Premium
Association between Selenium (Se) intake, plasma Se levels and disease progression in HIV‐infected adults in Miami
Author(s) -
Trivedi Riddhi,
Campa Adriana,
Martinez Sabrina Sales,
Page John Bryan,
Lai Shenghan,
Baum Marianna K
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.1022.3
Subject(s) - viral load , medicine , selenium , human immunodeficiency virus (hiv) , antiretroviral therapy , disease , selenium deficiency , young adult , gastroenterology , immunology , endocrinology , physiology , chemistry , oxidative stress , organic chemistry , catalase , glutathione peroxidase
Objective Se deficiency is associated with increased mortality and disease progression in HIV/AIDS. We explored the relationship between inadequate Se intake (<55 mcg/daily) and plasma levels (>0.085 mg/L) with disease progression in HIV+ adults. Methods With IRB approval, a cross‐sectional secondary analysis of the de‐identified database from “Zinc Therapy in Zinc deficient HIV+ Adults in Miami” study was performed. Results Of 231 HIV+ adults, 144 were on ART; 73.2 % were male. Mean CD4 cell count was 373 SD±279 cells/μL, viral load was 4.0 SD ±1.0 log10 copies/mL and plasma Se levels were 0.121 SD±0.29 mg/L. Higher plasma selenium levels were associated with controlled viral load (β=0.002, p=0.022), and remained significant after controlling for diarrheal disease and C‐reactive protein (p=0.039), and were correlated with Se intake (r=0.3, p>0.001). No association was found between Se intake or plasma Se levels with CD4 cell count. There were no differences in Se status (intake or plasma) between those in early HIV stages (CD4>200 cells/μL) and those with advanced disease (CD4<200 or CD4<100 cells/μL). Conclusion Adequate Se status appears to depend on adequate Se intake and viral load control in HIV+ adults. Further studies on the effect of normalizing Se status and the mechanism through which adequate Se contributes to slower disease progression are needed. Funded by NIDA