Sarcoidosis following HIV infection: Evidence for CD4⁺ lymphocyte dependence

Background: The chronic granulomatous inflammation of sarcoidosis has been hypothesized to depend on the CD4⁺ T-helper lymphocyte. HIV infection, which depletes these cells, has been reported to attenuate the manifestations of sarcoidosis. Study objectives: We asked whether the development of symptomatic sarcoidosis in the context of preexisting HIV infection was dependent on the CD4⁺ lymphocyte count. Design: We performed a retrospective standardized chart review of all patients who developed granulomatous inflammation following HIV infection at an urban academic referral center. Measurements: We identified seven patients with sarcoidosis within this cohort and compared their CD4⁺ lymphocyte count to that in a cohort of 16 patients in whom similar granulomatous inflammation was found but who did not have sarcoidosis. We then compared our cases to all reported cases using a systematic literature review. Results: The CD4⁺ lymphocyte count was > 200 cells/μL in all of our patients with HIV infection when they developed subsequent sarcoidosis. In contrast, specific etiologies for granulomatous inflammation were found in all 10 HIV-infected patients who presented with granulomatous inflammation and a CD4⁺ lymphocyte count of < 200 cells/μL, with infectious etiologies found in 8 patients. Similarly, there was relative preservation of the CD4⁺ lymphocyte count in previously reported cases, with 14 of 19 patients (74%) having an absolute CD4⁺ lymphocyte count of > 200 cells/μL. Conclusions: We conclude that the development of the chronic granulomatous inflammation of sarcoidosis appears to depend on the preservation or restoration of the peripheral CD4⁺ lymphocyte count and that in most cases the CD4⁺ lymphocyte count exceeds 200 cells/μL. Furthermore, alternative specific etiologies of granulomatous inflammation are generally identifiable in HIV-infected patients with peripheral CD4⁺ lymphocyte counts of < 200 cells/μL.