Hernández-Lorenzo Z, Mancillas-Adame L, González-González J, Garza-Muñoz R, Villarreal-Pérez J

Language: Spanish
References: 16
Page: 25-29
PDF size: 79.48 Kb.

ABSTRACT

The plasma concentration of calcium is controlled strictly by the parathyroid hormone (PTH) and vitamin D, along with the calcitonin. The lithium is a drug widely used to treat affective disorders. Even when the thyroid dysfunction is the endocrine side effect more frequently reported associated with lithium therapy, hypercalcemia and a clinical setting very similar to hyperparathyroidism (HPT) can develop. To this date approximately 50 cases have been reported. 10-15% of the patients under lithium therapy develop hypercalcemia with HPT, and the underlying mechanism has not been elucidated. The hypercalcemia and HPT symptoms resolve when lithium therapy is stopped, but this can take up to 8.5 weeks, especially in cases treated for more than 5 years with this drug. In general, it is recommended a routine bilateral neck exploration, along with inspection of the four parathyroid glands, given the possible multiglandular involvement. We must limit the excision to cases with evident disease. The use of cinacalcet has been suggested as a first line therapy in resistant cases of hyperparathyroidism associated with lithium therapy or relapse after surgery, but more clinical evidence is needed.

REFERENCES

1. DeGroot LJ, Jameson JL. Parathyroid hormone and parathyroid hormone-related peptide. In: DeGroot LJ, Jameson JL, eds. Endocrinology. 5th ed. Philadelphia; Elsevier-Saunders: 2006; 2: 1378-1384.

2. Peacock M. Calcium metabolism in health and disease. Clin J Am Soc Nephrol 2010; 5: S23–S30.

3. Wilting I, Souverein PC, Nolen WA, Egberts AC, Heerdin ER. Changes in outpatient lithium treatment in the Netherlands during 1996–2005. J Affect Disord 2008; 111: 94–99.

4. Bendz H, Sjodin L, Toss G, Berglund K. Hyperparathyroidism and long term lithium therapy – a cross sectional study and the effects of lithium withdrawal. J Intern Med 1999; 240: 357–365.

5. Cade JF. Lithium salts in treatment of psychotic excitement. Med J Aust 1949; 2: 349–352.

6. Garfinkel PE, Ezrin C, Stancer HC. Hypothyroidism and hyperparathyroidism associated with lithium. Lancet 1973; 2(7824): 331-332.

7. Mallette LE, Khouri K, Zengotita H, Hollis BW, Malini S. Lithium treatment increases intact and mid region parathyroid hormone and parathyroid volume. J Clin Endocrinol Metab 1989; 68: 654-660.

8. Awad SS, Miskulin J, Thompson N. Parathyroid adenomas versus four-gland hyperplasia as the cause of primary hyperparathyroidism in patients with prolonged lithium therapy. World J Surg 2003; 27: 486–488.

9. Szalat A, Mazeh H, Freund HR. Lithium-associated hyperparathyroidism: report of four cases and review of the literature. Eur J Endocrinol 2009; 160: 317-323.

10. Turan MT, Esel E, Tutus A, Sofuoglu S, Gonul AS. Lithium-induced alterations in parathormone function in patients with bipolar disorder. Bull Clin Psychopharmacol 2001; 11: 96–100.

11. Lenox RH, McNamara RK, Papke RL, Manji HK. Neurobiology of lithium: an update. J Clin Psychiatry 1998; 59: 37–47.

12. Misra M, Papakostas GI, Klibanski A. Effects of psychiatric disorders and psychotropic medications on prolactin and bone metabolism. J Clin Psychiatry 2004; 65: 1607–1618.

13. Nordenstrom J, Elvius M, Bagedahl-Strindlund M, Zhao B, Torring O. Biochemical hyperparathyroidism and bone mineral status in patients treated long term with lithium. Metabolism 1994; 43: 1563–1567.

14. Perrier ND. Asymptomatic hyperparathyroidism: a medical misnomer? Surgery 2005; 137: 127-131.

15. Rifai MA, Moles JK, Harrington DP. Lithium-Induced hypercalcemia and parathyroid dysfunction. Psychosomatics 2001; 42: 359-361.

16. Gregoor PS, de Jong GM. Lithium hypercalcemia, hyperparathyroidism, and cinacalcet. Kidney Int 2007; 71: 470.