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Immunoendocrinology: Scientific and Clinical Aspects pp 501–517Cite as

Hypoparathyroidism

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Part of the book series: Contemporary Endocrinology ((COE))

Abstract

Hypoparathyroidism is an important component of the differential diagnosis of hypocalcemia. It refers to a heterogeneous group of disorders that have in common a relative or absolute deficiency in the quantity of secreted parathyroid hormone (PTH) or in its peripheral actions. The disorder may be due to iatrogenic, infiltrative, developmental, signaling, autoimmune, or genetic abnormalities, which make etiological differentiation important as this has implications for diagnosis, therapy, counseling, and prevention of complications. Autoimmunity is an important cause of hypoparathyroidism, either as an isolated endocrinopathy or as a component of autoimmune polyglandular syndromes (e.g., APS1 and 2, and in some classifications, 3 and 4) (1, 2) with a prevalence ranging from 1:600 to 1:90,000 (2, 3).

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References

  1. Betterle C. Parathyroid and autoimmunity. Ann Endocrinol (Paris). 2006;67:147–154.

    Article  CAS  Google Scholar 

  2. Whyte MP. Autoimmune hypoparathyroidism. In: Bilezikian JP, Marcus R, Levine MA, eds. The Parathyroids. 2nd ed. San Diego: Academic Press. 2001;791–805.

    Chapter  Google Scholar 

  3. Myhre AG, Halonen M, Eskelin P, Ekwall O, Hedstrand H, Rorsman F, et al. Autoimmune polyendocrine syndrome type 1 (APS I) in Norway. Clin Endocrinol (Oxf). 2001;54:211–217.

    Article  CAS  Google Scholar 

  4. Irvine WJ, Scarth L. Antibody to the oxyphil cells of the human parathyroid in idiopathic hypoparathyroidism. Clin Exp Immunol. 1969;4:505–510.

    PubMed  CAS  Google Scholar 

  5. Betterle C, Caretto A, Zeviani M, Pedini B, Salviati C. Demonstration and characterization of anti-human mitochondria autoantibodies in idiopathic hypoparathyroidism and in other conditions. Clin Exp Immunol. 1985;62:353–360.

    PubMed  CAS  Google Scholar 

  6. Posillico JT, Wortsman J, Srikanta S, Eisenbarth GS, Mallette LE, Brown EM. Parathyroid cell surface autoantibodies that inhibit parathyroid hormone secretion from dispersed human parathyroid cells. J Bone Miner Res. 1986;1:475–483.

    Article  PubMed  CAS  Google Scholar 

  7. Brandi ML, Aurbach GD, Fattorossi A, Quarto R, Marx SJ, Fitzpatrick LA. Antibodies cytotoxic to bovine parathyroid cells in autoimmune hypoparathyroidism. Proc Natl Acad Sci U S A. 1986;83:8366–8369.

    Article  PubMed  CAS  Google Scholar 

  8. Fattorossi A, Aurbach GD, Sakaguchi K, Cama A, Marx SJ, Streeten EA, et al. Anti-endothelial cell antibodies: detection and characterization in sera from patients with autoimmune hypoparathyroidism. Proc Natl Acad Sci U S A. 1988;85:4015–4019.

    Article  PubMed  CAS  Google Scholar 

  9. Alimohammadi M, Bjorklund P, Hallgren A, Pontynen N, Szinnai G, Shikama N, et al. Autoimmune polyendocrine syndrome type 1 and NALP5, a parathyroid autoantigen. N Engl J Med. 2008;358:1018–1028.

    Article  PubMed  CAS  Google Scholar 

  10. Kifor O, McElduff A, LeBoff MS, Moore FD, Jr., Butters R, Gao P, et al. Activating antibodies to the calcium-sensing receptor in two patients with autoimmune hypoparathyroidism. J Clin Endocrinol Metab. 2004;89:548–556.

    Article  PubMed  CAS  Google Scholar 

  11. Goswami R, Brown EM, Kochupillai N, Gupta N, Rani R, Kifor O, et al. Prevalence of calcium sensing receptor autoantibodies in patients with sporadic idiopathic hypoparathyroidism. Eur J Endocrinol. 2004;150:9–18.

    Article  PubMed  CAS  Google Scholar 

  12. Kifor O, Moore FD, Jr., Delaney M, Garber J, Hendy GN, Butters R, et al. A syndrome of hypocalciuric hypercalcemia caused by autoantibodies directed at the calcium-sensing receptor. J Clin Endocrinol Metab. 2003;88:60–72.

    Article  PubMed  CAS  Google Scholar 

  13. Leonard M. Chronic Idiopathic hypoparathyroidism with superimposed Addison’s disease in a child. J Clin Endocrinol Metab. 1946;6:493–506.

    Article  PubMed  CAS  Google Scholar 

  14. Craig J, Schiff L, Boone J. Chronic Moniliasis associated with Addison’s disease. Am J Dis Child. 1955;89:669–684.

    CAS  Google Scholar 

  15. Whitaker L, Landing B, Esselborn V, Williams R. The syndrome of familial juvenile hypoadrenocorticism and superficial moniliasis. J Clin Endocrinol Metab. 1956;16:1374–1387.

    Article  PubMed  Google Scholar 

  16. Blizzard RM, Chee D, Davis W. The incidence of parathyroid and other antibodies in the sera of patients with idiopathic hypoparathyroidism. Clin Exp Immunol. 1966;1:119–128.

    PubMed  CAS  Google Scholar 

  17. Swana GT, Swana MR, Bottazzo GF, Doniach D. A human-specific mitochondrial antibody its importance in the identification of organ-specific reactions. Clin Exp Immunol. 1977;28:517–525.

    PubMed  CAS  Google Scholar 

  18. Li Y, Song YH, Rais N, Connor E, Schatz D, Muir A, et al. Autoantibodies to the extracellular domain of the calcium sensing receptor in patients with acquired hypoparathyroidism. J Clin Invest. 1996;97:910–914.

    Article  PubMed  CAS  Google Scholar 

  19. Mayer A, Ploix C, Orgiazzi J, Desbos A, Moreira A, Vidal H, et al. Calcium-sensing receptor autoantibodies are relevant markers of acquired hypoparathyroidism. J Clin Endocrinol Metab. 2004;89:4484–4488.

    Article  PubMed  CAS  Google Scholar 

  20. Gavalas NG, Kemp EH, Krohn KJ, Brown EM, Watson PF, Weetman AP. The calcium-sensing receptor is a target of autoantibodies in patients with autoimmune polyendocrine syndrome type 1. J Clin Endocrinol Metab. 2007;92:2107–2114.

    Article  PubMed  CAS  Google Scholar 

  21. Soderbergh A, Myhre AG, Ekwall O, Gebre-Medhin G, Hedstrand H, Landgren E, et al. Prevalence and clinical associations of 10 defined autoantibodies in autoimmune polyendocrine syndrome type I. J Clin Endocrinol Metab. 2004;89:557–562.

    Article  PubMed  Google Scholar 

  22. Gylling M, Kaariainen E, Vaisanen R, Kerosuo L, Solin ML, Halme L, et al. The hypoparathyroidism of autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy protective effect of male sex. J Clin Endocrinol Metab. 2003;88:4602–4608.

    Article  PubMed  CAS  Google Scholar 

  23. Hauache OM. Extracellular calcium-sensing receptor: structural and functional features and association with diseases. Braz J Med Biol Res. 2001;34:577–584.

    Article  PubMed  CAS  Google Scholar 

  24. Egbuna OI, Brown EM. Hypercalcaemic and hypocalcaemic conditions due to calcium-sensing receptor mutations. Best Pract Res Clin Rheumatol. 2008;22:129–148.

    Article  PubMed  CAS  Google Scholar 

  25. Makita N, Sato J, Manaka K, Shoji Y, Oishi A, Hashimoto M, et al. An acquired hypocalciuric hypercalcemia autoantibody induces allosteric transition among active human Ca-sensing receptor conformations. Proc Natl Acad Sci U S A. 2007;104:5443–5448.

    Article  PubMed  CAS  Google Scholar 

  26. Pallais JC, Kifor O, Chen YB, Slovik D, Brown EM. Acquired hypocalciuric hypercalcemia due to autoantibodies against the calcium-sensing receptor. N Engl J Med. 2004;351:362–369.

    Article  PubMed  CAS  Google Scholar 

  27. Bjerneroth G, Juhlin C, Gudmundsson S, Rastad J, Akerstrom G, Klareskog L. Major histocompatibility complex class II expression and parathyroid autoantibodies in primary hyperparathyroidism. Surgery. 1998;124:503–509.

    Article  PubMed  CAS  Google Scholar 

  28. Campbell JM, Knutsen AP, Becker BA. A 39-year-old father is diagnosed in adulthood as having partial DiGeorge anomaly with a combined T- and B-cell immunodeficiency after diagnosis of the condition in his daughter. Ann Allergy Asthma Immunol. 2008;100:620–621.

    Article  PubMed  Google Scholar 

  29. Keppen LD, Fasules JW, Burks AW, Gollin SM, Sawyer JR, Miller CH. Confirmation of autosomal dominant transmission of the DiGeorge malformation complex. J Pediatr. 1988;113:506–508.

    Article  PubMed  CAS  Google Scholar 

  30. Bowl MR, Nesbit MA, Harding B, Levy E, Jefferson A, Volpi E, et al. An interstitial deletion-insertion involving chromosomes 2p25.3 and Xq27.1, near SOX3, causes X-linked recessive hypoparathyroidism. J Clin Invest. 2005;115:2822–2831.

    Article  PubMed  CAS  Google Scholar 

  31. AndrewNesbit M, Bowl MR, Harding B, Schlessinger D, Whyte MP, Thakker RV. X-linked hypoparathyroidism region on Xq27 is evolutionarily conserved with regions on 3q26 and 13q34 and contains a novel P-type ATPase. Genomics. 2004;84:1060–1070.

    Article  PubMed  CAS  Google Scholar 

  32. Trump D, Dixon PH, Mumm S, Wooding C, Davies KE, Schlessinger D, et al. Localisation of X linked recessive idiopathic hypoparathyroidism to a 1.5 Mb region on Xq26-q27. J Med Genet. 1998;35:905–909.

    Article  PubMed  CAS  Google Scholar 

  33. Shoback D. Clinical practice. Hypoparathy-roidism. N Engl J Med. 2008;359:391–403.

    Article  PubMed  CAS  Google Scholar 

  34. Mannstadt M, Bertrand G, Muresan M, Weryha G, Leheup B, Pulusani SR, et al. Dominant-negative GCMB mutations cause an autosomal dominant form of hypoparathyroidism. J Clin Endocrinol Metab. 2008;93:3568–3576.

    Article  PubMed  CAS  Google Scholar 

  35. Thomee C, Schubert SW, Parma J, Le PQ, Hashemolhosseini S, Wegner M, et al. GCMB mutation in familial isolated hypoparathyroidism with residual secretion of parathyroid hormone. J Clin Endocrinol Metab. 2005;90:2487–2492.

    Article  PubMed  CAS  Google Scholar 

  36. Ding C, Buckingham B, Levine MA. Familial isolated hypoparathyroidism caused by a mutation in the gene for the transcription factor GCMB. J Clin Invest. 2001;108:1215–1220.

    PubMed  CAS  Google Scholar 

  37. Canaff L, Zhou X, Mosesova I, Cole DE, Hendy GN. Glial Cells Missing-2 (GCM2) transactivates the calcium-sensing receptor gene: effect of a dominant-negative GCM2 mutant associated with autosomal dominant hypoparathyroidism. Hum Mutat. 2009; 30(1):85–92.

    Article  PubMed  CAS  Google Scholar 

  38. Sunthornthepvarakul T, Churesigaew S, Ngowngarmratana S. A novel mutation of the signal peptide of the preproparathyroid hormone gene associated with autosomal recessive familial isolated hypoparathyroidism. J Clin Endocrinol Metab. 1999;84:3792–3796.

    Article  PubMed  CAS  Google Scholar 

  39. Arnold A, Horst SA, Gardella TJ, Baba H, Levine MA, Kronenberg HM. Mutation of the signal peptide-encoding region of the preproparathyroid hormone gene in familial isolated hypoparathyroidism. J Clin Invest. 1990;86:1084–1087.

    Article  PubMed  CAS  Google Scholar 

  40. Parkinson DB, Thakker RV. A donor splice site mutation in the parathyroid hormone gene is associated with autosomal recessive hypoparathyroidism. Nat Genet. 1992;1:149–152.

    Article  PubMed  CAS  Google Scholar 

  41. Chen CJ, Anast CS, Posillico JT, Brown EM. Effects of extracellular calcium and magnesium on cytosolic calcium concentration in fura-2-loaded bovine parathyroid cells. J Bone Miner Res. 1987;2:319–327.

    Article  PubMed  CAS  Google Scholar 

  42. Wei M, Esbaei K, Bargman JM, Oreopoulos DG. Inverse correlation between serum magnesium and parathyroid hormone in peritoneal dialysis patients: a contributing factor to adynamic bone disease? Int Urol Nephrol. 2006;38:317–322.

    Article  PubMed  CAS  Google Scholar 

  43. Navarro JF, Mora C, Macia M, Garcia J. Serum magnesium concentration is an independent predictor of parathyroid hormone levels in peritoneal dialysis patients. Perit Dial Int. 1999;19:455–461.

    PubMed  CAS  Google Scholar 

  44. Donovan EF, Tsang RC, Steichen JJ, Strub RJ, Chen IW, Chen M. Neonatal hypermagnesemia: effect on parathyroid hormone and calcium homeostasis. J Pediatr. 1980;96:305–310.

    Article  PubMed  CAS  Google Scholar 

  45. Quitterer U, Hoffmann M, Freichel M, Lohse MJ. Paradoxical block of parathormone secretion is mediated by increased activity of G alpha subunits. J Biol Chem. 2001;276:6763–6769.

    Article  PubMed  CAS  Google Scholar 

  46. Wade JS, Fourman P, Deane L. Recovery of parathyroid function in patients with “transient” hypoparathyroidism after thyroidectomy. Br J Surg. 1965;52:493–496.

    Article  PubMed  CAS  Google Scholar 

  47. Mora-Fernandez C, Navarro JF. PTH decrease after radioiodine treatment in a patient with end-stage renal disease. Clin Nephrol. 1999;52(5):337–338.

    PubMed  CAS  Google Scholar 

  48. O’Regan S, Carson S, Chesney RW, Drummond KN. Electrolyte and acid-base disturbances in the management of leukemia. Blood. 1977;49(3):345–353.

    PubMed  Google Scholar 

  49. Wadler S, Haynes H, Beitler JJ, Goldberg G, Holland JF, Hochster H, et al. Management of hypocalcemic effects of WR2721 administered on a daily times five schedule with cisplatin and radiation therapy. The New York Gynecologic Oncology Group. J Clin Oncol. 1993;11(8):1517–1522.

    PubMed  CAS  Google Scholar 

  50. Koiwa F, Kakuta T, Tanaka R, Yumita S. Efficacy of percutaneous ethanol injection therapy (PEIT) is related to the number of parathyroid glands in haemodialysis patients with secondary hyperparathyroidism. Nephrol Dial Transplant. 2007;22(2):522–528.

    Article  PubMed  CAS  Google Scholar 

  51. Vamvakas S, Teschner M, Bahner U, Heidland A. Alcohol abuse: potential role in electrolyte disturbances and kidney diseases. Clin Nephrol. 1998;49(4):205–213.

    PubMed  CAS  Google Scholar 

  52. Laitinen K, Lamberg-Allardt C, Tunninen R, Karonen SL, Tahtela R, Ylikahri R, et al. Transient hypoparathyroidism during acute alcohol intoxication. N Engl J Med. 1991;324(11):721–727.

    Article  PubMed  CAS  Google Scholar 

  53. Multicentre study on prevalence of endocrine complications in thalassaemia major. Italian Working Group on Endocrine Complications in Non-endocrine Diseases. Clin Endocrinol (Oxf). 1995;42(6):581–586.

    Google Scholar 

  54. Carpenter TO, Carnes DL, Jr., Anast CS. Hypoparathyroidism in Wilson’s disease. N Engl J Med. 1983;309(15):873–877.

    Article  PubMed  CAS  Google Scholar 

  55. Lienhardt A, Bai M, Lagarde JP, Rigaud M, Zhang Z, Jiang Y, et al. Activating mutations of the calcium-sensing receptor: management of hypocalcemia. J Clin Endocrinol Metab. 2001;86(11):5313–5323.

    Article  PubMed  CAS  Google Scholar 

  56. Pollak MR, Brown EM, Estep HL, McLaine PN, Kifor O, Park J, et al. Autosomal dominant hypocalcaemia caused by a Ca(2+)-sensing receptor gene mutation. Nat Genet 1994;8(3):303–307.

    Article  PubMed  CAS  Google Scholar 

  57. Finegold DN, Armitage MM, Galiani M, Matise TC, Pandian MR, Perry YM, et al. Preliminary localization of a gene for autosomal dominant hypoparathyroidism to chromosome 3q13. Pediatr Res. 1994;36(3):414–417.

    Article  PubMed  CAS  Google Scholar 

  58. Lienhardt A, Garabedian M, Bai M, Sinding C, Zhang Z, Lagarde JP, et al. A large homozygous or heterozygous in-frame deletion within the calcium-sensing receptor’s carboxylterminal cytoplasmic tail that causes autosomal dominant hypocalcemia. J Clin Endocrinol Metab. 2000;85(4):1695–1702.

    Article  PubMed  CAS  Google Scholar 

  59. Albright F, Burnett C, Smith P. Pseudohypoparathyroidism: an example of ‘Seabright-Bantam syndrome’. Endocrinology. 1942;30:922–932.

    CAS  Google Scholar 

  60. Tashjian AH, Jr., Frantz AG, Lee JB. Pseudohypoparathyroidism: assays of parathyroid hormone and thyrocalcitonin. Proc Natl Acad Sci U S A. 1966;56(4):1138–1142.

    Article  PubMed  CAS  Google Scholar 

  61. Chase LR, Melson GL, Aurbach GD. Pseudohypoparathyroidism: defective excretion of 3′,5′-AMP in response to parathyroid hormone. J Clin Invest. 1969;48(10):1832–1844.

    Article  PubMed  CAS  Google Scholar 

  62. Spiegel AM, Levine MA, Aurbach GD, Downs RW, Jr., Marx SJ, Lasker RD, et al. Deficiency of hormone receptor-adenylate cyclase coupling protein: basis for hormone resistance in pseudohypoparathyroidism. Am J Physiol. 1982;243(1):E37–E42.

    PubMed  CAS  Google Scholar 

  63. Levine MA, Ahn TG, Klupt SF, Kaufman KD, Smallwood PM, Bourne HR, et al. Genetic deficiency of the alpha subunit of the guanine nucleotide-binding protein Gs as the molecular basis for Albright hereditary osteodystrophy. Proc Natl Acad Sci U S A. 1988;85(2):617–621.

    Article  PubMed  CAS  Google Scholar 

  64. Schwindinger WF, Miric A, Zimmerman D, Levine MA. A novel Gs alpha mutant in a patient with Albright hereditary osteodystrophy uncouples cell surface receptors from adenylyl cyclase. J Biol Chem. 1994;269(41):25387–25391.

    PubMed  CAS  Google Scholar 

  65. Carter A, Bardin C, Collins R, Simons C, Bray P, Spiegel A. Reduced expression of multiple forms of the alpha subunit of the stimulatory GTP-binding protein in pseudohypoparathyroidism type Ia. Proc Natl Acad Sci USA. 1987;84(20):7266–7269.

    Article  PubMed  CAS  Google Scholar 

  66. Davies SJ, Hughes HE. Imprinting in Albright’s hereditary osteodystrophy. J Med Genet. 1993;30(2):101–103.

    Article  PubMed  CAS  Google Scholar 

  67. Liu J, Nealon JG, Weinstein LS. Distinct patterns of abnormal GNAS imprinting in familial and sporadic pseudohypoparathyroidism type IB. Hum Mol Genet. 2005;14(1):95–102.

    Article  PubMed  CAS  Google Scholar 

  68. Yu S, Yu D, Lee E, Eckhaus M, Lee R, Corria Z, et al. Variable and tissue-specific hormone resistance in heterotrimeric Gs protein alpha-subunit (Gsalpha) knockout mice is due to tissue-specific imprinting of the gsalpha gene. Proc Natl Acad Sci USA. 1998;95(15):8715–8720.

    Article  PubMed  CAS  Google Scholar 

  69. Hayward BE, Kamiya M, Strain L, Moran V, Campbell R, Hayashizaki Y, et al. The human GNAS1 gene is imprinted and encodes distinct paternally and biallelically expressed G proteins. Proc Natl Acad Sci USA. 1998;95(17):10038–10043.

    Article  PubMed  CAS  Google Scholar 

  70. Wroe SF, Kelsey G, Skinner JA, Bodle D, Ball ST, Beechey CV, et al. An imprinted transcript, antisense to Nesp, adds complexity to the cluster of imprinted genes at the mouse Gnas locus. Proc Natl Acad Sci USA. 2000;97(7):3342–3346.

    Article  PubMed  CAS  Google Scholar 

  71. Shalitin S, Davidovits M, Lazar L, Weintrob N. Clinical heterogeneity of pseudohypoparathyroidism: from hyper- to hypocalcemia. Horm Res. 2008;70(3):137–144.

    Article  PubMed  CAS  Google Scholar 

  72. Levine MA. Pseudohypoparathyroidism: from bedside to bench and back. J Bone Miner Res. 1999;14(8):1255–1260.

    Article  PubMed  CAS  Google Scholar 

  73. Weinstein LS, Yu S, Warner DR, Liu J. Endocrine manifestations of stimulatory G protein alpha-subunit mutations and the role of genomic imprinting. Endocr Rev. 2001;22(5):675–705.

    Article  PubMed  CAS  Google Scholar 

  74. Weinstein LS, Liu J, Sakamoto A, Xie T, Chen M. Minireview: GNAS: normal and abnormal functions. Endocrinology. 2004;145(12):5459–5464.

    Article  PubMed  CAS  Google Scholar 

  75. Juppner H, Bastepe M. Different mutations within or upstream of the GNAS locus cause distinct forms of pseudohypoparathyroidism. J Pediatr Endocrinol Metab. 2006;19(Suppl 2):641–646.

    PubMed  CAS  Google Scholar 

  76. Lania A, Mantovani G, Spada A. G protein mutations in endocrine diseases. Eur J Endocrinol. 2001;145(5):543–559.

    Article  PubMed  CAS  Google Scholar 

  77. Bringhurst FR, Demay MB, Kronenberg HM. Hormones and disorders of mineral metabolism. In: Wilson JD, Foster DW, Kronenberg HM, Larsen PR, eds. Williams Textbook of Endocrinology. 9th ed. Philadelphia: W.B. Saunders. 1998;1155–1209.

    Google Scholar 

  78. Winer KK, Ko CW, Reynolds JC, Dowdy K, Keil M, Peterson D, et al. Long-term treatment of hypoparathyroidism: a randomized controlled study comparing parathyroid hormone-(1-34) versus calcitriol and calcium. J Clin Endocrinol Metab. 2003;88(9):4214–4220.

    Article  PubMed  CAS  Google Scholar 

  79. Nemeth EF. Calcimimetic and calcilytic drugs: just for parathyroid cells? Cell Calcium. 2004;35(3):283–289.

    Article  PubMed  CAS  Google Scholar 

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Acknowledgments

Ogo Egbuna is supported by an NIH career development award DK076733, and Edward Brown is supported by NIH grant, DK078331.

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  1. Endocrinology Department, Brigham and Women’s Hospital, Boston, MA, USA

    Ogo I. Egbuna

  2. Division of Endocrinology, Diabetes and Hypertension, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, MA, USA

    Edward M. Brown

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  1. Health Sciences Center, Children's Hospital, University of Colorado, East 9th Avenue 4200, Denver, 80262, Colorado, USA

    George S. Eisenbarth

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Egbuna, O.I., Brown, E.M. (2011). Hypoparathyroidism. In: Eisenbarth, G. (eds) Immunoendocrinology: Scientific and Clinical Aspects. Contemporary Endocrinology. Humana Press, Totowa, NJ. https://doi.org/10.1007/978-1-60327-478-4_30

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