Dermatology Online Journal

HIV photodermatitis presenting with widespread vitiligo-like depigmentation
Rebecca C Philips MD¹, Kiran Motaparthi MD¹, Bhuvaneswari Krishnan MD^2,3, Sylvia Hsu MD¹
Dermatology Online Journal 18 (1): 6

1. Department of Dermatology, Baylor College of Medicine, Houston, Texas
2. Department of Pathology, Baylor College of Medicine, Houston, Texas
3. Michael E DeBakey VA Medical Center, Houston, Texas

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Abstract

HIV photodermatitis encompasses a variety of clinical manifestations. We report a rare clinical presentation of HIV photodermatitis with widespread vitiligo-like depigmentation.

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Case report

Figure 1	Figure 2
Figure 1. Depigmented patches with hyperpigmented border on dorsal forearms Figure 2. Depigmented patches with hyperpigmented border on posterior neck

A 60-year-old man presented with a 1-year history of an intensely pruritic eruption. Past medical history was significant for HIV/AIDS with a CD4 T-lymphocyte count of 7 cells/µl. The patient had never received highly active antiretroviral therapy (HAART). Hydroxyzine was previously prescribed for pruritus without relief. The patient was taking no other medications. Physical exam revealed photodistributed, depigmented macules and patches with a hyperpigmented border on the dorsal forearms (Figure 1), posterior neck (Figure 2), and “V” area of the chest. A 4 mm punch biopsy was performed from a patch on the dorsal forearm. Histopathologic examination revealed spongiotic dermatitis with abundant eosinophils (Figures 3 and 4). Based on the clinicopathologic correlation, the diagnosis of HIV photodermatitis was made.

Figure 3	Figure 4
Figure 3. Spongiotic dermatitis (H&E, x40) Figure 4. Spongiotic dermatitis with abundant eosinophils (H&E, x400)

Discussion

HIV photodermatitis occurs in approximately 5 percent of HIV-seropositive patients [1]. This entity encompasses a variety of clinical manifestations, including polymorphic light eruption, actinic prurigo, chronic actinic dermatitis, porphyria cutanea tarda, photosensitive granuloma annulare, and lichenoid photoeruption [2, 3]. Sun-exposed areas, such as the face, ears, scalp, posterior neck, upper back, “V” area of the chest, extensor arms, and dorsal hands, are involved [1]. Photosensitivity typically occurs in patients who have a CD4 T lymphocyte count ≤ 50 cells/µl and worsens as the immunodeficiency progresses [1, 3, 4]. The propensity to develop HIV photodermatitis varies by race. In one study, African-American patients with HIV were 6.68 times more likely to develop photodermatitis than all other races combined [1]. Native Americans are also thought to be at higher risk to develop the disease [4]. Certain medications, such as trimethoprim-sulfamethoxazole, NSAIDs, and HAART, can be photosensitizing and may increase the risk of photodermatitis. However, HIV photodermatitis also occurs without medication use [1, 3]. Histology varies based on clinical presentation, but may reveal subacute or chronic dermatitis and abundant eosinophils [5]. Treatment is often difficult. Initially, sun protection and topical steroids can be used. Treatment with thalidomide has been successful in refractory cases [3, 5]. It is important to note that thalidomide has been reported to increase the HIV viral load, although the clinical significance of this phenomenon is unknown. Therefore, the HIV RNA level should be monitored after the 1st and 3rd months of thalidomide treatment and subsequently every 3 months [6].

HIV photodermatitis with widespread vitiligo-like depigmentation, as observed in this patient, has rarely been reported in the literature. Kigonya et al reported a case of extensive, photodistributed and pruritic depigmentation in a patient with AIDS (CD4 T lymphocyte count of 2 cells/µl) with onset 1 month following the initiation of antiretroviral therapy with stavudine, lamivudine, and nevirapine. Repigmentation occurred in most areas after the antiretroviral regimen was changed to zidovudine, lamivudine, and efavirenz. The authors postulated that the photodistributed depigmentation was due to a photosensitizing effect of the medication [7]. Other studies have reported areas of depigmentation within chronic lichenoid photoeruptions in HIV patients. All of these noted a CD4 T-lymphocyte count < 400 cells/µl [8, 9, 10], and two studies specified counts < 50 cells/µl [8, 9]. A report of chronic photosensitivity marked by scaling, erythema, and concurrent vitiligo of the face, arms, and hands has been described in a patient prior to the diagnosis of HIV/AIDS. Both conditions improved with the use of sunscreen and topical steroids [11].

In the case presented herein, the differential diagnosis includes discoid lupus erythematosus, vitiligo, and lichen simplex chronicus. Discoid lesions of cutaneous lupus erythematosus can be photodistributed and are frequently characterized by central hypopigmentation with peripheral hyperpigmentation. Vitiligo-like depigmentation may also occur. However, the scarring that is often observed in discoid lupus is absent in HIV photodermatitis [12]. Additionally, the histopathology in this case, characterized by spongiosis and abundant eosinophils, is inconsistent with cutaneous lupus. Active lesions of discoid lupus most commonly feature a dense lymphocytic dermal infiltrate admixed with plasma cells [13]. Vitiligo was considered in the differential diagnosis given the patient’s extensive depigmentation [14]. Vitiligo, an autoimmune condition, rarely occurs in association with HIV [15]. However, the depigmentation in vitiligo is typically surrounded by normal skin, unlike the hyperpigmented border observed in our patient. Photodistribution would be unusual for vitiligo, which may occur anywhere on the body, especially in areas of frequent trauma, pressure, or friction [14]. It is also important to note that the histopathology in this case is inconsistent with vitiligo, which typically demonstrates decreased or absent melanocytes at the dermal-epidermal junction [16]. Lichen simplex chronicus was also considered as a diagnosis given the patient’s complaint of intense pruritus and histologic features of spongiotic dermatitis. However, the morphology of lichen simplex chronicus is classically described as hyperpigmented, lichenified plaques. The photodistribution and complete depigmentation with hyperpigmented borders observed in this patient are also inconsistent with lichen simplex chronicus [17, 18].

In conclusion, a myriad of clinical presentations are associated with HIV photodermatitis, which should be considered in patients with HIV/AIDS who present with a pruritic, photodistributed eruption. Rarely, HIV photodermatitis may present with depigmentation, mimicking vitiligo [5]. In these cases, immunodeficiency, photodistribution, and histology demonstrating spongiotic dermatitis with eosinophils distinguish HIV photodermatitis from vitiligo.

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