Review
HIV-associated psoriasis: pathogenesis, clinical features, and management

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Summary

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.

Introduction

The Joint UN Programme on HIV/AIDS and WHO reported that there were 33·4 million people with HIV infection worldwide in 2008;1 sub-Saharan Africa accounts for 67% of this number. According to the UK Health Protection Agency, there are 77 400 individuals infected with HIV in the UK.2

The immune dysfunction associated with HIV results in several cutaneous disorders, with progressive immunocompromise resulting in AIDS. Dermatological disorders such as psoriasis can be the presenting feature of HIV infection and can provide clinical clues to the degree of immune dysfunction. In this Review, we discuss the pathogenesis, clinical features, and management of psoriasis with HIV.

Section snippets

Classic psoriasis

Psoriasis is a chronic inflammatory skin disease and is prevalent in 1–2% of northern European populations.3 The common phenotype, psoriasis vulgaris, is characterised by symmetrical, erythematosus, scaly plaques typically found on the extensor surfaces of the skin although any site can be affected. Concomitant psoriatic arthritis happens in 5–42% of patients.4 Histologically, psoriasis is characterised by amplified proliferation of basal keratinocytes, a thickened epidermis, premature

HIV and psoriasis

The prevalence of HIV-associated psoriasis and HIV-associated psoriatic arthritis may or may not be the same as in the general population.23, 24, 25, 26, 27, 28 Psoriasis might worsen or be detected for the first time with HIV. It can be very severe, but can regress before death.23, 29 The development of HIV-associated psoriasis and HIV-associated psoriatic arthritis might be associated with poor prognosis in untreated patients, with a mean expectancy ranging from 4 months to 24 months after

Pathogenesis

Although psoriasis can present throughout the range of immunodeficiency, it tends typically to present late with increasing immunodysfunction,26 and CD4-cell counts are less than 100 cells per μL in many patients.24 This finding is paradoxical since the pathogenesis of psoriasis is associated with the activation of T cells and treatments that decrease T-cell counts improve psoriasis.33 Contributing to the paradox is that psoriasis is characterised by T cells that produce type-1 cytokines

Clinical features

The classic signs of plaque psoriasis are symmetrical erythematous (so-called salmon pink) patches or plaques with silver scales. Nail signs include coarse pitting, onycholysis, subungual hyperkeratosis, splinter haemorrhages, and frank onychodystrophy. A yellow subungual discolouration due to nail bed involvement (oil-drop lesion) is the only specific sign of nail psoriasis. Care must be taken to exclude onychomycosis (also common in HIV) since the clinical features can be similar to nail

Differential diagnosis

Annular psoriasis might be confused with ringworm; skin scrapings for fungal microscopy and culture help distinguish the latter. Microscopy can also be helpful to exclude crusted (Norwegian) scabies, to which patients with HIV are prone and which is highly contagious if undiagnosed. The clinical presentation can mimic psoriasis since the lesions are often non-pruritic and present as scaly plaques on the skin (figure 6), scalp, and nails.63

Papulosquamous secondary syphilis might clinically and

Histology and treatment

The histological features of HIV-associated psoriasis might be identical to classic psoriasis; however, diagnosis might be difficult. A psoriasiform dermatitis with few neutrophilic microabscesses, irregular acanthosis, and a perivascular infiltrate of lymphocytes, macrophages, and multinucleated giant cells might be seen.24, 65 Typically in HIV-associated psoriasis, there are few T cells, dyskeratotic keratinocytes, and lymphocytoclasis; but plasma cells are common. Since plasma cells are

Conclusions

The immunological dysfunction associated with HIV creates an environment that is conducive to developing psoriasis in those individuals constitutively susceptible by virtue of their immunogenotype. The main postulated mechanisms are a T-cell imbalance characterised by decreased CD4 T cells and a relative increase in CD8 memory T cells, a cytokine milieu predominantly mediated by interferon γ, superantigen stimulation of autoimmunity by HIV or other viral and bacterial infections and HLA Cw0602

Search strategy and selection criteria

We searched PubMed, Medline, and Cochrane databases with English keywords “psoriasis”, “HIV”, “psoriatic arthritis”, “pathogenesis”, “treatment”, “clinical features”, and “diagnosis”. We reviewed the reference lists of all articles retrieved, together with those in our personal reference libraries. An updated search was done on April 16, 2010.

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