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Print version ISSN 0365-0596On-line version ISSN 1806-4841
An. Bras. Dermatol. vol.78 no.6 Rio de Janeiro Nov./Dec. 2003
Regression of psoriasis in HIV patient after antiretroviral therapy*
Maria de Fátima Amorin RuizI; Débora GaburriII; José Roberto Paes de AlmeidaIII; Luiza Keiko OyafusoIV
student of masters degree at the Dermatology Service, "Escola Paulista de Medicina,
IIResident M.D. at the Dermatology Service of the Hospital Guilherme Álvaro - "Faculdade de Ciências Médicas de Santos"
IIIAssistant Lecturer of Dermatology, "Faculdade de Ciências Médicas de Santos - UNILUS"
IVM.D. dermato logist at the "Instituto de Infectologia Emílio Ribas". Post graduate student of doctorate course at the Dermatology Service of the "Escola Paulista de Medicina, UNIFESP".
Immunodeficiency syndrome was first described as a new disease in 1981 because an unusual association of Kaposi's Sarcoma and Pneumocystis carinii pneumonia in men. The skin is a frequent site of diseases due to this infection. Psoriasis is a chronic dermatitis that affects 1.3-5% of HIV-positive patients. The case is described of a 44-year-old man with onset of erythematous scaly lesions in scalp, elbows, knees, hands, feet and nails following HIV infection. After diagnosis of psoriasis was confirmed and antiretroviral therapy instigated, he presented improvement of the psoriasis lesions.
Key words: psoriasis; Acquired Immunodeficiency Syndrome.
Acquired immunodeficiency syndrome was recognized for the first time as a new disease during 1981, in the United States of America and one year later in Brazil, following the atypical association of Kaposi's sarcoma and pneumonia due to Pneumocystis carinii in men.1 Today, it is considered that some million people are infected by HIV in the USA.2 Psoriasis is a chronic dermatosis that affects approximately 1.5 to 2%3 of the world population and 1.3 to 5%3,4 of all patients infected with HIV and is considered to be a sign of a poor prognosis.3 The clinical presentations can be more serious9-11 and even disfiguring.6 Hence, the importance of constant attention to an association of these pathologies in order to reach the diagnosis as early as possible.
Male patient, Caucasian, 44 years of age, natural and resident in Guarujá. Eighteen months previously there was onset of migraine and progressive weight loss and one year ago lesions appeared in the scalp, palmoplantar region and nails that caused him to seek medical attendance at the authors' service. The prior pathological history was negative for dermatological diseases, including psoriasis. Dermatological exam showed erythematous-desquamative lesions in the scalp, elbows, knees, palm of hands and soles of feet, and unguinal involvement of all 20 nails, with onycholysis and subunguinal hyperkeratosis. (Figures 1 and 2) The diagnostic hypothesis of psoriasis was confirmed by histopathological exam. Due to the evident consumptive state, HIV test was performed, with positive result, besides CD4 count and viral load, which were 7cell/mm3 and 7,000 copies RNA/ml, respectively. In view of the intense immunodepresson, topical treatment with coal tar was initiated and the patient was referred to the Infectology Service, in the hope of achieving an improvement in the lesions with anti-retroviral medication (indinavir 1.2gr/day, lamivudine 300mg/day and zidovudine 600mg/day). After six months of periodic attendance, notable regression of the lesions was observed (Figures 3 and 4) that coincided with a reduction in the viral load (3,400 copies RNA/ml) and increased CD4 45cell/mm3. To date, the patient presents remission of the lesions, without use of topical medication, but is undergoing treatment for neurotoxoplasmosis.
Cutaneous diseases are observed in approximately 92%3 of patients infected with HIV, these can be the initial4 and sometimes only manifestation5,6 that the patient presents during the course of the disease. They continue to be one of the most important clinical markers of the syndrome,1 serving as a predictive factor of the infection5 or sign of advanced disease. Its frequency and gravity increases as the disease progresses, and the immune function diminishes.6,7 The majority of cutaneous manifestations appear when the CD4 count is less than 100 cell/mm3, as in the reported case.3 However, some authors have not observed significant differences in the prevalence or gravity of the disease between asymptomatic patients and those with Aids.3
Dermatoses in these patients can present in atypical form and the therapeutic response be less than expected.3
The most common mucocutaneous infections are histoplasmosis, oro-esophageal candidiasis, oral pilar leukoplasia, dermatophytosis, herpes simplex, scabies, infection by human papilloma virus and molluscum contagiosum.5,8 Other frequent dermatoses include seborrheic dermatitis, Kaposi's sarcoma, oral ulcer, xerosis and psoriasis.8
Psoriasis is a chronic pathology that affects about 1.5 to 2%3 of the world population and 1.3 to 5%3,4 of patients infected with HIV, a segment of the population in which it is frequent and considered to be a sign of poor prognosis,3 a fact observed in the patient described here, who at the present moment is being treated for neurotoxoplasmosis. Although not observed in the case reported here, these patients present a higher incidence of arthritis, reaching about 10%,4 while among immunocompetent patients, such clinical findings only occur in 1%. Usually, the clinical forms are more serious9-11 and even disfiguring,6 with secondary complications9,11 or exacerbation of prior disease.12,13 Such tardive appearance of the disease without familial history or risk factors, as in the patient described here, necessitates investigation for this infection.12 Two main clinical forms can be found: 1) psoriasis guttata or long plaques and sometimes both guttata and vulgar forms can be observed in the same patient; 2) diffuse psoriasiform dermatitis, in general associated with palmoplantar keratoderma that can course with generalized disease,3 as in the patient of this case report. The initial presentation can be atypical, manifesting in the form of inverted psoriasis.3
The histopathological findings are similar to those of the classic form.4
Association of psoriasis is demonstrated with HLA-CW6 and CW7, especially HLA-CW0602, the latter being more frequent in psoriasis associated to HIV, although further studies are necessary.13
Treatment of these patients is a complex and delicate task. The response to topical treatment can be poor14 and certain medicines should be avoided, either because they are immunosuppressant,3 or can provoke a cross reaction.
Topical treatment with coal tar, salicylic acid,4 triamcinolone4 or their equivalent can be effective, mainly in association with anti-retroviral therapy, as the authors observed in the patient.
Etretinate followed by Reverse-PUVA has been indicated as the most effective systemic therapy, with rare adverse effects.16 Side effects of Etretinate include migraine and alterations of hepatic enzymes.3
Although exactly how the use of the ultraviolet light (UV) alters the natural course of the infection17 has not been fully clarified and no significant increase in the viremia was observed during and after treatment,14 it is believed that activation of the virus can occur,1 as well as an increase in the viral load and decrease in the CD4 count, with potentiation of opportunist infections and acceleration of the Aids.17
Experiments in animal models have demonstrated that UVB and PUVA are immunosuppressants due to the stimulation of the replication or activation of HIV.18 UVB seems to be more effective in inducing activation of the virus in human skin than PUVA.18
The effect of UV therapy on the progression of the disease seems to vary considerably between the patients in tardive state of the disease, when the immunity is considerably impaired and the viral load is high in relation to those with disease in the initial phase,18 thus it is necessary to identify these differing populations when selecting the optimal therapy.
Methotrexate is effective in some cases, however it can lead to hematological toxicity 16 or the appearance of Kaposi's sarcoma,3 besides increasing the risk of opportunist infection.19
Cyclosporin acts by interfering in the translocation of the nuclear pre-integration complex and in the production of viral particles. It presents moderate effectiveness and does not lead to the progression of their disease.16 However, the immunosuppressant action is considered a high risk factor for opportunist infection.19
Carbamazepine allows fast regression of the lesions, representing a good option for these patients, since it does not interfere in the immunity. Inhibition of the neuropeptide secretion seems to be the responsible for regression of the lesions and reduction of the erythema.19
Zidovudine is considered by some authors to be the therapeutic choice,3 because with the increased CD4 rate and principally reduced viral load, a significant improvement is observed in the lesions, as was verified in this case, although recurrence is common.4,15
The authors opted for the association of anti-retroviral agents with topical medication, in an attempt not to interfere with the already very weakened immunity of the patient. Fortunately, there was a notable improvement in the lesions, thereby avoiding the need to use other therapies.
Patients with psoriasis that present exacerbated clinical forms and are resistant to therapeutic response should be tested for a possible HIV infection. After introduction of antiretroviral agents, there is generally a marked improvement in the psoriasis lesions.
1. Duvic M. Human immunodeficiency virus and the skin: selected controversies. J Invest Dermatol 1995;105:117s-121S. [ Links ]
2. Jewell ME, Sweet DE. Oral and dermatologic manifestations of HIV infection. Postgrad Med 1994;96(5):105-8, 111, 114-6. [ Links ]
3. Mark J Zalla, W P Daniel SU, Fransway AF. Dermatologic Manifestations of Human Immunodeficiency Virus Infection. Mayo Clin Proc 1992;67:1089-1108. [ Links ]
4. Porras B, Costner M, Friedman-Kien AE, Cockerell CJ. Update on Cutaneous Manifestations of HIV Infection. Medical Clinics of North Ameica 1998;82(5):1033-1080. [ Links ]
5. Jing W, Ismail R. Mucocutaneous manifestations of HIV infection: a retrospective analysis of 145 cases in a Chinese population in Malaysia. Int J Dermatol 1999;38(6):457-63. [ Links ]
6. Myskowski PL, Ahkami R. Dermatologic complications of HIV infection. Med Clin North Am 1996;80(6):1415-35. [ Links ]
7. Rosatelli JB, Machado AA, Roselino AM. Dermatoses among Brazilian HIV-positive patients: correlation with the evolutionary phases of AIDS. Int J Dermatol 1997;36(10):729-34. [ Links ]
8. Singh A, Thappa DM, Hamide A. The spectrum of mucocutaneous manifestations during the evolutionary phases of HIV disease: an emerging Indian scenario. J Dermatol 1999;26(5):294-304. [ Links ]
9. Liapi C, Takahashi N, Raynaud F, Evain-Brion D, Anderson WB. Effects of [D-Ala1] peptide T-NH2 and HIV envelope glycoprotein gp120 on cyclic AMP dependent protein kinases in normal and psoriatic human fibroblasts. J Invest Dermatol 1998;110(4):332-7. [ Links ]
10. Arruda LHF, Campbell GAM, Takahashi MDF. Psoríase. An bras Dermatol 2001;76(2):141-165. [ Links ]
11. Silva-Vergara ML, Pineli MR, Galati MC, Correia D. Psoríase em paciente HIV positivo. Rev Soc Bras Med Trop 1996;29(6):599-602. [ Links ]
12. Passeron T, Bahadoran P, Lacour JP, Ortonne JP. Psoriasis. Clinical cutaneous aspects. Presse Med 1999;28(23):1246-50. [ Links ]
13. Mallon E, Young D, Brunce M, Gotch F, Brook PE, Newson R, et al. HLA-CW*0602 and HIV associated psoriasis. Br J Dermatol 1998;139(3):527-33. [ Links ]
14. Pechere M, Yerly S, Lemonnier E, Krischer J, Perrin L, Saurat JH. Impact of PUVA therapy on HIV viremia: a pilot study. Dermatology 1997;195(1):84-5. [ Links ]
15. Duvic M, Cranne M, Conant M, Mahoney SE, Reveille JD, Lehrman S. Zidovudine improves psoriasis in human immunodeficiency virus-positive males. Arch Dermatol 1994;130(4):447-51. [ Links ]
16. Romani J, Puig L, Baselga E, De Moragas JM. Reiter's syndrome-like pattern in AIDS-associated psoriasiform dermatitis. Int J Dermatol 1996;35(7):484-8. [ Links ]
17. Maurer TA, Zackheim HS, Tuffanelli L, Berger TG. The use of methotrexate for treatment of psoriasis in patients with HIV infection. J Am Acad Dermatol 1994;31(2 Pt 2):372-5. [ Links ]
18. Stern RS, Mills DK, Krell K, Zmudzka BZ, Beer JZ. HIV-positive patients differ from HIV-negative patients in indications for and type of UV therapy used. J Am Acad Dermatol 1998;39(1):48-55. [ Links ]
19. Smith KJ, Decker C, Yeager J, Skelton HG, Baskin S. Therapeutic efficacy of carbamazepine in a HIV-1-positive patient with psoriatic erythroderma [see comments]. J Am Acad Dermatol 1997;37(5 Pt 2):851-4. [ Links ]
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Received in June,
04th of 2001
Approved by the Consultive Council and accepted for publication in September, 03rd of 2002
* Work done at "Hospital Guilherme Álvaro - Faculdade de Ciências Médicas de Santos/UNILUS" and "Hospital Dia William Rocha - Guarujá - SP".