Unintentional discontinuation of topical corticosteroids after emergency hospitalization can exacerbate adrenal insufficiency

Dear Editor,

We read with great interest the case report by Iwamoto et al. on adrenal insufficiency associated with hypothalamic-pituitary-adrenal (HPA) axis suppression following the tapering of topical corticosteroids for skin disease [1]. This report is particularly important for clinicians involved in the management of glucocorticoid preparations. In addition to this crucial finding, we would like to highlight another important situation of which all medical professionals should be aware: the need to confirm whether steroid ointments are being used in cases of emergency hospitalization or hospitalization accompanied by impaired consciousness.

A 73-year-old man with headache, vomiting, and dizziness was urgently admitted to a local hospital. On admission, his serum sodium concentration was markedly low at 120 mEq/L. Despite sodium supplementation, he developed worsening hyponatremia of unknown origin and was subsequently transferred to our hospital. His vital signs were normal, and he showed no physical changes, including signs of Cushing’s syndrome. Laboratory tests revealed marked hyponatremia (117 mmol/L), hypoosmolality, and low plasma glucose (52 mg/dL) despite no history of diabetes treatment. Although under stress, his basal serum cortisol (5.01 μg/dL) and plasma adrenocorticotropic hormone (ACTH) levels (10.0 pg/mL) were not elevated, suggesting possible adrenal insufficiency. The cortisol response to a rapid ACTH stimulation test (250 μg) was abnormally low, and neither ACTH nor cortisol responded to a corticotropin-releasing hormone stimulation test, indicating HPA axis suppression (Table 1). Imaging evaluations, including computed tomography and magnetic resonance imaging, revealed no obvious abnormalities in the adrenal or pituitary glands. A careful re-review of his medication history revealed that multiple topical corticosteroid ointments—including diflucortolone valerate (very strong), difluprednate (very strong), and triamcinolone acetonide (mild)—had been prescribed by a dermatologist for seborrheic dermatitis. He had applied approximately 2 g of each prescription daily to his trunk, limbs, genitals, and buttocks for 2 months, likely suppressing his HPA axis. However, these treatments were discontinued without being recognized by the primary care team at the time of his emergency admission to the previous hospital. Once the situation was clarified, intravenous high-concentration saline and glucocorticoid replacement therapy were initiated, gradually normalizing his serum sodium and plasma glucose levels. He was discharged on 15 mg/day of hydrocortisone.

Table 1 Laboratory test results after admission

Variable	Value	Reference range
White blood cells (/μL)	6,920	3,300–8,600
Hemoglobin (g/dL)	15.2	13.7–16.8
Platelets (/μL × 104)	18.1	15.8–34.8
BUN (U/L)	14.8	8.0–20.0
Creatinine (mg/dL)	0.63	0.65–1.07
Sodium (mEq/L)	117	138–145
Potassium (mEq/L)	3.3	3.6–4.8
Chloride (mEq/L)	87	101–108
Glucose (mg/dL)	52	73–109
TSH (μIU/mL)	0.53	0.50–5.00
Free T3 (pg/mL)	1.55	2.30–4.00
Free T4 (ng/dL)	1.80	0.90–1.70
ACTH (pg/mL)	10.0	7.2–63.3
Cortisol (μg/dL)	5.01	6.24–18.00
PRA (ng/mL/hour)	0.2	0.2–2.3
PAC (pg/mL)	25.4	4.0–82.1
Rapid ACTH test
Cortisol (basal)	3.25	6.24–18.00
Cortisol (peak)	9.91	≥18.00
CRH stimulation test
ACTH (basal)	20.7	7.2–63.3
ACTH (peak)	24.0	N/A
Cortisol (basal)	3.43	6.24–18.00
Cortisol (peak)	4.27	N/A

BUN, blood urea nitrogen; TSH, thyroid-stimulating hormone; T3, triiodothyronine; T4, thyroxine; ACTH, adrenocorticotropic hormone; PRA, plasma renin activity; PAC, plasma aldosterone concentration; CRH, corticotropin-releasing hormone; N/A, not applicable.

In patients with adrenal insufficiency, lack of cortisol prevents suppression of hypothalamic arginine vasopressin, leading to impaired renal free water clearance and hyponatremia [2]. It is well established that supraphysiological doses of glucocorticoids suppress the HPA axis, and discontinuation can cause secondary adrenal insufficiency [3]. As reported by Iwamoto et al. [1], topical corticosteroid ointments may also lead to adrenal insufficiency. Risk factors include the amount, frequency, and extent of application, as well as long-term use [4].

In this case, long-term topical steroid use suppressed the HPA axis, and discontinuation upon hospitalization exacerbated adrenal insufficiency. If signs of Cushing’s syndrome are present, adrenal insufficiency due to reduction or discontinuation of corticosteroid ointments can often be inferred from the clinical picture. However, in cases such as ours, where no obvious Cushingoid features are present, the diagnosis may be overlooked unless both a careful medication history and endocrine evaluation are performed. In clinical practice, there may be many patients facing similar risks. When patients are admitted, topical medications—particularly those prescribed by other hospitals—may be discontinued either by patients themselves or by healthcare professionals. It is essential for clinicians to recognize that stopping topical corticosteroids during hospitalization for acute illness can precipitate adrenal insufficiency.

Acknowledgment

A draft of this manuscript was edited by Angela Morben, DVM, ELS, from Edanz (https://jp.edanz.com/ac).

Disclosure statement

The authors declare no conflict of interest.

Funding information

The work submitted did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors.

References

• 1   Iwamoto  Y,  Komi  M,  Fushimi  Y,  Kimura  T,  Shimoda  M, et al. (2025) A case of Hailey-Hailey disease accompanied by Cushing’s syndrome and adrenal insufficiency due to long-term usage of topical steroids with review of literature. Endocr J doi: 10.1507/endocrj.EJ25-0164. Online ahead of print.
• 2   Charoensri  S,  Auchus  RJ (2024) A contemporary approach to the diagnosis and management of adrenal insufficiency. Endocrinol Metab (Seoul) 39: 73–82.
• 3   Dinsen  S,  Baslund  B,  Klose  M,  Rasmussen  AK,  Friis-Hansen  L, et al. (2013) Why glucocorticoid withdrawal may sometimes be as dangerous as the treatment itself. Eur J Intern Med 24: 714–720.
• 4   Tempark  T,  Phatarakijnirund  V,  Chatproedprai  S,  Watcharasindhu  S,  Supornsilchai  V, et al. (2010) Exogenous Cushing’s syndrome due to topical corticosteroid application: case report and review literature. Endocrine 38: 328–334.