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Association between Protease Inhibitor Use and Increased Cardiovascular Risk in Patients Infected with Human Immunodeficiency Virus: A Systematic Review

  1. David C. Rhew1,2,3,
  2. Myriam Bernal2,
  3. Daniel Aguilar2,
  4. Uchenna Iloeje4, and
  5. Matthew Bidwell Goetz1,3
  1. 1Veterans Affairs Greater Los Angeles Healthcare System, Division of Infectious Diseases, Los Angeles
  2. 2Zynx Health, Cedars-Sinai Departments of Medicine and Health Services Research, Beverly Hills
  3. 3David Geffen UCLA School of Medicine, Los Angeles, California
  4. 4Bristol-Myers Squibb, Outcomes Research, Wallingford, Connecticut
  1. Reprints or correspondence: Dr. David C. Rhew, Zynx Health, 9100 Wilshire Blvd., Ste. 655E, Beverly Hills, CA 90212 (DRHEW{at}cerner.com).
 
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Abstract

Some studies have shown that currently available protease inhibitors (PIs) are associated with an increased risk of cardiovascular disease. We have systematically reviewed the published literature and conference abstracts for studies evaluating cardiovascular risk factors and events in patients receiving highly active antiretroviral therapy, with and without PIs. The majority of studies showed that the use of PIs was associated with increased levels of total cholesterol (36 [75%] of 48 studies), triglycerides (35 [73%] of 48 studies), and low-density lipoprotein (12 [100%] of 12 studies). PI use was often associated with morphological signs of cardiovascular disease, such as increased carotid intima thickness or atherosclerotic lesions (7 [88%] of 8 studies). Finally, 2 (67%) of 3 long-term observational studies that met our inclusion criteria demonstrated an association between use of PIs and subsequent myocardial infarction. The benefits of the currently available PIs should be balanced against the long-term risk of cardiovascular disease.

HAART regimens that include protease inhibitors (PIs) have greatly improved clinical outcomes for patients with HIV infection [1–3]. However, there is a growing concern about the associated side effects of HAART. In particular, the use of PIs is associated with dyslipidemia [4], hyperglycemia [5], increased insulin resistance [6], and increased risk for cardiovascular disease (CVD) [7], although not all studies have reported such links [8–12]. Furthermore, elevated lipid levels have also been associated with HIV infection itself [9, 13, 14], as well as with the use of nonnucleoside reverse-transcriptase inhibitors (NNRTIs) [15, 16] and nucleoside reverse-transcriptase inhibitors (NRTIs) [17–21], although at least 1 study has shown that there is no association between the use of either NNRTIs or NRTIs and elevated lipid levels [22]. Finally, substantial variations in study design complicate the analysis of the associations among PIs, dyslipidemia, and the risk of CVD.

To understand the strength of the evidence linking PI therapy to increased lipid levels and/or the risk of CVD in HIV-infected persons, we performed a systematic review of studies that have examined these associations, drawing from both the published literature and abstracts from conference proceedings. We organized the data on the basis of study design and derived conclusions from properly controlled studies, with a particular focus on randomized, controlled trials (RCTs).

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Materials And Methods

We included published articles and conference abstracts in our systematic review. The Medical Subject Headings and other text items used in the search were developed in collaboration with an experienced medical librarian. We also searched all conference abstracts from scientific meetings. Our full search strategy and the list of the reviewed scientific meetings are provided in the Appendix.

To be included, studies had to have a study population of ⩾25 HIV-infected subjects and a follow-up period for patients receiving PI therapy, or a duration of PI therapy, of ⩾48 weeks. However, the latter criterion was omitted for observational studies because the majority of these did not report the per-patient duration of PI exposure. The studies were classified into 4 categories: (1) RCTs, (2) large observational studies (⩾2000 patients), (3) 2-group non-RCTs (i.e., nonrandomized studies that compared outcomes in patients receiving versus those not receiving PIs), and (4) 1-group non-RCTs (i.e., nonrandomized, crossover studies). Each included study had ⩾2 patient groups: one receiving antiretroviral therapy (ART) that included ⩾1 PI, and the other receiving ART without the use of PIs. For 1-group studies of treatment-naive patients who initiated PI therapy, the control arm could consist of treatment-naive subjects. To be included, all studies had to include a formal statistical analysis of the differences in the relevant outcomes between the groups who received or did not receive PIs. Statistical significance was defined when the P value was reported <.05, or when a nonoverlapping 95% CI was reported.

Abstracts were excluded if the studies they described did not include HIV-infected individuals, did not address cardiovascular risk factors or cardiovascular-related events, or failed to specifically provide results for subjects who received PIs. Studies that covered HIV treatment during pregnancy or maternal-fetal HIV transmission and studies of HIV-infected children or adolescents were also excluded.

For publications that potentially represented the same study, the “better” publication was selected on the basis of the following hierarchy: (1) a more recently published peer-reviewed article, (2) the report with the longest follow-up time, and (3) the report with the largest sample size.

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Results

The initial search yielded 76,977 abstracts, 5954 (7.7%) of which came from peer-reviewed articles and 71,023 (92.3%) of which came from conference proceedings. After applying the predetermined selection criteria, 71 studies were accepted: 14 RCTs, 6 large observational studies (i.e., those with ⩾2000 subjects), 37 two-group studies, and 19 one-group studies (figure 1). It should be noted that 3 two-group studies [23–25] and 2 one-group studies [26, 27] were counted as large studies and assessed separately for the occurrence of clinical end points.

Figure 1
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Figure 1

Selection of included articles. An initial search yielded 76,977 potential studies, of which 71 studies were chosen for inclusion. *Three 2-group studies were also counted as large studies (i.e., studies with ⩾2000 subjects) [23–25], and 2 one-group studies were also counted as large studies [26, 27]. RCTs, randomized, controlled trials; X-over, cross-over; X-sectional, cross-sectional.

RCTs. The 14 RCTs and their baseline characteristics are listed in table 1. Eight were reported in abstracts [10, 11, 16, 28–32], and 6 were reported in published articles [33–38]. Six of the studies were conducted with PI-naive patients [10, 11, 16, 29, 30, 34], and 8 involved PI-experienced patients [28, 31–33, 35–38].

Table 1
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Table 1

Characteristics of randomized, controlled trial studies reporting metabolic changes and cardiovascular events.

Thirteen of the RCTs reported changes in total cholesterol level [10, 11, 16, 28–31, 33–38], of which 9 (69%) [11, 28, 29, 31, 33–36, 38] reported significant worsening in the PI group or improvement when the PI treatment was suspended (table 2, figure 2). Four studies evaluated changes in low-density lipoprotein (LDL) or high-density lipoprotein (HDL) cholesterol levels (table 3). Kumar et al. [29] found that antiretroviral treatment—naive patients who were provided nelfinavir in combination with either zidovudine-lamivudine or stavudine-lamivudine had an increase in the mean LDL cholesterol level, whereas patients receiving zidovudine-lamivudine in combination with abacavir (3 NRTIs) had a decease in the mean LDL cholesterol level. Negredo et al. [35] found a significant decrease in LDL cholesterol levels in patients who discontinued treatment with PI in favor of nevirapine, but not in those who substituted the PI with efavirenz. van der Valk et al. [32] reported that, among patients receiving stavudine and didanosine plus either nevirapine, lamivudine, or indinavir, subjects in the nevirapine and lamivudine arms had an increase in HDL cholesterol levels at 96 weeks (46% and 14%, respectively), whereas those in the indinavir arm had no increase in the HDL cholesterol level. Finally, Opravil et al. [38] found no significant change in HDL cholesterol levels between PI-experienced patients who did and those who did not switch to a non-PI regimen.

Table 2
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Table 2

Randomized, controlled trials reporting changes in the cholesterol level in groups receiving protease inhibitors (PIs) and in groups that did not receive PIs.

Figure 2
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Figure 2

Cholesterol levels in randomized, controlled trials. P values are provided for the protease inhibitor (PI) group versus no-PI group. Data from Garcia et al. [34] are not included because of insufficient data (values for non-PI group not reported). NS, not significant.

Table 3
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Table 3

Data from studies showing worsening on lipid, metabolic, and cardiovascular measures with protease inhibitor use.

Of the 12 RCTs that examined triglyceride (TG) levels [11, 16, 28–31, 33–38], 7 (58%) [28, 29, 33–36, 38] reported a significant worsening of TG levels for PI-naive patients who initiated PI therapy, or a significant improvement in the TG level for patients who suspended PI treatment (table 4). In the study by Ruiz et al. [37], substitution of a PI with nevirapine resulted in a significant decrease in the TG level, in contrast to patients continuing to receive a PI. Negredo et al. [35] found improvements in both total cholesterol and TG levels when the PI was replaced with nevirapine, but not when it was replaced with efavirenz. The patients receiving efavirenz experienced a greater increase in TG levels than did those receiving a PI. In another study [29], patients receiving a PI had a greater increase (for naive patients) and a greater decrease (for experienced patients who discontinued the PI) in TG levels, compared with those not receiving a PI.

Table 4
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Table 4

Randomized, controlled trials reporting triglyceride changes in groups receiving protease inhibitor (PI) therapy versus non-PI groups.

Three RCTs [11, 34, 35] reported no significant difference in glucose metabolism in groups treated with or without a PI. Only 1 [11] of these RCTs provided statistical analysis for the change from baseline glucose levels and was eligible for inclusion in table 3. Two RCTs [31, 38] found increased insulin sensitivity when PI therapy was discontinued. No RCT examined the rates of cardiovascular events, hypertension, atherosclerosis, or cerebrovascular events.

Large observational studies with ⩾2000 patients. Six observational studies met the inclusion criteria. Three of these studies [23–25] were also included in the “2-group non-RCT” category; 2 were included in the “1-group” category [26, 27]; and the sixth large study [39] did not include length of follow-up and was not included in any other previous category.

Holmberg et al. [40] examined the incidence of myocardial infarction, angina, and cerebrovascular accidents in 5676 HIV-positive patients in the United States during 1993–2001. Compared with persons not receiving PIs, patients receiving PIs had an increased risk for developing an myocardial infarction (adjusted OR, 4.92; 95% CI, 1.3–32.3; P = .04), but not for angina and cerebrovascular accidents. A study of 19,795 HIV-infected French men receiving a PI [23] found that relative to patients exposed to PIs for <18 months, the standardized morbidity ratios were 2.0 (95% CI, 1.2–3.2) and 3.7 (95% CI, 2.0–6.3) for patients exposed to PIs for 18–30 months and >30 months, respectively. Compared with the general population, the standardized morbidity ratios were 1.7 (95% CI, 1.0–2.7) and 3.1 (95% CI, 1.7–5.4) for patients exposed to PIs for 18–30 months and >30 months, respectively. Another study of 4157 HIV-infected patients in United States between 1996 and 2001 [26] found that rates of myocardial infarction and coronary heart disease were not elevated among persons receiving PIs (table 5).

Table 5
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Table 5

Data from large studies (i.e., those with ⩾2000 patients) reporting cardiovascular risk for protease inhibitors (PIs).

In a study of 17,852 subjects [39], when compared with ART-naive patients, patients exposed to PIs demonstrated an OR of 2.10 (95% CI, 1.65–2.67) for elevated total cholesterol level; 1.49 (95% CI, 1.15–1.92), for lowered HDL cholesterol level; and 2.20 (95% CI, 1.80–2.68), for elevated TG level. After a median of 14 months' follow-up, of 3734 treatment-naive HIV-infected patients initiating PI therapy [27], the mean increases in total cholesterol and TG levels were 1.9 mg/dL per month (95% CI, 1.5–2.3 per month) and 1.7 mg/dL per month (95% CI, 0.7–2.5 per month), respectively. Finally, in a cohort of 2625 HIV-positive women, Justman et al. [25], found that PI use was associated with increased incidence of diabetes mellitus (P = .081), compared with NRTIs alone.

Two-group non-RCT studies. Thirty-seven nonrandomized studies with ⩾2 comparison groups met the inclusion criteria. Twenty were published in peer-reviewed journals [5, 6, 9, 41–57], and 17 were reported in conference abstracts [8, 23–25, 58–70]. Thirty-one studies [5, 6, 8, 9, 23–25, 41–45, 49–66, 68] were observational or cross-sectional studies, and 6 [46–48, 67, 69, 70] were prospective non-RCTs.

Twenty-six of these studies reported changes in the levels of ⩾1 type of lipid [5, 6, 41–45, 47, 48, 50–57, 60, 61, 64–70]. Nineteen (73%) of 26 studies reported a worsening with PI use [5, 6, 41, 43–45, 48, 51, 53–57, 60, 64–68], 3 (12%) of 26 reported no significant worsening with PIs [61, 69, 70], and 4 (15%) of 26 reported mixed results [42, 47, 50, 52].

The effect of PI use on glucose levels was examined in 11 of the 2-group non-RCT studies [5, 25, 44, 50, 51, 54, 56, 57, 60, 68, 70], of which 7 (64%) found a worsening in the PI group [5, 25, 44, 51, 54, 57, 68], and 4 (36%) saw no significant changes [50, 56, 60, 70]. Four studies reported on insulin resistance [50, 54, 64, 67], with 3 (75%) of these 4 studies reporting a worsening in the PI group [54, 64, 67].

Single-group (crossover) non-RCT studies. Nineteen studies had a crossover design and met the inclusion criteria as single-group non-RCT studies. Four studies were reported in published articles [26, 71–73], and 15 were reported in conference abstracts [27, 74–87]. In 7 of the studies [72, 78, 79, 81–83, 85], the patients were PI-experienced patients who were assessed before and after discontinuing PI therapy. Of the remaining 12 studies [26, 27, 71, 73–77, 80, 84, 86, 87], 2 [27, 71] reported results in PI-naive patients initiating a PI-based HAART regimen, and 2 other studies [76, 84] reported results in a mix of patients, some of whom were PI experienced (and continued receiving their PI regimen) and others who were PI naive (and initiated therapy with a PI). All other studies [26, 73–75, 77, 80, 86, 87] did not specify whether patients were PI naive or PI experienced at baseline.

The majority of single-group crossover studies reported worsening of lipid levels with PIs (table 3). Twelve studies examined total cholesterol levels [27, 72–75, 78, 79, 81, 83–85, 87], of which 9 (75%) reported worsening with PI use [27, 72–75, 83–85, 87]. Eleven examined TG levels [27, 71–73, 75, 78, 79, 81, 83, 85, 87], of which 9 (82%) reported worsening with PI use [27, 71–73, 75, 81, 83, 85, 87]. One of these studies [81] reported worsening of TG levels but not total cholesterol levels. One additional study [76] (which reported TG data but is not included in the 9) reported simply on a change in lipid levels, which were not worse in the PI group. In one of the 2 “mixed” studies [76, 84], investigators observed that lipid levels worsened for those initiating PIs and improved for those discontinuing PIs.

Seven (37%) of the 19 studies reported data on glucose level changes [73–76, 79, 85, 86], of which 4 (57%) showed a worsening within the PI group [74, 75, 85, 86]. Four studies [73, 79, 82, 85] examined changes in insulin resistance, but none reported worsening in the PI group. In addition, 1 study [77] examined changes in hypertension and found worsening in the PI group; 1 study [80] examined carotid intima media thickness and found worsening in the PI group; and 1 study [26] examined rates of coronary heart disease and myocardial infarction and did not find worsening in the PI group.

Summary of studies. A summary of all the studies included in our analysis demonstrated that 36 (75%) of 48 showed worsening in the total cholesterol level, 35 (73%) of 48 showed worsening in the TG level, 4 (40%) of 10 showed worsening in the HDL cholesterol level, and 12 (100%) of 12 showed worsening in the LDL cholesterol level. Nineteen studies assessed hyperglycemia or diabetes mellitus, with 11 (58%) studies reporting worsening in the PI group. Eight studies measured carotid intima thickness or atherosclerotic lesions, and 7 (88%) of 8 studies reported worsening in the PI group. Two (67%) of 3 studies addressing endothelial dysfunction showed worsening in the PI group. Three studies evaluated the effect of PIs on the incidence of myocardial infarction, and 2 (67%) of the 3 studies reported worsening in the PI group. Three studies reported total number of cardiovascular events and coronary artery disease (without specifying exactly which cardiovascular events occurred), and none found worsening in patients receiving PIs.

Effect of specific PIs. Fourteen studies [5, 6, 27, 43, 47, 48, 50, 52–54, 56, 57, 59, 65] compared the effects of specific PIs on lipid levels, insulin resistance, or blood pressure changes (table 6). Ritonavir was consistently associated with elevated lipid levels [5, 43, 48, 50, 54, 56]. In some studies [27, 48, 53, 54, 65], saquinavir was associated with elevated cholesterol and/or elevated TG levels, but to a lesser degree than were other PIs (especially ritonavir). Saquinavir in combination with ritonavir was associated with significantly elevated TG levels [6] and higher lipid levels [52]. One study [59] found that patients receiving indinavir experienced a statistically significant increase in blood pressure, compared with those receiving nelfinavir.

Table 6
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Table 6

Data from studies reporting cardiovascular risk for specific protease inhibitors.

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Discussion

Of the 14 RCTs that studied the effects of initiating or stopping PIs in ⩾25 subjects for a period of ⩾48 weeks, PIs were associated with increased total cholesterol levels in 9 (69%) of 13 studies, increased TG levels in 7 (58%) of 12 studies, and increased LDL cholesterol levels in 2 of 2 studies. The RCTs consisted of 2 basic study designs: (1) initiation of a PI regimen in PI-naive patients [10, 11, 16, 29, 30, 34, 35], or (2) discontinuation of the PI in PI-experienced patients [28, 31–33, 36–38]. In the former design, lipid levels often increased in both the PI and non-PI groups, but usually more so in the PI group (figure 2). In treatment-experienced patients, lipid levels usually decreased regardless of whether patients were switched to a non—PI-containing regimen, although the decreases were greater in subjects who discontinued PI therapy.

The results of the RCT studies were corroborated by 37 two-group non-RCT studies with concurrent controls and 19 one-group non-RCT studies. These studies demonstrated that PIs were associated with increased total cholesterol levels in 27 (79%) of 34 studies, increased TG levels in 29 (83%) of 35 studies, and increased LDL cholesterol levels in 10 of 10 studies. The results were supplemented by analyses of large observational studies (i.e., those with ⩾2000 subjects). These studies showed that PI use was associated with increased total cholesterol or TG levels in 1 of 2 studies for each. Furthermore, the use of PIs was associated with increased incidence of myocardial infarction in 2 of the 3 studies [23, 24, 26]. One study [23] found this to be true only for those who had taken PIs for ⩾18 months. In terms of markers associated with increased risk for CVD, 11 of the 19 studies that evaluated markers of diabetes mellitus found an association between the use of PIs and hyperglycemia or frank diabetes mellitus. Both studies that examined the effect of PIs on blood pressure found such an association [59, 77]. It should be noted that all of the RCTs, large studies, and 2-group studies contained a control arm of ART without a PI (e.g., 2 NRTIs plus 1 NNRTI, or 3 NRTIs), as opposed to no ART.

We emphasize the results of RCTs because results from RCTs are most likely to represent true differences between comparison arms [88]. However, the statistical power of RCTs to detect differences in rare events is limited. To assess the relationship between PI use and important clinical outcomes, we evaluated large observational studies that examined the rates of myocardial infarction in patients who did or did not receive PIs.

Our review has several limitations. First, to provide a current assessment of the topic, we included abstracts from conference proceedings. Indeed, the majority of studies (92.3%) reviewed came from such abstracts. However, abstracts often do not present all of the relevant details and are not as rigorously peer-reviewed as journal articles. Second, data from abstracts were only derived from the abstract itself and not from the posters. It is possible that some additional data pertaining to the effect of PIs on cardiovascular outcomes may have been missed by this approach. Third, we had hoped to perform a meta-analysis of the RCT data because meta-analyses can provide unbiased estimates of the risks of adverse events [88, 89]. However, we were unable to do so because many of the studies did not provide sufficient statistical data on cardiovascular parameters. Moreover, our attempts to collect the required information by contacting investigators of RCTs did not yield sufficient data. Therefore, we were unable to quantify the extent of change associated with PIs for each outcome. Fourth, the accompanying use of specific NRTIs may potentially influence the development of dyslipidemia [19, 29]. Unfortunately, most of the studies did not identify the accompanying antiretroviral agents. Fifth, the results of our systematic review may have been influenced by publication bias, which could have resulted in over- or underestimation of the effects of PIs on various cardiovascular outcomes.

Finally, it should be noted that, by excluding studies that did not have a control arm that excluded PI use, our review did not capture all studies that have examined the association of PIs with cardiovascular risk. For instance, atazanavir, a PI that was recently approved by the US Food and Drug Administration, has been shown to have a favorable effect on the lipid profile and no insulin resistance [90–92], but the primary studies evaluating the effect of this agent on lipid values compared a PI (atazanavir) with another PI (nelfinavir). Furthermore, we excluded 2 large studies [12, 93] from our analysis because they did not compare the effect of ART with PI versus ART without PI on the rates of CVD and myocardial infarction. One of these studies [93] showed that, although overall rates of coronary heart disease did not increase in 28,513 Medicare patients with HIV infection during 1995–2000, use of ART was associated with increased risk in younger individuals (i.e., those aged 18–30 years). The other study [12] demonstrated in a large cohort of HIV-infected patients (n = 36,766) in the Veteran Affairs Health system that rates of myocardial infarction hospitalizations had not increased since 1997, despite the substantial use of PIs.

In summary, although the preponderance of the evidence suggests that currently available PIs do elevate cardiovascular risk, the PI class remains a very effective class of drugs for treating HIV infection, and, as such, PIs will continue to be an important treatment option. However, physicians should evaluate their HIV-infected patients for cardiovascular risk factors before prescribing a PI-containing regimen and should closely monitor patients receiving PIs, especially those with additional risk factors for CVD. Treatment options include the use of pharmacological and nonpharmacological methods for managing dyslipidemia and hyperglycemia, as well as considering lipid-neutral HAART regimens for their patients, especially with the availability of drugs in this class with less adverse lipid profiles.

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Acknowledgments

We thank Dr. Moon Kim for her assistance in the collection of data and Dr. Naomi Ruff for her assistance in the preparation of the manuscript.

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Footnotes

  • Financial support: Bristol Myers-Squibb, Outcomes Research.

  • Received February 18, 2003.
  • Accepted June 4, 2003.
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Appendix

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Literature Search Method

• Search 1: Medical Subject Headings and Subject Heading

• Anti HIV Agents OR HIV Protease Inhibitors OR lopinavir OR ritonavir OR nelfinavir OR amprenavir OR indinavir OR saquinavir OR tipranavir OR atazanavir OR PNU-140690 OR BMS-232632; AND

• Subject heading: Adverse effects; OR

• Adverse effect OR adverse effects OR secondary effect$ OR side effect$ OR side-effect$; OR

• Cardiovascular system OR cardiovascular diseases OR cardiovascular OR fat OR lipids OR glucose OR cholesterol OR triglycerides OR triglyceride OR lipodystrophy OR lipodystroph* OR dyslipidemia OR dyslipidemi* OR hyperlipidemia OR hyperlipidemi* OR hypercholesterolemia OR hypercholesterolemi* OR hypertriglyceridemia OR hypertriglyceridemi* OR blood pressure OR hypertension OR hypertensiv* OR hyperlactatemia OR hyperlactatemi* OR lipoatrophy OR lipoatrophi* OR hyperglycemia OR hyperglycemi*

Search 2: All Fields

Anti-HIV OR anti HIV OR anti AIDS anti-AIDS OR retroviral OR antiretroviral OR reverse transcriptase inhibitor$; AND

Cardiovascular system OR cardiovascular diseases OR cardiovascular OR fat OR lipids OR glucose OR cholesterol OR triglycerides OR triglyceride OR lipodystrophy OR lipodystroph* OR dyslipidemia OR dyslipidemi* OR hyperlipidemia OR hyperlipidemi* OR hypercholesterolemia OR hypercholesterolemi* OR hypertriglyceridemia OR hypertriglyceridemi* OR blood pressure OR hypertension OR hypertensiv* OR hyperlactatemia OR hyperlactatemi* OR lipoatrophy OR lipoatrophi* OR hyperglycemia OR hyperglycemi*

Search 3: All Fields

• Acquired immunodeficiency syndrome OR AIDS OR HIV; AND

• Drug$ OR therapy OR medication$ OR agent$ OR regimen OR pharmaceutical$; AND

• Cardiovascular system OR cardiovascular diseases OR cardiovascular OR fat OR lipids OR glucose OR cholesterol OR triglycerides OR triglyceride OR lipodystrophy OR lipodystroph* OR dyslipidemia OR dyslipidemi* OR hyperlipidemia OR hyperlipidemi* OR hypercholesterolemia OR hypercholesterolemi* OR hypertriglyceridemia OR hypertriglyceridemi* OR blood pressure OR hypertension OR hypertensiv* OR hyperlactatemia OR hyperlactatemi* OR lipoatrophy OR lipoatrophi* OR hyperglycemia OR hyperglycemi*

Search 4: All Fields

• Acquired immunodeficiency syndrome OR aids OR HIV; AND

• Antiviral$ OR protease inhibitor$; AND

• Cardiovascular system OR cardiovascular diseases OR cardiovascular OR fat OR lipids OR glucose OR cholesterol OR triglycerides OR triglyceride OR lipodystrophy OR lipodystroph* OR dyslipidemia OR dyslipidemi* OR hyperlipidemia OR hyperlipidemi* OR hypercholesterolemia OR hypercholesterolemi* OR hypertriglyceridemia OR hypertriglyceridemi* OR blood pressure OR hypertension OR hypertensiv* OR hyperlactatemia OR hyperlactatemi* OR lipoatrophy OR lipoatrophi* OR hyperglycemia OR hyperglycemi*

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Combine Searches 1–4 and Limit to the Following

Language: English

Date: 1996 through September 2002

Medical subject headings: NOT Animal

Publication type: NOT Review, letter, editorial

We also searched all conference abstracts from the following scientific meetings: Conference on Retrovirus and Opportunistic Infections (1996–2002), Interscience Conference on Antimicrobial Agents and Chemotherapy (1996–2002), Infectious Diseases Society of America Annual Meeting (1996–2002), International Workshop on Adverse Drug Reactions and Lipodystrophy (1999–2002), International Workshop on Drug Resistance and Treatment Strategies (2000–2001), International Workshop on Salvage Therapy for HIV Infection (2000), International AIDS Society Conference (1996–2002), American Heart Association Scientific Sessions (1998–2001), American College of Cardiology Annual Scientific Session (1998–2002), and Congress of the European Atherosclerosis Society (1998–2002).

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  1. Clin Infect Dis. (2003) 37 (7): 959-972. doi: 10.1086/378064
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