Solitary violaceous plaque over the abdomen.

A 60-year-old man presented with a 2-year history of a single, nonpruritic, light-brown colored plaque over the lower abdomen. There was no history of similar eruption in the past, prior drug intake, trauma, or insect bite. Past medical and family history was noncontributory. Dermatologic examination revealed a solitary, oval-shaped, 3 × 4 cm sized sharply-demarcated annular plaque over the lower right side of anterior abdomen. The plaque was violaceous to brown-colored in the center with raised erythematous borders [Figure 1]. The surface had a wrinkled appearance with mild scaling. On palpation, it was mildly indurated with intact sensations. Examination of the mucosae and rest of the physical examination were normal. Histopathological features on hematoxylin and eosin (H and E) staining from a biopsy specimen are shown in Figures 2 and 3. Treatment with 0.05% clobetasol propionate cream twice-a-day for 3 weeks resulted in complete resolution with no recurrence till 6 months of follow-up.

Figure 1

Solitary oval-shaped 3 × 4 cm sized sharply-demarcated annular plaque over the anterior abdomen with violaceous to brown-colored center, raised erythematous borders, and a wrinkled surface with mild scaling

Figure 2

Mild hyperkeratosis, focal parakeratosis, and hypergranulosis with flattening of rete ridges, Max-Joseph space formation, and dense band-like lymphohistiocytic inflammation at dermoepidermal junction (hematoxylin and eosin (H and E), ×100)

Figure 3

Dense lymphohistiocytic inflammation at dermoepidermal junction with numerous melanophages in the upper dermis. Vacuolar degeneration of basal layer and colloid bodies (arrow) are also visible (H and E, ×400)

Question

What is the diagnosis?

Answer

Solitary benign lichenoid keratosis (plaque-like variant).

Histopathological findings

Epidermis showed mild hyperkeratosis, focal parakeratosis, and hypergranulosis with flattening of rete ridges, and Max–Joseph space formation [Figure 2]. There was dense, band-like lymphohistiocytic inflammation at dermoepidermal junction with numerous melanophages in the upper dermis. Vacuolar degeneration of basal layer, and colloid bodies were prominent [Figure 3]. There was no evidence of solar elastosis or any features suggestive of solar lentigo at the lesional margins.

Discussion

Solitary benign lichenoid keratosis (SBLK), first described in 1966 by Shapiro and Ackerman as ‘lichen planus-like keratosis’ (LPLK) and by Lumpkin and Helwig as ‘solitary lichen planus’, consists of a nonpruritic papule or slightly indurated plaque predominantly occurring in adults (between the 5th and 7th decade), with female preponderance.[12] Though typically solitary with predilection for sun-exposed sites of trunk and upper extremities, multiple lesions and involvement of sun-protected sites have been well reported. Clinically, many morphological types have been described: Erythematous, papulokeratotic, and plaque-like (PL) type by Panizzon and Skaria; and PL, flat erythematous (FE) and flat pigmented (FP) type by Bugatti and Filosa.[34] Based on duration, it may be acute (<3 month's duration), subacute (3 months – 1 year), and chronic (>1 year). Acute lesions are mostly erythematous, subacute are erythematous to violaceous, while chronic lesions are usually macular with regularly or irregularly distributed hyperpigmentation.

Though the clinical appearance is often distinctive enough for diagnosis, certain conditions share clinical as well as histological features and may be differentiated on histopathology and dermoscopy. The most important differentials include lichen planus (LP), lichenoid actinic keratosis (LAK), seborrheic keratosis (SK), lupus erythematosus, regressing melanocytic lesions, basal cell carcinoma, and Bowen's disease. Histopathological differentiation from LP is not straightforward, because LPLK also shows epidermal acanthosis, lichenoid infiltrate at the dermoepidermal junction, and colloid bodies. However, hypergranulosis (which is typical in LP) is not prominent in SBLK; whereas, focal parakeratosis is usually present. Five histopathological variants of LPLK have been described with each type displaying a characteristic clinical picture: Classic, bullous, atypical, early or interface, and atrophic or senescent.[5] Dermoscopy of suspected lesions not only aids in correct clinical recognition of SBLK, it also closely correlates with the evolution of a baseline lesion like SK into SBLK or its regression.[4] A pigmented granular pattern is characteristic of SBLK or areas of SBLK within a lesion of SK. Though Langerhans cells (LCs) are relatively increased in lesions of SBLK, the role of immunohistochemical staining for S100 protein (for LCs) in differentiating it from LP and LAK is not very convincing.[6]

The exact cause of SBLK is unknown. Though many authors consider it to represent a lymphocyte-mediated regression of a preexisting solar lentigo, an end-stage evolution of a reticulated SK, or even other suspected precursor lesions like warts or actinic keratosis; recent detailed histological and immmunohistochemical staining-based studies have doubted this concept and suggest it to be a specific disorder.[7] Though it is known that SBLK tends to regress spontaneously, treatment with potent topical steroids results in early resolution. Prophylactic surgical removal and submission of the entire specimen for histopathology is recommended if a malignant melanocytic lesion is suspected.

Learning points

SBLK or LPLK is clinically characterized by a solitary (sometimes multiple) violaceous to brownish plaque(s) predominantly affecting adults with female preponderance

It may represent the end-stage evolution of a reticulated SK or regression of a preexisting solar lentigo-specific disorder, but may be a specific disorder in itself

Differentiation from LP and LAK is difficult due to overlapping clinical and histopathological features. Presence of focal parakeratosis favors its diagnosis, but not in all cases

Dermoscopic features of pigmented granular pattern are helpful in diagnosis

Spontaneous resolution is well-known, though topical steroids also induce resolution. Surgical excision is ideal for any suspicious lesion.