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| __NOTOC__
| | Mutations in the MEN1 gene cause multiple endocrine neoplasia type 1. This gene provides instructions for producing a protein called menin. Menin acts as a tumor suppressor, which means it normally keeps cells from growing and dividing too rapidly or in an uncontrolled way. Although the exact function of menin is unknown, it is likely involved in cell functions such as copying and repairing DNA and regulating the activity of other genes. When mutations inactivate both copies of the MEN1 gene, menin is no longer available to control cell growth and division. The loss of functional menin allows cells to divide too frequently, leading to the formation of tumors characteristic of multiple endocrine neoplasia type 1. It is unclear why these tumors preferentially affect endocrine tissues. |
| {{CMG}}; {{AE}} {{Ajay}}
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| ==Family Tree==
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| {{familytree/start}}
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| {{familytree | | | | | | | | | |A01 | | | | | |A01='''Familial Hypocalciuric Hypercalcemia'''}}
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| {{familytree | | | | | | | | | | |!| | | | | | | | }}
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| {{familytree | | | | | |,|-|-|-|-|+|-|-|-|-|.| | | }}
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| {{familytree | | | | | A01 | | | A02 | | | A03 | | | | |A01=Type 1 FHH|A02=Type 2 FHH|A03=Type 3 FHH}}
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| {{familytree | | | | | |!| | | | |!| | | | |!| | |A01=Type 1 FHH|A02=Type 2 FHH|A03=Type 3 FHH}}
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| {{familytree | | | | | B01 | | | B02 | | | B03 | | | | |B01=Mutations of the calcium-sensing receptor|B02=Mutation in the GNA11 gene|B03=Mutation in the AP2S1 gene}}
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| {{familytree/end}}
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| {| style="border: 0px; font-size: 90%; margin: 3px;" align="center"
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| | colspan="6" style="background: #4479BA; text-align: center;" | {{fontcolor|#FFF|'''Laboratory Findings of Familial Hypocalciuric Hypercalcemia'''}}
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| |+
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| ! colspan="1" rowspan="1" style="background: #4479BA; padding: 5px 5px;" | {{fontcolor|#FFFFFF|Condition}}
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| ! colspan="1" rowspan="1" style="background: #4479BA; padding: 5px 5px;" | {{fontcolor|#FFFFFF|PTH}}
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| ! colspan="1" rowspan="1" style="background: #4479BA; padding: 5px 5px;" | {{fontcolor|#FFFFFF|Serum Calcium}}
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| ! colspan="1" rowspan="1" style="background: #4479BA; padding: 5px 5px;" | {{fontcolor|#FFFFFF|Serum phosphate}}
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| ! colspan="1" rowspan="1" style="background: #4479BA; padding: 5px 5px;" | {{fontcolor|#FFFFFF|Urine Calcium}}
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| ! colspan="1" rowspan="1" style="background: #4479BA; padding: 5px 5px;" | {{fontcolor|#FFFFFF|Urine Calcium/Serum Creatinine Ratio}}
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| |-
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| | colspan="1" rowspan="1" style="background: #4479BA; padding: 5px 5px;" |{{fontcolor|#FFFFFF|Familial Hypocalciuric Hypercalcemia}}
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| | style="padding: 5px 5px; background: #F5F5F5;" | Normal
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| | style="padding: 5px 5px; background: #F5F5F5;" | Normal or ↑
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| | style="padding: 5px 5px; background: #F5F5F5;" | Normal
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| | style="padding: 5px 5px; background: #F5F5F5;" | ↓
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| | style="padding: 5px 5px; background: #F5F5F5;" | ↓
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| |-
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| | colspan="1" rowspan="1" style="background: #4479BA; padding: 5px 5px;" |{{fontcolor|#FFFFFF|Primary Hyperparathyroidism}}
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| | style="padding: 5px 5px; background: #F5F5F5;" | ↑
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| | style="padding: 5px 5px; background: #F5F5F5;" | ↑
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| | style="padding: 5px 5px; background: #F5F5F5;" | ↓
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| | style="padding: 5px 5px; background: #F5F5F5;" | Normal
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| | style="padding: 5px 5px; background: #F5F5F5;" | ↑
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| |}
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| https://academic.oup.com/labmed/article/41/11/683/2504912/Urine-Calcium-Laboratory-Measurement-and-Clinical?searchresult=1
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| ==Differentials==
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| Familial hypocalciuric hypercalcemia should be differentiated from other causes of hypercalcemia. Causes of hypercalcemia include:
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| Parathyroid-related
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| '''Hyperparathyroidism'''
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| -[[Primary hyperparathyroidism]]
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| [[Primary hyperparathyroidism|-Secondary hyperparathyroidism]]
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| [[Primary hyperparathyroidism|-Tertiary hyperparathyroidis]][[Primary hyperparathyroidism-Secondary hyperparathyroidism-Tertiary hyperparathyroidism|m]]
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| '''Non-parathyroid related'''
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| -Malignancy
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| -Humoral hypercalcemia of malignancy
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| -Osteolytic tumors
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| -Production of calcitriol by tumors
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| -Ectopic parathyroid hormone production
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| '''Medication-induced'''
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| -Thiazide diuretics
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| -Lithium
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| '''Other'''
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| -Nutritional
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| -Milk-alkali syndrome
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| -Vitamin D toxicity
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| -[[Granulomatous disease]]
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| -[[Sarcoidosis]]
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| -Surgical
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| -Immobilization
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| {| class="wikitable"
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| ! colspan="9" style="background: #4479BA; text-align: center;" |{{fontcolor|#FFF||Differential diagnosis of Familial Hypocalciuric Hypercalcemia on the basis of hypercalcemia}}
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| |-
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| ! colspan="2" rowspan="2" style="background: #7d7d7d; text-align: center;" |{{fontcolor|#FFF|Disorder}}
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| ! rowspan="2" style="background: #7d7d7d; text-align: center;" |{{fontcolor|#FFF|Mechanism of hypercalcemia}}
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| ! rowspan="2" style="background: #7d7d7d; text-align: center;" |{{fontcolor|#FFF|Clinical features}}
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| ! colspan="4" style="background: #7d7d7d; text-align: center;" |{{fontcolor|#FFF|Laboratory findings}}
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| ! rowspan="2" style="background: #7d7d7d; text-align: center;" |{{fontcolor|#FFF|Imaging & diagnostic modalities}}
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| |-
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| ! style="background: #7d7d7d; text-align: center;" |{{fontcolor|#FFF|PTH}}
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| ! style="background: #7d7d7d; text-align: center;" |{{fontcolor|#FFF|Calcium}}
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| ! style="background: #7d7d7d; text-align: center;" |{{fontcolor|#FFF|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="background: #F0FFFF; text-align: center;" |'''Familial hypocalciuric hypercalcemia'''
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| | style="background: #DCDCDC;" |
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| * This is a genetic disorder caused my mutation in calcium-sensing receptor gene.
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| | style="background: #DCDCDC;" |
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| * This is a benign condition and does not require treatment.
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| | style="background: #DCDCDC; text-align: center;" |Normal/↑
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| | style="background: #DCDCDC; text-align: center;" |Normal/↑
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| | style="background: #DCDCDC; text-align: center;" |
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| | style="background: #DCDCDC; text-align: center;" | --
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| | style="background: #DCDCDC;" |
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| * Calcium/creatinine clearance ratio
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| |-
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| | rowspan="3" style="background: #F0FFFF; text-align: center;" |'''Hyperparathyroidism'''
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| | style="background: #F0FFFF; text-align: center;" |Primary hyperparathyroidism
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| | style="background: #DCDCDC;" |Increase in [[secretion]] of [[parathyroid hormone]] (PTH) from a primary process in [[parathyroid gland]]. Parathyroid hormone causes increase in serum calcium.
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| | style="background: #DCDCDC;" |
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| * Usually asymptomatic
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| * Hypercalcemia detected on routine biochemical panel
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| | style="background: #DCDCDC; text-align: center;" |↑
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| | style="background: #DCDCDC; text-align: center;" |↑
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| | style="background: #DCDCDC; text-align: center;" |↓/Normal
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| | style="background: #DCDCDC; text-align: center;" |Normal/↑ calcitriol
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| | rowspan="3" style="background: #DCDCDC;" |Findings of bone resorption:
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| * X-ray
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| * DXA
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| Preoperative localization of hyperfunctioning parathyroid gland:
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| * Non-Invasive
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| ** Tc-99m sestamibi scintigraphy
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| ** Neck ultrasound
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| ** 4D-CT
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| ** SPET(P-SPECT)
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| ** PET
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| ** MRI
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| * Invasive:
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| ** Super sensitive venous sampling
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| ** Selective arteriography
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| ** Angiography
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| Predicting post-operative success:
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| * Intraoperative parathyroid hormone monitoring
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| |-
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| | style="background: #F0FFFF; text-align: center;" |Secondary hyperparathyroidism
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| | style="background: #DCDCDC;" |Increase in [[secretion]] of [[parathyroid hormone]] (PTH) from a secondary process. Parathyroid hormone causes increase in serum calcium.
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| | style="background: #DCDCDC;" |
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| * May present with history of:
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| ** Chronic renal failure
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| ** Vitamin D deficiency
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| | style="background: #DCDCDC; text-align: center;" |↑
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| | style="background: #DCDCDC; text-align: center;" |↓/Normal
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| | style="background: #DCDCDC; text-align: center;" |↑
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| | style="background: #DCDCDC; text-align: center;" | --
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| |-
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| | style="background: #F0FFFF; text-align: center;" |Tertiary hyperparathyroidism
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| | style="background: #DCDCDC;" |Continuous elevation of [[parathyroid hormone]] (PTH) even after successful treatment of the secondary cause of elevated parathyroid hormone. Parathyroid hormone causes increase in serum calcium.
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| | style="background: #DCDCDC;" |
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| * Usually present with history of:
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| ** Kidney transplant
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| * Usually hyperplasia of all four parathyroid glands
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| | style="background: #DCDCDC; text-align: center;" |↑
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| | style="background: #DCDCDC; text-align: center;" |↑
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| | style="background: #DCDCDC; text-align: center;" |↑
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| | style="background: #DCDCDC; text-align: center;" | --
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| |-
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| | rowspan="4" style="background: #F0FFFF; text-align: center;" |'''Malignancy'''<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>
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| | style="background: #F0FFFF; text-align: center;" |Humoral hypercalcemia of malignancy<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>
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| | style="background: #DCDCDC;" |Tumor cells secretes parathyroid hormone related protein (PTHrP) which has similar action as parathyroid hormone.
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| | style="background: #DCDCDC;" |
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| * Most common cause of malignancy related hypercalcemia.
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| * Usually present in solid tumors
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| | style="background: #DCDCDC; text-align: center;" | --
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| | style="background: #DCDCDC; text-align: center;" |↑
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| | style="background: #DCDCDC; text-align: center;" |↓/Normal
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| | style="background: #DCDCDC; text-align: center;" |↑ PTHrP
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| Normal/↑ calcitriol
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| | style="background: #DCDCDC;" |
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| * Chest X-ray
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| * CT scan
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| * MRI
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| |-
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| | style="background: #F0FFFF; text-align: center;" |Osteolytic tumors
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| | style="background: #DCDCDC;" |Multiple myeloma produces osteolysis of bones causing hypercalcemia. Osteolytic metastasis can cause bone resorption causing hypercalcemia.
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| | style="background: #DCDCDC;" |
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| * Most commonly present in multiple myeloma and breast cancer.
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| | style="background: #DCDCDC; text-align: center;" |↓
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| | style="background: #DCDCDC; text-align: center;" |↑
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| | style="background: #DCDCDC; text-align: center;" | --
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| | style="background: #DCDCDC; text-align: center;" | --
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| | style="background: #DCDCDC;" |
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| * DXA
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| * X-ray
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| * Mammography
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| * Ultrasound
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| * ESR
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| * Serum protein electrophoresis
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| |-
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| | style="background: #F0FFFF; text-align: center;" |Production of calcitirol
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| | style="background: #DCDCDC;" |Some tumors has ectopic activity of 1-alpha-hydroxylase leading to increased production of calcitriol. Calcitriol is active form of vitamin D and causes hypercalcemia.
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| | style="background: #DCDCDC;" |
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| * Most commonly present in lymphomas and in some ovarian germ cell tumors.
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| | style="background: #DCDCDC; text-align: center;" | --
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| | style="background: #DCDCDC; text-align: center;" |↑
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| | style="background: #DCDCDC; text-align: center;" | --
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| | style="background: #DCDCDC; text-align: center;" |↑ Calcitriol
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| | style="background: #DCDCDC;" |
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| * CT scan
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| * MRI
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| |-
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| | style="background: #F0FFFF; text-align: center;" |Ectopic parathyroid hormone<ref name="pmid16263810">{{cite journal |vauthors=VanHouten JN, Yu N, Rimm D, Dotto J, Arnold A, Wysolmerski JJ, Udelsman R |title=Hypercalcemia of malignancy due to ectopic transactivation of the parathyroid hormone gene |journal=J. Clin. Endocrinol. Metab. |volume=91 |issue=2 |pages=580–3 |year=2006 |pmid=16263810 |doi=10.1210/jc.2005-2095 |url=}}</ref>
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| | style="background: #DCDCDC;" |Some tumors leads to ectopic production of parathyroid hormone.
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| | style="background: #DCDCDC;" |
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| * In rare instances, small cell carcinoma of lung may produce hypercalcemia by this process.
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| | style="background: #DCDCDC; text-align: center;" |↑
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| | style="background: #DCDCDC; text-align: center;" |↑
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| | style="background: #DCDCDC; text-align: center;" |↓/Normal
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| | style="background: #DCDCDC; text-align: center;" |Normal/↑ Calcitriol
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| | style="background: #DCDCDC;" |
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| * Chest X-ray
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| * CT scan
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| * MRI
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| |-
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| | rowspan="2" style="background: #F0FFFF; text-align: center;" |'''Medication induced'''
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| | style="background: #F0FFFF; text-align: center;" |Lithium<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>
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| | style="background: #DCDCDC;" |Lithium lowers urinary calcium and causes hypercalcemia. Lithium has been reported to cause an increase in parathyroid hormones and enlargement if parathyroid gland after weeks to months of therapy.
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| | style="background: #DCDCDC;" |
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| * History of mood disorder
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| | style="background: #DCDCDC; text-align: center;" |↑
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| | style="background: #DCDCDC; text-align: center;" |↑
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| | style="background: #DCDCDC; text-align: center;" | --
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| | style="background: #DCDCDC; text-align: center;" | --
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| | style="background: #DCDCDC;" |
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| * Lithium levels
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| |-
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| | style="background: #F0FFFF; text-align: center;" |Thiazide diuretics
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| | style="background: #DCDCDC;" |Thiazide diuretics lowers urinary calcium excretion and causes hypercalcemia
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| | style="background: #DCDCDC;" |
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| * History of cardiac disorder
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| * Rarely causes hypercalcemia
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| | style="background: #DCDCDC; text-align: center;" | --
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| | style="background: #DCDCDC; text-align: center;" |↑
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| | style="background: #DCDCDC; text-align: center;" | --
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| | style="background: #DCDCDC; text-align: center;" | --
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| | style="background: #DCDCDC;" | --
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| |-
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| | rowspan="2" style="background: #F0FFFF; text-align: center;" |'''Nutritional'''
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| | style="background: #F0FFFF; text-align: center;" |Milk-alkali syndrome
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| | style="background: #DCDCDC;" |Hypercalcemia is be caused by high intake of calcium carbonate
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| | style="background: #DCDCDC;" |
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| * History of
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| ** High milk intake
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| ** Excess calcium intake for treating:
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| *** Osteoporosis
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| *** Dyspepsia
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| * May lead to metabolic alkalosis and renal insufficiency.
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| | style="background: #DCDCDC; text-align: center;" | --
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| | style="background: #DCDCDC; text-align: center;" |↑
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| | style="background: #DCDCDC; text-align: center;" | --
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| | style="background: #DCDCDC; text-align: center;" | --
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| | style="background: #DCDCDC;" |
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| * Renal function test
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| |-
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| | style="background: #F0FFFF; text-align: center;" |Vitamin D toxicity
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| | style="background: #DCDCDC;" |Excess vitamin D causes increased absorption of calcium from intestine causing hypercalcemia.
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| | style="background: #DCDCDC;" |
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| * History of:
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| ** Excess intake vitamin D
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| ** Excess milk fortified with vitamin D<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>
| |
| ** Topical application of vitamin D analogue analogue calcipotriol<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>
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| | style="background: #DCDCDC; text-align: center;" | --
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| | style="background: #DCDCDC; text-align: center;" |↑
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| | style="background: #DCDCDC; text-align: center;" | --
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| | style="background: #DCDCDC; text-align: center;" |↑ Vitamin D (calcidiol and/or calcitriol)
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| | style="background: #DCDCDC;" | --
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| |-
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| | style="background: #F0FFFF; text-align: center;" |'''Granulomatous disease'''
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| | style="background: #F0FFFF; text-align: center;" |Sarcoidosis<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>
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| | style="background: #DCDCDC;" |Hypercalcemia is causes by endogeous production of calcitriol by disease-activated macrophages.
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| | style="background: #DCDCDC;" |
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| * History of:
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| ** Cough
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| ** Dyspnea
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| ** Chest pain
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| ** Tiredness or weakness
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| ** Fever
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| ** Weight loss
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| | style="background: #DCDCDC; text-align: center;" | --
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| | style="background: #DCDCDC; text-align: center;" |↑
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| | style="background: #DCDCDC; text-align: center;" | --
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| | style="background: #DCDCDC; text-align: center;" |
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| * ↑ Calcitriol
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| * ↑ ACE levels
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| | style="background: #DCDCDC;" |
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| * Chest X-ray
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| * Biopsy
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| |}
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| * The complications associated with primary hyperparathyroidism, like osteopenia and nephrolithiasis, is not increased in persons with benign familial hypocalciuric hypercalcemia, and the rates are similar to those in the general population.
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| * Rarely, a severe form of this disease, neonatal severe primary hyperparathyroidism is seen in infants with homozygous CASR mutations.<ref name="pmid21478088">{{cite journal |vauthors=Varghese J, Rich T, Jimenez C |title=Benign familial hypocalciuric hypercalcemia |journal=Endocr Pract |volume=17 Suppl 1 |issue= |pages=13–7 |year=2011 |pmid=21478088 |doi=10.4158/EP10308.RA |url=}}</ref>
| |
| * Very rarely FHH is associated with<ref name="pmid7311809">{{cite journal |vauthors=Marx SJ, Attie MF, Levine MA, Spiegel AM, Downs RW, Lasker RD |title=The hypocalciuric or benign variant of familial hypercalcemia: clinical and biochemical features in fifteen kindreds |journal=Medicine (Baltimore) |volume=60 |issue=6 |pages=397–412 |year=1981 |pmid=7311809 |doi= |url=}}</ref><ref name="pmid3977197">{{cite journal |vauthors=Law WM, Heath H |title=Familial benign hypercalcemia (hypocalciuric hypercalcemia). Clinical and pathogenetic studies in 21 families |journal=Ann. Intern. Med. |volume=102 |issue=4 |pages=511–9 |year=1985 |pmid=3977197 |doi= |url=}}</ref><ref name="pmid2673770">{{cite journal |vauthors=Heath H |title=Familial benign (hypocalciuric) hypercalcemia. A troublesome mimic of mild primary hyperparathyroidism |journal=Endocrinol. Metab. Clin. North Am. |volume=18 |issue=3 |pages=723–40 |year=1989 |pmid=2673770 |doi= |url=}}</ref>
| |
| *Pancreatitis
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| *Chondrocalcinosis
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| *Gallstones
| |