Asymptomatic Pigmented Plaque over the Index Finger in Human Immunodeficiency Virus (HIV) Infected Patient : Indian Dermatology Online Journal

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Clinicopathologic Challenge

Asymptomatic Pigmented Plaque over the Index Finger in Human Immunodeficiency Virus (HIV) Infected Patient

Haritha, Kollipara; Rao, Gandikota R.1,; Attili, Sasi K.2

Author Information
Indian Dermatology Online Journal: Nov–Dec 2020 - Volume 11 - Issue 6 - p 1034-1035
doi: 10.4103/idoj.IDOJ_89_20
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Clinical Findings

A 39-year-old HIV infected women on anti-retroviral therapy (CD4 = 185 cells/μL; viral load = 57385 copies) presented with a single asymptomatic scaly, pigmented plaque of 2 × 1.5 cm size over the volar aspect of left index finger of 6 years duration [Figure 1]. There were no similar lesions elsewhere over the body and no regional lymphadenopathy. Systemic examination was normal. All relevant hematological and biochemical investigations were within normal limits. Lesional biopsy revealed full thickness epidermal dysplasia with loss of polarity, a few abnormal mitotic figures without evidence of dermal invasion and pigment incontinence in papillary dermis [Figure 2a and b].

Figure 1:
Pigmented scaly plaque over the index finger
Figure 2:
(a) H and E ×100 showing regular psoriasiform acanthosis associated with marked orthohyperkeratosis. (b) H and E ×400 showing loss of polarity with dysmaturation of keratinocytes, numerous mitotic figures including abnormal mitoses. Marked pigment incontinence is seen in the papillary dermis

Diagnosis: Pigmented bowens disease

Bowen's disease (BD) is a form of intraepidermal (in situ) squamous cell carcinoma (SCC) of the skin. It was first described by John Bowen in 1912. BD arises in the outer layers of the epidermis and the risk of progression to invasive SCC is relatively low at about 3% of typical cases. Pigmented BD, an uncommon variant presents clinically as an asymptomatic well demarcated, pigmented, flat, scaly plaque. It constitutes less than 2% of all cases of BD.[1] In a review of 420 cases of BD, pigmented variant was rare and was present in 1.7% of cases.[2] Of 951 histopathologically verified cases of BD, pigmented BD was seen only in 52 (5.5%) cases.[3] It is characterized by increased melanin pigment in the epidermis or papillary dermis in addition to the typical findings of BD like abnormal mitoses in the thickened epidermis, dyskeratosis, and presence of proliferating atypical cells without dermal invasion. Although the exact cause of pigmentation is unknown, various theories are proposed.[4] According to the theory of “colonization,” the pigment occurs due to the presence of an enhanced melanocytic hyperplasia within the hypertrophic dendritic processes dispersed through the tumor. Another hypothesis suggests that specific growth factors or cytokines produced by atypical keratinocytes, which induce the proliferation of melanocytes and stimulate melanin production. BD most frequently develops on sun-exposed areas of face, neck, and also affects non-exposed areas like trunk, extremities, perianal area, umbilicus, scrotum, and nails. Palmar location is uncommon. Risk factors include sun exposure, arsenic exposure, radiotherapy, history of trauma; infection with HIV, HPV, and organ transplants.[5] The pigmented BD poses a clinical challenge as a close differential with other pigmented lesions particularly melanoma. Though dermoscopy is a useful tool to differentiate these pigmented conditions, but the findings of pigmented BD are variable.[3] Therefore, histopathology remains the gold standard in confirming the diagnosis of pigmented BD.

The association of HIV with BD is not clearly established. In majority of the cases[67] including ours, BD was seen in patients with low CD4 counts. In addition to immunosupression, persistent subclinical HPV infection may be one of the reasons for developing BD (in situ SCC) in HIV patients. In general 3–10% of untreated BD may progress to invasive carcinoma, usually SCC, of which 13% patients will develop metastasis and 10% end in death.[1] However, presence of pigmentation does not alter the metastatic potential of BD. Management options for BD include topical 5-fluorauracil, topical Imiquimod, cryotherapy, electrodessication and curettage, laser ablation, photodynamic therapy and surgical excision. Our patient was treated with 5% 5-fluorouracil cream three applications a week for 12 weeks. A good response was observed [Figure 3].

Figure 3:
Regression of lesion after-treatment

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Conflicts of interest

There are no conflicts of interest.


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