Bilateral avascular necrosis of the head of the femur after intradermal triamcinolone acetonide injection for alopecia areata: A first-of-its-kind case report

INTRODUCTION

Alopecia areata is an autoimmune disease that presents with circumscribed patches of hair loss. The first line of management is intralesional corticosteroids such as Triamcinolone Acetonide.^[1] Although avascular necrosis (AVN) of the head of the femur is a well-known complication of systemic corticosteroid therapy, such a complication is yet to be recorded with intralesional corticosteroids, as is commonly used in many dermatological conditions.

CASE REPORT

A 35-year-old man with no known medical comorbidities presented with patchy circumscribed hair loss with preserved follicles from the beard and moustache region for the last 3 months [Figure 1]. He was non-diabetic, non-obese, not a smoker and had never drunk alcohol. There was also no history of intravenous drug use. Due to the presence of atopy, he was classified as alopecia areata Ikeda subtype atopic and was prescribed intralesional Triamcinolone acetonide 10 mg/mL diluted to 5 mg/mL repeated once monthly till improvement. He subsequently improved with 3 injections. He was co-prescribed oral zinc 50 mg twice daily. His alopecia resolved completely, and he was put off therapy after 3 months.

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Figure 1: Hairless patches on the moustache area with preserved follicles and relative sparing of white hairs.

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After 7 months of the last intralesional injection, he developed hip pain and stiffness in both hip joints, exacerbated on crossing legs. There was no history of trauma at the site. A serum cortisol revealed suppressed cortisol levels. The adrenocorticotropin (ACTH) stimulation test was normal. His antinuclear antibody profile, antiphospholipid antibody profile, protein C, protein S, and dual-energy x-ray absorptiometry scan were summarily normal. X-ray showed subluxation of hip joints, and due to strong suspicion of AVN of the head of the femur, he was advised to undergo magnetic resonance imaging (MRI) of both hip joints. MRI showed subchondral ischemic foci surrounded by a double line sign on T2-weighted images in the right femoral head. T1-weighted images showed hypointense wedge-shaped subchondral ischemic areas with central marrow fat intensity surrounded by a T1 hypointense peripheral band [Figure 2]. Also, the right femoral head spherical shape was not maintained.

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Figure 2: Magnetic resonance imaging scan showing loss of the rounded contour of the femoral head with a few opacities.

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Ficat stage III AVN of the head of the femur was diagnosed in both hip joints. He was subsequently scheduled for total hip arthroplasty of both joints. Causality assessment with the Naranjo algorithm was done, which showed a score of +6.

We established causality by the fact that serum cortisol remained suppressed at the end of 7 months, pointing towards Iatrogenic causes and by exclusion of other causes of AVN, such as antiphospholipid antibody syndrome syndrome, protein C and S defect. Idiopathic Cushing's disease was excluded by the ACTH stimulation test. The detailed Naranjo assessment is attached as a supplementary file.

DISCUSSION

Many mechanisms have been purported to explain AVN following systemic steroids, viz., development of a prothrombotic state with resultant microthrombi blocking the circulation of the femoral head with resultant hypoxia and osteonecrosis, intraosseous hypertension due to excess marrow fat induced by corticosteroids with resultant demand-supply mismatch resulting in osseous hypoxia and consequent osteonecrosis, excess weight bearing on the joint, genetic susceptibility, etc.^[2] Risk factors for vascular necrosis of the head of the femur have been exclusively elucidated and include being overweight, type 2 diabetes mellitus, preexisting bone disease such as osteopetrosis, hypercoagulable thrombophilias such as protein C, protein S deficiencies, hyperhomocysteinemia, elevated LP(a) levels, factor V leiden mutations, former episodes of deep venous thrombosis and other related conditions. Dosage analyses of steroids taken in any form show that there is probably no safe lower limit of steroid exposure. Daily low-dose steroids were found to be more vasculopathic than a larger dose taken over a shorter period. Injectable forms carried a higher risk compared to oral doses, which in turn was associated with a higher risk than topical therapy.^[3] Doses as low as 10 mg of a single dose of prednisolone have been documented to cause AVN, as do steroids applied over a large surface area or inhaled.^[2,4,5] To the best of our knowledge, after searching “AVN of head of femur” and “intralesional steroid” on PubMed, Medline and Embase databases, we could not identify any other case reports, although a case report exists where systemic therapy was instituted for alopecia areata, which resulted in AVN of the femoral head.^[6] While numerous case reports and evidence exist of the occurrence of AVN of the head of the femur after systemic steroids, sometimes in doses as low as 10 mg/day for a single day via intra-articular, oral and intramuscular routes, this occurrence after intralesional use is particularly alarming for dermatologists who routinely use intralesional steroids for a variety of disorders ranging from alopecia areata to vitiligo.^[1]

CONCLUSION

Intralesional corticosteroids have the potential to cause AVN of the head of the femur. Hence, dermatologists should exercise more caution while injecting steroids intradermally.