Abstract
Secondary hyperparathyroidism (SHP) occurs in multiple disorders, most commonly renal and gastrointestinal disease, to defend against hypocalcemia and hyperphosphatemia. If such disorders are left untreated or are undertreated, chronic stimulation of parathyroid tissue may lead to parathyroid hyperplasia. Medical therapy to correct hypocalcemia or hyperphosphatemia or to directly suppress parathyroid gland growth usually corrects SHP. Occasionally, sufficient parathyroid cell mass is achieved such that even basal (i.e., suppressed) PTH production is in excess of requirements to correct hypocalcemia. Monoclonal expansion of chief cells with reduced expression of vitamin D and calcium-sensing receptors may also contribute to parathyroid autonomy and hypercalcemia that may ensue. This state, referred to as tertiary hyperparathyroidism (THP), may require surgical treatment as hypercalcemia may limit options for medical therapy. Pseudohypoparathyroidism (PHP) is an uncommon disorder characterized by resistance to PTH action leading to hypocalcemia, hyperphosphatemia, secondary elevations in PTH and, rarely, THP. In PHP, the medical and surgical approaches to THP must be carefully planned, given that normalization of PTH concentrations may not be desirable.
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References
Brown EM, Gamba G, Riccardi D, Lombardi M, Butters R, Kifor O, et al. Cloning and characterization of an extracellular Ca2+-sensing receptor from bovine parathyroid. Nature. 1993;366(6455):575–80.
Grant F, Conlin P, Brown E. Rate and concentration dependence of parathyroid hormone dynamics during stepwise changes in serum ionized calcium in normal humans. J Clin Endocrinol Metab. 1990;71:370–8.
Jüppner H, Gardella T, Brown E. Parathyroid hormone and parathyroid hormone-related peptide in the regulation of calcium homeostasis and bone development. In: DeGroot L, Jameson J, editors. Endocrinology: adult and pediatric. 7th ed. Philadelphia: Elsevier; 2015.
Goodman WG, Quarles LD. Development and progression of secondary hyperparathyroidism in chronic kidney disease: lessons from molecular genetics. Kidney Int. 2007;74:276–88.
Moallem E, Kilav R, Silver J, Naveh-Many T. RNA-protein binding and post-transcriptional regulation of parathyroid hormone gene expression by calcium and phosphate. J Biol Chem. 1998;273:5253–9.
Mallette LE. Synthetic human parathyroid hormone 1-34 fragment for diagnostic testing. Ann Intern Med. 1988;109:800–4.
Stone MD, Hosking DJ, Garcia-Himmelstine C, White DA, Rosenblum D, Worth HG. The renal response to exogenous parathyroid hormone in treated pseudohypoparathyroidism. Bone. 1993;14:727–35.
Ish-Shalom S, Rao LG, Levine MA, Fraser D, Kooh SW, Josse RG, et al. Normal parathyroid hormone responsiveness of bone-derived cells from a patient with pseudohypoparathyroidism. J Bone Miner Res. 1996;11:8–14.
Zvi F. Pseudohypohyperparathyroidism-pseudohypoparathyroidism type Ib. J Bone Miner Res. 1999;14:1016.
Tollin SR, Perlmutter S, Aloia JF. Serial changes in bone mineral density and bone turnover after correction of secondary hyperparathyroidism in a patient with pseudohypoparathyroidism type Ib. J Bone Miner Res. 2000;15:1412–6.
Park-Sigal J, Don BR, Porzig A, Recker R, Griswold V, Sebastian A, et al. Severe hypercalcemic hyperparathyroidism developing in a patient with hyperaldosteronism and renal resistance to parathyroid hormone. J Bone Miner Res. 2013;28:700–8.
Bleskestad IH, Bergrem H, Leivestad T, Gøransson LG. Intact parathyroid hormone levels in renal transplant patients with normal transplant function. Clin Transplant. 2011;25:E566–70.
Krause MW, Hedinger CE. Pathologic study of parathyroid glands in tertiary hyperparathyroidism. Hum Pathol. 1985;16:772–84.
Grzela T, Chudzinski W, Lasiecka Z, Niderla J, Wilczynski G, Gornicka B, et al. The calcium-sensing receptor and vitamin D receptor expression in tertiary hyperparathyroidism. Int J Mol Med. 2006;17:779–83.
Palmer SC, McGregor DO, Macaskill P, Craig JC, Elder GJ, Strippoli GFM. Meta-analysis: vitamin D compounds in chronic kidney disease. Ann Intern Med. 2007;147:840–53.
Zisman AL, Ghantous W, Schinleber P, Roberts L, Sprague SM. Inhibition of parathyroid hormone: a dose equivalency study of paricalcitol and doxercalciferol. Am J Nephrol. 2005;25:591–5.
Indridason OS, Quarles LD. Comparison of treatments for mild secondary hyperparathyroidism in hemodialysis patients. Kidney Int. 2000;57:282–92.
Lindberg JS, Moe SM, Goodman WG, Coburn JW, Sprague SM, Liu W, et al. The calcimimetic AMG 073 reduces parathyroid hormone and calcium x phosphorus in secondary hyperparathyroidism. Kidney Int. 2003;63:248–54.
Koizumi M, Komaba H, Nakanishi S, Fujimori A, Fukagawa M. Cinacalcet treatment and serum FGF23 levels in haemodialysis patients with secondary hyperparathyroidism. Nephrol Dial Transplant. 2012;27:784–90.
Pitt SC, Sippel RS, Chen H. Secondary and tertiary hyperparathyroidism, state of the art surgical management. Surg Clin North Am. 2009;89:1227–39.
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© 2016 Mayo Foundation for Medical Education and Research
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Kennel, K.A., Clarke, B.L. (2016). Tertiary Hyperparathyroidism. In: Kearns, A., Wermers, R. (eds) Hyperparathyroidism. Springer, Cham. https://doi.org/10.1007/978-3-319-25880-5_20
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DOI: https://doi.org/10.1007/978-3-319-25880-5_20
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