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Case Report
2002:68:6;356-357
PMID: 17657002

Intralesional corticosteroid induced perilesional and perilymphatic hypopigmentation

Sukhjot Kaur, Gurvider P Thami
 Department of Dermatology and Venereology Government Medical College and Hospital, Sector 32 B, Chandigarh, India

Correspondence Address:
Gurvider P Thami
Department of Dermatology and Venereology Government Medical College and Hospital, Sector 32 B, Chandigarh
India
How to cite this article:
Kaur S, Thami GP. Intralesional corticosteroid induced perilesional and perilymphatic hypopigmentation . Indian J Dermatol Venereol Leprol 2002;68:356-357
Copyright: (C)2002 Indian Journal of Dermatology, Venereology, and Leprology

Abstract

Intralesional corticosteroid administration is a commonly used therapeutic modality in dermatology. PeriIesionoI streaky depigmentation and/or atrophy is a distinct, though rare adverse effect resulting from lymphatic uptake of corticosteroid crystals. The pathogenesis and its self-limiting clinical course are discussed.
Keywords: Corticosteroids, Intralesional, Perilesional Hypopigmentation

Introduction

Corticosteroid is one of the most potent and effective anti-inflammatory drugs used in current day clinical dermatologic practice.[1] When used intralesionally, these have the advantage of achieving high local concentration with prolonged depot effects and minimal systemic absorption and adverse effects.[1] The various cutaneous changes reported after intralesional corticosteroid administration include dermal or subcutaneous atrophy, hypopigmentation, alopecia, infection, ulceration and localized dystrophic calcification.[1],[2] Occurrence of perilesional linear atrophy and / or hypopigmentation is a distinct and an interesting local adverse effect following intralesional corticosteroid therapy.[3],[4],[5],[6],[7] A patient with this pattern of hypopigmentation and atrophy is presented.

Case Report

A 17-year-old male presented for treatment of a post burn keloid over the ventral aspect of left wrist. It was treated with intralesional injection of triamcinolone acetonide 40 mg/ml twice at three weeks interval. The volume injected was 0. 4 ml and 0. 5 ml on the two occasions respectively. One month later there was approximately 80% reduction in the thickness of the keloid. However, approximately 6 cm long, linear, streaky, atrophic hypopigmention was observed in the perilesional area extending proximally towards the cubital fossa [Figure - 1]. There was lesional hypopigmentation and few telangiectasias were also noted. There were no other areas of atrophy or hypopigmentation. No vein or cord was palpable beneath the line of depigmentation and the skin was free from underlying structures.

There was no personal or family history of vitiligo. With these features a diagnosis of corticosteroid-induced perilymphatic hypopig-mentation and atrophy was considered. Consent for a biopsy was not given. Further injections were withheld and the patient was counseled regarding the nature of the disorder and was kept under observation. A gradual repigmentation was observed at 3 months follow up.

Discussion

Intralesional injections of corticosteroids are associated with various local adverse effects.[1],[2] Occasionally, the atrophy and color changes instead of remaining confined to the site of injection radiate outwards in the perilesional area in a linear streaky pattern termed as ′perilesional lymphatic hypopigmentation or atrophy′.[3],[4],[5],[6],[7] It Is a distinctive adverse effect that may develop after a variable latency period ranging from a few weeks to months.[3] It has been observed following a single, a few or even after several intralesional corticosteroid injections.[3] The color changes are more prominent in dark skinned individuals and they extend both proximally and distally for variable distances.[4],[5],[6],[7] Depigmentation up to two feet from the site of injection has also been reported.[7] In its natural course these changes gradually regress and up to one year may elapse before complete resolution occurs.[3]

While the exact pathogenesis is not known it is postulated that the spread of corticosteroid crystals along the cutaneous lymphatic vessels is the underlying mechanism.[3] Kikuchi and Horikawa injected Evans blue dye or alphazurine into the atrophic lesions and concluded that the lesion was related to lymphatic vessels.[6] Thami and Sharma emphasized the additive or synergistic role of hyaluronidase in breaking the connective tissue barriers and facilitating the absorption into lymphatic vessels. ′Triamcinolone acetonide is the most commonly associated preparation, probably because it is most widely administered form.[1]

There is no specific treatment for this condition. Further injections should be withheld and the patients should be kept under observation. It is emphasized that while administering the intralesional corticosteroid injections care should be taken not to inject excess of the drug and to avoid injecting too deep into the underlying dermis and subcutaneous tissue.

References
1.
Firooz A, Tehranchi-Nia Z, Ahmed AR. Benefits and risks of intralesional corticosteroid injection in the treatment of dermatologic diseases. Clin Exp Dermatol 1995;20 363-370.
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Carruthers J, Jevon G, Prendivilie J. Localized dystrophic periocular calcification: a complication of intralesional corticosteroid therapy for infantile periocular hemangiomas. Pediatr Dermatol 1998; 15:23-26.
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Friedman SJ, Butler DF, P ttelkow MR. Perilesional linear atrophy and hypopigmentation after intralesional corticosteroid therapy. Report of two cases and review of literature. J Am Acad Dermatol 1988; 19:537-541.
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Gupta Ak, Rasmussen JE. Perilesional linear atrophic streaks associated with intralesional corticosteroid injections in a psoriatic plaque. Pediatr Dermatol 1987;4:259-260.
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Kikuchi I, Hirikawa S. Perilyrnphotic atrophy of skin: a side effect of topical corticosteroid injection therapy. Arch Dermatol 1974;109:558-559.
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Thami GP Sharma RC. Perilymphatic iotrogenic depigmentotion. Indian J Dermatol Venereal Leprol 1995;61:183-184.
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