Parathyroid disorders: Difference between revisions
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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]].<ref name=" | * 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> |
Revision as of 21:29, 10 October 2017
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. 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, 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 | ↑ | ↓ | ↑ |
|
Acrodysostosis type 2 | ↑ | ↓ | ↑ |
| |
Blomstrand chondrodysplasia | ↑ | ↓ | ↑ |
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.[1][3][4][5][6][7][8][9][10][11][12][13][14][15][16][17][18][19][20][21][22][23][24]
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 polyendocrinopathy syndrome or Isolated autoimmune hypoparathyroidism | Hypoparathyroidism related to other genetic causes | Other causes of hypoparathyroidism should bbe evaluted (for other causes of hypoparathyroidims, click here) | Sepsis | Acute pancreatitis | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
- ↑ 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.
- ↑ Marx SJ (2000). "Hyperparathyroid and hypoparathyroid disorders". N. Engl. J. Med. 343 (25): 1863–75. doi:10.1056/NEJM200012213432508. PMID 11117980.
- ↑ 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.
- ↑ 4.0 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.
- ↑ 5.0 5.1 Shoback D (2008). "Clinical practice. Hypoparathyroidism". N. Engl. J. Med. 359 (4): 391–403. doi:10.1056/NEJMcp0803050. PMID 18650515.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
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- ↑ 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.