Aldosterone Producing Adenoma Associated Hypercalcemia and Rhabdomyolysis

Case Report

Austin Endocrinol Diabetes Case Rep. 2023; 7(1): 1019.

Aldosterone Producing Adenoma Associated Hypercalcemia and Rhabdomyolysis

Shahnaz Ahmad Mir; Pooran Sharma*; Md Ejaz Ala

Department of Endocrinology, GMC, Srinagar, India

*Corresponding author: Pooran Sharma Department of Endocrinology, GMC, Srinagar, India. Email: puran.k.sharma@gmail.com

Received: April 03, 2023 Accepted: May 01, 2023 Published: May 08, 2023

Abstract

Aldosterone producing adenomas are rare in children’s with less than 20 cases reporting in literature present a 15-year female who presenting with polyuria and proximal muscle weakness. Investigations revealed severe hypokalaemia, raised creatinine phosphokinase suggestive of hypokalaemia induced rhabdomyolysis. Further patient’s investigations showed raised aldosterone and suppressed renin and CT abdomen was suggestive of left adrenal adenoma which was removed laparoscopically. We will review all cases in literature of childhood onset aldosteronomas.

Keywords: Aldosteronoma; Hypokalaemia; Rhabdomyolysis; Polyuria

Introduction

It is well known that marked hypokalaemia manifests as muscle weakness, but rhabdomyolysis is a rare presentation of hypokalaemia. The causes of rhabdomyolysis are various; usage of laxatives and diuretics, anorexia, chronic alcoholism, infectious enterocolitis, renal tubular acidosis and aldosteronism has been reported to be possible causes of hypokalaemia rhabdomyolysis [1,2]. However, aldosterone-producing adrenal tumours are extremely rare in children, considering the cause of hypokalaemia. Here, we report a case of primary hyperaldosteronism due to unilateral aldosterone producing adenoma in a 15-year-old girl who developed rhabdomyolysis following hypokalaemia.

Case Report

13 year female presented with Polyuria, (documented urine output 7.5 lit], increase thirst for 6 months; severe myalgias and inability to stand from sitting position for 2 months. No history of failure to thrive, or any alternative medicine intake, hyper or hypothyroid symptoms, or any problem with hearing. No significant family history, two other siblings normal. Anthropometry: Height-153cm [10-25%], Weight [48kg]. Puberty completed, no clinical evidence of rickets or any bone disease, Pulse 78 regular B.P-140/90mmHg (both upper limbs), Chest- WNL CVS; WNL, Bulk normal, both upper and lower limbs Tone normal, Power grade 4- in all muscle groups of upper and lower limbs. Gower's sign was positive. Reflexes diminished. Patient serum electrolytes revealed hypokalaemia, metabolic acidosis and hypernatermia. Patient had normal liver and kidney function tests. Serum LDH was 680U/L and CPK of 3320U/L. Patient had calcium of 10.2 and phosphorus of 3.8mg/dl. 2hr urinary calcium was 550mg/day. ECG revealed U waves and USG abdomen showed Anderson cork kidney. Serum vitamin D was 48ng/ml and serum PTH of 110pg/ml. Patients workup for hyperaldosteronism revealed serum aldosterone of 1182pg/ml and renin of 0.013ng/ml/hr. CECT abdomen showed a (1.2×1.8cm) left adrenal mass (Figure 1). Laparoscopic adrenalectomy was done which showed a (2×1.3cm) tumor found in left adrenal gland. Histopathology confirmed left adrenal adenoma (Figure 2). Patient is on follow-up off any treatment for 6 months.

Citation: Mir SA, Sharma P, Alam ME. Aldosterone Producing Adenoma Associated Hypercalcemia and Rhabdomyolysis. Austin Endocrinol Diabetes Case Rep. 2023; 7(1): 1019.