Clinico- histopathological study of subacute cutaneous lupus erythematous

Introduction

SCLE was described as a subset of LE, intermediate in severity between DLE and acute cutaneous lupus erythematosus (ACLE) in genetically predisposed.[1] Clinically SCLE is characterised by photosensitivity, bilateral symmetrical, recurring, superficial, non-scarring either papulosquamous or annular plaques on photoexposed areas. In addition EM-like, pityriasiform, vitiligo, mouth ulcers, non-scarring alopecia, Raynaud′s phenomenon may develop singly or in combination.[2]

Histopathologically SCLE is characterised by more of epidermal atrophy and damage while DLE lesions demonstrated greater hyperkeratosis, basement membrane thickening, follicular plugging and both superficial and deep inflammatory cell infiltrate.[3] Pilosebaceous atrophy seen in DLE is found to be statistically significant criteria for differentiation from SCLE.[4] Histopathologically interface dermatitis, vacuolisation of basal cells, satellite cell necrosis and prominent colloid body formation of epidermis are salient features of SCLE.[5]

Materials and Methods

Fourteen cases of SCLE were selected from Dermato-Venereology department of Rajindra Hospital, Patiala during the last 2½ years. Detailed history, dermatological, general physical and systemic examinations were done. Routine investigations in detail and histopathological examination after biopsy were done in all cases. All 14 cases were treated with 10-15mg prednisolone daily, medium potency topical corticosteroids and sunscreens.

Results

Female to male sex ratio was 2.5;1 and age range was 12-65 years [Table - 1]. All cases gave positive history of photosensitivity and family history was negative in all cases. Annular lesions were present in all, 6 cases had scaly annular plaques (SAP), 2 cases had EM-like lesions, 2 had SAP + DLE, 2 had SAP + vitiligo, 1 had SAP + EM and 1 had pityriasis rosea - like plaques + EM. Face was involved in all, forearms in 12, dorsa of hands in 8, trunk in 6, neck in 5 and thigh in 1 case. Five cases had mucosal ulcers on palate and posterior buccal mucosa and 1 case had pigmented plaques on tongue. Associated arthralgia was present in 4 cases, haemorrhagic crusting of lips in 1, rheumatoid arthritis in 1, cicatricial alopecia in 1, telangiectasia in 1, ichthyosis in 1 and hypertrichosis in 1 case.

Routine investigations were normal in all 14 cases except evidence of UTI in 1 case. ESR ranged from 30-60mm. Slight derangement of SGOT/SGPT was observed in 2 cases, RA factor was positive in 1:40 dilutions in 1 case. Test for ANA was done in 7/14 cases and were negative in all.

Histopathologically all 14 cases revealed variable degree of epidermal atrophy, basket weave hyperkeratosis, delling, variable degree of epidermal cell damage seen as perinuclear vacuolisation, homogenisation or eosinophilic necrosis of epidermal cells. Interface dermatitis with variable degree of basal cell degeneration (14), lichenoid dermal infiltration close to dermo-epidermal junction (11), lymphohistiocytic vasculitis of dermal vessels (14) incontinence of melanin (14), colloid bodies (prominent in 8, moderate in 3 and occasional in 3) and dermal oedema were also observed (all cases).

Discussion

Present study revealed that SCLE is a definite entity which can be differentiated from both DLE and SLE clinically as well as histopathologically. Histopathologically epidermal atrophy, interface dermatitis, colloid bodies, melanin incontinence and lymphohistiocytic vasculitis were regularly observed. All cases responded favourably to 10-15mg prednisolone daily which was later reduced to maintenance dose of 5-7.5 mg prednisolone daily without any significant side effects. Most of the patients needed prolonged maintenance doses as relapses occurred after variable interval of stopping systemic corticosteroids.