Cocaine may hasten disease progression. The first study below isn't
comparing to HIV-negative but there is no reason to believe that it
causes CD4 counts to decline. Just that they may faster with chronic
use associated with HIV disease.

Obviously, not everyone with HIV is using cocaine. And not everyone
with a drug habit has HIV.

        George M. Carter

**
Larrat EP, Zierler S, Mayer K.  Cocaine use and HIV disease
progression among heterosexuals. Pharmacoepidemiol Drug Saf. 1996
Jul;5(4):229-36.

Department of Community Health, Brown University, School of Medicine,
USA.

   Evidence derived fromin vitro experiments would suggest that
cocaine exposure may hasten the progression of HIV disease among
infected individuals. Epidemiologic support for this association is
equivocal at best. We examined the relationship between cocaine use
and decline in CD4 cell counts over a 6-month period in a cohort of 81
heterosexually active men and women who were infected with HIV.
Overall, cocaine users were 1.4 times (90% CI=1.0-2.1) more likely to
experience a decline in CD4 count than were non-cocaine users. Cocaine
users with a baseline CD4 count of greater than 500 cells/mm(3) were
at 1.6 times (90% CI=1.2-2.3) greater risk for a CD4 decline than
non-cocaine users at this baseline CD4 level. Concurrent treatment
with an antiretroviral agent [AZT] modified the strength of this
association, as evidenced by a cumulative incidence ratio (CIR) of 0.4
(90% CI=0.1-1.3) among AZT users and a CIR=2.2 (90% CI=1.5-3.2) among
those not undergoing AZT treatment. The results of this study raise
concerns about the negative effects of cocaine on people living with
HIV infection, particularly those not receiving antiretroviral therapy
who entered our study with a relatively intact immune system.

**
J Acquir Immune Defic Syndr. 2003 Aug 1;33(4):500-5.     Related
Articles, Links
   Click here to read
   Drug use patterns over time among HIV-seropositive and
HIV-seronegative women: the HER study experience.

   Macalino GE, Ko H, Celentano DD, Hogan JW, Schoenbaum EE, Schuman
P, Rich JD; HER Study Group.

   Brown University Medical School, Providence, Rhode Island 02912,
USA. Grace_Macalino@Brown.edu

   BACKGROUND: Drug use, particularly among women, is a public health
issue given its health effects and its impact on HIV transmission.
Becoming HIV seropositive could lead to differing patterns of drug use
over time. HIV infection may decrease drug use due to an increased
access to health services. Alternatively, increased drug use may occur
due to depression associated with being HIV infected, leading to
despair, hopelessness, and a lack of motivation to become drug free.
METHODS: We evaluated the potential association between HIV serostatus
and drug use among a cohort of 1310 women who were part of a
multicenter collaborative study on the natural history of HIV
infection. Eight hundred seventy-one HIV-seropositive women and 439
HIV-seronegative women were enrolled at four sites (New York,
Providence, Baltimore, and Detroit). We defined drug use as any heroin
or cocaine use reported at the baseline visit (enrollment). RESULTS:
Drug use was found to decrease during earlier visits (months 1-24) and
remained stable at 20% thereafter (months 30-84). No significant
differences in change of drug use were noted by HIV serostatus, using
generalized estimating equation-based logistic regression analyses.
CONCLUSIONS: HIV-seropositive status did not affect drug use patterns
over time within our population of high-risk women.

**
Herning RI, Tate K, Better W, Cadet JL. Cerebral blood flow
pulsatility deficits in HIV+ poly substance abusers: differences
associated with antiviral medications. Drug Alcohol Depend. 2002 Jan
1;65(2):129-35.

Molecular Neuropsychiatry Section, Division of Intramural Research,
National Institute on Drug Abuse, National Institutes of Health, PO
Box 5180, Baltimore, MD 21224, USA. rherning@intra.nida.nih.gov

   This study examines the influence of HIV-seropositivity and
antiviral medications on cerebral blood flow in cocaine abusers.
Forty-five HIV negative (HIV-) cocaine abusers, 36 HIV positive (HIV+)
cocaine abusers (CD4; mean 378, +/-229) and 27 control HIV- subjects
were studied. Blood flow velocity and pulsatility were determined for
the anterior and middle cerebral arteries using transcranial Doppler
sonography (TCD). Psychological assessments, which included the
psychiatric symptom checklist (SCL-90R), hopelessness (Beck) and
well-being (Ellison) questionnaires revealed greater psychiatric
distress in HIV+ cocaine abusers than the other groups. HIV- cocaine
abusers and HIV+ cocaine abusers not receiving antiviral medications
(n=25 of 36) had elevated pulsatility values, indicating increased
resistance in the cerebral blood vessels in comparison to control
subjects. HIV+ cocaine abusers using antiviral medications (n=11 of
36) had pulsatility values similar to HIV- control subjects.
Interestingly, there was no significant relationship between intensity
of psychiatric distress reported by HIV+ cocaine abusers and perfusion
deficits. Our findings suggest that unmedicated HIV+ cocaine abusers
have cerebrovascular deficits, which are similar to HIV- cocaine
abusers. In addition, the use of antiviral medications appears to be
associated with a reduction of these deficits in HIV+ cocaine abusers.
Nevertheless, more studies will be needed before any conclusion can be
reached regarding possible beneficial effects of these agents on the
cerebral vasculature.

**
Wang GJ, Chang L, Volkow ND, Telang F, Logan J, Ernst T, Fowler JS.
Decreased brain dopaminergic transporters in HIV-associated dementia
patients. Brain. 2004 Nov;127(Pt 11):2452-8. Epub 2004 Aug 19.

 Medical and Chemistry Departments, Brookhaven National Laboratory,
Upton, NY, USA.

   HIV has a propensity to invade subcortical regions of the brain,
which may lead to a subcortical dementia termed HIV-cognitive motor
complex. Therefore, we aimed to assess whether dopamine (DA) D2
receptors and transporters (DAT) are affected in the basal ganglia of
subjects with HIV, and how these changes relate to dementia status.
Fifteen HIV subjects (age 44.5 +/- 11 years; CD4 185 +/- 130/mm3)) and
13 seronegative controls (42 +/- 12 years) were evaluated with PET to
assess availability of DAT ([11C]cocaine) and DA D2 receptor
([11C]raclopride). HIV patients with associated dementia (HAD), but
not those without dementia (ND) had significantly lower DAT
availability in putamen (-19.3%, P = 0.009) and ventral striatum
(-13.6%, P = 0.03) compared with seronegative controls. Higher plasma
viral load in the HIV dementia patients correlated with lower DAT in
the caudate (r = -0.7, P = 0.02) and putamen (r = -0.69, P = 0.03). DA
D2 receptor availability, however, showed mild and non-significant
decreases in HIV patients. These results provide the first evidence of
DA terminal injury in HIV dementia patients, and suggest that
decreased DAT may contribute to the pathogenesis of HIV dementia. The
greater DAT decrease in the putamen than in the caudate parallels that
observed in Parkinson's disease. The inverse relationship between
viral burden and DAT availability further supports HIV-mediated
neurotoxicity to dopaminergic terminals.