Sir,

Lichen planus is a cutaneous inflammatory disease of unknown etiology, classically characterized by polygonal papules forming purpuric and pruritic plaques, with Wickham striae as a distinctive finding. There are more than ten clinical variants of this condition, which are less common but present a diagnostic challenge [1].

A 64-year-old male was referred to the dermatology department for a widespread dermatosis with an 8-month evolution, affecting the trunk and lower extremities, specifically involving the back, abdomen, and anterior aspects of both legs in a symmetrical distribution. The dermatosis was characterized by multiple circular and oval, non-confluent plaques with peripheral erythema and scaling, but with a pale, atrophic center, with no associated pruritus or prior treatment interventions (Figs. 1a – 1d). The biopsy revealed a lichenoid interface dermatitis with areas of epidermal atrophy, scaling, and focal lymphocytic parakeratosis, consistent with annular lichen planus (Figs. 2a – 2d). Treatment was initiated with medium-potency corticosteroids for four weeks, followed by a calcineurin inhibitor. The patient returned for follow-up six months later, having completed corticosteroid therapy and remaining on calcineurin inhibitor treatment. On physical examination, there was significant improvement. The dermatosis was now only localized to the lower extremities, affecting the anterior and distal lateral aspects bilaterally and symmetrically. The lesions were characterized by residual annular plaques, some with scaling, and only one with a persistent erythematous border. Maintenance therapy with a calcineurin inhibitor continued, and a follow-up appointment was scheduled in four months.

	Figure 1: (a-d) Widespread dermatosis characterized by multiple, circular and oval, non-confluent plaques with peripheral erythema and scaling, but with a pale, atrophic center.
	Figure 2: (a-d) Lichenoid interface dermatitis with areas of epidermal atrophy, scaling, and focal lymphocytic parakeratosis, consistent with annular lichen planus.

Lichen planus is a cutaneous inflammatory disease of unknown etiology. Among its more than ten clinical variants, three are particularly relevant to this case: annular lichen planus (ALP), atrophic lichen planus (aLP), and annular atrophic lichen planus (AaLP).

ALP represents a rare variant, accounting for less than 10% of cases. It is characterized by violaceous, annular plaques with a thin border and a central clearing, typically affecting the penis and intertriginous areas [2]. In a case series of 20 patients, the most frequent location was the axillae (35%), followed by the penis (25%) and extremities (25%). The border was mainly described as purpuric or white, with only one of the 20 patients presenting atrophic centers. Additionally, four patients had more than ten lesions, none exhibited the Koebner phenomenon or generalized lesions, and only 26% reported pruritus [2].

Two prevailing theories have been proposed to explain the formation of these lesions, summarized as: ‘rings resulting from papules’ versus ‘papules forming ring-like patterns.’ The latter is the more widely accepted theory, suggesting that annular lesions may arise from the central involution of a papule or plaque, which simultaneously expands peripherally with an advancing raised border. Histologically, typical features of lichen planus are only observed in the periphery, while the center of the lesion shows pronounced epidermal atrophy. Additionally, the characteristic findings of lichen planus are often present, indicating that ALP may also be associated with epidermal atrophy in itself [1].

On the other hand, aLP may represent the resolving phase of lichen planus, characterized by epidermal thinning rather than the degeneration of elastic fibers [3].

Finally, AaLP is a highly rare clinical variant with a morphology similar to the two previous entities. However, it is histologically distinct due to secondary atrophy resulting from the loss of elastic fibers in the papillary dermis, driven by elastases released by macrophages. It is proposed that the annular configuration of these lesions is a consequence of the elastolytic activity of infiltrating inflammatory cells in the center, with peripheral expansion of the active process. Given that AaLP is already an uncommon variant, some authors suggest not further subdividing it. Nevertheless, AaLP is recognized for its worse prognosis due to resistance to conventional treatments [4].

ALP is a rare variant of lichen planus. A translesional biopsy that includes the center, periphery, and healthy skin is recommended, as typical histopathological findings are usually located in the periphery, while the center only shows epidermal atrophy. aLP may represent the resolving phase of lichen planus, in which the atrophy corresponds to epidermal thinning. In contrast, AaLP presents atrophy secondary to the loss of elastic fibers due to the elastolytic activity of macrophages [1–4].

The clinical relevance of distinguishing these variants lies in their prognosis. AaLP is associated with a worse outcome due to a poor response to conventional treatments, whereas ALP tends to resolve spontaneously within one to two years, leaving residual hyperpigmentation [3,4]. Distinguishing ALP from atrophic or annular atrophic variants is clinically relevant due to their differing prognoses and responses to treatment.

REFERENCES

1.Böer-Auer A, Lütgerath C. [Lichen planus:Fundamentals, clinical variants, histological features, and differential diagnosis]. Hautarzt. 2020;71:1007-21.

2.Reich HL, Nguyen JT, James WD. Annular lichen planus:A case series of 20 patients. J Am Acad Dermatol. 2004;50:595-9.

3.Shiohara T, Mizukawa Y:Liquen plano y dermatosis liquenoides, [w:] Dermatología, 4ªed., J.L. Bolognia, J.L. Jorizzo, J.V. Schaffer (red.), Elsevier, España, 2019:188–207.

4.Santhosh P, George M. Annular atrophic lichen planus:A review of the literature. Int J Dermatol. 2022;61:1213-7.