Case reportTenosynovitis as a possible feature of immune reconstitution syndrome during highly active antiretroviral treatment (HAART)
Introduction
An immune reconstitution syndrome (IRS) occurs in between 10% and 25% of patients starting highly active antiretroviral treatment (HAART) [1]. It appears to be due to the reconstitution of specific immunity to certain antigens, both microbial and non microbial, in patients with immunological and/or genetic risk factors [2]. This syndrome was first described with opportunistic pathogens such as cytomegalovirus, Cryptococcus neoformans and other bacteria [3]. Immunoinflammatory and rheumatic manifestations have also been reported, including sarcoidosis and thyroid disorders (Hashimoto and Basedow's disease), aseptic inflammatory arthritis and lupus-like connective tissue inflammation [3], [4], [5]. Malignant and septic arthritis (lymphoma, Kaposi's sarcoma) now represent more than 50% of the rheumatologic disorders observed in HIV-infected patients since the advent of HAART [6]. However, peripheral inflammatory disorders such as tenosynovitis have not yet been reported in this setting. Here, we describe a case that adds to the already broad spectrum of inflammatory rheumatologic disorders associated with HIV infection.
Section snippets
Case report
A 49-year-old Cameroonian man was diagnosed with HIV-1 infection in August 2006, after developing persistent diarrhea along with an altered general state. We noticed former attacks of gout. His CD4+ cell count was 53/mm3 (10%), the CD8+ cell count was 345/mm3 (65%), the CD4/CD8 ratio was 0.2 and the viral load was 800 000 copies/mm3 (5.83 log10). Treatment with lamivudine, tenofovir, fosamprenavir and ritonavir was started in late August 2006. Six weeks later he presented with a painful and swollen
Discussion
This patient's history, clinical manifestations and biological findings were suggestive of aseptic arthritis and bilateral tenosynovitis associated with an IRS. Based on previously described criteria [1], the main supporting arguments were the following: the chronology (onset 6 weeks after starting boosted protease inhibitor therapy), the patient's young age, the profound immunodepression at the outset of antiretroviral treatment, the rapid decline in viral load (reduction of 2.7 log10 in a
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