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Letter to the Editor

Single‐Dose Dexamemthasone‐Induced Adrenocortical Suppression in an Intentional Self‐Poisoning—Case Report

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Page 895 | Published online: 30 Oct 2003

To the Editor:

Hypothalamic‐pituitary‐adrenal (HPA) axis suppression is a common undesirable effect of long‐term corticosteroid treatment and has also been noted following short‐term use (1,2). Although even a single dose of dexamethasone can decrease cortisol levels, it has never been associated with serious impairment of the HPA axis (3–5) and, to our knowledge has not been noted following intentional self‐poisoning.

A 15‐year‐old female was hospitalized following the ingestion of 36 1‐mg dexamethasone tablets and 12 diazepinum tablets. Following a symptom‐free 3‐day period, she became febrile (39.2°C) approximately 85 hr postingestion, and rapidly developed symptoms of shock (blood pressure 70/50 mmHg, pulse 125/min and weak, heart tones soft and unclear), and confusion. An emergent gastrointestinal endoscopy ruled out frank bleeding.

Intravenous saline, with 80 mg methylprednisolone by bolus, was administered and the patient's symptoms resolved within 15 min. Admission serum chemistry values were Na+ 130 mmol/L, K+ 5.2 mmol/L, and glucose 3.8 mmol/L. Two hours later, they were 142, 4.8, and 6.2 mmol/L, respectively. Other causes of acute shock (acute poisoning, sepsis, central nervous system and cardiovascular abnormalities, acute hemorrhage, ruptured ectopic pregnancy) were ruled out. Over the next 2 days, the patient received oral corticosteroid replacement therapy. Unfortunately, blood cortisol and corticotropin studies were drawn but not analyzed because of technical difficulties. The child was discharged on the seventh day and lost to follow‐up.

Dexamethasone is a potent, long‐acting corticosteroid shown to alter adrenal response within a few days of use or even following a single dose (6–9). This condition is transient HPA suppression characterized by blunted corticosteroid response and an adrenal hyporesponsiveness (3,8). In this case, slow absorption of the long‐acting synthetic corticosteroid probably contributed to the delay in initial symptoms. The fever itself perhaps acted as the stressor, heralding the subsequent evident crisis of adrenal insufficiency. Clinicians are well advised to closely observe those patients with intentional corticosteroid overdose for signs of HPA axis alteration.

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