Psoriasis regression in terminal AIDS

Colebunders, R; Blot, K; Mertens, Veerle; Dockx, P.

doi:10.1016/0140-6736(92)90701-4

Cited by 34 publications

(13 citation statements)

References 2 publications

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“…53 However, psoriasis also tends to spontaneously improve during end-stage AIDS. 52,55 The relationship between HIV infection and psoriasis is complicated. While an expansion of CD8 cells in advanced HIV might explain the exacerbation of psoriasis, 56 there is now evidence that psoriasis patients are enriched for genetic variants that protect against HIV-1 disease.…”

Section: Psoriasis and Hivmentioning

confidence: 99%

Psoriasis: epidemiology, natural history, and differential diagnosis

Basko-Plluska¹,

Petronic‐Rosic²

2012

PTT

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Psoriasis is a chronic, immune-mediated, inflammatory disease which affects primarily the skin and joints. It occurs worldwide, but its prevalence varies considerably between different regions of the world. Genetic susceptibility as well as environmental factors play an important role in determining the development and prognosis of psoriasis. Genomewide association studies have identified many genetic loci as potential psoriasis susceptibility regions, including PSORS1 through PSORS7. Histocompatibility antigen (HLA) studies have also identified several HLA antigens, with HLA-Cw6 being the most frequently associated antigen. Epidemiological studies identified several modifiable risk factors that may predispose individuals to developing psoriasis or exacerbate pre-existing disease. These include smoking, obesity, alcohol consumption, diet, infections, medications and stressful life events. The exact mechanism by which they trigger psoriasis remains to be elucidated; however, existing data suggest that they are linked through Th1-mediated immunological pathways. The natural history of psoriasis varies depending on the clinical subtype as well as special circumstances, including pregnancy and HIV infection. In general, psoriasis is a chronic disease with intermittent remissions and exacerbations. The differential diagnosis is vast and includes many other immunemediated, inflammatory disorders.

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Section: Psoriasis and Hivmentioning

confidence: 99%

Psoriasis: epidemiology, natural history, and differential diagnosis

Basko-Plluska¹,

Petronic‐Rosic²

2012

PTT

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“…Previous studies reported that QOL improved following heart transplantation and significantly correlated with functional ability at 1-year follow-up [32, 33]. This may contribute to the ceiling effects, since QOL in our OHT recipients was already comparable to normal subjects [27].…”

Section: Discussionmentioning

confidence: 85%

Efficacy of a Home-Based Exercise Program for Orthotopic Heart Transplant Recipients

Chien

Chou

et al. 2008

Cardiology

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Background:A hospital-based cardiac rehabilitation program can significantly improve the cardiopulmonary endurance and quality of life (QOL) in patients after orthotopic heart transplantation (OHT). Home-based programs for these patients have advantages of low cost and high accessibility, but little is known about their efficacy. This prospective study was designed to evaluate the effect of an 8-week home-based exercise program on muscular strength and endurance of lower limbs, aerobic capacity and QOL in OHT recipients. Methods:Thirty-seven OHT recipients were randomized into exercise (n = 14) or control (n = 23) groups. Exercise group subjects were to exercise at least 3 times a week for 8 weeks. Each subject was evaluated by Cybex testing of right quadriceps strength and endurance, 1-min sit-to-stand test, a symptom-limited maximal exercise test and QOL assessment before and after 8 weeks. Results: Subjects in the exercise group improved significantly in sit-to-stand test, fatigue index of the right quadriceps, maximal workload achieved and physical domain of QOL compared to controls after 8 weeks, regardless of older age and lower value for sit-to-stand test at baseline. Conclusions: OHT recipients can significantly improve their muscular endurance, sit-to-stand test scores and QOL after a medically directed home-based exercise program.

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“…[3] However, it may appear for the first time or pre-existing psoriasis may undergo severe exacerbation in HIV disease, and psoriasis reportedly becomes more severe with progression of immunodeficency but may remit in the terminal phase. [4] The prognosis of AIDS in patients with HIV-associated psoriasis has also been reported to be poor. [3] The mechanism of exacerbation of psoriasis in HIV disease is unclear.…”

Section: Exacerbation Of Psoriasis In Aidsmentioning

confidence: 99%

Paradoxical Exacerbation of Psoriasis in AIDS: Proposed Explanations Including the Potential Roles of Substance P and Gram-negative Bacteria

Namazi

2004

Autoimmunity

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Psoriasis, a TH1-induced disorder, is not more common in human immunodeficiency virus (HIV) infection than in the general population. However, it may appear for the first time or pre-existing psoriasis may worsen and be difficult to treat in HIV disease. The paradoxical exacerbation of psoriasis in AIDS has not been fully explained. Various explanations have been proposed including (a) the reduction of Langerhans' cells (LCs) in HIV disease, (b) the direct epidermal proliferative effect of HIV, (c) the altered cytokine profile in HIV disease, (d) HIV-induced macrophage nitric oxide (NO) production, (e) the increased CD8/CD4 T-cell ratio in HIV infection and (f) the increased colonization of skin by Staphylococcus aureus. However, the observations that (a) LCs cells play an important role in the pathogenesis of psoriasis and a variety of topical and systemic psoriasis treatments cause a reversible decrease in LC function, (b) psoriasis may improve in end-stage HIV infection, (c) overproduction of some TH2 cytokines and underproduction of IL-2 in HIV infection, and (d) the presence of NO favors a TH2 response over a TH1 response make the first four explanations difficult to interpret. Since psoriasis is exacerbated in HIV infection possibly due to the increased staphylococcal colonization, and psoriatic keratinocytes could aggravate HIV infection through production of TNF-alpha, it could be reasoned that in HIV-positive psoriatics a strong vicious cycle is present between the degree of immune deficiency and the staphylococcal colonization, explaining the poor prognosis of both AIDS and psoriasis in these patients. With reference to the studies which indicate significant involvement of substance P (SP) in the pathogenesis of psoriasis and on the other hand increased release of this agent by HIV-infected immune cells it is proposed that SP plays an important role in creating the paradox. Since in HIV-positive psoriatics the source of SP is largely immune cells not neurons, capsaicin, which exerts its action selectively on a subpopulation of neurons, could not be of significant therapeutic value. As SP significantly enhances HIV-1 replication in latently infected immune cells, psoriatic lesions, being heavily infiltrated with immune cells and having high concentrations of SP, could serve as high HIV-replication foci, with the resultant rapid progression of the infection towards AIDS. Additionally, given that lipopolysaccharide is supposed to exacerbate psoriasis, increase of gram-negative infections or cutaneous colonization with these organisms in AIDS may partly explain the paradox. Understanding the HIV-induced immunodysregulation that is associated with psoriasis in some HIV-seropositive patients may assist in the delineation of the immunopathogenesis of the disease in HIV-seronegative psoriatics.

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Psoriasis regression in terminal AIDS

Cited by 34 publications

References 2 publications

Psoriasis: epidemiology, natural history, and differential diagnosis

Psoriasis: epidemiology, natural history, and differential diagnosis

Efficacy of a Home-Based Exercise Program for Orthotopic Heart Transplant Recipients

Paradoxical Exacerbation of Psoriasis in AIDS: Proposed Explanations Including the Potential Roles of Substance P and Gram-negative Bacteria

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