Rheumatic and autoimmune disease is a well known association of HIV disease. Entities include vasculitis, arthropathy, arthritis, myopathy, psori-atic disease, and diseases resembling sarcoidosis and Sjogren's disease. This is likely caused by both manifestation of primary disease and resultant dysregulation and hyperactivity of immune response and a consequence of subsequent effective immune reconstitution with highly active antiretroviral therapy [165,166].
Rheumatic disease in HIV prompts consideration of treatment with immunosuppressive therapy in patients who are at risk for life-threatening deterioration of immune defense. TNF-a is required for host response to intracellular pathogens, suggesting use of anti-TNF agents in HIV disease is a worrisome prospect. Anti-TNF therapy has been used successfully in HIV-positive patients with progressive psoriatic arthritis [167,168] and Reiter syndrome . Etanercept given as pretreatment against immune activation of IL-2 revealed no effect on HIV viral load . As in other chronic viruses, circulating TNF levels are found to be elevated in HIV disease proportionately to degree of compromise and presence of opportunistic infections. TNF-a may facilitate lymphocyte depletion and dysfunction and viral replication [166,171]. Etanercept given adjuvantly to TB therapy in HIV-positive patients not on highly active antiretroviral therapy was without adverse events and increased CD4+ T-cells by 25%; however, there was no reduction of viral load . Oral anti-TNF-alpha agents with a half-life of mere hours requiring twice daily dosing may be imminently available and confer a safer treatment profile for HIV rheumatic disease. Further studies regarding the use of anti-TNF therapy in HIV rheumatic disease are warranted.
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