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 Table of Contents  
CASE REPORT
Year : 2012  |  Volume : 1  |  Issue : 4  |  Page : 274-280

Management of difficult uncommon dermatoses in HIV/AIDS clinical setting: A case series


1 Department of Dermatology, MVJ Medical College and Research Hospital, Hoskote, Bangalore, India
2 Department of Dermatology, Andhra Medical College, Visakhapatnam, India

Date of Web Publication27-Feb-2013

Correspondence Address:
G R Rao
Department of Dermatology, Andhra Medical College, Consultant Dermatologist, Surya Skin Care and Research Centre, Gopal Sadan, 15-1-2, Naoroji Road, Maharanipeta, Visakhapatnam - 530 002, Andhra Pradesh
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/2278-344X.107903

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  Abstract 

Skin disease may provide the first suspicion of diagnosis of HIV infection. Infection with HIV has great impact on skin diseases. In the context of HIV, the clinical presentation of dermatoses assumes either a classic or an uncommon form. Herein, we report six dermatological cases in the setting of HIV, with varied presentation and outcome after treatment. Knowledge of changing disease pattern with HIV may help the clinician to identify dermatoses and act in appropriate manner in the case management to support the patient.

Keywords: Difficult dermatoses, HIV/AIDS, management, uncommon presentations


How to cite this article:
Kumar H, Rao G R. Management of difficult uncommon dermatoses in HIV/AIDS clinical setting: A case series. Int J Health Allied Sci 2012;1:274-80

How to cite this URL:
Kumar H, Rao G R. Management of difficult uncommon dermatoses in HIV/AIDS clinical setting: A case series. Int J Health Allied Sci [serial online] 2012 [cited 2021 Sep 27];1:274-80. Available from: https://www.ijhas.in/text.asp?2012/1/4/274/107903


  Introduction Top


Infection with HIV or AIDS has great impact on skin diseases, not only by affecting immune system and thereby affecting host defense against various infections, but also by changing tumor immune response. HIV-infected patients can pose diagnostic challenges, as their altered immune status may lead to atypical presentations of common cutaneous diseases, as well as the occurrence of uncommon or opportunistic skin disorders. [1],[2],[3],[4],[5],[6] Management of cutaneous disease in sero-positive patients can also be challenging, as the dermatological manifestations may be more severe, may recur with greater frequency, and may be refractory to standard treatment. [7] Herein, we report our clinical experience in six cases. [Table 1]
Table 1: Case details

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  Case Reports Top


Case 1

A 55 year old male presented with multiple discrete annular well-defined hyperkeratotic scaly plaques, rupoid like lesions present bilaterally over chest, abdomen, and upper and lower limbs. Scalp, palms and soles had hyperkeratotic scaly plaques, nails showed subungual hyperkeratosis since three months [Figure 1]. Diagnosis of rupoid psoriasis was made with a suspicion of HIV and blood investigation revealed HIV seropositive with CD4 count - 120 cells/mm 3 . Patient was treated with oral Acitretin - 25 mg OD along with ART. All the lesions cleared remarkably after four weeks of Acitretin therapy [Figure 2].
Figure 1: A case of Rupoid psoriasis showing multiple discrete well-defined hyperkeratotic scaly plaques

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Figure 2: After 4 weeks of Acetretin treatment, complete clearance of lesions

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Case 2

A 40-year old male presented with discrete annular well-defined hyperkeratotic plaques, rupoid like lesions present over chest, abdomen, and upper and lower limbs. Scalp, palms and soles had hyperkeratotic scaly plaques, nails showed subungual hyperkeratosis since 1 month [Figure 3]. Patient was diagnosed with HIV 6 months back with CD4 count - 132 cells/cm 3 . With our previous experience with Acitretin even in this case, we treated in similar lines with good response [Figure 4].
Figure 3: Rupoid ( Limpet like) hyperkeratotic scaly plaques in a HIV seropositive patient

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Figure 4: Complete resolution of lesions, after 4 weeks of acetretin treatment

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Case 3

A 25-year old male, known HIV seropositive with CD4 count - 104 cells/mm 3 , presented with multiple erythematous well-defined scaly plaques, bilateral distributed over chest, abdomen, trunk, and upper and lower limbs. Scalp, palms, and soles showed diffuse hyperkeratotic plaques since 1 year [Figure 5]. A diagnosis of psoriasis vulgaris was made and was started on zidovudine containing ART-regimen based on few reports of successful outcome. After 4 weeks of ART, all the lesions had cleared without any other adjuvant treatment for psoriasis [Figure 6].
Figure 5: A case of psoriasis vulgaris with HIV, showing erythematous well-defined scaly plaques

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Figure 6: Complete clearance after 4 weeks of zidovudine containing ART regimen with no adjuvant treatment

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Case 4

A 23-year old female presented with multiple discrete vesicles and bullae of varying sizes present over chest, abdomen, trunk, and upper and lower limbs with large areas of denuded skin [Figure 7]. Nikolsky sign was positive. She was diagnosed to be HIV +ve - 1 month back with CD4 count - 640 cells/mm 3 and had developed toxic epidermal necrosis. She was treated with IV systemic steroids (dexamethasone 1cc TID), tapered slowly over 4 weeks under antibiotic cover (ceftriaxone 1g BD) along with proper fluid management. There were no side effects or any drug interactions noted. The patient recovered and all the lesions healed with hyperpigmentation [Figure 8].
Figure 7: Multiple discrete vesicles and bullae of varying sizes present all over the body with large areas of denuded skin. oxic epidermal necrolysis in a HIV patient

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Figure 8: Response with systemic steroids, tapered slowly over 4 weeks. Healing with post inflammatory hyperpigmentation

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Case 5

A 35-year old male presented with multiple papules and vesicular lesions present over the chest, abdomen, trunk, and upper and lower limbs. Grouped vesicles over lips and around mouth, over genitals and scrotum were present. Marked congestion of eyes was seen [Figure 9]. Diagnosed as HIV +ve 3 years ago, and his CD4 count - 176 cells/mm 3 . Serology for HSV IgG - 3.50 OD ratio and HSV IgM - 0.82 OD ratio confirmed diagnosis of disseminated herpes simplex. Patient was treated with Tab Acyclovir - 800 mg, 5 times/day. After 8 weeks of therapy all the lesions became verrucous and healed with scarring [Figure 10].
Figure 9: Multiple papules and vesicular lesions with grouped vesicles over lips, and around mouth. Also, marked congestion of eyes seen in a case of Disseminated herpes simplex with HIV

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Figure 10: Response after 8 weeks of acyclovir, healing with verrucous growths and scarring

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Case 6

A 30-year old male, known HIV with CD4 count 160 cells/mm 3 , presented with multiple large well-defined ulcers over soft palate covered with slough and surrounded by erythematous rim of 3 months duration, [Figure 11] resistant to all topical and systemic antibiotics and steroid therapy. Later Tab Thalidomide - 100 mg BD for 2 weeks was given for these chronic apthous stomatitis and a remarkable improvement was noticed after 2 weeks treatment [Figure 12].
Figure 11: Multiple large well-defined ulcers over soft palate covered with slough and surrounded by erythematous rim in an HIV individual

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Figure 12: Complete clearance after 2 weeks of thalidomide therapy

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  Discussion Top


Skin disorders are commonly encountered in HIV-infected patients, and they may be the first manifestation of HIV disease. Up to 90% of HIV-infected persons suffer from skin diseases during their course of illness. [1] The spectrum of skin disorders depends on:

  1. Immunologic stage, as reflected by CD4 count
  2. Concurrent use of HAART
  3. Pattern of endemic infections


In general, declining immunity is associated with increased number and severity of skin disorders. [3] Skin lesions are more likely to have unusual appearance in advanced HIV infection.

The prevalence of psoriasis (PS) in HIV-infected individuals is the same or slightly higher than that seen in noninfected individuals, but its clinical presentation can be more severe. [8],[9] The severity of presentation often correlates with the degree of immunosuppression. HIV-positive patients with pre-existing psoriasis may see a flare of lesions as their CD4 count decreases and their viral load increases. A higher frequency of guttate and inverse psoriasis, rupoid type, as well as cases of generalized erythrodermic type psoriasis, have been reported in HIV-positive patients. Psoriasis has been the presenting manifestation of HIV in some individuals, thus HIV testing should be considered in patients that present with de novo psoriasis. [8]

Treatment of psoriasis in HIV-positive patients can be challenging as it is often refractory to standard psoriasis treatments. [7] When started on HAART, patients' psoriasis tends to improve as the immune system is reconstituted. Ten case reports have shown a dramatic and rapid improvement of psoriasis in HIV-positive patients who have been either started or restarted on HAART. [7],[9] Even in our case series, patient with psoriasis with HIV, started on Zidovudine containing ART, showed remarkable improvement in psoriatic lesions with no other adjuvant treatment. In our institutional setup, all HIV infected patients with CD4 counts below 200 cells/mm 3 are started with ART (lamuvudine, stavudine/zidovudine, and nevirapine) as first line, which is supplied by the government and dispensed in Integrated Counseling and Testing centres (ICTC). Acitretin is a safe and effective treatment for PS-HIV. Both skin and joint manifestations of PS-HIV responded to acitretin therapy in most patients. The adverse effects are moderate and well-tolerated. Acitretin does not appear to have immunosuppressive properties. [10] Even in our cases of rupoid psoriasis, patients tolerated Acetretin well and good response was noted after 4 weeks of therapy with complete clearance of lesions.

Cutaneous drug eruptions are the most common manifestation of drug hypersensitivity. The incidence of drug reaction is higher in patient with HIV infection. Morbilliform rash is the commonest type of drug rash, Steven Johnson syndrome and toxic epidermal necrolysis (TEN) are also well known. [11] TEN is rare, with an overall incidence of 1-2 cases per million population per year. Patients with the acquired immunodeficiency syndrome (AIDS) appear to be at increased risk for adverse drug reactions. These kinds of reactions, however, seem to occur more often in patients with a more advanced immunodeficiency state. The mortality rate from toxic epidermal necrolysis remains significant despite improvements in the care of patients with acute renal failure. The main prognostic factors are age, area of necrolysis, and elevated blood urea. [12]

The role of corticosteroids in the management of toxic epidermal necrolysis in HIV individuals is controversial due to the potential risk of further immunosuppression in these already immunodeficient patients with the use of corticosteroids. [13] Our patient of TEN tolerated high corticosteroid doses (dexamethasone 1cc TID), which was tapered over a period of four weeks. The lesions healed completely with hyperpigmentation. There appears to be no difference in immunosuppression by steroids for toxic epidermal necrolysis as compared to HIV negative cases. Diagnosis of TEN is by clinical assessment, supplemented by histopathology and by exclusion. Management involves withdrawal of culprit drug and supportive measures are most important. [13]

Infection with HSV is extremely common in HIV disease. It usually represents the reactivation of latent virus. The usual manifestations are orolabial vesicles, anogenital disease or herpetic whitlow. [14] In advanced HIV disease, HSV is more likely to be persistent and atypical in appearance: Verrucous erosions, deep ulcers or large ulcer reaching 20 cm in diameter. Disseminated cutaneous HSV can be the first presentation of AIDS. Atypical cutaneous HSV lesions should be considered in all AIDS patients with unusual or difficult-to-diagnose skin lesions. Empiric treatment with acyclovir is essential, when clinical suspicion is high or pathologic findings are non-diagnostic because of the high risk-to-benefit ratio when treatment is delayed or prescribed not at all. [15] In our case too, patient was started on acyclovir, patient showed improvement after 8 weeks of therapy, with healing of lesions noted with verrucous growths and scarring.

Cutaneous HSV in early HIV disease is typical, affecting mucocutaneous areas, whereas in advanced HIV when immunity is compromised, the presentation is more often atypical, chronic, more disseminated, recurrent, and acyclovir-resistant. Although the CDC criteria for AIDS with regard to cutaneous HSV requires the existence of chronic. HSV mucocutaneous ulcerations persisting for more than one month, studies suggest that cutaneous HSV are considered atypical where the lesions are unusual in appearance and location and disseminated usually signifies a profound reduction in cellular immunity. [16] Hence, finding of any atypical cutaneous HSV presentation should prompt a search for HIV disease. The differential diagnosis of a cutaneous lesion resembling HSV in an AIDS patient is diverse and includes cutaneous tuberculosis, l neurotic excoriations,8 whitlow (staphylococal infections), impetigo when secondary impetiginization occurs, and herpes zoster. [14] Treatment response to acyclovir is often less marked than the immunocompetent individual. Continuous suppressive treatment with acyclovir 400 mg bid is considered for frequent relapses, such as >6 episodes/year. Some clinicians prefer the use of valacyclovir or famciclovir because of improved pharmacokinetics and convenience of administration. For acyclovir-resistant HSV, intravenous foscarnet or cidofovir can be used. [15]

Aphthous stomatitis, also known as aphthous ulcers, represents a potentially debilitating disorder in HIV-infected persons. When these lesions develop on a recurring basis, it is referred to as recurrent aphthous stomatitis, or recurrent aphthous ulcers. [17] Immunocompetent persons can also develop painful aphthous oral lesions, but they typically have a more self-limited course than seen with HIV-infected persons, particularly those with advanced immunosuppression. Compared with immunocompetent persons, HIV-infected individuals characteristically have oral ulcers that are larger, more painful, heal more slowly, and recur more frequently. [18],[19] Aphthous lesions generally appear as round or oval ulcerations of variable depth, with a raised red border. The center of the ulcer is often covered by a pseudomembrane that can appear white, yellow, or gray. They most often develop on mobile non-keratinized mucosal surfaces in the mouth, though in HIV-infected patients, they may also occur in the esophagus and anogenital region. The oral lesions typically cause intense pain and can interfere with eating, speaking, and swallowing, even leading to significant anorexia and weight loss in some patients. [17]

The diagnosis of aphthous stomatitis is usually made based on clinical findings combined with an exclusion of other disorders that have a similar clinical presentation. Oral herpes simplex virus infection can manifest as ulcers that closely resemble aphthous lesions, thus the initial evaluation of an oral ulcer should include a fluorescent antibody and culture for herpes simplex virus. Other less frequently seen causes of oral ulcerations include cytomegalovirus infection, syphilis, systemic fungal infections, neoplasm, Behet's syndrome, and the antiretroviral drug zalcitabine. [17] Although biopsy can provide a definitive diagnosis, it is infrequently performed. Management of aphthous stomatitis depends on the severity of the lesions. Minor lesions can usually be treated topically with a product that combines a mucosal binding agent and a topical steroid. Topical anesthetics play an important adjunctive role for pain control. Unfortunately, topical therapy often produces inconsistent response rates and high rates of relapse. More recently, several case reports have noted successful treatment of aphthous lesions with antiretroviral therapy. [19] Severe ulcers and those not responding to topical therapy may require more aggressive management consisting of systemic corticosteroids, intralesional corticosteroids, or systemic immunomodulators, such as thalidomide. [20]

Randomized clinical trials have demonstrated the efficacy of thalidomide, an antagonist of tumor necrosis factor-alpha, for the treatment of oral and esophageal aphthous lesions in HIV-infected patients. [20],[21] The use of thalidomide is typically reserved for the treatment of ulcers that fail to respond to systemic corticosteroid therapy, or in patients who have recurrent severe lesions, particularly when they require repeated courses of systemic corticosteroids. Because of the well-established teratogenic effects of thalidomide, the S.T.E.P.S. (System for Thalidomide Education and Prescribing Safety) program has been designed by Celgene to ensure the safe and effective dispensing of thalidomide. [21] Our case too, showed excellent response with complete clearance of the ulcers after 2 weeks of therapy with no further recurrences followed upto six months.

Finally the discussion would be incomplete without the mention of Leprosy and tuberculosis, which are two common diseases in India. The prevalence of tuberculosis is estimated to be 4.0 and 16.0 per thousand for bacteriologically and radiologically active tuberculosis cases, respectively, while the national prevalence rate of leprosy in India is 0.88/10,000. [22] Early in the HIV epidemic, it was feared that the disease would undermine leprosy control as has occurred with tuberculosis. It was predicted that patients with leprosy and HIV coinfection would have an increased risk of lepromatous disease and a faster clinical evolution, and that the leprosy would be more dificult to treat, the interaction between HIV and Mycobacterium leprae seems to be far more subtle than that between HIV and tuberculosis. [23] The published epidemiological data are limited in quality, but show neither an increased HIV prevalence among leprosy cases nor an alteration in clinical spectrum of leprosy among coinfected patients. Some data suggest that immune-mediated reactions that complicate leprosy occur at a higher frequency in coinfected patients. Leprosy has now been reported to present as immune reconstitution disease among patients commencing highly active antiretroviral treatment. These observations suggest that cell-mediated immune responses to M leprae are preserved at the site of disease despite of the evidence that these responses are abrogated systemically by contrast with tuberculosis, in which the host granulomatous response is impaired by HIV coinfection. [24]

Tuberculosis and HIV have been closely linked since the emergence of AIDS. HIV infection has contributed to a significant increase in the worldwide incidence of tuberculosis. [25] By producing a progressive decline in cell-mediated immunity, HIV alters the pathogenesis of tuberculosis, greatly increasing the risk of developing disease in coinfected individuals and leading to more frequent extrapulmonary involvement and atypical radiographic manifestations. Although HIV-related tuberculosis is both treatable and preventable, incidence rates continue to climb in developing nations, where HIV infection and tuberculosis are endemic and resources are limited. Worldwide, tuberculosis is the most common opportunistic infection affecting HIV-seropositive individuals, and it is the most common cause of death in patients with AIDS. [26]


  Conclusion Top


In our case series, varied manifestations of dermatological diseases in HIV are presented with diagnostic and management difficulties. HIV infection can lead to a myriad of dermatoses with complicated clinical presentations. The altered immune status of HIV-infected individuals leads to diagnostic and therapeutic challenges. As dermatologists, it is important to be aware of the varied dermatoses associated with HIV as well as their management. The presentations may be atypical and less responsive to routine treatment, and hence a thorough knowledge is required to manage persons with HIV infection. Additionally, recognition of the need for more intensive therapy in these patients can provide improved care, and ultimately, improved patient outcomes with quality of life in patients living with HIV AIDS.

 
  References Top

1.Cockerell CJ, Friedman-kien. Cutaneous manifestations of HIV infection. In: Merigan TC Jr, Barlett JG, Bolognesi D, editors. Textbook of AIDS Medicine. 2 nd ed. Baltimore: Williams and Wilkins; 1999. p. 499-520.  Back to cited text no. 1
    
2.Coldiron BM, Bergstresser PR. Prevalence and clinical spectrum of skin disease in patients infected with human immunodeficiency virus. Arch Dermatol 1989;125: 357-61.  Back to cited text no. 2
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6.Rigopoulos D, Paparizos V, Katsambas A. Cutaneous markers of HIV infection. Clin Dermatol 2004;22:487-98.  Back to cited text no. 6
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10.Buccheri L, Katchen BR, Karter AJ, Cohen SR. Acitretin therapy is effective for psoriasis associated with human immunodeficiency virus infection. Arch Dermatol 1997;133:711-5.  Back to cited text no. 10
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11.Roujeau JC, Stern RS. Severe adverse cutaneous reactions to drugs. N Engl J Med 1994;331:1272-85.  Back to cited text no. 11
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12.Roujeau JC, Revuz J. Toxic epidermal necrolysis: An expanding field of knowledge. J Am Acad Dermatol 1994;31:301-2.  Back to cited text no. 12
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19.MacPhail LA, Greenspan D, Greenspan JS. Recurrent aphthous ulcers in association with HIV infection. Diagnosis and treatment. Oral Surg Oral Med Oral Pathol 1992;73:283-8.  Back to cited text no. 19
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21.Jacobson JM, Greenspan JS, Spritzler J, Ketter N, Fahey JL, Jackson JB, et al. Thalidomide for the treatment of oral aphthous ulcers in patients with human immunodeficiency virus infection. National Institute of Allergy and Infectious Diseases AIDS Clinical Trials Group. N Engl J Med 1997;336:1487-93.  Back to cited text no. 21
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23.Corbett EL, Watt CJ, Walker N, Maher D, Williams BG, Raviglione MC, et al. The growing burden of Tuberculosis: Global trends and interactions with the HIV epidemic. Arch Intern Med 2003;163:1009-21.  Back to cited text no. 23
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24.Ustianowski AP, Lawn SD, Lockwood DN. Interactions between HIV infection and leprosy: A paradox. Lancet Infect Dis 2006;6:350-60.  Back to cited text no. 24
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25.Raviglione MC, Narain JP, Kochi A. HIV-associated tuberculosis in developing countries: Clinical features, diagnosis, and treatment. Bull WHO 1992;70:515-26.  Back to cited text no. 25
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26.Raviglione MC, Snider DE Jr, Kochi A. Global epidemiology of tuberculosis: Morbidity and mortality of a worldwide epidemic. Bull WHO 2002;80:501-2.  Back to cited text no. 26
    


    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7], [Figure 8], [Figure 9], [Figure 10], [Figure 11], [Figure 12]
 
 
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