Effects of Alcohol and Crack Cocaine Use on Virological and Immunological Disease Progression in a C - PowerPoint PPT Presentation

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Effects of Alcohol and Crack Cocaine Use on Virological and Immunological Disease Progression in a C

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Effects of Alcohol and Crack Cocaine Use on Virological and Immunological ... Department of Psychiatry. Presented at AIDS 2006 XVI International AIDS Conference ... – PowerPoint PPT presentation

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Title: Effects of Alcohol and Crack Cocaine Use on Virological and Immunological Disease Progression in a C


1
Effects of Alcohol and Crack Cocaine Use on
Virological and Immunological Disease Progression
in a Cohort of U.S. Women with HIV/AIDS
  • Judith A. Cook, Ph.D.
  • University of Illinois at Chicago
  • Department of Psychiatry
  • Presented at AIDS 2006 XVI International AIDS
    Conference
  • Toronto, Canada
  • August 15, 2006

2
Collaborators
  • Jane K. Burke-Miller
  • Dennis D. Grey
  • Mardge H. Cohen
  • Robert Cook
  • David Vlahav
  • Farzana Kapadia
  • Tracey Wilson
  • Rebecca Schwartz
  • Elizabeth Golub
  • Kathy Anastos
  • Claudia Ponath
  • Lakshmi Goparaju
  • Jean Richardson

Funded by U.S. National Institute of Allergy
Infectious Diseases National Institute on Drug
Abuse
3
Study Background
  • Heavy and at-risk alcohol use are associated with
    lesser likelihood of HAART use adherence (R.
    Cook et al., 2001 Samet et al., 2004)
  • Crack/cocaine use is associated with lesser
    likelihood of HAART use adherence (J. Cook et
    al, 2006)
  • Some evidence suggests that alcohol use
    crack/cocaine use are associated with faster HIV
    disease progression AIDS-related mortality
    (Samet et al., 2003 Farbris et al., 2000 J.
    Cook et al., 2002)
  • Given the foregoing, do alcohol crack/cocaine
    use, together or separately, have an effect on
    disease progression that is independent of their
    effects on HAART use adherence?

4
Direct or Indirect Effects of Alcohol Crack Use
on HIV Disease Progression?
At-Risk Alcohol Crack Use
?
?
?
Crack Use Alone
HIV Disease Progression
HAART Use Adherence
?
At-Risk Alcohol Use Alone
?
?
5
Study Purpose
  • To explore whether alcohol and crack/cocaine use,
    alone or in combination, are associated with
    HIV-positive womens virologic and immunologic
    disease progression

6
Hypotheses
  • Women using alcohol, crack/cocaine, or both have
    higher HIV RNA viral loads and negative CD4 cell
    count slopes over time.
  • These effects are not modified by the influence
    of highly active antiretroviral therapy (HAART)
    use and adherence.

7
Womens Interagency HIV Study (WIHS)
  • Cohort study of HIV-positive women recruited in 6
    cities Chicago, Los Angeles, San Francisco,
    Bronx, Brooklyn, Washington, DC
  • Data collection bi-annually beginning in 1994
    until present
  • In-person interviews, physical exam, blood work,
    gynecological exam
  • Data come from 1996 through 2002
  • Funded by U.S. National Institute of Allergy
    Infectious Diseases National Institute on Drug
    Abuse

8
Characteristics of WIHS Cohort Used in Analysis
(N1,691)
  • African American 56
  • Hispanic/Latina 24
  • Caucasian 18
  • Other 2
  • High School Ed 63
  • Average Age 37 years
  • On HAART 68
  • ARV Adherencegt95 66
  • IDU 7
  • Tobacco Use 56
  • Income lt12,000/yr 62
  • Probable depression 41
  • Viral Load gt100,000 19
  • CD4lt200 6

Current time
Study baseline
9
Independent Dependent Variables
  • Alcohol use measured by self-reported number of
    drinks per week (with 8 drinks per week defined
    as at-risk drinking per NIAAA guidelines)
  • Crack use measured as any self-reported use in
    the past 6 months
  • Plasma HIV-RNA copies categorized as gt100,000 vs.
    lt100,000
  • CD4 slope calculated from biannual CD4 counts

10
Control Variables
  • study site
  • time
  • age
  • race/ethnicity
  • income
  • education
  • tobacco use
  • injection drug use
  • depressive symptoms
  • CD4 as appropriate
  • HIV RNA as appropriate

11
Use of Alcohol and Crack/Cocaine at Baseline
12
HIV RNA Viral Load Over Time by Use of
Crack/Cocaine At-Risk Drinking
Mean HIV RNA Viral Load
Study Visit (1994-2004)
13
CD4 Over Time by Use of Crack/Cocaine At-Risk
Drinking
Mean CD4 Level
Study Visit (1994-2004)
14
Effects of At-Risk Alcohol Crack Use on HAART
Use Adherencea
  • Variable HAART USE
    ADHERENCE
  • At-risk alcohol crack -0.64 -0.65
  • At-risk alcohol alone -0.59 -0.60
  • Crack alone -0.45 -0.58
  • a Mixed effects logistic regression controlling
    for time, age, African American, Latina, income,
    education, tobacco use, IDU, depressive symptoms
  • plt.05, plt.01, plt.001

15
Effects of At-Risk Alcohol Crack Use on HIV RNA
Viral Load CD4 Slopea
  • Variable HIV RNA Viral Loadb
    CD4c Slope
  • At-risk alcohol crack 0.69 -0.09
  • At-risk alcohol alone 0.28 -0.01ns
  • Crack alone 0.10ns -0.04
  • a Mixed effects regression controlling for
    time, age, African American, Latina, income,
    education, tobacco use, IDU, depressive symptoms
  • b Controls for CD4lt200 c Controls for
    VLgt100,000
  • plt.05, plt.01, plt.001, plt.10

16
Effects of At-Risk Alcohol Crack on HIV Disease
Progression Controlling for HAART Use Adherencea
  • Variable Viral Loadb CD4 Slopec
  • At-risk alcohol crack 1.08 -0.13
  • At-risk alcohol alone 0.20ns -0.06
  • Crack alone 0.41ns -0.08
  • HAART -2.29 -0.01ns
  • Adherent -0.41 -0.03ns
  • a Mixed effects regression controlling for
    time, age, African American, Latina, income,
    education, tobacco use, IDU, depressive symptoms
  • b Controls for CD4lt200 c Controls for
    VLgt100,000
  • plt.05, plt.01, plt.001, plt.10

17
Conclusions
  • HIV women engaging in at-risk alcohol use
    crack/cocaine use are at considerable risk of
    rapid virological immunological disease
    progression
  • The effects of at-risk alcohol crack use are
    independent of HAART use adherence
  • Alcohol crack use may affect disease
    progression through health behaviors (nutrition,
    exercise), psychological factors (depression,
    anxiety), HAART use adherence, or through
    direct biological effects
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