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.


OBJECTIVE
We asked whether the development of symptomatic sarcoidosis in the context of preexisting HIV infection was dependent on the CD4+ lymphocyte count.


METHODS
We performed a retrospective standardized chart review of all patients who developed granulomatous inflammation following HIV infection at an urban academic referral center.


METHODS
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/ microL 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/ microL, 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/ microL.


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/ microL. Furthermore, alternative specific etiologies of granulomatous inflammation are generally identifiable in HIV-infected patients with peripheral CD4+ lymphocyte counts of < 200 cells/ microL.
Morris
David G
DG
Interstitial Lung Disease Program, Department of Medicine, San Francisco General Hospital, University of California-San Francisco, San Francisco, CA 94142-0854, USA. dmorris@itsa.ucsf.edu
Jasmer
Robert M
RM
Huang
Laurence
L
Gotway
Michael B
MB
Nishimura
Stephen
S
King
Talmadge E
TE
D017088:AIDS-Related Opportunistic Infections / Q000276:immunology; D000328:Adult; D018791:CD4 Lymphocyte Count; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology*; D005260:Female; D015658:HIV Infections / Q000276:immunology*; D006801:Humans; D017563:Lung Diseases, Interstitial / Q000276:immunology; D008297:Male; D008875:Middle Aged; D012189:Retrospective Studies; D012307:Risk Factors; D012495:San Francisco; D017565:Sarcoidosis, Pulmonary / Q000276:immunology*; D014397:Tuberculosis, Pulmonary / Q000276:immunology