Dr. Norman B. Gaylis

Reiter’s syndrome is an acute inflammatory arthritis with no standard treatment options for patients unresponsive to nonsteroidal antiinflammatory drugs (NSAID). In patients positive for Human Inmunodeficiency Virus (HIV), HIV-RNA levels have been correlated with elevated tumor necrosis factor-α (TNF-α) levels. We investigated the safety and actvitiy of infliximab, an anti-TNF-α chimeric monoclonal antibody, in the treatment of an HIV-positive patient with Reiter’s refractory to NSAID therapy. A 41-year-old HIV positive patient with Reiter’s syndrome was treated with infliximab 300 mg intravenously at Week 0, 2 and 6 and then every 6 to 7 weeks thereafter. He presented with severe fatigue, pain, muscle wasting, synovitis of the elbows, wrists and knees, a scaly rash in the groin area, burning during urination, and severe onycholysis on all digits. Laboratory assessment revealed hemoglobin 7.8 g/dl, erythrocyte sedimentation rate (ESR) 152 mm/h, white blood cell count 5700 cells/ mm3 , and C-reactive protein (CRP) 65.7 mg/dl. HIV viral load on presentation was 1600 quantitative:ultrasensitive (Qn:US) copies/ml, decreased from a maximum of 428,000 Qn:US copies at the start of antiretroviral therapy. After 6 months taking infliximab, all complaints resolved, nails regrew, and the rash cleared. CRP decreased to 0.8 mg/dl and ESR to 22 mm/h. Durign this 6-month period, antiretroviral therapy remained unchanged, and the viral titer remained below 400 Qn:US copies/ml.

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