Cushing syndrome secondary to topical glucocorticoids
Published Web Locationhttps://doi.org/10.5070/D33ns8x0t5
Cushing syndrome secondary to topical glucocorticoidsFrom the Ronald O. Perelman Department of Dermatology, New York University
Edwin K Joe MD
Dermatology Online Journal 9(4): 16
An 11-year-old boy with a history of psoriasis presented with Cushingoid stigmata, which included weight gain, central obesity, violaceous striae, and facial plethora. It was discovered that he had used potent topical glucocorticoids for two months prior to the onset of his weight gain. Laboratory studies were consistent with adrenal suppression that improved after discontinuation of the use of topical glucocorticoids.
History.—An 11-year-old boy presented with a 9-month history of skin changes involving the head, neck, trunk, axillae, inguinal folds, and thighs. Over the last 9 months, since June 2001, the patient experienced weight gain without any change in eating habits or activity level. The weight gain was noted to be most prominent on his central trunk. Facial rounding and fullness as well as red-purple striae on the axillae, abdomen, and upper thighs were reported.
Past medical history included a 2-year history of psoriasis, which was treated with topical medications. Recent topical therapy included at least 275 g of halobetasol propionate (0.05 %) and 100 g of betamethasone dipropionate (0.05 %) between April and October 2001. The patient also received prednisone orally, 10mg/day, for 10 days in September 2001.
He was evaluated at the dermatology clinics at Bellevue Hospital Center and at the Charles C. Harris Skin and Cancer Pavilion. Topical glucocorticoids were discontinued, and he was started on calcipotriene (0.005 %) ointment for his body, ketoconazole (2 %) cream for his face, and ketoconazole (2 %) shampoo for his scalp; he also was started on adapalene (0.1 %) gel for his axillary striae. After 2 weeks, his psoriasis worsened, and a punch biopsy was obtained. His treatment regimen was continued and some improvement was noted over the next week. Tazarotene (0.1 %) cream was added to his regimen, and further improvement was noted. The axillary striae improved with adapalene (0.1 %) gel.
|Figure 1||Figure 2|
Physical examination.—Central obesity, facial plethora, and increased soft tissue on his breasts and between his scapulae were noted. Red-violaceous striae were noted on the abdomen, upper thighs, inguinal folds, and axillae. Erythematous, scaly, guttate papules involved his trunk and extremities, with thicker plaques on his knees and patchy involvement on his central face and scalp.
Laboratory data.—A complete blood count, basic metabolic panel, serum calcium level, and lipid profile were normal. Plasma cortisol levels were undetectable in October 2001. An ACTH stimulation test was performed in November 2001 and repeated in January 2002, 5 weeks after discontinuing topical glucocorticoids.November 2001 January 2002 0 min. 60 mins. 0 min. 60 mins. Cortisol (µg/dl) < 0.2 (nl: 5-23) 3.08 (nl: increase > 10) 4.9 19.45
Cranial magnetic resonance imaging was normal. The adrenals could not be visualized by ultrasound.
Histopathology.—There is a superficial perivascular, predominantly lymphocytic infiltrate, which extends to the overlying slightly hyperplastic epidermis, where there is mild spongiosis and parakeratosis with a few neutrophils in the cornified layer. Many suprabasal mitoses are present. A periodic-acid Schiff stain failed to show fungal elements.
Diagnosis.— Cushing syndrome secondary to topical glucocorticoids.
Cushing syndrome  is categorized as adrenocorticotropin hormone (ACTH) dependent or ACTH independent (Table 1) . The most common symptom of Cushing syndrome is weight gain, which is usually manifested by central obesity. Muscle weakness, bruising, hypertension, facial rounding, and plethora eventually occur (Table 2) . Because high glucocorticoid concentrations interfere with growth, children may exhibit higher than normal weights with stunted linear growth. (3)
|ACTH dependent |
If iatrogenic causes are not apparent, initial evaluation of excessive glucocorticoid production is usually accomplished with a 24-hour urine collection for urinary free cortisol or a dexamethasone suppression test. A late-afternoon plasma ACTH level will determine whether the pathologic state is ACTH dependent (elevated levels) or ACTH independent (depressed levels). Computed tomographic scanning and magnetic resonance imaging aid in localizing pituitary, adrenal, or other masses .
Cushing syndrome is most commonly caused by the therapeutic administration of exogenous systemic glucocorticoids. However, there have been a few reports, mostly in children, of iatrogenic Cushing syndrome caused by potent topical corticosteroids . In such cases, further exposure to exogenous glucocorticoids should be limited or avoided entirely. Oral glucocorticoid supplementation may be required, however, for several months until hypothalamic-pituitary-adrenal function recovers, with possibly increased dosage requirements during periods of stress and illness. Patients should wear appropriate medical alert labels . It has been suggested that systemic adverse reactions caused by potent topical glucocorticoids could be avoided by restricting usage to 50 g per week in adults and 15 g per week in children .
References1. Boscaro M, et al. Cushing's syndrome. Lancet 2001;357:783.
2. Kirk LF Jr, et al. Cushing's disease: Clinical manifestations and diagnostic evaluation. Am Fam Physician 2000;62:1119.
3. Ohnishi T, et al. Erythrodermic psoriasis associated with hyperuricemia and iatrogenic Cushing's syndrome due to topical corticosteroid therapy. Int J Dermatol 1996;35-379.
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