Program Schedule

1602
Impact of IGF-1 and Sex Steroids on Bone Health in HIV- and HCV-Infected US Male Veterans

Session: Poster Abstract Session: HIV: Comorbidities and Coinfections
Saturday, October 11, 2014
Room: The Pennsylvania Convention Center: IDExpo Hall BC
Posters
  • ID Week 2014 Bone Health Final.pdf (419.3 kB)
  • Background:

    The mechanisms of decreased bone mineral density (BMD) in HIV or HCV infections remain poorly understood. While HIV increases bone turnover markers (BTM), HCV does not.  Insulin-like growth factor-1 (IGF-1), testosterone (T) and estradiol (E2) also play key roles in osteogenesis.  In this analysis, we explored if their levels are associated with BMD in HIV or HCV.
    Methods:

    This cross-sectional study recruited 298 US male veterans with HIV, HCV, HIV/HCV and non-infected controls. All HIV patients were virally suppressed on HAART. Subjects underwent BMD testing and analysis of serum biomarkers (Figure 1).  The association of HIV or HCV with BMD and BTMs was evaluated in multivariable models adjusting for IGF-1, T and E2 in addition to age, race, BMI, smoking status.  Correlations between IGF-1, T or E2 with BMD and BTMs were also calculated. 
    Results:

    HCV was associated with decreased levels of IGF-1 (p<0.01), but HIV was associated with increased levels (p=0.03). In all groups, IGF-1 levels were negatively correlated with severity of liver disease (r=-0.214; p<0.01).  However, in multivariate modeling including IGF-1, bioavailable T (or E2), neither hormone was associated with BMD, nor did they attenuate the effect of HIV or HCV on lower femoral neck BMD (model 2-4, in table 1). IGF-1 was associated with higher bone specific alkaline phosphatase (BSAP; p=0.04) and a trend toward higher osteocalcin (OC; p=0.09), but not with C-telopeptide (CTX; p=0.13). T and E2 were associated with lower BSAP (p<0.01 and p=0.02), but not with OC or CTX.
    Conclusion:

    IGF-1 was lower in patients with HCV or greater severity of liver disease, likely representing decreased hepatic production.  However, levels of IGF-1, T or E2 do not appear to explain bone loss in in HIV or HCV. 

     

     

    Table 1: Multivariate models examining the impact of HIV and HCV on femoral neck BMD

    Model 1
    (HIV, HCV, BMI, Race, Age, Smoking)

    Model 2

    (Model 1 + IGF-1)

    Model 3

    (Model 1 + Bioavailable T)

    Model 4

    (Model 1 + Bioavailable E2)

    HIV

    -0.041 (p=0.02)

    -0.044 (p=0.01)

    -0.041 (p=0.02)

    -0.042 (p=0.02)

    HCV

    -0.041 (p=0.01)

    -0.044 (p=0.01)

    -0.042 (p=0.01)

    -0.039 (p=0.01)

    IGF-1

    -0.000 (p=0.80)

    Bioavailable T

    -0.000 (p=0.45)

    Bioavailable E2

    -0.000 (p=0.27)

    James Cutrell, MD1,2, Naim Maalouf, MD3, Song Zhang, PhD4, Martha Carvour, MD, PhD5, Henning Drechsler, MD1,2, Pablo Tebas, MD6 and Roger Bedimo, MD1,2, (1)Infectious Diseases, VA North Texas Health Care System, Dallas, TX, (2)Infectious Diseases, University of Texas Southwestern Medical School, Dallas, TX, (3)Mineral Metabolism, University of Texas Southwestern Medical School, Dallas, TX, (4)Clinical Science, University of Texas Southwestern Medical School, Dallas, TX, (5)Medicine, University of Texas Southwestern Medical School, Dallas, TX, (6)Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA

    Disclosures:

    J. Cutrell, None

    N. Maalouf, None

    S. Zhang, None

    M. Carvour, None

    H. Drechsler, None

    P. Tebas, None

    R. Bedimo, Merck & Co.: Grant Investigator and Scientific Advisor, Consulting fee, Grant recipient and Research grant
    Bristol Myers Squibb: Grant Investigator and Scientific Advisor, Consulting fee, Grant recipient and Research grant
    ViiV Healthcare: Scientific Advisor, Consulting fee

    Findings in the abstracts are embargoed until 12:01 a.m. EDT, Oct. 8th with the exception of research findings presented at the IDWeek press conferences.

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