Context.—

Hypertrophic lichen planus (HLP) is a variant of lichen planus that can be difficult to diagnose based on histopathologic features alone. Thus, patient clinical history and clinicopathologic correlation are essential considerations to make the correct diagnosis.

Objective.—

To discuss the clinical and histologic presentation of HLP and provide a thorough review of commonly encountered mimickers in the differential diagnosis.

Data Sources.—

Data were derived from a literature review, personal clinical and research experiences, and a review of cases in the archives of a tertiary care referral center.

Conclusions.—

In general, HLP involves the lower extremities and is characterized by thickened, scaly nodules and plaques that are often pruritic and chronic in nature. HLP affects both males and females and is most common in adults 50 to 75 years of age. Unlike conventional lichen planus, HLP tends to have eosinophils and classically displays a lymphocytic infiltrate most concentrated around the tips of rete ridges. The differential diagnosis for HLP is broad and encompasses numerous entities in many different categories, including premalignant and malignant neoplasms, reactive squamoproliferative tumors, benign epidermal neoplasms, connective tissue disease, autoimmune bullous disease, infection, and drug-related reactions. Therefore, a high index of suspicion must be maintained to avoid a misdiagnosis and potential inappropriate treatments.

Hypertrophic lichen planus (HLP), also known as lichen planus verrucosus or lichen planus hypertrophicus, is a variant of lichen planus (LP) not infrequently encountered in routine dermatologic practice. HLP can be difficult to correctly diagnose on histology alone, and patient clinical history is essential to make the appropriate diagnosis. HLP most commonly involves the bilateral shins, ankles, or dorsal feet and is characterized by hyperkeratotic nodules and plaques with overlying thick adherent scale. These lesions are often pruritic and chronic in nature owing to repeated scratching and/or rubbing. HLP can be seen in both men and women, most commonly in adults 50 to 75 years of age. Histologically, HLP shows compact hyperkeratosis, hyperorthokeratosis, hypergranulosis, and pseudoepitheliomatous hyperplasia. Unlike conventional LP, HLP demonstrates the presence of eosinophils and usually lacks the underlying dense bandlike lymphocytic inflammatory infiltrate. Instead, the lymphocytic infiltrate is most prominent and/or confined to the tips of rete ridges. The clinical and histologic differential diagnosis for HLP is quite broad and includes malignant squamous and benign epidermal neoplasms, lupus erythematosus, drug eruptions, and fungal infections, among other entities. A high index of suspicion must be maintained to avoid a misdiagnosis and potential inappropriate treatments. The primary objective of this article is to provide an update on HLP and provide practical dermatopathology knowledge on how to differentiate HLP from common mimickers and avoid similar but distinct pitfall diagnoses.

LP is an idiopathic autoimmune inflammatory condition that can affect the skin, nails, hair, and oral and anogenital mucous membranes.1,2  While both men and women can be affected by LP, there is a female predominance (female to male ratio of 3:1) and tends to be more frequent in individuals of European descent. Less commonly, children can be affected by LP. Previous studies exploring the prevalence of LP were limited and/or inaccurate because they included only certain variants of LP, excluded certain populations of people, lacked clear inclusion or diagnostic criteria in studies, and lacked uniform methods. However, more recent analyses estimate that the prevalence of LP worldwide is approximately 0.22% to 5%, while the prevalence of LP among US adults was between 0.36% and 0.42%, but varied by age and race or ethnicity.36  These results are somewhat similar to the results from another study examining parts of Sweden, which estimated the prevalence of LP to be 0.1% to 0.3%.7  While older reports state that LP is most common in middle-aged adults, this cross-sectional study found that LP prevalence is highest among patients who are older (≥75 years) and that LP prevalence increases with increasing age.36 

While the exact etiology and pathogenesis of LP have yet to be fully elucidated, it is believed to be host T-lymphocyte mediated. Specifically, it is hypothesized that skin-infiltrating T cells, including both T cells migrating through the circulation as well as those T cells residing indigenously within the skin (ie, cytotoxic CD8+ T cells), cause direct tissue damage to the epidermis within a milieu of inflammatory cytokines like interferon-γ and tumor necrosis factor α.79  A number of contributing factors have been linked to the development of HLP, including infections (particularly viral), certain environmental exposures (such as contact allergens), and medications.79  It is thought that there is an interplay between the host immune system and one of the previously listed factors such that it generates an autoimmune reaction resulting in clinical manifestation of LP. Furthermore, it has been hypothesized that eosinophils may play more of a role in the development of HLP than previously thought.10  Lastly, the Koebner phenomenon is also believed to be involved in the development of HLP lesions.2 

LP is a papulosquamous disorder of the skin and mucous membranes. The characteristic clinical morphology, anatomic distribution, and histopathologic features all tend to differ slightly, based on the specific variant of LP. Classic LP clinically presents with numerous monomorphic, pruritic, purple, polygonal, flat-topped, scaly papules and plaques and tends to favor the wrists, upper extremities, and distal lower extremities.1  LP lesions characteristically have adherent, white reticulated scale called Wickham striae.11  There are numerous described clinical variants of LP, including annular LP, actinic LP, atrophic LP, oral LP, nail LP, genital LP, erosive LP, hypertrophic LP, inverse LP, bullous LP, LP pigmentosus, LP pemphigoides, follicular LP (lichen planopilaris or frontal fibrosis alopecia), and drug-induced LP.1,2,1216 

HLP is a less common variant of LP that favors the lower extremities, but less commonly may be seen elsewhere on the body. Clinically, HLP begins as single or multiple papules, nodules, or plaques on the shins, ankles, and feet with overlying thick, adherent, reticulated scale (known as Wickham striae), which may have an erythematous base (Figure 1). Lesions can be asymptomatic, but are commonly pruritic and tender or painful, especially when traumatized. Given a predilection for sun-exposed sites on the lower legs and similar clinical appearance, HLP is often mistakenly initially diagnosed as hypertrophic actinic keratosis, keratoacanthoma, or invasive squamous cell carcinoma (SCC). A common clinical scenario may involve a patient presenting with multiple keratotic lesions on the bilateral shins, histologically diagnosed as invasive SCCs, and referred for Mohs micrographic surgery or surgical excision. Management of HLP differs drastically from that of malignant squamous neoplasms; thus, clinicopathologic correlation is of the utmost importance. An incorrect diagnosis can lead to inappropriate treatment and unnecessary surgery on sensitive anatomic sites. Further complicating this scenario are reports of keratoacanthoma and invasive SCC arising within HLP lesions.

Figure 1

Thickened, scaly papulonodule on the lower extremity with prominent adherent scale, known as Wickham striae, which is a distinct clinical feature of lichen planus.

Figure 2. Histopathologic features of hypertrophic lichen planus, which include pseudoepitheliomatous hyperplasia, dense lymphocytic infiltrate most prominent at the tips of rete ridges with apoptotic keratinocytes, and scattered eosinophils (hematoxylin-eosin, original magnification ×2).

Figure 3. Dense lymphocytic infiltrate most prominent at the tips of rete ridges with apoptotic keratinocytes seen in hypertrophic lichen planus (hematoxylin-eosin, original magnification ×10).

Figure 4. Lymphocytes and scattered eosinophils in hypertrophic lichen planus (hematoxylin-eosin, original magnification ×40).

Figure 1

Thickened, scaly papulonodule on the lower extremity with prominent adherent scale, known as Wickham striae, which is a distinct clinical feature of lichen planus.

Figure 2. Histopathologic features of hypertrophic lichen planus, which include pseudoepitheliomatous hyperplasia, dense lymphocytic infiltrate most prominent at the tips of rete ridges with apoptotic keratinocytes, and scattered eosinophils (hematoxylin-eosin, original magnification ×2).

Figure 3. Dense lymphocytic infiltrate most prominent at the tips of rete ridges with apoptotic keratinocytes seen in hypertrophic lichen planus (hematoxylin-eosin, original magnification ×10).

Figure 4. Lymphocytes and scattered eosinophils in hypertrophic lichen planus (hematoxylin-eosin, original magnification ×40).

Close modal

In general, the histologic hallmark of LP is the presence of an interface dermatitis, a histologic reaction pattern that includes a heterogeneous group of skin conditions. Interface dermatitis shows a dense, bandlike lymphocytic inflammatory infiltrate obscuring the dermal-epidermal junction, resulting in apoptosis of keratinocytes due to cellular destruction along the basement membrane zone. This lymphocytic inflammation leads to cytoplasmic vacuolization and edema with separation of the epidermal basal cells from the underlying lamina densa, creating gaps called Max Joseph spaces. In addition, there is hyperorthokeratosis, irregular psoriasiform acanthosis, pseudoepitheliomatous hyperplasia, wedge-shaped hypergranulosis, and saw-toothing of rete ridges.

Conventional LP displays a lichenoid interface dermatitis, which is defined by the presence of a dense, confluent, bandlike lymphocytic inflammatory infiltrate obscuring the dermal-epidermal junction. There are also eosinophilic amorphous dyskeratotic cells, which represent dead or dying keratinocytes in the epidermis, along with hyperorthokeratosis, irregular psoriasiform acanthosis, wedge-shaped hypergranulosis, saw-toothing of rete ridges, and Max Joseph spaces along the basement membrane zone. Idiopathic LP customarily lacks parakeratosis and eosinophils. In contrast, HLP often demonstrates the presence of eosinophils and classically lacks the underlying prominent bandlike lymphocytic inflammatory infiltrate in the dermis. Instead, the lymphocytic infiltrate is most prominent at the tips of rete ridges in HLP and displays a discontinuous pattern of inflammation (Figures 2 and 3). HLP can display variable numbers of eosinophils even in the absence of medication/drug history (Figure 4).10,17,18  Dyskeratotic cells, hyperorthokeratosis, irregular psoriasiform acanthosis, wedge-shaped hypergranulosis, and saw-toothing of rete ridges are still seen in HLP.

The clinicopathologic differential diagnosis for HLP is quite broad and requires direct correlation between clinical presentation and microscopic findings to make the correct diagnosis. HLP can mimic premalignant and malignant neoplasms (hypertrophic actinic keratosis, keratoacanthoma, and invasive SCC), reactive squamoproliferative entities (prurigo nodularis/lichen simplex chronicus), connective tissue diseases (hypertrophic lupus erythematosus), benign epidermal neoplasms (benign lichenoid keratosis), autoimmune bullous diseases (pemphigoid nodularis), and those associated with human papillomaviruses such as viral verrucae. HLP may also imitate skin processes due to exposure to certain chemical compounds and even infections, including halogenoderma (eg, bromoderma, iododerma) and infections with cutaneous involvement (eg, deep fungal such as blastomycosis, chromoblastomycosis, and mycobacterial). Additionally, owing to the presence of eosinophils, HLP can be mistaken for drug-related reactions (lichenoid drug eruption). Owing to the large number of entities in the differential diagnosis for HLP, a sufficient sample is critical to fully assess the base of the lesion and any important features in the dermis or subcutaneous tissue. A broad shave biopsy or excisional biopsy is recommended to obtain adequate sampling.

HLP, hypertrophic actinic keratosis, keratoacanthoma, and invasive SCC can share many overlapping features, both clinically and histopathologically, thus making clinicopathologic correlation essential for appropriate and timely initiation of the correct treatment.1931  Hypertrophic actinic keratosis and keratoacanthoma exhibit prominent irregular acanthosis, parakeratosis, and orthokeratosis, which are features seen in prurigo nodularis/lichen simplex chronicus due to chronic, repetitive rubbing or scratching. Cytology in hypertrophic actinic keratosis and keratoacanthoma can have little atypia, while prurigo nodularis/lichen simplex chronicus is entirely bland. An underlying dermal lymphocytic infiltrate can be present in hypertrophic actinic keratosis, keratoacanthoma, and invasive SCC, indicating irritation and/or inflammation, but the characteristic features of LP (ie, dyskeratotic cells, hyperorthokeratosis, irregular psoriasiform acanthosis, wedge-shaped hypergranulosis, and saw-toothing of rete ridges) are lacking. Invasive SCC can exhibit varying degrees of cytologic atypia (ranging from well, moderately, to poorly differentiated) and invasion may range from the superficial dermis down into subcutaneous fat and beyond. There may or may not be perineural involvement. HLP can also be easily misdiagnosed as SCC, but there are also reports of keratoacanthoma and SCC arising in long-standing HLP.1931  In another study, HLP was compared to invasive SCC to assess the utility of certain histopathologic features in distinguishing the entities from one another.21  Hyperorthokeratosis, wedge-shaped hypergranulosis, and irregular hyperplasia were significantly associated with HLP (Figure 5), while parakeratosis, solar elastosis, deep extension, and perforating elastic fibers were significantly associated with SCC (Figure 6).21  The presence of eosinophils, cytologic atypia, lichenoid dermatitis, and hypogranulosis, however, was not found to be statistically significant and these were seen in both HLP and SCC.21 

Figure 5

More prominently well-developed lesion of hypertrophic lichen planus mimicking squamous cell carcinoma but lacking cytologic atypia and increased mitotic figures (hematoxylin-eosin, original magnification ×2).

Figure 6. Pseudoepitheliomatous hyperplasia with keratinocyte atypia, pleomorphism, increased mitotic figures, and paradoxical maturation characteristic of invasive well-differentiated squamous cell carcinoma (hematoxylin-eosin, original magnification ×2).

Figure 5

More prominently well-developed lesion of hypertrophic lichen planus mimicking squamous cell carcinoma but lacking cytologic atypia and increased mitotic figures (hematoxylin-eosin, original magnification ×2).

Figure 6. Pseudoepitheliomatous hyperplasia with keratinocyte atypia, pleomorphism, increased mitotic figures, and paradoxical maturation characteristic of invasive well-differentiated squamous cell carcinoma (hematoxylin-eosin, original magnification ×2).

Close modal

Another common entity in the differential diagnosis for idiopathic LP and HLP includes benign lichenoid keratosis, which is also known as LP-like keratosis. Clinically, benign lichenoid keratoses represent solitary lesions that most commonly present on the trunk or proximal extremities. Histopathologically, benign lichenoid keratoses demonstrate a lichenoid infiltrate of lymphocytes and occasionally may exhibit parakeratosis; dyskeratotic keratinocytes may be present in the epidermis (Figure 7).32,33  Benign lichenoid keratoses do not typically contain eosinophils, unlike HLP. Additionally, in comparison, idiopathic LP presents as multiple lesions most commonly involving the distal extremities like the wrists and ankles.

Figure 7

Lichenoid interface dermatitis with cytoid bodies at the dermal-epidermal junction and mild reactive keratinocyte atypia seen in benign lichenoid keratosis/lichen planus–like keratosis (hematoxylin-eosin, original magnification ×10).

Figure 8. Lichenoid to vacuolar interface dermatitis with cytoid bodies seen in hypertrophic lupus erythematosus (hematoxylin-eosin, original magnification ×20).

Figure 9. Prominent pseudoepitheliomatous hyperplasia with mixed dermal inflammatory infiltrate and characteristic Medlar, or sclerotic, bodies that resemble copper pennies seen in cutaneous infection with chromoblastomycosis (hematoxylin-eosin, original magnification ×20).

Figure 10. Vacuolar to lichenoid interface dermatitis with cytoid bodies at the dermal-epidermal junction, mild spongiosis, pigment incontinence, and scattered eosinophils seen in lichenoid drug eruption (hematoxylin-eosin, original magnification ×20).

Figure 7

Lichenoid interface dermatitis with cytoid bodies at the dermal-epidermal junction and mild reactive keratinocyte atypia seen in benign lichenoid keratosis/lichen planus–like keratosis (hematoxylin-eosin, original magnification ×10).

Figure 8. Lichenoid to vacuolar interface dermatitis with cytoid bodies seen in hypertrophic lupus erythematosus (hematoxylin-eosin, original magnification ×20).

Figure 9. Prominent pseudoepitheliomatous hyperplasia with mixed dermal inflammatory infiltrate and characteristic Medlar, or sclerotic, bodies that resemble copper pennies seen in cutaneous infection with chromoblastomycosis (hematoxylin-eosin, original magnification ×20).

Figure 10. Vacuolar to lichenoid interface dermatitis with cytoid bodies at the dermal-epidermal junction, mild spongiosis, pigment incontinence, and scattered eosinophils seen in lichenoid drug eruption (hematoxylin-eosin, original magnification ×20).

Close modal

Hypertrophic lupus erythematosus is an autoimmune connective tissue disease that affects the skin and is characterized by the presence of a dense lymphocytic inflammatory infiltrate in the underlying superficial dermis. Hypertrophic lupus erythematosus is a rare variant of chronic cutaneous lupus erythematosus that may be confused histologically with HLP. Similar to classic chronic cutaneous lupus, hypertrophic lupus erythematosus features irregular epidermal hyperplasia (pseudoepitheliomatous hyperplasia) and vacuolar interface changes with a dense, bandlike, lymphocytic inflammatory infiltrate, but frequently demonstrates reactive squamous atypia of the basal cell layer, placing it in the differential diagnosis of atypical squamoproliferative lesions including HLP (Figure 8).3436  There may be varying numbers of apoptotic keratinocytes present in hypertrophic lupus erythematosus, as well as hyperkeratosis, follicular plugging, basement membrane thickening, dermal mucin, and plasma cells.3436  These are useful clues to the diagnosis of hypertrophic lupus erythematosus when present; however, when absent it may be quite difficult to distinguish this entity from HLP. The number of plasmacytoid dendritic cells is increased and they form discrete aggregates within the dermis in hypertrophic lupus erythematosus; CD123 may be used to highlight these clusters.37 

Pemphigoid nodularis is an extremely rare variant of pemphigoid and clinically presents with hyperkeratotic papules and nodules with evidence of excoriation involving the trunk and extremities. Unlike bullous pemphigoid, non–bullous pemphigoid nodularis does not present with vesicles or bullae. On histology, the typical features mimic those seen with prurigo nodularis and include acanthosis, hyperkeratosis, focal spongiosis, and a mixed superficial perivascular inflammatory infiltrate.3841  Eosinophils are almost never a prominent feature.38  There is no keratinocyte atypia and no subepidermal split. The immunopathologic findings are identical to bullous pemphigoid with antibodies directed against the hemidesmosome structure, specifically bullous pemphigoid antigen 1 (BP 230) and bullous pemphigoid antigen 2 (BP 180). Direct immunofluorescence on perilesional skin can be helpful in distinguishing pemphigoid nodularis from other entities and displays linear deposition of immunoglobulin G and/or C3 along the basement membrane zone.38 

Human papillomaviruses encompass a large group of DNA viruses that infect the epithelium of skin and mucosa. Most commonly, these viruses cause benign papillomas or warts; however, they can also cause malignancy including cervical cancer, anogenital carcinoma, and some oropharyngeal SCCs. In terms of the skin, warts can have several different clinical presentations, such as flat warts (verruca plana), common warts (verruca vulgaris), plantar warts (verruca plantaris), and myrmecial or mosaic warts. In general, histopathologic features of warts include well-circumscribed, papillomatous (steeply sloping “church spires”) papule or plaque with heaped up orthokeratosis and parakeratosis. The parakeratosis is most commonly concentrated, overlying the tops of the “church spires” of papillomatosis along with intracorneal hemorrhage. Additionally, acanthosis, elongated rete ridges, hypergranulosis, prominent course “chunky” keratohyaline granules within the granular layer of the epidermis, and dilated ectatic superficial dermal blood vessels concentrated within dermal papillae are seen in warts. Koilocytes may or may not be seen; however, their presence is not required for diagnosis. Owing to the presence of papillomatosis, orthokeratosis, parakeratosis, hypergranulosis, and acanthotic architecture, warts may be confused with HLP. If the wart has been irritated or is inflamed, then there may be a superficial dermal lymphocytic inflammatory infiltrate, which may further the microscopic similarity between warts and HLP.

Halogenoderma is a category of uncommon dermatoses (bromoderma, fluoroderma, iododerma) that are due to exposure to certain chemicals (bromides, fluorides, iodides/iodine-containing compounds, respectively). These compounds are found in agents used in the medical field, especially as hyperthyroidism treatment, expectorants, radiation protectants, contrast media, wound disinfectants, supplements/medications including amiodarone, and sedatives. The exact pathogenesis of halogenoderma is unknown; however, it is believed that accumulation of the culprit halogenide plays a key role in the development of disease. An identified risk factor that also seems to contribute to halogenoderma is the presence of acute or chronic kidney disease. Halogenoderma can have a variable clinical presentation, ranging from acneiform eruptions and pustules to granulomatous and vegetative plaques. On histopathology, halogenoderma can also demonstrate hyperplasia of the epidermis (pseudoepitheliomatous hyperplasia), which mimics that seen with squamous cell carcinoma and HLP. Adnexal epithelium may become elongated and thickened, appearing as irregular projections down into the dermis. There is also often hypergranulosis, orthokeratosis, and parakeratosis. Notably, halogenoderma displays a predominance of dermal neutrophils as well as intraepidermal collections of neutrophils forming microabscesses, which helps distinguish this entity from HLP. Measurement of serum levels of bromide or iodine may aid in the diagnosis of halogenoderma when pathology is nonspecific.

Certain infections with cutaneous involvement can simulate HLP because they often display pseudoepitheliomatous hyperplasia, akin to several aforementioned entities. Classic infectious processes that present with pseudoepitheliomatous hyperplasia include deep fungal infections and mycobacterial infections.42  Deep fungal infections like histoplasmosis, blastomycosis, coccidioidomycosis, chromoblastomycosis, and paracoccidioidomycosis show irregular acanthosis and a dense underlying lymphohistiocytic inflammation infiltrate with numerous neutrophils (Figure 9). Fungal elements vary in size, shape, and ease of identification based on the species of fungi causing pathology. Similarly, cutaneous tuberculosis demonstrates pseudoepitheliomatous hyperplasia but with the addition of dermal epithelioid granulomas with surrounding mixed inflammatory infiltrate. Ultimately, speciation of deep fungal and mycobacterial infections is based on correlation with tissue culture results. HLP can be distinguished from cutaneous deep fungal and mycobacterial infections by the absence of neutrophils and lack of granulomas.

The presence of eosinophils is a hallmark feature of drug-induced LP and lichenoid drug eruption, but can also be seen in the setting of hypertrophic lichenoid dermatitis due to immune checkpoint inhibition therapy. In several studies, a higher number of apoptotic cells, plasma cells, and eosinophils were found to characterize lichenoid drug eruptions when compared to idiopathic LP (Figure 10).43,44  Similarly, HLP can also have eosinophils present on histopathologic examination.3  In another study, HLP demonstrated a wide histopathologic spectrum, ranging from none to a few eosinophils (similar to idiopathic LP) to numerous eosinophils (average of 10.5 eosinophils per 10 × 20 fields, more comparable to lichenoid drug eruption).3  Thus, HLP can have zero to many eosinophils and therefore it should be considered in the differential diagnosis for any lichenoid interface dermatitis with eosinophils in the appropriate clinical setting. Hypertrophic lichenoid dermatitis is an emerging entity that can be seen in the setting of treatment with immune checkpoint inhibition.4549  These immunotherapy agents, which include programmed death receptor-1 (PD-1), programmed death ligand-1 (PD-L1), and cytotoxic T-lymphocyte–associated protein 4 (CTLA-4) inhibitors, are commonly used to treat metastatic malignancies including melanoma and SCC. Clinically, there are multiple thickened to verrucous papules, nodules, and plaques that can appear on the trunk and extremities, with a mean onset of 42 days from drug initiation, although these lesions may appear anywhere within 1 to 75 days of starting the culprit agent.46  Histologically, hypertrophic lichenoid dermatitis can have almost identical features to HLP and lichenoid drug eruptions, and in addition to a dense bandlike lymphocytic infiltrate in the dermis, also usually has eosinophils present. Helpful clues that may point toward a diagnosis of hypertrophic lichenoid dermatitis include a known history of being treated with an immune checkpoint inhibitor within an appropriate period (between start of the medication and onset of the cutaneous eruption) and the presence of overlying epidermal spongiosis. Clinicopathologic correlation is essential in making the correct diagnosis.

HLP is a clinical variant of LP, which has a predilection for the lower extremities, particularly the shins. It is usually a chronic skin condition, often requiring topical, intralesional, and/or systemic intervention. If initially misdiagnosed as invasive SCC, patients may undergo a procedure such as a wide local excision or Mohs micrographic surgery in an attempt to “clear the cancer.” However, because HLP is not considered to be a malignancy and there tends to be more than 1 lesion present, the patient may ultimately go through multiple surgeries for a nonmalignant condition. This potentially leads to an increase in slowly healing, sometimes poorly healing, or even nonhealing lower leg wounds that can become a significant burden for the patient and health care system in general. Unfortunately, the shins are a high-risk site for infection with less common organisms (including Pseudomonas, Enterococcus, gram-negative organisms, and methicillin-resistant Staphylococcus aureus) and the healing process is often slowed down by older/advanced age and the presence of 1 or more comorbid conditions like diabetes mellitus, lymphedema, heart failure, and peripheral vascular disease. Patients often require weeks to months of wound care, either from visiting home health nurses or weekly visits to wound care clinics, which may or may not be located near a patient's home.

If diagnosed correctly, surgery can be appropriately avoided, wherein HLP treatment can be much less invasive and less likely to lead to chronic, poorly healing to nonhealing lower leg wounds and ulcers. Initial treatments for HLP generally start with topical agents including potent topical corticosteroid application under occlusion but alitretinoin gel has been reported to be effective.5052  Intralesional corticosteroid injections can be used, especially if there are numerous lesions. If widespread and/or patient factors prevent the use of topical or intralesional therapies, phototherapy (especially narrowband ultraviolet B radiation) and/or systemic agents like prednisolone, acitretin, methotrexate, mycophenolate mofetil, tofacitinib, and thalidomide have also been reported for LP treatment.5361  Overall, HLP has a good prognosis, and patients normally do well after treatment with resolution of most, if not all, lesions. However, close observation and routine skin examination are recommended to monitor for development of keratoacanthoma and SCC if HLP lesions do not resolve completely.

LP is an idiopathic inflammatory condition that can affect the skin, nails, hair, and mucous membranes. HLP is an uncommon variant of LP that is frequently misdiagnosed as SCC owing to overlapping similarities, both clinically and histopathologically. HLP demonstrates hyperorthokeratosis, hypergranulosis, and pseudoepitheliomatous hyperplasia. Unlike conventional LP, HLP can have a variable number of eosinophils present and notably lacks an underlying prominent bandlike lymphocytic inflammatory infiltrate. The differential diagnosis for HLP is quite broad and, thus, requires both a high index of suspicion and clinicopathologic correlation to make the correct diagnosis.

1.
Le Cleach
L,
Chosidow
O.
Lichen planus
.
N Engl J Med
.
2012
;
366
(8)
:
723
732
.
2.
Weston
G,
Payette
M.
Update on lichen planus and its clinical variants
.
Int J Womens Dermatol
.
2015
;
1
(3)
:
140
149
.
3.
Bhattacharya
M,
Kaur
I,
Kumar
B.
Lichen planus: a clinical and epidermiological study
.
J Dermatol
.
2000
;
27
(9)
:
576
582
.
4.
Leasure
AC,
Cohen
JM.
Prevalence of lichen planus in the United States: a cross-sectional study of the All of Us Research Program
.
J Am Acad Dermatol
.
2022
;
87
(3)
:
686
687
.
5.
Hellgren
L.
The prevalence of lichen ruber planus in different geographical areas in Sweden
.
Acta Derm Venereol
.
2019
;
50
(5)
:
374
380
.
6.
Pandhi
D,
Singal
A,
Bhattacharya
SN.
Lichen planus in childhood: a series of 316 patients
.
Pediatr Dermatol
.
2014
;
31
(1)
:
59
67
.
7.
Gilhar
A,
Pillar
T,
Winterstein
G,
Etzioni
A.
The pathogenesis of lichen planus
.
Br J Dermatol
.
1989
;
120
(4)
:
541
544
.
8.
Shiohara
T,
Mizukawa
Y,
Takahashi
R,
Kano
Y.
Pathomechanisms of lichen planus autoimmunity elicited by cross-reactive T cells
.
Curr Dir Autoimmun
.
2008
;
10
:
206
226
.
9.
Rana
S,
Gupta
R,
Singh
S,
Mohanty
S,
Gupta
K,
Kudesia
M.
Localization of T-cell subsets in cutaneous lichen planus: an insight into pathogenetic mechanism
.
Indian J Dermatol Venereol Leprol
.
2010
;
76
(6)
:
707
709
.
10.
Alomari
A,
McNiff
JM.
The significance of eosinophils in hypertrophic lichen planus
.
J Cutan Pathol
.
2014
;
41
(4)
:
347
352
.
11.
Steffen
C,
Dupree
ML.
Wickham
Louis-Frederic
and the Wickham's striae of lichen planus
.
Skinmed
.
2004
;
3
(5)
:
287
289
.
12.
Sharma
A,
Białynicki-Birula
R,
Schwartz
RA,
Janniger
CK.
Lichen planus: an update and review
.
Cutis
.
2012
;
90
(1)
:
17
23
.
13.
Gorouhi
F,
Davari
P,
Fazel
N.
Cutaneous and mucosal lichen planus: a comprehensive review of clinical subtypes, risk factors, diagnosis, and prognosis
.
ScientificWorldJournal
.
2014
;
30
:
742826
.
14.
Tziotzios
C,
Brier
T,
Lee
JYW,
et al .
Lichen planus and lichenoid dermatoses: conventional and emerging therapeutic strategies
.
J Am Acad Dermatol
.
2018
;
79
(5)
:
807
818
.
15.
Tziotzios
C,
Lee
JYW,
Brier
T,
et al .
Lichen planus and lichenoid dermatoses: clinical overview and molecular basis
.
J Am Acad Dermatol
.
2018
;
79
(5)
:
789
804
.
16.
Lehman
JS,
Tollefson
MM,
Gibson
LE.
Lichen planus
.
Int J Dermatol
.
2009
;
48
(7)
:
682
694
.
17.
Parihar
A,
Sharma
S,
Bhattacharya
SN,
Singh
UR.
A clinicopathological study of cutaneous lichen planus
.
J Derm Dermatol Surg
.
2015
;
19
(1)
:
21
26
.
18.
Guillen-Climent
S,
Porcar Saura S, Monteagudo C, Ramón Quiles MD. Hypertrophic lichen planus: importance of follow-up and clinicopathologic correlation
.
Actas Dermosifiliogr (Engl Ed)
.
2021
;
112
(2)
:
184
185
.
19.
Badell A Marcoval J, Gallego I, Moreno A, Peyri J
.
Keratoacanthoma arising in hypertrophic lichen planus
.
Br J Dermatol
.
2000
;
142
(2)
:
380
382
.
20.
Allen
JV,
Callen
JP.
Keratoacanthoma arising in hypertrophic lichen planus: a case report
.
Arch Dermatol
.
1981
;
117
(8)
:
519
521
.
21.
Astudillo
MG,
Hoang
MP,
Nazarian
RM,
Foreman
RK.
Distinction between hypertrophic lichen planus and squamous cell carcinoma requires clinicopathologic correlation in difficult cases
.
Am J Dermatopathol
.
2021
;
43
(5)
:
349
355
.
22.
Levandoski
KA,
Nazarian
RM,
Asgari
MM.
Hypertrophic lichen planus mimicking squamous cell carcinoma: the importance of clinicopathologic correlation
.
JAAD Case Rep
.
2017
;
3
(2)
:
151
154
.
23.
Mozafari
N,
Bidari-Zerehpoosh
F,
Movahedi
M,
Dadkhahfar
S.
Hypertrophic lichen planus on lip mimicking SCC
.
Clin Case Rep
.
2022
;
10
:
e06191
.
24.
Sigurgeirsson
B,
Lindelof
B.
Lichen planus and malignancy: an epidemiologic study of 2,071 patients and a review of the literature
.
Arch Dermatol
.
1991
;
127
(11)
:
1684
1688
.
25.
Haenen
CCP,
Buurma
AAJ,
Genders
RE,
Quint
KD.
Squamous cell carcinoma arising in hypertrophic lichen planus
.
BMJ Case Rep
.
2018
;
1
3
.
26.
Totonchy
MB,
Levanthal
JS,
Ko
CJ,
Leffell
DJ.
Hypertrophic lichen planus and well-differentiated squamous cell carcinoma: a diagnostic conundrum
.
Dermatol Surg
.
2018
;
44
(11)
:
1466
1470
.
27.
Knackstedt
TJ,
Collins
LK,
Li
Z,
Yan
S,
Samie
FH.
Squamous cell carcinoma arising in hypertrophic lichen planus: a review and analysis of 38 cases. Dermatol Surg.
2015
;
2015;
41
(12)
:
1411
141
.
28.
Sing
SK,
Saikia
UN,
Ajith
C,
Kumar
B.
Squamous cell carcinoma arising from hypertrophic lichen planus
.
J Eur Acad Dermatol Venereol
.
2006
;
20
(6)
:
745
746
.
29.
Manz
B,
Paasch
U,
Sticherling M. squamous cell carcinoma as a complication of long-standing hypertrophic lichen planus
.
Int J Dermatol
.
2005
;
44
(9)
:
773
774
.
30.
Jayaraman
M,
Janaki
VR,
Yesudian
P.
Squamous cell carcinoma arising from hypertrophic lichen planus
.
Int J Dermatol
.
1995
;
34
(1)
:
70
71
.
31.
Tan
E,
Malik
R,
Quirk
CJ.
Hypertrophic lichen planus mimicking squamous cell carcinoma
.
Australas J Dermatol
.
1998
;
39
(1)
:
45
47
.
32.
Jang
KA,
Kim
SH,
Choi
JH,
Sung
KJ,
Moon
KC,
Koh
JK.
Lichenoid keratosis: a clinicopathologic study of 17 patients
.
J Am Acad Dermatol
.
2000
;
43
(3)
:
511
516
.
33.
Morgan
MB,
Stevens
GL,
Switlyk
S.
Benign lichenoid keratosis: a clinical and pathologic reappraisal of 1040 cases
.
Am J Dermatopathol
.
2005
;
27
(5)
:
387
392
.
34.
Arps
DP,
Patel
RM.
Cutaneous hypertrophic lupus erythematosus: a challenging histopathologic diagnosis in the absence of clinical information
.
Arch Pathol Lab Med
.
2013
;
137
(9)
:
1205
1210
.
35.
Daldon
PEC,
Macedo de Souza
E,
Cintra
ML.
Hypertrophic lupus erythematosus: a clinicopathologic study of 14 cases
.
J Cutan Pathol
.
2003
;
30
(7)
:
443
448
.
36.
Riahi
RR,
Cohen
PR.
Hypertrophic lichen planus mimicking verrucous lupus erythematosus
.
Cureus
.
2018
;
10
(11)
:
e3555
.
37.
Tomasini
D,
Mentzel
T,
Hantschke
M,
et al .
Plasmacytoid dendritic cells: an overview of their presence and distribution in different inflammatory skin diseases, with special emphasis on Jessner's lymphocytic infiltrate of the skin and cutaneous lupus erythematosus
.
J Cutan Pathol
.
2010
;
37
(11)
:
1132
1139
.
38.
Szymanski
K,
Adaszewska
A,
Jakubowska
B,
Kowalewski
C,
Pietrzyk
E,
Wozniak
K.
Case report: pemphigoid nodularis-five patients with many years of follow-up and review of the literature
.
Front Immunol
.
2022
;
13
:
885023
.
39.
Tani
M,
Murata
Y,
Masaki
H.
Pemphigoid nodularis
.
J Am Acad Dermatol
.
1989
;
21
(5 pt 2)
:
1099
1104
.
40.
Vornicescu
C,
Şenilă SC, Cosgarea R, Candrea E, Pop AD, Ungureanu L. Pemphigoid nodularis—rare presentation of bullous pemphigoid: a case report and literature review
.
Exp Ther Med
.
2019
;
17
(2)
:
1132
1138
.
41.
Powell
AM,
Albert
S,
Gratian
MJ,
Bittencourt
R,
Bhogal
BS,
Black
MM.
Pemphigoid nodularis (non-bullous): a clinicopathological study of five cases
.
Br J Dermatol
.
2002
;
147
(2)
:
343
349
.
42.
Zayour
M,
Lazova
R.
Pseudoepitheliomatous hyperplasia: a review
.
Am J Dermatopathol
.
2011
;
33
(2)
:
112
124
.
43.
Lage
D,
Juliano
PB,
Metze
K,
de Souza
EM,
Cintra
ML.
Lichen planus and lichenoid drug-induced eruption: a histological and immunohistochemical study
.
Int J Dermatol
.
2012
;
51
(10)
:
1199
1205
.
44.
Halevy
S,
Shai
A.
Lichenoid drug eruptions
.
J Am Acad Dermatol
.
1993
;
29
(2 pt 1)
:
249
255
.
45.
Ameri
AH,
Foreman
RK,
Vedak
P,
Chen
S,
Miller
DM,
Demehri
S.
Hypertrophic lichen planus with histological features of squamous cell carcinoma associated with immune checkpoint blockade therapy
.
Oncologist
.
2020
;
25
(5)
:
366
368
.
46.
Marques-Piubelli
ML,
Tetzlaff
MT,
Nagarajan
P,
et al .
Hypertrophic lichenoid dermatitis immune-related adverse event during combined immune checkpoint and exportin inhibitor therapy: a diagnostic pitfall for superficially invasive squamous cell carcinoma
.
J Cutan Pathol
.
2020
;
47
(10)
:
954
959
.
47.
Coscarart
A,
Martel
J,
Lee
MP,
Wang
AR.
Pembrolizumab-induced pseudoepitheliomatous eruption consistent with hypertrophic lichen planus
.
J Cutan Pathol
.
2020
;
47
(3)
:
275
279
.
48.
Honda
R,
Fujii
K,
Uchida
Y,
et al .
Hypertrophic lichenoid dermatitis during pembrolizumab treatment
.
J Cutan Immunol Allergy
.
2021
;
4
(4)
:
95
96
.
49.
Chapman
S,
Ashack
K,
Dapprich
DC.
Hypertrophic lichen planus-like eruption following pembrolizumab
.
Cutis
.
2021
;
107
(1)
:
E10
E11
.
50.
Norris
DA.
Mechanisms of action of topical therapies and the rationale for combination therapy
.
J Am Acad Dermatol
.
2005
;
53
(1)
:
S17
S25
.
51.
Theodosiou
G,
Papageorgiou
M,
Vakirlis
E,
Mandekou-Lefaki
I.
Successful treatment of hypertrophic lichen planus with betamethasone under occlusion and TCA-peelings
.
Dermatol Ther
.
2016
;
29
(5)
:
338
340
.
52.
Yoo
SA,
Park
HE,
Kim
M.
Alitretinoin for hypertrophic lichen planus
.
Ann Dermatol
.
2022
;
34
(3)
:
235
236
.
53.
Horio
T.
Indications and action mechanisms of phototherapy
.
J Dermatol Sci
.
2000
;
23
(1)
:
S17
S21
.
54.
Iraji
F,
Faghihi
G,
Asilian
A,
Siadat
AH,
Larijani
FT,
Akbari
M.
Comparison of the narrow band UVB versus systemic corticosteroids in the treatment of lichen planus: a randomized clinical trial
.
J Res Med Sci
.
2011
;
16
(12)
:
1578
1582
.
55.
Kellett
JK,
Ead
RD.
Treatment of lichen planus with a short course of oral prednisolone
.
Br J Dermatol
.
1990
;
123
(4)
:
550
551
.
56.
Alamri
A,
Alsenaid
A,
Ruzicka
T,
Wolf
R.
Hypertrophic lichen planus: successful treatment with acitretin
.
Dermatol Ther
.
2016
;
29
(3)
:
173
176
.
57.
Laurberg
G,
Geiger
JM,
Hjorth
N,
et al .
Treatment of lichen planus with acitretin: a double-blind, placebo-controlled study in 65 patients
.
J Am Acad Dermatol
.
1991
;
24
(3)
:
434
437
.
58.
Kanwar
AJ,
De
D.
Methotrexate for treatment of lichen planus: old drug, new indication
.
J Eur Acad Dermatol Venereol
.
2013
;
27
(3)
:
e410
e413
.
59.
Seiringer
P,
Lauffer
F,
Pilz
AC,
Boehmer
D,
Biedermann
T,
Eyerich
K.
Tofacitinib in hypertrophic lichen planus. Acta Derm Venereol.
2020
;
100(14):adv00220.
60.
Moura
AKA,
Moure
ERD,
Romiti
R.
Treatment of cutaneous lichen planus with thalidomide
.
Clin Exp Dermatol
.
2009
;
34
(1)
:
101
103
.
61.
Atzmony
L,
Reiter
O,
Hodak
E,
Gdalevich
M,
Mimouni
D.
Treatments for cutaneous lichen planus: a systematic review and meta-analysis
.
Amer J Clin Dermatol
.
2016
;
17
(1)
:
11
22
.

Author notes

The authors have no relevant financial interest in the products or companies described in this article.

Presented at the New Frontiers in Pathology Conference; October 26–28, 2022; Ann Arbor, Michigan.