COMMENTARY

HIV-Associated Rheumatic Conditions

John G. Bartlett, MD

Disclosures

June 01, 2009

This Viewpoint presents highlights of an article that describes rheumatic diseases associated with HIV infection that is based largely on a literature review with 165 references.

Rheumatic Conditions in Human Immunodeficiency Virus Infection

Walker UA, Tyndall A, Daikeler T
Rheumatology (Oxford). 2008;47:952-959. Epub 2008 Apr 15

Article Summary

The authors reviewed rheumatic diseases associated with HIV infection. The following are highlights.

HIV-associated arthritis: This is a nonerosive oligoarthritis of the legs of unknown etiology found in up to 1% of patients.[1] This condition is usually self-limited and lasts less than 6 weeks.

Reiter's syndrome (reactive arthritis): This appears to be more common in persons with HIV infection who are usually HLA-B27 positive. The best treatment is HIV suppression and tumor necrosis factor (TNF)-alpha antagonists.[2]

Septic arthritis: The largest reviews comprising 14-30 cases have shown no clear association with CD4 count; major joints affected are the sternoclavicular and leg joints.[3,4]

Indinavir-associated hyperuricemia and arthralgia:Indinavir has been implicated in this condition, but crystals were not detected.[5,6]

Gout: Hyperuricemia is common with HIV, with an annual incidence of gout of 0.5% reported, and ritonavir boosting has been implicated.[7]

Rhabdomyolysis: This may complicate primary HIV infection[8] or complicate statin use in patients receiving highly active antiretroviral therapy (HAART).[9]

HIV-associated polymyositis: Polymyositis has been reported in as many as 2% to 7% of persons with HIV infection.[10]Muscle biopsy shows CD8 cell infiltrates and viral antigen.[11] HIV-associated polymyositis has been reported to be clinically and histologically identical to idiopathic polymyositis, but has a good prognosis and responds well to immunosuppressive treatment. About half also have diffuse infiltrative lymphocytosis syndrome.[12]

Zidovudine myopathy: This is seen exclusively with zidovudine and is characterized by muscle weakness and normal or slightly elevated creatine kinase levels. Electron microscopy shows abnormal mitochondria that resolves with drug discontinuation.[13]

Vasculitis: This is described in early HIV disease in patients with high CD4 counts, as well as later in patients with severe immunosuppression.[14] Biopsies show nonspecific neutrophilic or monocytic vascular inflammation and often other clinical features, such as rash or peripheral neuropathy or both. Some patients have cryoglobulinemia; some have HIV-associated polyarteritis nodosa[15]; and some have large-vessel complications, including aneurysms or strokes.[16,17]

Diffuse infiltrative lymphocytosis syndrome: Prevalence in the HIV population is approximately 3%.[18] Many patients present with bilateral painless parotid gland enlargement, lacrimal gland enlargement, and sicca symptoms. The pathogenesis is thought to be an excessive response to HIV with CD8 lymphocytosis,[19] and it may be associated with lymphoid interstitial pneumonia in up to 31%, or involvement of muscles or liver.[20] HAART appears to be effective given that the incidence is decreasing in the current era.[21]

Systemic lupus erythematosus: This condition usually improves in patients with untreated HIV infection, which fits the current concepts of the importance of CD4 cells in pathogenesis.[22] However, this can also be a component of immune reconstitution inflammatory syndrome. Systemic lupus erythematosus may also be the source of a false-positive screening test for HIV, but not the confirmatory Western blot.[23]

Sarcoidosis: When sarcoidosis coexists with HIV, most patients who are symptomatic have CD4 counts exceeding 200 cells/µL, which is consistent with the current concept of the role of CD4 cell lymphocytes in the pathogenesis of granuloma formation.[24,25] At present, most patients with active sarcoidosis have this as a result of immune reconstitution inflammatory syndrome.[24,26]

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