1147452 |doi= |url=}}</ref>
===Hypercalcemia===
===Hypercalcemia===
<br><br>
<br><br>
Line 195: Line 197:
{{Family tree| | | G01 | | | G02 | | | G03 | | | | | | | | | | |!| | | | | | | |G01=Drug induced [[hypocalcemia]]<br>([[bisphosphonates]], [[cisplatin]], [[antiepileptics]], [[aminoglycosides]], [[proton pump inhibitors]])|G02=[[Hypomagnesemia]] <br> (sometimes [[hypermagnesemia]])|G03=[[Calcium]] levels reaches normal after [[transfusion]] is stopped}}
{{Family tree| | | G01 | | | G02 | | | G03 | | | | | | | | | | |!| | | | | | | |G01=Drug induced [[hypocalcemia]]<br>([[bisphosphonates]], [[cisplatin]], [[antiepileptics]], [[aminoglycosides]], [[proton pump inhibitors]])|G02=[[Hypomagnesemia]] <br> (sometimes [[hypermagnesemia]])|G03=[[Calcium]] levels reaches normal after [[transfusion]] is stopped}}
{{Family tree| | | | | | | | | | | | | | | | | | | | | | | | | |!| | | | | | | |}}
{{Family tree| | | | | | | | | | | | | | | | | | | | | | | | | |!| | | | | | | |}}
{{Family tree| | | | | | | | | |,|-|-|-|-|-|-|-|-|-|-|-|-|-|-|-|^|.| | | | | | | |}}
{{Family tree| | | | | | | | | |,|-|-|-|-|-|-|-|-|-|-|-|-|-|-|-|^|-|-|-|.| | | | |}}
{{Family tree| | | | | | | | | K01 | | | | | | | | | | | | | | | K02 | | | | | | |K01=↓ [[PTH]]|K02=↑  [[PTH]]}}
{{Family tree| | | | | | | | | K01 | | | | | | | | | | | | | | | | | | K02 | | | |K01=↓ [[PTH]]|K02=↑  [[PTH]]}}
{{Family tree| | | | | | | | | |!| | | | | | | | | | |,|-|-|-|-|-|+|-|-|-|-|.| | |}}
{{Family tree| | | | | | | | | |!| | | | | | | | | | |,|-|-|-|-|-|v|-|-|^|-|-|v|-|-|-|-|.| | | | | | |}}
{{Family tree| | | | | | | | | H01 | | | | | | | | | H02 | | | | H03 | | | H04 | |H01=[[Hypoparathyroidism]]|H02=History of [[chronic kidney disease]]|H03=[[↓ 25-hydroxy vitamin D]]|H04=Genetic testing}}
{{Family tree| | | | | | | | | H01 | | | | | | | | | H02 | | | | H03 | | | | H04 | | | H05||H01=[[Hypoparathyroidism]]|H02=History of [[chronic kidney disease]]|H03=↓ [[25-hydroxy vitamin D]]|H04=Genetic testing|H05=Inflammatory conditions}}
{{Family tree| |,|-|-|-|-|v|-|-|^|-|v|-|-|-|-|.| | | |!| | | | | |!| | | | |!| | |}}
{{Family tree| |,|-|-|-|-|v|-|-|^|-|v|-|-|-|-|.| | | |!| | | | | |!| | | | |!| | | | |!| | }}
{{Family tree| I01 | | | I02 | | | I03 | | | I04 | | I05 | | | | I06 | | | I07 | |I01=History of anterior neck surgery|I02=Associated with [[autoimmunity]]|I03=Family history present|I04=None of these present|I05=Secondary hyperparathyroidism<br> (may have ↓/normal [[calcium]])|I06=[[Vitamin D deficiency|Hypovitaminosis D]]|I07=[[Pseudohypoparathyroidism|PTH resistance disorders]]}}
{{Family tree| I01 | | | I02 | | | I03 | | | I04 | | I05 | | | | I06 | | | I07 | | | |!| | |I01=History of anterior neck surgery|I02=Associated with [[autoimmunity]]|I03=Family history present|I04=None of these present|I05=Secondary hyperparathyroidism<br> (may have ↓/normal [[calcium]])|I06=[[Vitamin D deficiency|Hypovitaminosis D]]|I07=[[Pseudohypoparathyroidism|PTH resistance disorders]]}}
{{Family tree| |!| | | | | |!| |,|-|^|.| | | |!| | | | | | | | | | | | | | | | | |}}
{{Family tree| |!| | | | | |!| |,|-|^|.| | | |!| | | | | | | | | | | | | |,|-|-|-|-|-|(| | | |}}
{{Family tree| J01 | | | | | J02 | | J03 | | J04 | | | | | | | | | | | | | | | | |J01=Post-surgical hypoparathyroidism|J02=[[Autoimmune polyglandular endocrinopathy]]<br>or<br>Isolated autoimmune hypoparathyroidism|J03=Hypoparathyroidism related to other genetic causes|J04=Other causes of hypoparathyroidism should bbe evaluted<br> (for other causes of hypoparathyroidims, click [[Hypoparathyroidism causes|here]])}}
{{Family tree| J01 | | | | | J02 | | J03 | | J04 | | | | | | | | | | | | J05 | | | | J06 | |J01=[[Hypoparathyroidism classification|Post-surgical hypoparathyroidism]]|J02=[[Autoimmune polyendocrine syndrome]]<br>or<br>Isolated autoimmune hypoparathyroidism|J03=Hypoparathyroidism related to other genetic causes|J04=Other causes of hypoparathyroidism should be evaluted<br> (for other causes of hypoparathyroidims, click [[Hypoparathyroidism causes|here]])|J05=[[Sepsis]]|J06=[[Acute pancreatitis]]}}
{{Family tree/end}}
{{Family tree/end}}
<br><br>
<br><br>
==References==
{{Reflist|2}}
{{WH}}
{{WS}}

Latest revision as of 16:06, 20 November 2018

Parathyroid disorders

Overview

Classification

Hyperparathyroidism
Familial hypocalciuric hypercalcemia
Hypoparathyroidism
Pseudohypoparathyroidism

Diagnosis

Differentiating Parathyroid Disorders

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Anmol Pitliya, M.B.B.S. M.D.[2], Usama Talib, BSc, MD [3], Seyedmahdi Pahlavani, M.D. [4]

Synonyms and keywords: Disorders of parathyroid gland; Parathyroid gland disorders.

Overview

The parathyroid glands are small endocrine glands in the neck, usually located behind the thyroid gland, which produce parathyroid hormone. These glands were first discovered in the Indian Rhinoceros by Richard Owen in 1852. The sole function of the parathyroid glands is to maintain the body's calcium level within a very narrow range, so that the nervous and muscular systems can function properly. When blood calcium levels drop below a certain point, calcium-sensing receptors in the parathyroid gland are activated to release hormone into the blood. Parathyroid hormone (PTH, also known as parathormone) is a small protein that takes part in the control of calcium and phosphate homeostasis, as well as bone physiology. Parathyroid hormone has effects antagonistic to those of calcitonin. It increases blood calcium levels by stimulating osteoclasts to break down bone and release calcium. It also increases gastrointestinal calcium absorption by activating vitamin D, and promotes calcium uptake by the kidneys. Hyperparathyroidism is overactivity of the parathyroid glands resulting in excess production of parathyroid hormone (PTH). Overactivity of one or more of the parathyroid glands causes high calcium levels (hypercalcemia) and low levels of phosphorus in the blood. Hyperfunctioning of the parathyroid glands could be due to adenoma, hyperplasia or, rarely, carcinoma of the parathyroid glands. Hyperparathyroidism may present with symptoms of hypercalcemia, such as painful bones, kidney stones, abdominal pain, psychic moans, and fatigue. An elevated concentration of serum calcium with elevated parathyroid hormone level is diagnostic of primary hyperparathyoidism. Surgical therapy is preferred over medical therapy in primary hyperparathyroidism. Hypoparathyroidism is a disorder characterized by hypocalcemia due to insufficient secretion of PTH. Most common cause for hypoparathyroidism is post-surgical including thyroidectomy, parathyroidectomy, and radical neck dissection. Second most common cause for hypoparathyroidism is autoimmune including polyglandular autoimmune syndrome type 1 and isolated autoimmune hypoparathyroidism. Hypoparathyroidism should be differentiated from other causes of hypocalcemia. Causes of hypocalcemia other than hypoparathyroidism include pseudohypoparathyroidism, hypomagnesemia, hypovitaminosis D, chronic kidney disease, and relative hypocalcemia due to hypoalbuminemia. The hallmark of acute hypocalcemia due to hypoparathyroidism is tetany. A positive history of neck surgery and symptoms of hypocalcemia is suggestive of hypoparathyroidism. The most common symptoms of hypoparathyroidism include tetany, paresthesia, carpopedal spasms, and circumoral numbness. Common symptoms of hypoparathyroidism include abdominal pain, biliary colic, fatigue, muscle cramps, myoclonic jerks, new onset seizure due to hypocalcemia or worsening of seizures, and painful menstruation. Diagnosis of hypoparathyroidism is made by measurement of serum calcium (total and ionized), serum albumin (for correction), phosphate, intact parathyroid hormone (PTH), and 25-hydroxy vitamin D levels. Normal or inappropriately low serum intact parathyroid hormone (PTH) concentration in patients with subnormal serum albumin corrected total or ionized calcium concentration diagnostic of hypoparathyroidism. Pharmacologic medical therapies for hypoparathyroidism include calcium and Vitamin D3 supplementation. Severe hypocalcemia, a potentially life-threatening condition, is treated as soon as possible with intravenous calcium (e.g. as calcium gluconate).

Classification

Parathyroid disorders may be classified as follows:[1][2]

 
 
 
 
 
 
 
 
 
 
 
 
 
Parathyroid disorders
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Hyperparathyroidism
 
 
 
Familial hypocalciuric hypercalcemia
 
 
 
Hypoparathyroidism
 
 
 
Parathyroid hormone resistance diseases
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Primary
 
Secondary
 
Tertiary
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Post-surgical
 
Autoimmune
 
Genetic defects associated
 
Functional
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Pseudohypoparathyroidism
 
 
 
Acrodysostosis
 
 
 
 
Blomstrand chondrodysplasia
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Pseudohypoparathyroidism type 1
 
 
 
Pseudohypoparathyroidism type 2
 
Acrodysostosis type 1
 
 
Acrodysostosis type 2
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Type 1A
 
 
Type 1B
 
 
 
Type 1C
 
 
Pseudopseudohypoparathyroidism
 

Diagnosis

The diagnosis of parathyroid disorders is mainly based on serum concentration of parathyroid hormone, calcium, and phosphate.[3][4][5]

Disorder Laboratory findings
Parathyroid hormone Serum calcium Serum phosphate Other findings
Hyperparathyroidism Primary hyperparathyroidism ↑ ↑ ↓/Normal
Secondary hyperparathyroidism ↑ ↓/Normal ↑ --
Tertiary hyperparathyroidism ↑ ↑ ↑ --
Familial hypocalciuric hypercalcemia Normal/↑ Normal/↑ --
Hypoparathyroidism ↓ ↓ ↑
Pseudohypoparathyroidism Type 1A ↑ ↓ ↑
Type 1B ↑ ↓ ↑
Type 1C ↑ ↓ ↑
Pseudopseudohypoparathyroidism Normal Normal Normal --
Type 2 ↑ ↓ ↑
Acrodysostosis Acrodysostosis type 1 ↑ ↓ ↑
  • Multiple hormone resistance
Acrodysostosis type 2 ↑ ↓ ↑
  • Multiple hormone resistance
Blomstrand chondrodysplasia ↑ ↓ ↑

Differentiating Parathyroid Disorders

Hypercalcemia



 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Hypercalcemia
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Repeat (Check ionized calcium or calcium corrected for albumin)
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Hypercalcemia confirmed
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Measure intact parathyroid hormone (PTH)
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
↑ PTH
 
 
 
 
 
 
 
Mildly ↑ PTH
 
 
 
 
 
 
↓ PTH
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Hyperparathyroidism
 
 
 
 
 
 
 
Urinary calcium creatinine ratio
 
 
 
 
 
 
Measure parathyroid hormone-related protein (PTHrP) and vitamin D metabolites
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
↑ serum phosphate
History of renal transplantation
 
 
 
↓/Normal phosphate levels
 
↑ Urinary calcium creatinine ratio
 
 
 
↓ Urinary calcium creatinine ratio
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Tertiary hyperparathyroidism
 
 
 
 
 
Primary hyperparathyroidism
 
 
 
 
 
Familial hypocalciuric hypercalcemia
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
↑ PTHrP
 
 
↑ 1,25-dihydroxy vitamin D
 
 
↑ 25-hydroxy vitamin D
 
 
↓ 1,25-dihydroxy vitamin D
 
 
 
 
 
Normal PTHrP and vitamin D metabolites
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Humoral hypercalcemia of malignancy
 
 
Chest X-ray, ACE levels
 
 
Hypervitaminosis D
 
 
History of high milk intake,
excess calcium intake for treating osteoporosis or dyspepsia
 
Serum protein electrophoresis
 
Mammography
 
Check medications
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Check for malignancies
 
 
Bilateral hilar lymphadenopathy, ↑ ACE levels
 
 
 
 
 
 
 
Milk-alkali syndrome
 
Multiple myeloma
 
Breast cancer
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Sarcoidosis
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Lithium induced hypercalcemia
 
 
 
Thiazide diuretic induced hypercalcemia
 



Hypocalcemia

 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Hypocalcemia
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Repeat (check ionized calcium or calcium corrected for albumin)
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Hypocalcemia confirmed
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Look for reversible cause
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Reversible cause present
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Reversible cause absent
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
History of drug use
 
 
Serum magnesium levels
 
 
Blood transfusion
 
 
 
 
 
 
 
 
 
Measure intact parathyroid hormone (PTH)
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Drug induced hypocalcemia
(bisphosphonates, cisplatin, antiepileptics, aminoglycosides, proton pump inhibitors)
 
 
Hypomagnesemia
(sometimes hypermagnesemia)
 
 
Calcium levels reaches normal after transfusion is stopped
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
↓ PTH
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
↑ PTH
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Hypoparathyroidism
 
 
 
 
 
 
 
 
History of chronic kidney disease
 
 
 
↓ 25-hydroxy vitamin D
 
 
 
Genetic testing
 
 
Inflammatory conditions
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
History of anterior neck surgery
 
 
Associated with autoimmunity
 
 
Family history present
 
 
None of these present
 
Secondary hyperparathyroidism
(may have ↓/normal calcium)
 
 
 
Hypovitaminosis D
 
 
PTH resistance disorders
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Post-surgical hypoparathyroidism
 
 
 
 
Autoimmune polyendocrine syndrome
or
Isolated autoimmune hypoparathyroidism
 
Hypoparathyroidism related to other genetic causes
 
Other causes of hypoparathyroidism should be evaluted
(for other causes of hypoparathyroidims, click here)
 
 
 
 
 
 
 
 
 
 
 
Sepsis
 
 
 
Acute pancreatitis
 



References

  1. ↑ 1.0 1.1 Bilezikian JP, Khan A, Potts JT, Brandi ML, Clarke BL, Shoback D, Jüppner H, D'Amour P, Fox J, Rejnmark L, Mosekilde L, Rubin MR, Dempster D, Gafni R, Collins MT, Sliney J, Sanders J (2011). "Hypoparathyroidism in the adult: epidemiology, diagnosis, pathophysiology, target-organ involvement, treatment, and challenges for future research". J. Bone Miner. Res. 26 (10): 2317–37. doi:10.1002/jbmr.483. PMC 3405491. PMID 21812031.
  2. ↑ Marx SJ (2000). "Hyperparathyroid and hypoparathyroid disorders". N. Engl. J. Med. 343 (25): 1863–75. doi:10.1056/NEJM200012213432508. PMID 11117980.
  3. ↑ 3.0 3.1 Silverberg SJ, Bilezikian JP (1996). "Evaluation and management of primary hyperparathyroidism". J. Clin. Endocrinol. Metab. 81 (6): 2036–40. doi:10.1210/jcem.81.6.8964825. PMID 8964825.
  4. ↑ 4.0 4.1 Marx SJ, Spiegel AM, Brown EM, Koehler JO, Gardner DG, Brennan MF, Aurbach GD (1978). "Divalent cation metabolism. Familial hypocalciuric hypercalcemia versus typical primary hyperparathyroidism". Am. J. Med. 6http://www.sciencedirect.com/science/article/pii/0002934378908148?via%3Dihub5 (2): 235–42. doi:10.1016/0002-9343(78)90814-8. PMID 686009.
  5. ↑ 5.0 5.1 Shoback D (2008). "Clinical practice. Hypoparathyroidism". N. Engl. J. Med. 359 (4): 391–403. doi:10.1056/NEJMcp0803050. PMID 18650515.
  6. ↑ Yamamoto M, Akatsu T, Nagase T, Ogata E (2000). "Comparison of hypocalcemic hypercalciuria between patients with idiopathic hypoparathyroidism and those with gain-of-function mutations in the calcium-sensing receptor: is it possible to differentiate the two disorders?". J. Clin. Endocrinol. Metab. 85 (12): 4583–91. doi:10.1210/jcem.85.12.7035. PMID 11134112.
  7. ↑ Marx SJ, Stock JL, Attie MF, Downs RW, Gardner DG, Brown EM, Spiegel AM, Doppman JL, Brennan MF (1980). "Familial hypocalciuric hypercalcemia: recognition among patients referred after unsuccessful parathyroid exploration". Ann. Intern. Med. 92 (3): 351–6. PMID 7356229.
  8. ↑ Mirrakhimov AE (2015). "Hypercalcemia of Malignancy: An Update on Pathogenesis and Management". N Am J Med Sci. 7 (11): 483–93. doi:10.4103/1947-2714.170600. PMC 4683803. PMID 26713296.
  9. ↑ Ratcliffe WA, Hutchesson AC, Bundred NJ, Ratcliffe JG (1992). "Role of assays for parathyroid-hormone-related protein in investigation of hypercalcaemia". Lancet. 339 (8786): 164–7. doi:10.1016/0140-6736(92)90220-W. PMID 1346019.
  10. ↑ Ikeda K, Ohno H, Hane M, Yokoi H, Okada M, Honma T, Yamada A, Tatsumi Y, Tanaka T, Saitoh T (1994). "Development of a sensitive two-site immunoradiometric assay for parathyroid hormone-related peptide: evidence for elevated levels in plasma from patients with adult T-cell leukemia/lymphoma and B-cell lymphoma". J. Clin. Endocrinol. Metab. 79 (5): 1322–7. doi:10.1210/jcem.79.5.7962324. PMID 7962324.
  11. ↑ Horwitz MJ, Tedesco MB, Sereika SM, Hollis BW, Garcia-Ocaña A, Stewart AF (2003). "Direct comparison of sustained infusion of human parathyroid hormone-related protein-(1-36) [hPTHrP-(1-36)] versus hPTH-(1-34) on serum calcium, plasma 1,25-dihydroxyvitamin D concentrations, and fractional calcium excretion in healthy human volunteers". J. Clin. Endocrinol. Metab. 88 (4): 1603–9. doi:10.1210/jc.2002-020773. PMID 12679445.
  12. ↑ Mallette LE, Khouri K, Zengotita H, Hollis BW, Malini S (1989). "Lithium treatment increases intact and midregion parathyroid hormone and parathyroid volume". J. Clin. Endocrinol. Metab. 68 (3): 654–60. doi:10.1210/jcem-68-3-654. PMID 2918061.
  13. ↑ Jacobus CH, Holick MF, Shao Q, Chen TC, Holm IA, Kolodny JM, Fuleihan GE, Seely EW (1992). "Hypervitaminosis D associated with drinking milk". N. Engl. J. Med. 326 (18): 1173–7. doi:10.1056/NEJM199204303261801. PMID 1313547.
  14. ↑ Hoeck HC, Laurberg G, Laurberg P (1994). "Hypercalcaemic crisis after excessive topical use of a vitamin D derivative". J. Intern. Med. 235 (3): 281–2. PMID 8120527.
  15. ↑ Dusso AS, Kamimura S, Gallieni M, Zhong M, Negrea L, Shapiro S, Slatopolsky E (1997). "gamma-Interferon-induced resistance to 1,25-(OH)2 D3 in human monocytes and macrophages: a mechanism for the hypercalcemia of various granulomatoses". J. Clin. Endocrinol. Metab. 82 (7): 2222–32. doi:10.1210/jcem.82.7.4074. PMID 9215298.
  16. ↑ Levine MA (2012). "An update on the clinical and molecular characteristics of pseudohypoparathyroidism". Curr Opin Endocrinol Diabetes Obes. 19 (6): 443–51. doi:10.1097/MED.0b013e32835a255c. PMC 3679535. PMID 23076042.
  17. ↑ Mantovani G (2011). "Clinical review: Pseudohypoparathyroidism: diagnosis and treatment". J. Clin. Endocrinol. Metab. 96 (10): 3020–30. doi:10.1210/jc.2011-1048. PMID 21816789.
  18. ↑ Lee S, Mannstadt M, Guo J, Kim SM, Yi HS, Khatri A, Dean T, Okazaki M, Gardella TJ, Jüppner H (2015). "A Homozygous [Cys25]PTH(1-84) Mutation That Impairs PTH/PTHrP Receptor Activation Defines a Novel Form of Hypoparathyroidism". J. Bone Miner. Res. 30 (10): 1803–13. doi:10.1002/jbmr.2532. PMC 4580526. PMID 25891861.
  19. ↑ Jahnen-Dechent W, Ketteler M (2012). "Magnesium basics". Clin Kidney J. 5 (Suppl 1): i3–i14. doi:10.1093/ndtplus/sfr163. PMC 4455825. PMID 26069819.
  20. ↑ Freitag JJ, Martin KJ, Conrades MB, Bellorin-Font E, Teitelbaum S, Klahr S, Slatopolsky E (1979). "Evidence for skeletal resistance to parathyroid hormone in magnesium deficiency. Studies in isolated perfused bone". J. Clin. Invest. 64 (5): 1238–44. doi:10.1172/JCI109578. PMC 371269. PMID 227929.
  21. ↑ Navarro JF, Mora C, Jiménez A, Torres A, Macía M, García J (1999). "Relationship between serum magnesium and parathyroid hormone levels in hemodialysis patients". Am. J. Kidney Dis. 34 (1): 43–8. doi:10.1053/AJKD03400043. PMID 10401014.
  22. ↑ Li K, Xu Y (2015). "Citrate metabolism in blood transfusions and its relationship due to metabolic alkalosis and respiratory acidosis". Int J Clin Exp Med. 8 (4): 6578–84. PMC 4483798. PMID 26131288.
  23. ↑ Zaloga GP, Chernow B (1987). "The multifactorial basis for hypocalcemia during sepsis. Studies of the parathyroid hormone-vitamin D axis". Ann. Intern. Med. 107 (1): 36–41. PMID 3592447.
  24. ↑ Weir GC, Lesser PB, Drop LJ, Fischer JE, Warshaw AL (1975). "The hypocalcemia of acute pancreatitis". Ann. Intern. Med. 83 (2): 185–9. PMID 1147452.

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