J Korean Med Sci.  2009 Dec;24(6):1220-1223. 10.3346/jkms.2009.24.6.1220.

Symptomatic Hypocalcemia in Primary Hyperaldosteronism: A Case Report

• Pai SG
• Shivashankara K
• Pandit V
• Sheshadri

• KMID: 1783161
• DOI: http://doi.org/10.3346/jkms.2009.24.6.1220

Abstract

The metabolic alterations caused by hyperaldosteronism are being increasingly recognized and have generated considerable interest among the medical fraternity. Hyperaldosteronism is suspected to have a pivotal role in the patho-physiology of congestive cardiac failure where it has been studied extensively. But its effects on calcium metabolism, parathyroid metabolism and renal handling of calcium are less well described. Recent experimental models have shed light into the roles played by previously unknown mechanisms in causing these metabolic alterations. We hereby report a case of primary hyperaldosteronism due to adrenal adenoma (Conn's syndrome) who presented with a myriad of clinical features including symptomatic hypocalcemia, significant weight loss along with uncontrolled hypertension for a prolonged period before eventually detected to have primary hyperaldosteronism. Surgical removal of the causative tumor resulted in prompt disappearance of all the symptoms and signs and regain of lost weight.

Keyword

Primary Aldosteronism; Hypocalcemia; Weight Loss

MeSH Terms

Adrenal Cortex Neoplasms/*complications/diagnosis/pathology/surgery
Adrenocortical Adenoma/*complications/diagnosis/pathology/surgery
Adult
Female
Humans
*Hyperaldosteronism/complications/etiology/physiopathology
Hypocalcemia/*etiology
Pregnancy
Treatment Outcome

Figure

• 

  Fig. 1 (A) Plain computed tomography image of the abdomen showing a mass measuring 3×3×3 cm in the supra renal region on the left side (arrow). (B) Contrast CT of the same region showing a non enhancing nature of the mass lesion in the same area.

• 

  Fig. 2 Gross operative specimen showing a 3×3 cm exophytic adrenal mass excised from the left suprarenal area.

• 

  Fig. 3 Microscopy after HE stain showing rounded lipid rich clear cells resembling those of normal zona fasciculate.

Reference

1. Vidal A, Sun Y, Bhattacharya SK, Ahokas RA, Gerling IC, Weber KT. Calcium paradox of aldosteronism and the role of the parathyroid glands. Am J Physiol Heart Circ Physiol. 2006. 290:H286–H294.

2. Rossi E, Sani C, Perazzoli F, Casoli MC, Negro A, Dotti C. Alternations of calcium metabolism and of parathyroid function in primary aldosteronism, and their reversal by spironolactone or by surgical removal of aldosterone-producing adenomas. Am J Hypertens. 1995. 8:884–893.

3. Chhokar VS, Sun Y, Bhattacharya SK, Ahokas RA, Myers LK, Xing Z, Smith RA, Gerling IC, Weber KT. Hyperparathyroidism and the calcium paradox of aldosteronism. Circulation. 2005. 111:871–878.

4. Chhokar VS, Sun Y, Bhattacharya SK, Ahokas RA, Myers LK, Xing Z, Smith RA, Gerling IC, Weber KT. Loss of bone minerals and strength in rats with aldosteronism. Am J Physiol Heart Circ Physiol. 2004. 287:H2023–H2026.

5. Conn JW. Presidential address: painting background: primary aldosteronism, new clinical syndrome. J Lab Clin Med. 1955. 45:3–17.

6. Kabadi UM. Renal calculi in primary aldosteronism. J Postgrad Med. 1995. 41:17–18.

7. Toraya S, Nomura K, Kono A, Aiba M, Ogasawara M, Kikuchi C, Demura H. Characteristics of aldosterone-producing adenoma responsive to upright posture. Endocr J. 1995. 42:481–487.

8. Rastegar A, Agus Z, Connor TB, Goldberg M. Renal handling of calcium and phosphate during mineralocorticoid "escape" in man. Kidney Int. 1972. 2:279–286.

9. Jakob F, Seufert J, Haack D, Schröder K, Ludwig J, Rendl J, Vecsei P. Unilateral autonomous aldosterone production in hyperaldosteronism suppressible by dexamethasone. Dtsch Med Wochenschr. 1993. 118:1837–1843.

10. Smith RJ, Faulkner WL. Primary aldosteronism caused by an adrenal tumor: a correctable cause of hypertension. J Natl Med Assoc. 1993. 85:761–763.

11. Weber KT. Aldosterone in congestive heart failure. N Engl J Med. 2001. 345:1689–1697.