Pediatric Hypercalcemia Medication

  • Author: Ilene A Claudius, MD; Chief Editor: Stephen Kemp, MD, PhD   more...
 
Updated: Apr 3, 2012
 

Calcimimetic agents

Class Summary

These agents increase sensitivity of the calcium-sensing receptor to extracellular calcium by changing the configuration.

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Cinacalcet (Sensipar in the US, Mimpara in Europe)

 

Directly lowers iPTH levels by increasing sensitivity of calcium-sensing receptor on chief cell of parathyroid gland to extracellular calcium. Also results in concomitant decrease of serum calcium levels by affecting renal reabsorption. Indicated for secondary hyperparathyroidism in patients with chronic kidney disease. Pediatric data are limited.

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Loop diuretics

Class Summary

These augment urinary elimination.

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Furosemide (Lasix)

 

Used to induce calciuresis. First line for hypercalcemia with concomitant intense hydration. For IV dosing, diuretic effect begins within 5 min and peaks at 2 h.

Administer IV for emergency treatment of hypercalcemia.

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Bone-resorption inhibitors

Class Summary

These agents decrease serum calcium levels. They inhibit bone resorption and, thus, have a hypocalcemic effect. Used in the treatment of conditions associated with increased bone resorption, such as osteoporosis, Paget disease of bone, and management of hypercalcemia (especially that associated with malignancy). Recent reports have linked these medications with osteonecrosis of the jaw, delayed oral wound healing, and renal compromise.[9]

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Etidronate (Didronel)

 

Bisphosphonate that inhibits formation, growth, and dissolution of hydroxyapatite crystals by chemisorption to calcium phosphate surfaces; can be used IV short term or PO long term.

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Pamidronate (Aredia)

 

A bisphosphonate. Same mechanism as etidronate. Inhibits formation, growth, and dissolution of hydroxyapatite crystals by chemisorption to calcium phosphate surfaces. Only IV use is approved, although a few studies have attempted PO.

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Gallium nitrate (Ganite)

 

A naturally occurring heavy metal. The mechanism by which it inhibits calcium resorption from bone is unclear but may involve reducing increased bone turnover.

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Calcium-lowering hormones

Class Summary

These are secreted by the thyroid gland and help maintain calcium homeostasis by increasing calcium mineral stores in bone and increasing calcium renal excretion.

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Calcitonin (Calcimar, Miacalcin)

 

Acts primarily on bone but also on the kidney and GI tract to decrease serum calcium levels. Also lowers serum alkaline phosphatase levels by inhibiting bony turnover. Calcium-lowering effect begins 2 h after the first injection and lasts 6-8 h. The effect is maintained for 5-8 d.

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Contributor Information and Disclosures
Author

Ilene A Claudius, MD  Assistant Professor of Pediatrics, Division of Emergency Medicine, Children's Hospital, Los Angeles

Ilene A Claudius, MD is a member of the following medical societies: Alpha Omega Alpha

Disclosure: Nothing to disclose.

Coauthor(s)

Oved Fattal, MD  Staff Physician, Department of Pediatrics, Kaiser Permanente Medical Group

Oved Fattal, MD is a member of the following medical societies: American Academy of Pediatrics

Disclosure: Nothing to disclose.

Jon Nakamoto, MD  Consulting Staff, Department of Pediatric Endocrinology, Quest Diagnostics

Jon Nakamoto, MD is a member of the following medical societies: Alpha Omega Alpha

Disclosure: Nothing to disclose.

Pisit (Duke) Pitukcheewanont, MD  Associate Professor of Clinical Pediatrics, University of Southern California, Keck School of Medicine, Childrens Hospital Los Angeles

Pisit (Duke) Pitukcheewanont, MD is a member of the following medical societies: American Academy of Pediatrics, American Diabetes Association, American Medical Association, American Society for Bone and Mineral Research, Endocrine Society, and Pediatric Endocrine Society

Disclosure: Nothing to disclose.

Specialty Editor Board

Thomas A Wilson, MD  Professor of Clinical Pediatrics, Chief and Program Director, Division of Pediatric Endocrinology, Department of Pediatrics, The School of Medicine at Stony Brook University Medical Center

Thomas A Wilson, MD is a member of the following medical societies: Endocrine Society, Pediatric Endocrine Society, and Phi Beta Kappa

Disclosure: Nothing to disclose.

Mary L Windle, PharmD  Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

George P Chrousos, MD, FAAP, MACP, MACE, FRCP(London)  Professor and Chair, First Department of Pediatrics, Athens University Medical School, Aghia Sophia Children's Hospital, Greece; UNESCO Chair on Adolescent Health Care, University of Athens, Greece

George P Chrousos, MD, FAAP, MACP, MACE, FRCP(London) is a member of the following medical societies: American Academy of Pediatrics, American College of Endocrinology, American College of Physicians, American Pediatric Society, American Society for Clinical Investigation, Association of American Physicians, Endocrine Society, Pediatric Endocrine Society, and Society for Pediatric Research

Disclosure: Nothing to disclose.

Merrily P M Poth, MD  Professor, Department of Pediatrics and Neuroscience, Uniformed Services University of the Health Sciences

Merrily P M Poth, MD is a member of the following medical societies: American Academy of Pediatrics, Endocrine Society, and Pediatric Endocrine Society

Disclosure: Nothing to disclose.

Chief Editor

Stephen Kemp, MD, PhD  Professor, Department of Pediatrics, Section of Pediatric Endocrinology, University of Arkansas for Medical Sciences College of Medicine, Arkansas Children's Hospital

Stephen Kemp, MD, PhD is a member of the following medical societies: American Academy of Pediatrics, American Association of Clinical Endocrinologists, American Pediatric Society, Endocrine Society, Phi Beta Kappa, Southern Medical Association, and Southern Society for Pediatric Research

Disclosure: Nothing to disclose.

References

  1. [Guideline] Hawley C, Elder G. Calcium. Westmead NSW (Australia): CARI - Caring for Australasians with Renal Impairment; 2005 Oct. [Full Text].

  2. Vezzoli G, Soldati L, Gambaro G. Roles of calcium-sensing receptor (CaSR) in renal mineral ion transport. Curr Pharm Biotechnol. Apr 2009;10(3):302-10. [Medline].

  3. Hsu YH, Chen HI. Acute respiratory distress syndrome associated with hypercalcemia without parathyroid disorders. Chin J Physiol. Dec 2008;51(6):414-8. [Medline].

  4. Arico M, Egeler RM. Clinical aspects of Langerhans cell histiocytosis. Hematol Oncol Clin North Am. Apr 1998;12(2):247-58. [Medline].

  5. Bennett MT, Sirrs S, Yeung JK, Smith CA. Hypercalcemia due to all trans retinoic acid in the treatment of acute promyelocytic leukemia potentiated by voriconazole. Leuk Lymphoma. Dec 2005;46(12):1829-31. [Medline].

  6. Picolos MK, Lavis VR, Orlander PR. Milk-alkali syndrome is a major cause of hypercalcaemia among non-end-stage renal disease (non-ESRD) inpatients. Clin Endocrinol (Oxf). Nov 2005;63(5):566-76. [Medline].

  7. Gatti D, Viapiana O, Idolazzi L, Fracassi E, Adami S. Neridronic acid for the treatment of bone metabolic diseases. Expert Opin Drug Metab Toxicol. Oct 2009;5(10):1305-11. [Medline].

  8. Faggiano A, Tavares LB, Tauchmanova L, Milone F, Mansueto G, Ramundo V et al. Effect of treatment with depot somatostatin analogue octreotide on primary hyperparathyroidism in MEN1 patients. Clin Endocrinol. May 2008;Epub:[Medline].

  9. Landesberg R, Cozin M, Cremers S, Woo V, Kousteni S, Sinha S, et al. Inhibition of oral mucosal cell wound healing by bisphosphonates. J Oral Maxillofac Surg. May 2008;66(5):839-47. [Medline].

  10. Oski F, DeAngelis CD, Feigin RD. Principles and Practice of Pediatrics. 2nd ed. 1994.

  11. Barkin RM, Capto GL, Jaffe DM, eds. Pediatric Emergency Medicine: Concepts and Clinical Practice. 2nd ed. 1997.

  12. Beer TM, Javle M, Lam GN, et al. Pharmacokinetics and tolerability of a single dose of DN-101, a new formulation of calcitriol, in patients with cancer. Clin Cancer Res. Nov 1 2005;11(21):7794-9. [Medline].

  13. Behrman RE, Kliegman R, eds. Nelson Textbook of Pediatrics. 16th ed. WB Saunders Co; 2000.

  14. Benjamin RW, Moats-Staats BM, Calikoglu's A, Savendahl L, Chrysis D. Hypercalcemia in children. Pediatr Endocrinol Rev. Mar 2008;5(3):778-84. [Medline].

  15. Braverman LE. Werner and Ingbar's The Thyroid: A Fundamental and Clinical Text. 7th ed. 1997.

  16. Cheung M. Drugs used in paediatric bone and calcium disorders. Endocr Dev. 2009;16:218-232. [Medline].

  17. Cotran RS, Kumar V, Robbins SL. Pathologic Basis of Disease. 5th ed. 1994.

  18. Dambro MR. Griffith's 5 Minute Clinical Consult. Lippincott, Williams & Wilkins; 1999.

  19. Dong BJ. Cinacalcet: An oral calcimimetic agent for the management of hyperparathyroidism. Clin Ther. Nov 2005;27(11):1725-51. [Medline].

  20. Ellenhorn M. Ellenhorn's Medical Toxicology: Diagnosis and Treatment of Human Poisoning. 2nd ed. 1997.

  21. Feldman M, Sleisenger M, Scharschmidt BF, et al, eds. Sleisenger and Fordtran's Gastrointestinal and Liver Disease: Pathophysiology/Diagnosis/Management. 6th ed. WB Saunders Co; 1997.

  22. Guyton AC. Human Physiology and Mechanisms of Disease. 5th ed. 1992.

  23. Isselbacher KJ, Braunwald E, Wilson JD. Harrison's Principles of Internal Medicine. 13th ed. 1994.

  24. Lee GR, Foerster J, Lukens J, eds. Wintrobe's Clinical Hematology. 10th ed. 1999.

  25. Lteif AN, Zimmerman D. Bisphosphonates for treatment of childhood hypercalcemia. Pediatrics. Oct 1998;102(4 Pt 1):990-3. [Medline].

  26. Mosby. Mosby's GenRx. 10th ed. 1998.

  27. Mundy GR. Calcium Homeostasis: Hypercalcemia and Hypocalcemia. 1989.

  28. Muscheites J, Wigger M, Drueckler E, Fischer DC, Kundt G, Haffner D. Cinacalcet for secondary hyperparathyroidism in children with end-stage renal disease. Pediatr Nephrol. Oct 2008;23(10):1823-9. [Medline].

  29. Pizzo P, Poplack DG, eds. Principles and Practice of Pediatric Oncology. 3rd ed. 1996.

  30. Poon G. Cinacalcet hydrochloride (Sensipar). Proc (Bayl Univ Med Cent). Apr 2005;18(2):181-4. [Medline].

  31. Rakel R. Robert Conn's Current Therapy. WB Saunders Co; 1999.

  32. Robinson DM, Scott LJ. Spotlight on paricalcitol in secondary hyperparathyroidism. Treat Endocrinol. 2005;4(3):185-6. [Medline].

  33. Rockwood C, ed. Rockwood and Greens' Fractures in Adults. 4th ed. 1996.

  34. Rodd C, Goodyer P. Hypercalcemia of the newborn: etiology, evaluation, and management. Pediatr Nephrol. Aug 1999;13(6):542-7. [Medline].

  35. Shaw NJ, Bishop NJ. Bisphosphonate treatment of bone disease. Arch Dis Child. May 2005;90(5):494-9. [Medline].

  36. The Johns Hopkins Hospital. Harriet Lane Handbook: A Manual for Pediatric House Officers. 2000.

  37. Townsend C, ed. Sabiston Textbook of Surgery. 15th ed. 1997.

  38. Wallach J. Interpretation of Diagnostic Tests. 5th ed. 1992.

  39. Wilson J, ed. William's Textbook of Endocrinology. 1998.

  40. Yee YK, Chintalacharuvu SR, Lu J, Nagpal S. Vitamin D receptor modulators for inflammation and cancer. Mini Rev Med Chem. Aug 2005;5(8):761-78. [Medline].

  41. Zisman AL, Ghantous W, Schinleber P, et al. Inhibition of parathyroid hormone: a dose equivalency study of paricalcitol and doxercalciferol. Am J Nephrol. Nov-Dec 2005;25(6):591-5. [Medline].

 
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Investigations flowchart.
Table 1
Laboratory Test Reference Range Normal Response to Increased Calcium
Serum calcium8.5-10.2 mg/dLNA
Ionized calcium1-1.3 mmol/LNA
PTH (intact)10-55 pg/mL*Decrease
Serum phosphateAge-dependentIncrease
1,25-dihydroxyvitamin D36-108 pmol/LDecrease
Alkaline phosphatase68-217 U/LNormal
Urine calcium4 mg/kg/dIncrease
Urine Ca/Cr ratioSee note†Increase
Urine cAMP‡< 5 molDecrease
*Note that 1 mmol/L equals 4 mg/dL. †In infants younger than 7 months, the reference range is less than 0.86; in infants aged 7-18 months, the reference range is less than 0.6. By age 6-7 years, the adult reference range of less than 0.21 is reached.‡The urine cAMP level generally parallels the PTH level.
Table 2
Condition Serum Phosphorus Serum Alkaline Phosphatase Urine Calcium Urine Phosphate PTH
HyperparathyroidismLowNormal-highHigh*HighHigh
Vitamin D excessNormal-highLowHighHigh
MalignancyOften lowHigh † VariableHigh
Granulomatous diseaseNormal-highNormal-highHighNormal
Milk alkali syndromeNormal-highNormalNormalNormal
FHHNormal or lowNormalLow (< 200mg/d)NormalLow
*67% of the time



† Except hematologic malignancies, in which alkaline phosphatase is normal



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