Share this article on:

Vitamin D insufficiency may impair CD4 recovery among Women's Interagency HIV Study participants with advanced disease on HAART

Aziz, Mariam; Livak, Britt; Burke-Miller, Jane; French, Audrey L.; Glesby, Marshall J.; Sharma, Anjali; Young, Mary; Villacres, Maria C.; Tien, Phyllis C.; Golub, Elizabeth T.; Cohen, Mardge H.; Adeyemi, Oluwatoyin M.

doi: 10.1097/QAD.0b013e32835b9ba1
Clinical Science

Background: Recent studies in HIV-infected men report an association between low vitamin D (25OH-D) and CD4 recovery on HAART. We sought to test this relationship in the Women's Interagency HIV Study (WIHS).

Methods: We examined 204 HIV-infected women with advanced disease, who started HAART after enrollment in the WIHS. We measured vitamin D (25OH-D) levels about 6 months prior to HAART initiation. The relationship between CD4 recovery (defined as increases of ≥50, 100, and 200 cells at 6, 12, and 24 months) and exposure variables was examined using logistic regression models at 6, 12 and 24 months post-HAART initiation in unadjusted and adjusted analyses, and using multivariable longitudinal Generalized Estimating Equations (GEE). Vitamin D insufficiency was defined as 25OH-D levels at least 30 ng/ml.

Results: The majority were non-Hispanic black (60%) and had insufficient vitamin D levels (89%). In adjusted analyses, at 24 months after HAART, insufficient vitamin D level (OR 0.20, 95% CI 0.05–0.83) was associated with decreased odds of CD4 recovery. The undetectable viral load (OR 11.38, 95% CI 4.31–30.05) was associated with CD4 recovery. The multivariable GEE model found that average immune reconstitution attenuated significantly (P < 0.01) over time among those with insufficient vitamin D levels compared with those with sufficient vitamin D levels.

Conclusion: Vitamin D insufficiency is associated with diminished late CD4 recovery after HAART initiation among US women living with advanced HIV. The mechanism of this association on late CD4 recovery may be late vitamin D-associated production of naive CD4 cells during immune reconstitution.

aRush University Medical Center

bJohn H Stroger Hospital, Chicago, Illinois

cWeill Cornell Medical College, New York

dSUNY Downstate Medical Center, Brooklyn, New York

eGeorgetown University Medical Center, Washington, DC

fUniversity of Southern California, Los Angeles

gUniversity of California

hVeterans Affairs Medical Center, San Fransisco, California

iJohns Hopkins University, Baltimore, Maryland, USA.

Correspondence to Mariam Aziz, MD, Section of Infectious Diseases, Rush University Medical Center, 600 S Paulina Suite 143, Chicago, IL 60612, USA. Tel: +1 312 942 5865; fax: +1 312 942 8200; e-mail:

Received 25 May, 2012

Revised 10 October, 2012

Accepted 16 October, 2012

Study was presented in part at the Conference on Retroviruses and Opportunistic Infections, Seattle WA, 2012.

Copyright © 2013 Wolters Kluwer Health, Inc.