Exp Clin Endocrinol Diabetes 2009; 117(3): 142-145
DOI: 10.1055/s-2008-1078741
Article

© J. A. Barth Verlag in Georg Thieme Verlag KG Stuttgart · New York

Hypercalcemia of Primary Hyperparathyroidism was Treated by Cinacalcet in a Patient with Liver Cirrhosis

B. Akinci 1 , A. Comlekci 1 , E. Tankurt 2
  • 1Division of Endocrinology and Metabolism, Department of Internal Medicine, Dokuz Eylul University Medical School, Izmir, Turkey
  • 2Division of Gastroenterology and Hepatology, Department of Internal Medicine, Dokuz Eylul University Medical School, Izmir, Turkey
Further Information

Publication History

received 15.02.2008 first decision 11.04.2008

accepted 15.05.2008

Publication Date:
17 June 2008 (online)

Abstract

Cinacalcet is a type II calcimimetic agent which is an allosteric modulator of the calcium-sensing receptor (CaR) located on the surface of the parathyroid cells. Cinacalcet increases the sensitivity of CaR via binding to the transmembrane region of CaR. Increasing sensitivity of CaR causes reduced secretion of parathyroid hormone (PTH) and suppression of serum calcium levels. Cinacalcet has recently been approved by Federal Drug Administration (FDA) for the treatment of patients with secondary hyperparathyroidism on maintenance dialysis and hypercalcemia in patients with parathyroid cancer. It is used also in Europe for both indications. Several controlled studies have shown that cinacalcet is effective in normalizing serum calcium levels also in primary hyperparathyroidism. Cinacalcet is metabolized primarily in the liver by N-dealkylation leading to carboxylic acid and oxidation of naphthalene ring to form dihydrodiols. The safety and optimal dosage of the drug in hypercalcemic patients with liver impairment remains unclear. We present a patient with Child-Pugh B class primary biliary cirrhosis who presented with moderate hypercalcemia and was diagnosed as primary hyperparathyroidism. As she refused having parathyroid surgery for her parathyroid adenoma at first, her hypercalcemia was treated successfully with 30 mg/day cinacalcet for 6 months. Cinacalcet was discontinued after 6 months. Her calcium level increased gradually. As she accepted surgery this time, her parathyroid adenoma was removed by minimally invasive parathyroidectomy. Parathyroid adenoma was confirmed pathologically. Her calcium levels maintained within the normal ranges after surgery.

References

  • 1 Coker LH, Rorie K, Cantley L, Kirkland K, Stump D, Burbank N, Tembreull T, Williamson J, Perrier N. Primary hyperparathyroidism, cognition, and health-related quality of life.  Ann Surg. 2005;  242 ((5)) 642-650
  • 2 Bilezikian JP, Potts Jr JT, Fuleihan Gel H, Kleerekoper M, Neer R, Peacock M, Rastad J, Silverberg SJ, Udelsman R, Wells SA. Summary statement from a workshop on asymptomatic primary hyperparathyroidism: a perspective for the 21st century.  J Clin Endocrinol Metab. 2002;  87 ((12)) 5353-5361
  • 3 Farford B, Presutti RJ, Moraghan TJ. Nonsurgical management of primary hyperparathyroidism.  Mayo Clin Proc. 2007;  82 ((3)) 351-355
  • 4 Shoback DM, Bilezikian JP, Turner SA, MacCary LC, Guo MD, Peacock M. The calcimimetic cinacalcet normalizes serum calcium in subjects with primary hyperparathyroidism.  J Clin Endocrinol Metab. 2003;  88 ((12)) 5644-5649
  • 5 Peacock M, Bilezikian JP, Klassen PS, Guo MD, Turner SA, Shoback D. Cinacalcet hydrochloride maintains long-term normocalcemia in patients with primary hyperparathyroidism.  J Clin Endocrinol Metab. 2005;  90 ((1)) 135-141
  • 6 Kumar GN, Sproul C, Poppe L, Turner S, Gohdes M, Ghoborah H, Padhi D, Roskos L. Metabolism and disposition of calcimimetic agent cinacalcet HCl in humans and animal models.  Drug Metab Dispos. 2004;  32 ((12)) 1491-1500
  • 7 Amgen Inc: . Sensipar® (cinacalcet HCL) Product Monograph. 2004; 
  • 8 Szmuilowicz ED, Utiger RD. A case of parathyroid carcinoma with hypercalcemia responsive to cinacalcet therapy.  Nat Clin Pract Endocrinol Metab. 2006;  2 ((5)) 291-296 , ; quiz 297
  • 9 Silverberg SJ, Bilezikian JP, Bone HG, Talpos GB, Horwitz MJ, Stewart AF. Therapeutic controversies in primary hyperparathyroidism.  J Clin Endocrinol Metab. 1999;  84 ((7)) 2275-2285
  • 10 Heath 3rd H. Familial benign (hypocalciuric) hypercalcemia. A troublesome mimic of mild primary hyperparathyroidism.  Endocrinol Metab Clin North Am. 1989;  18 ((3)) 723-740
  • 11 Law Jr WM, Heath 3rd H. Familial benign hypercalcemia (hypocalciuric hypercalcemia) Clinical and pathogenetic studies in 21 families.  Ann Intern Med. 1985;  102 ((4)) 511-519
  • 12 Crawford BA, Labio ED, Strasser SI, MacCaughan GW. Vitamin D replacement for cirrhosis-related bone disease.  Nat Clin Pract Gastroenterol Hepatol. 2006;  3 ((12)) 689-699
  • 13 Bingham CT, Fitzpatrick LA. Noninvasive testing in the diagnosis of osteomalacia.  Am J Med. 1993;  95 ((5)) 519-523
  • 14 Ring-Larsen H. Renal blood flow in cirrhosis: relation to systemic and portal haemodynamics and liver function.  Scand J Clin Lab Invest. 1977;  37 ((7)) 635-642
  • 15 Sansoe G, Biava AM, Silvano S, Ferrari A, Rosina F, Smedile A, Touscoz A, Bonardi L, Rizzetto M. Renal tubular events following passage from the supine to the standing position in patients with compensated liver cirrhosis: loss of tubuloglomerular feedback.  Gut. 2002;  51 ((5)) 736-741

Correspondence

B. AkinciMD 

Division of Endocrinology of Metabolism

Department of Internal Medicine

Dokuz Eylul University Medical School

Inciralti

35340 Izmir

Turkey

Phone: +90/232/412 37 44

Fax: +90/232/279 22 67

Email: baris.akinci@deu.edu.tr