Intralesional triamcinolone injections have been used to treat several different kinds of conditions including dermatologic (acne, alopecia areata, hypertrophic or keloid scarring), rheumatologic (rheumatoid arthritis, osteoarthritis), neurologic (multiple sclerosis), ophthalmologic (periocular capillary hemangioma, chalazion) and otolaryngologic (allergic rhinitis, nasal polyp) conditions1. These injections direct a high-concentration of drug to the lesion site, thereby avoiding many of the potential side effects associated with systemic administration, such as hypothalamus-pituitary-adrenal axis suppression, endocrine changes, growth inhibition, allergic reactions, syncope, and blindness2. However, local side effects may occur, such as pain, hemorrhage, ulceration, atrophy, pigmentary changes, calcification, secondary infection, granuloma formation, allergic reactions2, and, in very rare cases, the development of linear atrophy and hypopigmentation after intralesional or intraarticular injection of triamcinolone acetonide has been reported in the literature as a side effect3.

Here, we report the case of a 30-year-old woman with unresolved cutaneous linear hypopigmentation and atrophy along the left shin for 13 months that developed after an intralesional corticosteroid injection.

A 30-year-old woman visited our dermatology department for a linear hypopigmented patch with atrophy from her left foot to the lower margin of the knee. The patient had received a single injection of 40 mg/ml triamcinolone acetonide for the treatment of a painful nodule on the left foot dorsum 7 months prior. Three months after the injection of triamcinolone acetonide, a hypopigmented patch with atrophy appeared at the site of injection on the dorsum of the left foot (Fig. 1A). Five months after the injection, the lesions proximally extended from the left dorsal foot in multiple linear patches up to the lower margin of the knee. The streak of hypopigmentation and atrophy branched as it spread and was not overlapped by superficial veins (Fig. 1B). A biopsy specimen was taken from the border of the lesion. To compare the lesional side with the normal side, epidermal atrophy and flattening rete ridges were observed on the lesional side (Fig. 2A, C). Fontana-Masson stain revealed hypopigmentation of the basal layer on the lesional side when compared to the normal side (Fig. 2B, D). The patient did not receive any specific treatment, and 13 months after injection her hypopigmentation and atrophy showed little improvement upon physical examination.

Cutaneous changes after local corticosteroid administration may include dermal atrophy, hyperpigmentation, alopecia, and hypopigmentation4. However, the development of linear atrophy and hypopigmentation after intralesional or intraarticular injections of corticosteroids has only rarely been reported in the literature3. A Medline review of the English language literature from 1981 to 2009 yielded 12 cases of linear pattern hypopigmentation after corticosteroid injection. Skin atrophy develops due to the direct antiproliferative effects of corticosteroids on fibroblasts and keratinocytes, the disturbed metabolism of extracellular matrix proteins, and the perturbed synthesis of skin lipids5. Corticosteroid-induced vasoconstriction may also play a role. This enhanced vasoconstriction may facilitate local thrombosis or embolization and capillary closure with resultant local tissue hypoxia. These effects then produce local tissue atrophy, or, in extreme cases, necrosis2. Although the exact pathogenesis of hypopigmentation is unknown, the corticosteroid may reduce the number or activity of melanocytes1. Corticosteroids might also alter melanocyte function by inhibiting prostaglandin or cytokine production in various epidermal cells, and may suppress secretory metabolic products from melanocytes without causing their destruction6. The exact pathogenesis of linear hypopigmentation or atrophy is also unknown. The most widely accepted mechanism is the lymphatic spread of the corticosteroid suspension and resulting linear hypopigmentation or atrophy of skin tissues1. After injecting Evans Blue Dye or Alphazurine 2 G (Patent Blue) into atrophic lesions, Kikuchi and Horikawa7 concluded that the lesions were related to lymphatic vessels.

Linear hypopigmentation has been reported after single or multiple injections with a long latency period of several weeks to months8. There is a considerably increased risk of dermal atrophy when 40 mg/ml of triamcinolone is injected instead of 10 mg/ml1. In this case, linear atrophy and hypopigmentation appeared 3 months after a single 40 mg/ml injection of triamcinolone, and the lesions extended more broadly than in any other reported case. Hypopigmentation and atrophy generally begin to resolve without further treatment several months after the discontinuation of the steroid in the majority of cases, although a single reported case involved an area of unresolved hypopigmentation 1 year after injection9. In the present case, hypopigmentation and atrophy were not resolved 13 months after injection.

Linear pattern hypopigmentation and atrophy is a very rare side effect of intralesional triamcinolone injection. The present case is the first reported in Korea. Permanent hypopigmentation and atrophy are important cosmetic issues, and in this case, just a single injection caused broad branch-shaped hypopigmentation and atrophy around the injection site, with the lesions persisting for more than one year. Clinicians should be aware of this rare side effect and in particular, must be careful when injecting high concentrations of corticosteroids into patients.