HIV-Associated Rheumatic Conditions

John G. Bartlett, MD


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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