Endocrine Abstracts

Introduction: Rhabdomyolysis coexisting with Addison’s disease is a rare condition and the mechanism is not clearly defined. We report a patient presenting with sever rhabdomyolysis which resolved after steroid replacement therapy.

Case report: A 33-year-old man without accompanying comorbidity, presented with progressive myopathy and fatigue. He was hypotensive (RR 90/70), hypovolemic with hyponatremia (125 mmol/l, range 137–146), elevated serum CPK (12 560 U/I, range <177) and high serum (3003 μg/l, range 28–72) and urinary myoglobin (384 μg/l, range <30). The muscle biopsy and tests of humoral and cellular immunity were normal. The hormonal findings confirmed adrenal insufficiency: serum cortisol (33 nmol/l (0800 h) <20 nmol/l (0500 h), range 138–800), ACTH 415.7 pmol/l (range 2.0–13.3), serum aldosterone 28 pmol/l (range 105–868), urinary aldosterone <1.0 nmol/24 h (range 6.23–59.3), renin >300 pg/ml (range 3.5–65.5) (upright posture). The absence of neurological symptoms and a prompt remission following steroid administration were against adult-onset form of adrenoleukodystrophy. The PPD probe, chest X-ray and CT scan of adrenal glands were normal. The etiology of Addison’s disease was problably autoimmune; this hypothesis is supported by a positive anti 21-OH autoantibody. Normal values of testosterone, gonadotropins and blood glucose suggested that no other glands were involved in the autoimmune disease. The patient was treated with a high (200 mg), gradually decreasing dose of hydrocortisone i.v., then with 20+10 mg p.o. Finally, two months later, all laboratory signs of rhabdomyolysis disappeared with complete clinical recovery.

Conclusion: The association between Addison’s disease and rhabdomyolysis is not clearly understood. Hyponatremia has been blamed for myopathy due to maladaptive cellular mechanism in response to fluid hypoosmolality. Myopathy was described in hyponatremia resulting from water intoxication, but, in spite of hyponatremia we were unable to detect a syndrome of inappropriate ADH secretion. Possibly, a glucocorticoid deficiency per se, by a mechanism unknown, could be involved in rhabdomyolysis. This case suggests that, in patients with rhabdomyolysis, an adrenal failure should be considered. It also raises the question of potential benefit of a glucocorticoid administration in other forms of rhabdomyolysis.

Declaration of interest: The authors declare that there is no conflict of interest that could be perceived as prejudicing the impartiality of the research project.

Funding: This research did not receive any specific grant from any funding agency in the public, commercial or not-for-profit sector.