Dr. Norman B. Gaylis
Reiter’s syndrome is an acute inflammatory arthritis with no standard treatment options for patients unresponsive to nonsteroidal anti-inflammatory drugs (NSAID). In patients positive for Human Immunodeficiency Virus (HIV), HIV-RNA levels have been correlated with elevated tumor necrosis factor-α (TNF-α) levels. We investigated the safety and activity 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 of taking the infliximab, all complaints resolved, nails regrew, and the rash cleared. CRP decreased to 0.8 mg/dl and ESR to 22 mm/h. During this 6-month period, antiretroviral therapy remained unchanged, and the viral titer remained below 400 Qn: US copies/ml.