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Brief Report

Gut Structural Damage

an Ongoing Process in Chronically Untreated HIV Infection

El Kamari, Vanessa, MD*,†; Sattar, Abdus, PhD*; Mccomsey, Grace A., MD*,†

JAIDS Journal of Acquired Immune Deficiency Syndromes: February 1, 2019 - Volume 80 - Issue 2 - p 242–245
doi: 10.1097/QAI.0000000000001910
Translational Research
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Objective: To investigate the longitudinal changes of gut structural damage in chronically untreated HIV infection.

Design: This is a 96-week prospective, single-site, cohort study of antiretroviral therapy–naive HIV-infected participants.

Methods: Intestinal fatty acid-binding proteins (I-FABP) were used as a surrogate marker of gut structural damage. We assessed changes in I-FABP over 96 weeks and examined the associations between I-FABP, HIV variables, and inflammation. Spearman's correlations and linear mixed-effect models were used to study relationships among variables.

Results: A total of 63 HIV-infected, antiretroviral therapy–naive patients were included in this analysis. At baseline, 76% were male; 62% were African American, with median age and body mass index of 40 years and 27 kg/m2, respectively. Median HIV-RNA and CD4+ T-cell counts were 5520 copies per milliliter and 588 cells per mm3, respectively. I-FABP significantly increased from baseline to week 96 (mean change +333.9 pg/mL; P = 0.03), and this increase was associated with viral replication (rho = +0.4; P = 0.03). I-FABP levels were found to be associated with markers of inflammation: sTNFR-II (rho = 0.4, P = 0.02) and sVCAM-1 (rho = 0.04; P < 0.01) at all study time points. Lower baseline CD4+ T-cell counts was found to be independently associated with I-FABP progression after adjusting for baseline characteristic variables (P = 0.02).

Conclusion: Gut structural damage is an ongoing process in the chronic phase of untreated HIV infection and is largely dependent on viral replication. I-FABP was found to be associated with worse immune function, increased inflammation, and viremia in chronically untreated HIV infection, supporting its role as a biomarker of intestinal barrier dysfunction.

*Case Western Reserve University, Cleveland, OH; and

University Hospitals Cleveland Medical Center, Cleveland, OH.

Correspondence to: Grace A. McComsey, MD, Case Western Reserve School of Medicine, 11100 Euclid Avenue, Cleveland, OH 44106 (e-mail: grace.mccomsey@uhhospitals.org).

Supported by NIH Grant DK118757. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institute of Health.

G.A.M. has served as consultant for Gilead, Merck, and ViiV/GSK and received grant support to her institution from BMS, Roche, Merck, Astellas, and Gilead. The remaining authors have no conflicts of interest to disclose.

V. E. helped with study concept and design, performed the statistical analysis, and drafted the manuscript. Adbus Sattar helped with statistical analysis and G. A. M. conceived the study concept and design, obtained funding, oversaw all study procedures, and contributed to the manuscript.

Received June 05, 2018

Accepted October 22, 2018

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