HIV-associated psoriasis: pathogenesis, clinical features, and management. Lancet Infect Dis
Department of Dermatology, Chelsea and Westminster Hospital, 369 Fulham Road, London, UK. The Lancet Infectious Diseases
(Impact Factor: 22.43).
07/2010; 10(7):470-8. DOI: 10.1016/S1473-3099(10)70101-8
Psoriasis is a chronic papulosquamous skin disease that is thought to be a T-cell-mediated autoimmune disorder of keratinocyte proliferation. The association between psoriasis and HIV infection seems paradoxical, but insights into the role of T-cell subsets, autoimmunity, genetic susceptibility, and infections associated with immune dysregulation might clarify our understanding of the pathogenesis of psoriasis with HIV in general. HIV-associated psoriasis can be clinically confusing because several comorbid skin disorders in patients with HIV can mimic psoriasis. Phenotypic variants such as a Reiter's syndrome or fulminant erythroderma provide diagnostic clues to underlying immunodeficiency. The management of moderate and severe HIV-associated psoriasis is challenging, although patients typically improve with highly active antiretroviral therapy. Conventional systemic treatments might be contraindicated or need dose adjustment to avoid toxicity. New biological treatments in this setting are promising and warrant further study.
Available from: PubMed Central
- "Notably, exacerbation due to staphylococcal and streptococcal infection is more common among HIV-infected individuals [5, 6]. In the present case, psoriasis began suddenly and was immediately severe (involving 60% of body surface area) during the course of diminished immune function (CD4 count, 44/mm3) without other risk factors such as excessive alcohol intake, smoking, and the use of drugs such as lithium and β-blockers . No infectious complications occurred during treatment under close follow-up. "
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ABSTRACT: Psoriasis is a chronic inflammatory skin disease that involves immune-mediated cutaneous inflammation and keratinocyte hyperproliferation. Psoriasis in patients with HIV responds poorly to treatment and has a high morbidity rate, thus posing a challenge to clinicians. Until now, there have been no documented cases of acitretin therapy for HIV-associated psoriasis in Korea. Here, we report a case of safe and successful therapy with acitretin in a 52-year-old man with HIV-associated psoriasis that responded poorly to previous treatments including steroids and ultraviolet B phototherapy. We also review the relevant literature.
06/2014; 46(2):115-9. DOI:10.3947/ic.2014.46.2.115
Available from: Hayley G Evans
- "This is supported by observational data; patients with advanced human immunodeficiency virus (HIV) status and low CD4+ T cell counts may develop de novo or worsening PsA and/or psoriasis, whereas patients with CD4+ T cell–driven diseases such as RA have shown improvement at the onset of HIV infection (8,9). It has been suggested that the corresponding increase in memory CD8+ T cells, comprising up to 80% of the total T cell compartment in severe HIV infection, contributes to the development of PsA in this context (10). "
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Psoriatic arthritis (PsA) is associated with HLA class I genes, in contrast to the association with HLA class II in rheumatoid arthritis (RA). Since IL-17+ cells are considered important mediators of synovial inflammation, we sought to determine whether IL-17–producing CD8+ T cells may be found in the joints of patients with PsA and whether these cells might contribute to the disease process.
Mononuclear cells from paired samples of synovial fluid (SF) and peripheral blood (PB) from patients with PsA or patients with RA were stimulated ex vivo, and CD4− T cells were examined by flow cytometry for cytokine expression, cytotoxic markers, and frequencies of γ/δ or mucosal-associated invariant T cells. Clinical measures of arthritis activity (C-reactive protein [CRP] level, erythrocyte sedimentation rate [ESR], Disease Activity Score in 28 joints [DAS28]) and power Doppler ultrasound (PDUS) scores for the presence of active synovitis in the aspirated knee were recorded and assessed for correlations with immunologic markers.
Within the CD3+ T cell compartment, both IL-17+CD4− (predominantly CD8+) and IL-17+CD4+ T cells were significantly enhanced in the SF compared to the PB of patients with PsA (P = 0.0003 and P = 0.002, respectively; n = 21), whereas in patients with RA, only IL-17+CD4+ T cells were increased in the SF compared to the PB (P = 0.008; n = 14). The frequency of IL-17+CD4− T cells in PsA SF was positively correlated with the CRP level (r = 0.52, P = 0.01), ESR (r = 0.59, P = 0.004), and DAS28 (r = 0.52, P = 0.01), and was increased in patients with erosive disease (P < 0.05). In addition, the frequency of IL-17+CD4− T cells positively correlated with the PDUS score, a marker for active synovitis (r = 0.49, P = 0.04).
These results show, for the first time, that the PsA joint, but not the RA joint, is enriched for IL-17+CD8+ T cells. Moreover, the findings reveal that the levels of this T cell subset are correlated with disease activity measures and the radiographic erosion status after 2 years, suggesting a previously unrecognized contribution of these cells to the pathogenesis of PsA.
Arthritis and Rheumatology 05/2014; 66(5). DOI:10.1002/art.38376
Available from: Nicolas Alejandre
- "T cell-driven autoimmune diseases can occur in HIV carriers even in the presence of very low T cell counts. Psoriasis is an example and illustrates how HIV favors immune dysregulation . HAART therapy leads to restoration of T cell functions with general improvement in patient’s health. "
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ABSTRACT: The purpose of this study is to report a case of sympathetic ophthalmia (SO) in an HIV-infected patient on treatment with highly active antiretroviral therapy (HAART) 9 years after a penetrating eye injury.
The study utilized clinical course and histopathological findings.
Histopathology of the enucleated right eye showed a predominantly lymphocytic inflammatory infiltration with some plasma cells and epithelioid granulomata in the choroid, suggesting the diagnosis of SO.
SO seems to be driven by T lymphocytes, specifically by the CD4 subset of T cells. HIV-infected individuals suffer a decline in CD4 T cell numbers, leading to an acquired immunodeficiency that could halt the development of the inflammatory reaction responsible for SO. The restoration of the CD4 counts by HAART therapy makes HIV-infected individuals as susceptible to SO as non-infected ones. To the best of our knowledge, there are no cases of SO in HIV-infected patients reported in the literature.
Journal of Ophthalmic Inflammation and Infection 03/2012; 2(3):161-4. DOI:10.1007/s12348-012-0065-y
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