Case Presentation: A young man presented to the ED with four days of severe, sharp midsternal chest pain, fevers, diffuse arthralgias, bilateral conjunctivitis, diarrhea, and fatigue. He reported sexual intercourse with an HIV positive male partner four months prior to presentation and a history of multiple STI’s diagnosed in the past 6 years. Vitals: 101.5F, HR was 102 bpm, and respiratory rate was 20. He was normotensive with an O2s of 94% on RA Physical exam includes warmth and erythema of the anterior chest wall, tenderness to palpation of the sternum, right knee, left ankle, and left sacroiliac joint, and bilateral conjunctivitis. Labs demonstrated elevated inflammatory markers (WBC, ESR, and CRP) as well as positive anti RF and anti-CCP. Infectious work up was significant for positive stool PCR for E. Coli (EAEC), shigella, and giardia with positive rectal swab for chlamydia. HIV antibody testing was positive; diagnosis confirmed with an HIV viral load of 65,073 copies/mL with CD4 T-lymphocyte of 91 cell/mm3. Blood cultures, ocular, pharyngeal, and urethral swabs were negative. Viral hepatitis testing was negative. Chest CT demonstrated non-specific abdominal lymphadenopathy and mild hepatosplenomegaly. Chest MRI ruled out sternal osteomyelitis. He started on scheduled Naproxen, had improvement in his pain. It was not clear if the etiology of his symptoms was reactive arthritis or HIV associated arthritis. He was also started on HAART, appropriate prophylaxis, and antibacterial treatment of GI infection.

Discussion: The diagnostic dilemma stems from our patient meeting criteria of both reactive arthritis and HIV-associated arthritis. This patient’s asymmetric oligoarthritis in the lower extremity, diarrhea, and positive rectal swab for fulfilled the diagnostic criteria for reactive arthritis. Reactive arthritis is a rheumatic disorder that can occur one-to-six weeks following a GI or GU infection. HIV-associated arthropathy (HA) can present similarly to reactive arthritis in that it too can cause an asymmetric oligoarthritis predominantly in the lower extremities and generally follows a one-to-six-week time course. Differentiating between reactive arthritis and HIV-associated arthritis can be challenging based on musculoskeletal manifestations alone, and therefore requires consideration of all symptoms and a thorough lab evaluation to make an accurate diagnosis. Our patient’s presenting symptoms included oligoarthritis and bilateral painless conjunctivitis. However, the absence of GU symptoms at presentation initially kept reactive arthritis lower on the differentia. Urethritis can be the presenting symptomatic component of reactive arthritis in up to 80% of GI-induced reactive arthritis and may precede the onset of arthritis by up to one month. Our patient’s lack of urethritis highlights a key point that the absence of GU symptoms does not preclude a diagnosis of reactive arthritis.

Conclusions: Reactive arthritis should remain high on the differential in HIV/AIDS-positive patients presenting with undifferentiated arthritis. A thorough infectious workup to identify enteric or venereal arthritogenic pathogens should be carried out in all HIV/AIDS patients presenting with oligoarthritis. Should a patient meet the diagnostic criteria for reactive arthritis prompt treatment should be started as to prevent chronic destructive joint disease. The authors hope that our experience offers insight into improving the diagnosis and management of ReA in patients with HIV/AIDS.