Cushing syndrome is a known cause of short stature and usually presents with a characteristic body habitus. Rarely, the florid signs of Cushing syndrome may be absent leading to a missed or delayed diagnosis [1].

Two siblings, a 10-year old boy and 7-year old girl were referred to our pediatric endocrinology clinic for evaluation of short stature. There was a history of joint pains since early childhood and growth failure since the last many years. On examination, they had severe stunting (height-for-age Z-score -4.9 and -3.8, respectively), anemia, and delayed bone age and osteopenia on radiographs. The younger sibling had right eye posterior sub-capsular cataract and rickets as well. The etiology of growth failure was not evident from the initial diagnostic evaluation with evidence of multi-systemic involvement including pituitary dysfunction (including low serum T4 and TSH levels and suppressed hypothalamus-pituitary-adrenal (HPA) axis with low morning cortisol levels). However, detailed history revealed surreptitious over-the-counter intake of glucocorticoids in the form of oral prednisolone in a variable dose of 0.5-1 mg/kg off and on, since early childhood. The children had become dependent on glucocorticoids and had a characteristic withdrawal syndrome that accounted for their severe arthralgias and myalgias. Catch-up growth occurred once glucocorticoids were stopped and supplementation with physiological doses of hydrocortisone were given till recovery of the HPA axis.

Long-term use of glucocorticoids is known to suppress growth by direct toxic effect on the cartilage growth plate by decreasing vascular proliferation and inhibiting hypertrophy of chondrocytes [2]. Hyper-cortisolemia due to Cushing syndrome or chronic glucocorticoids intake can be associated with reversible pituitary dysfunction, including low T4 and TSH levels [3], GH deficiency, or panhypopituitarism [4].

The underlying condition for which the siblings began consuming steroids is still unclear. Detailed evaluation including inflammatory/autoimmune markers or effusion of the joints on ultrasound/aspiration did not reveal evidence of inflammation. We postulate that they suffered from a characteristic steroid withdrawal syndrome manifesting as severe myalgias and arthralgias [5], making it difficult to distinguish from the underlying condition for which the steroids were started. The dependence on glucocorticoids led to a vicious cycle of its over-the counter intake, withdrawal symptoms on discontinuation, and its further consumption.

These cases highlight the practice of over-the-counter sale and abuse of glucocorticoids preparations in countries with poor drug regulation system. Additionally, parents may self-medicate their children with corticosteroids to increase appetite and weight without knowing the deleterious side effects [6].

Clinicians need to keep a high index of suspicion for chronic glucocorticoid toxicity in the differential diagnosis of short stature and other unexplained clinical findings.

1. Lee PA, Weldon VV, Migeon CJ. Short stature as the only clinical sign of Cushing’s syndrome. J Pediatr. 1975;86:89-91.

2. Mushtaq T, Ahmed SF. The impact of corticosteroids on growth and bone health. Arch Dis Child. 2002;87:93-6.

3. Hara Y1, Sekiya M, Suzuki M, Hiwada K, Kato I, Kokubu T. A case of isolated thyrotropin deficiency with Cushing’s syndrome. Jpn J Med. 1989;28:727-30.

4. Watanabe K1, Adachi A, Nakamura R. Reversible panhypopituitarism due to Cushing’s syndrome. Arch Intern Med. 1988;148:1358-60.

5. Hochberg ZI, Pacak K, Chrousos GP. Endocrine withdrawal syndromes. Endocr Rev. 2003;24:523-38.