Multiple Hypertrophic Lichen Planus Mimicking Squamous Cell Carcinoma: A Case Report

Abstract

Introduction

Hypertrophic lichen planus (HLP) with pseudoepitheliomatous hyperplasia (PEH) can closely mimic well-differentiated squamous cell carcinoma (SCC), creating a clinically important diagnostic pitfall. Fewer than 26 case reports in the literature describe HLP initially misdiagnosed as SCC, underscoring the need for careful clinicopathologic correlation.

Case Presentation

A 77-year-old woman developed multiple hyperkeratotic nodules and plaques on both legs and feet over 4 months. A punch biopsy led to an initial diagnosis of well-differentiated SCC. An additional elliptical incisional biopsy from a separate plaque showed irregular acanthosis with hypergranulosis, endophytic well-differentiated squamous epithelium, and a dense lichenoid interface infiltrate with focal basal vacuolar change and Max-Joseph spaces, without destructive invasion or significant atypia – findings consistent with HLP with PEH. The lesions flattened with topical clobetasol propionate under occlusion for 6 weeks, and no recurrence was observed during a 3-month follow-up.

Conclusion

HLP can closely mimic well-differentiated SCC, making adequate tissue sampling and clinicopathologic correlation essential to avoid unnecessary surgery. This case adds to the limited literature on HLP misdiagnosed as SCC and highlights the need to also consider inflammatory mimickers.

Introduction

Hypertrophic lichen planus (HLP) is a chronic inflammatory dermatosis characterized by thick, verrucous plaques, often localized to the shins [1]. Histopathologically, HLP typically demonstrates hyperkeratosis, acanthosis, hypergranulosis, and occasionally pseudoepitheliomatous hyperplasia (PEH). A recent review of the literature identified fewer than 26 reported cases in which HLP was initially misdiagnosed as squamous cell carcinoma (SCC) [2], emphasizing the ongoing diagnostic challenge and the risk of unnecessary surgical intervention. We report a case of HLP presenting with rapidly developing, bilateral, multifocal plaques predominantly on the legs, in which a punch biopsy suggested SCC, whereas an elliptical incisional biopsy established HLP with PEH. We also outline key clinical and histologic discriminators between HLP, SCC, and inflammatory mimickers.

Case Report

The CARE Checklist has been completed by the authors for this case report, attached as online supplementary material (for all online suppl. material, see https://doi.org/10.1159/000550461). A 77-year-old woman presented with a 4-month history of hyperkeratotic eruption on the left leg. Similar lesions had appeared on the bilateral legs and feet within the preceding month. The lesions were intensely pruritic. Physical examination revealed numerous hyperkeratotic nodules and plaques with oyster shell-like hyperkeratosis on erythematous bases on the shin and dorsum of both feet (Fig. 1a, b). She had no history of varicose veins or chronic venous insufficiency; body mass index was 22.1. There was no history of sun damage, phototherapy, irradiation, or halogen-containing medication use. She reported no oral, nail, or scalp involvement. Histological examination of a punch biopsy specimen from a nodule on the right ankle revealed marked acanthosis with hyperkeratosis and inflammatory cell infiltration in the upper dermis (Fig. 2a). Hypergranulosis was observed in over half the area of the epidermis. Based on these findings, a diagnosis of well-differentiated SCC was initially rendered. To clarify the diagnosis, an elliptical incisional biopsy was performed on a left-leg plaque, which showed mild hyperkeratosis, irregular acanthosis with hypergranulosis, epidermal hyperplasia, and endophytic well-differentiated squamous epithelium with associated lichenoid inflammation (Fig. 2b). Focal basal cell vacuolar degeneration and small areas of artifactual separation between the epidermis and the dermis, known as Max-Joseph spaces, were seen. Laboratory examinations, including a full blood cell count, routine biochemistry, fasting blood sugar level, and urinalysis, gave normal results. Reconsidering the overall clinical and histopathological findings, a diagnosis of HLP with PEH was made, and the patient was treated with topical corticosteroid (clobetasol propionate) with occlusion for 6 weeks. This resulted in gradual resolution of the plaques and nodules, with no recurrence during a 3-month follow-up (Fig. 3).

Fig. 1.

a, b Numerous hyperkeratotic nodules and plaques overlying erythematous bases on the shin (a) and dorsum of both feet (b).

Fig. 2.

a A punch biopsy specimen from a nodule on the right ankle showed marked acanthosis with hyperkeratosis and inflammatory cell infiltration in the upper dermis (hematoxylin-eosin [HE]. original magnification, ×20). b An elliptical incisional biopsy specimen from plaque on the left leg showed mild hyperkeratosis, irregular acanthosis with hypergranulosis, epidermal hyperplasia, and endophytic well-differentiated squamous epithelium with associated lichenoid inflammation (HE. ×40).

Fig. 3.

Hyperkeratotic plaques and nodules showed almost complete resolution after 6 weeks treatment with topical corticosteroid with occlusion.

Discussion

Malignant transformation of long-standing HLP to SCC has been reported but remains uncommon; to date, at least 41 cases have been documented in the English literature [3–6]. Separately, recent literature documents fewer than 26 cases of HLP initially misdiagnosed as SCC, making the distinction clinically challenging [2]. Clinically, HLP usually presents as multiple hyperkeratotic plaques and causes pruritus. The presence of Wickham striae and associated typical lichen planus affecting the oral mucosa, nails, and other skin areas may be diagnostically informative. The present patient had no history of sun damage, phototherapy, irradiation, or factors predisposing to multiple SCC. Histologically, in HLP, marked epidermal hyperplasia and large rete ridges may be present alongside classic histological features of lichen planus in lesional tissue. HLP may be associated with PEH, the latter consisting of epidermal hyperplasia usually with jagged borders and a sharply pointed base [7]. Horn pearl formation may also be evident. Epidermal keratinocytes may show a minor degree of cytologic atypia, mostly in the epidermal basal layer, and keratinocyte necrosis is usually absent. Mitotic figures may be evident, but they are not numerous or atypical. However, in PEH, lymphovascular and perineural invasion, as seen in SCC, are not observed. Lichenoid dermatitis with eosinophils may be present [8]. Absence of perforating elastic fibers may suggest HLP rather than SCC [9]. In many cases, SCC develops in long-standing HLP, and the average lag time from HLP diagnosis to SCC presentation is 11 years [2]. In contrast, our patient developed numerous lesions within a few months, without chronic scarring or photodamage, supporting an inflammatory rather than neoplastic process.

In this case, the rapid bilateral and multifocal shin-predominant eruption with oyster shell-like hyperkeratosis and a lichenoid interface pattern without destructive invasion necessitated differentiation from inflammatory dermatoses. We also systematically considered inflammatory mimickers that clinically and histologically resemble HLP, as summarized in Table 1. Bromoderma typically requires halogen exposure and may show folliculocentric pustules or neutrophil-rich microabscesses; exposure history was absent and these features were not present [10]. Discoid lupus erythematosus often produces photo-distributed scarring plaques with follicular plugging and histologic basement-membrane thickening with dermal mucin; these clinical and histologic hallmarks were lacking [11]. Prurigo nodularis/lichen simplex chronicus cause lichenified nodules with dermal fibrosis and verticalized collagen bundles but no true lichenoid interface [12, 13]; in contrast, our biopsies showed a classic lichenoid pattern. Verrucous psoriasis exhibits regular psoriasiform acanthosis with parakeratosis and Munro microabscesses, which were absent in our specimens [14].

Table 1.

Differential diagnosis of HLP and its mimickers

​	HLP	SCC	Bromoderma	DLE	Prurigo nodularis/lichen simplex	Verrucous psoriasis
Typical location	Shins/ankles, distal lower legs	Often sun-exposed sites	Hands, forearms, face	Face, scalp, ears	Extensor limbs	Knees, elbows, shins
Number/distribution	Multiple, bilateral, symmetric	Usually solitary/few	Few, scattered	Localized scarring plaques	Multiple nodules	Symmetric plaques
Surface morphology	Hyperkeratotic, verrucous, violaceous	Keratotic, crusted; may ulcerate	Pustular/crusted, vegetating	Atrophic center, follicular plugging	Excoriated lichenified nodules	Thick scaly plaques
Symptoms	Intense pruritus	Variable	Tender/inflamed	Photosensitive	Severe pruritus	Pruritus variable
Histopathology	Lichenoid interface; wedge-shaped hypergranulosis; saw-tooth rete;±PEH	Invasive atypical squamous cells; keratin pearls; mitoses	Neutrophil-rich microabscesses; mixed infiltrate	Basement-membrane thickening; dermal mucin; periadnexal inflammation	Epidermal hyperplasia; vertical collagen bundles; no interface	Regular psoriasiform acanthosis; parakeratosis; Munro abscesses
Key discriminator	No destructive invasion; clinicopathologic correlation	Destructive invasion and cytologic atypia	Exposure history; neutrophils/eosinophils	Scarring, mucin, “lupus band” on DIF (if performed)	Lack of interface; fibrosis pattern	Neutrophils in stratum corneum, granular layer loss

DLE, discoid lupus erythematosus.

The mechanisms by which lichen planus evolves into HLP are not fully understood, but chronic mechanical irritation and circulatory factors are plausible contributors [15]. Mechanical irritation including koebnerization and pruritus-driven scratching has been implicated in the HLP; in this case, the patient reported marked pruritus, and an itch-scratch cycle may have promoted lichenification and epidermal hyperplasia. Circulatory factors such as venous insufficiency are also discussed particularly for lower-leg HLP [15]. Management should therefore address local factors by controlling pruritus and correcting venous stasis when present in addition to anti-inflammatory therapy.

Conclusion

HLP can closely mimic well-differentiated SCC. Although SCC is usually the first consideration, our case highlights the need to also consider inflammatory mimickers and to obtain adequate tissue – often with repeat deeper biopsy – so clinicopathologic correlation is secure. Recognizing this pattern helps avoid unnecessary surgery and enables effective conservative therapy.

Statement of Ethics

Ethical approval was not required for this study in accordance with the local or national guidelines. Written informed consent was obtained from the patient for the publication of this report in accordance with the journal’s patient consent policy.

Conflict of Interest Statement

The author has no conflicts of interest to declare.

Funding Sources

This study was not supported by any sponsor or funder.

Author Contributions

Sho Hirata: writing – original draft and writing – review and editing. Daisuke Watabe: writing – review and editing and visualization. Toshihide Akasaka: supervision and visualization. Hiroo Amano: supervision and visualization.

Funding Statement

This study was not supported by any sponsor or funder.

Data Availability Statement

The data that support the findings of this study are not publicly available due to privacy reasons but are available from the corresponding author upon request.