Lichen Planus-like Keratosis: Another Differential Diagnosis for Kaposi Sarcoma

Abstract

Epidemic Kaposi sarcoma is a common finding among HIV/AIDS patients that are not under antiretroviral treatment, and sometimes it is the first sign of the disease. However, it can be seen even in patients with undetectable viral load and high CD 4 cell count. Under these circumstances, the clinical presentation can be atypical in location or number. For this reason, the number of differential diagnosis is increased and biopsy of the suspicious lesions is essential for an accurate diagnosis and further apropiate treatment.

What was known?

Endemic SK is the most common presentation, and can be an initial manifestation of AIDS.

Introduction

Kaposi sarcoma (KS) was described in 1872 as a neoplasm originated from vascular and lymphatic endothelia. Since then, four types have been described: Classic, iatrogenic, endemic (African) and epidemic (AIDS related).[1]

Human herpes virus 8 is often detected in all types of KS lesions which clinically can be seen as a violaceous patch, plaque or nodule.[2]

Since the introduction of the combined antiretroviral therapy (cARV), the incidence of epidemic SK has dropped from 35% to only 3%, as reported in developed countries. However, it is still a common finding among recently diagnosed AIDS patients and remains the most common type of SK seen in clinical practice.[3]

On the other hand, lichenoid keratosis (LK), or benign lichenoid keratosis also known as lichen planus-like keratosis (LPLK), is a common lesion frequently seen as a single papule on the chest or upper extremities, more common in fair skinned women between 50 and 60 years-old. Its size varies between 3 and 10 mm, of light pink color, or intensely violaceous. It usually is a single lesion, and only 8% present two and less than 1% present three lesions.[4]

Although initially described in 1966 as an incomplete or frustrated form of lichen planus, several clinical differences have made it a separate entity. It has been suggested that LK may be the inflammatory stage of regressing solar lentigines or reticulated seborrheic keratosis, and possibly related to UV exposure.[5,6,7]

Some cases present spontaneous resolution although the usual treatment includes cryotherapy, curettage, electrosurgery and/or shaving.[7,8,9,10]

Case Report

We present the case of a 54-year-old male, diagnosed with HIV in 2002, under cARV therapy since February 2003 with emtricitavine, tenofovir and efavirenz.

He attended the dermatology office in January 2013 for presenting a 2-year evolution unique violaceous plaque on the right shin, oval shaped, that measured 2.5 × 3 cm, well demarcated and elevated, with some scale in the surface [Figure 1]. It was slowly growing and asymptomatic. A punch biopsy was taken with the clinical impression of KS.

Figure 1.

Clinical appearance. Violaceous patch on the right shin

At the time of consultation, the CD4 lymphocyte cell count was of 491 and the viral load undetectable.

The histopathologic diagnosis was compatible with LPLK [Figure 2].

Figure 2.

Histopathology of the lichen planus-like keratosis with the inflammatory band infiltrate (H and E ×20)

He received successful treatment with cryotherapy.

Discussion

KS is an AIDS-defining clinical condition, and as such, a very strong association between KS and immunosuppression has been documented, further supported by the results that cARV has diminished the KS incidence.

Several reports have noted KS regression after successful response to antiretroviral therapy with increases in CD4 lymphocyte counts and undetectable viral load. However, the contrast can also be seen. SK can manifest in patients receiving cARV with undetectable viral load and high CD4 lymphocyte cell count.[11]

As LPLK is a common and benign lesion, scarce recent articles are written about it. The importance of the correct diagnosis resides on the clinical differential diagnosis, which is primarily with malignant lesions of melanocytic origin or basal cell carcinoma, so one should keep this diagnosis in mind.[12,13]

The histopathological differential diagnosis should be with lichen planus, lichenoid drug eruption, lichenoid acral lupus erythematosus, lichenoid graft-versus-host disease, inflamed seborrheic keratosis, halo nevus and lichenoid regression of melanoma.[14]

Fortunately for our patient, the biopsy reported a benign and localized non-HIV-related dermatosis, but cases like this teach us that although the clinical picture may be compatible with KS, we must still perform a skin biopsy which will clarify the diagnosis and determine which further studies and treatment should be done, if necessary. Even if the patient is under good control for the HIV infection.

What is new?

Endemic SK continues to be a common finding even with high CD4 cell counts and undetectable viral load.