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Lipid-lowering Therapy Responses in HIV+ and HIV- Dyslipidemic Patients Enrolled in a Large Integrated Healthcare Delivery System
Michael Silverberg*, W Leyden, M Horberg, L Hurley, A Go, C Quesenberry, and D Klein
Kaiser Permanente, Oakland, CA, US
Background: Differences in responses to lipid lowering therapy (LLT) by HIV status and HAART class
are largely unknown.
Methods: In Kaiser
Permanente Northern California, we
identified HIV+ and HIV- patients treated with LLT from
1996 to 2005 in 3 cohorts defined by dyslipidemia type: total cholesterol (TC) ≥240 mg/dL; LDL
≥160 mg/dL or ≥130 if ≥2 coronary
heart disease (CHD) risk factors or ≥100 if CHD; and triglycerides (TG)
≥500 mg/dL. HIV+ patients aged ≥18 years and age-, sex-,
and year-matched HIV- patients were included. Exclusions
were prior dyslipidemia dialysis and prior LLT. Cohorts were not mutually
exclusive. In each cohort, we estimated adjusted
percentage of changes in lipids by HIV status 1 year after LLT start using
linear regression controlling for sex, age, baseline lipid levels, year, prior
CHD/diabetes/hepatitis dialysis, CHD risk factors, and LLT class and duration. Among
HIV+ patients, we estimated adjusted percentage changes in lipids by
HAART class with additional adjustments for baseline CD4, HIV RNA, and AIDS. Adjusted
odds ratios (OR) for achieving Adult Treatment Panel III (ATP III) lipid goals were
estimated using logistic regression controlling for the same factors.
Results: Cohorts included 6862 patients (907 HIV+)
with high TC, 6496 patients (695 HIV+) with high LDL, and 5182 patients
(511 HIV+) with high TG. The most common LLT were statins: 87%, 89%,
and 52% in the 3 cohorts, respectively. Of note, dosing of individual LLT was
similar by HIV status, but drugs used differed (eg,
HIV+ patients had more pravastatin use, p <0.001 for all 3 cohorts). HIV+ patients had
significantly smaller declines in TC, LDL, and TG compared to HIV- patients (see the table), although differences in percentage change
between HIV+ and HIV- patients were larger for TC
(4.4%) and TG (17.4%) than for LDL (1.8%).
HIV+ patients on PI+NNRTI had the smallest declines in TC and
TG compared to other HIV+ patients, but no differences by HAART
class were found for LDL (see the table). Compared to HIV- patients, HIV+ patients had lower odds of attaining ATP-III
lipid goals for TC (OR 0.57, p
<0.001), LDL (OR 0.81, p = 0.017),
and TG (OR 0.39, p <0.001).
Conclusions: Declines in LDL in response to LLT are similar in HIV+
and HIV- patients, but declines
in TC and TG levels are less prominent in HIV+ patients. Differences
in choice of LLT among HIV+ due to concerns of drug–drug
interactions and toxicity may in part explain results for TC. PI+NNRTI regimens also associated with
inferior TC and TG responses.
Adjusted Percentage Changes in Lipids 1 Year after LLT Initiation

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