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Clinical Investigations: SARCOIDOSIS |

Sarcoidosis Following HIV Infection*: Evidence for CD4+ Lymphocyte Dependence

David G. Morris; Robert M. Jasmer; Laurence Huang; Michael B. Gotway; Stephen Nishimura; Talmadge E. King, Jr
Author and Funding Information

*From the Interstitial Lung Disease Program (Drs. Morris, Gotway, Nishimura, and King) and the Division of Pulmonary and Critical Care Medicine (Drs. Jasmer and Huang), Department of Medicine, San Francisco General Hospital, University of California, San Francisco, CA.

Correspondence to: David G. Morris, MD, Box 0854, University of California, San Francisco, San Francisco, CA 94143-0854; e-mail: dmorris@itsa.ucsf.edu



Chest. 2003;124(3):929-935. doi:10.1378/chest.124.3.929
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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.


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