Hyper- and Hypocalcemia

作者: Benjamin Z. Leder , Joel S. Finkelstein

DOI: 10.1007/978-1-59259-293-7_12

关键词: HomeostasisCalciumChemistryParathyroid hormoneCalcitoninInternal medicineParathyroid glandCalcium metabolismHormoneBlood proteinsEndocrinology

摘要: Abnormalities in circulating levels of calcium are commonly encountered by the internist and endocrinologist. Ninety-nine percent body’s is found bone, with remaining fraction either extracellular or intracellular compartments all other tissues. Approximately half blood bound to serum proteins, but it nonbound (or ionized calcium) that tightly controlled homeostatic hormones. The role many cellular functions, including excitation nerves muscle contraction (including myocardium), directly relates symptoms both its excess insufficiency circulation. Because physiologic importance maintaining concentration a tight range, feedback loop controls homeostasis highly sensitive (Fig. 1). two main regulatory hormones parathyroid hormone (PTH) 1,25(OH)2 vitamin D. Calcitonin’s human physiology less clear. Similarly, role, if any, PTH-related protein (the peptide responsible for humoral hypercalcemia malignancy) normal has not yet been elucidated.

参考文章(37)
Janet Walls, Wendy A. Ratcliffe, A. Howell, N. J. Bundred, Parathyroid hormone and parathyroid hormone‐related protein in the investigation of hypercalcaemia in two hospital populations Clinical Endocrinology. ,vol. 41, pp. 407- 413 ,(1994) , 10.1111/J.1365-2265.1994.TB02569.X
Fredriech K.W. Chan, Lilia M.C. Koberle, Susan Thys-Jacobs, John P. Bilezikian, Differential diagnosis, causes, and management of hypercalcemia Current Problems in Surgery. ,vol. 34, pp. 445- 523 ,(1997) , 10.1016/S0011-3840(97)80008-1
P. L. Selby, M. Davies, J. S. Marks, E. B. Mawer, Vitamin D intoxication causes hypercalcaemia by increased bone resorption which responds to pamidronate Clinical Endocrinology. ,vol. 43, pp. 531- 536 ,(1995) , 10.1111/J.1365-2265.1995.TB02916.X
Jeffrey S. Flier, Lisa H. Underhill, Arthur E. Broadus, Marguerite Mangin, Kyoji Ikeda, Karl L. Insogna, Eleanor C. Weir, William J. Burtis, Andrew F. Stewart, Humoral Hypercalcemia of Cancer The New England Journal of Medicine. ,vol. 319, pp. 556- 563 ,(1988) , 10.1056/NEJM198809013190906
ROBERT K. RUDE, SUSAN B. OLDHAM, FREDERICK R. SINGER, FUNCTIONAL HYPOPARATHYROIDISM AND PARATHYROID HORMONE END‐ORGAN RESISTANCE IN HUMAN MAGNESIUM DEFICIENCY Clinical Endocrinology. ,vol. 5, pp. 209- 224 ,(1976) , 10.1111/J.1365-2265.1976.TB01947.X
P. M. J. McSHEEHY, T. J. CHAMBERS, Osteoblastic cells mediate osteoclastic responsiveness to parathyroid hormone. Endocrinology. ,vol. 118, pp. 824- 828 ,(1986) , 10.1210/ENDO-118-2-824
J. H. Friedman, M. I. Chiucchini, J. R. Tucci, Idiopathic hypoparathyroidism with extensive brain calcification and persistent neurologic dysfunction Neurology. ,vol. 37, pp. 307- 307 ,(1987) , 10.1212/WNL.37.2.307
A. Carter, C. Bardin, R. Collins, C. Simons, P. Bray, A. Spiegel, Reduced expression of multiple forms of the alpha subunit of the stimulatory GTP-binding protein in pseudohypoparathyroidism type Ia. Proceedings of the National Academy of Sciences of the United States of America. ,vol. 84, pp. 7266- 7269 ,(1987) , 10.1073/PNAS.84.20.7266
Martin R. Pollak, Edward M. Brown, Herschel L. Estep, Peter N. McLaine, Olga Kifor, Ji Park, Steven C. Hebert, Christine E. Seidman, J. G. Seidman, Autosomal dominant hypocalcaemia caused by a Ca 2+ -sensing receptor gene mutation Nature Genetics. ,vol. 8, pp. 303- 307 ,(1994) , 10.1038/NG1194-303