Fenofibrate in hyperlipidaemia secondary to HIV protease inhibitors

Luis, Daniel Antonio de; Bachiller, P; Aller, R.

doi:10.1016/s0899-9007(01)00582-2

Cited by 15 publications

(10 citation statements)

References 8 publications

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“…[83] A second investigation with fenofibrate noted a mean reduction in serum triglyceride levels from 11.2 to 3.0 mmol/L (-73%) in 9 protease inhibitor recipients. [84] Serum levels of total cholesterol were reduced from 6.5 to 5.9 mmol/L (-9%) in this cohort. Because mean baseline serum triglyceride levels ranged from 11.2 to 22.4 mmol/L in these patients, the risk of acute pancreatitis may have been lowered with fenofibrate.…”

Section: Therapeutic Intervention Datamentioning

confidence: 60%

“…[14,15,70,74,[79][80][81][82][83][84][85] Henry et al [81] used NCEP guidelines to treat 74 patients with elevated serum levels of total cholesterol and/or triglycerides. Patient management included dietary modification and exercise (n = 20), atorvastatin 10 mg/day to start (n = 10), gemfibrozil 600mg twice daily (n = 25), and atorvastatin plus gemfibrozil (n = 19).…”

Section: Therapeutic Intervention Datamentioning

confidence: 99%

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Management of Protease Inhibitor-Associated Hyperlipidemia

Penzak

Chuck

2002

American Journal of Cardiovascular Drugs

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Dyslipidemia, characterized by elevated serum levels of triglycerides and reduced levels of total cholesterol, low-density lipoprotein-cholesterol (LDL-C) and high-density lipoprotein-cholesterol, has been recognized in patients with human immunodeficiency virus (HIV) infection. It is thought that elevated levels of circulating cytokines, such as tumor necrosis factor-alpha and interferon-alpha, may alter lipid metabolism in patients with HIV infection. Protease inhibitors, such as saquinavir, indinavir and ritonavir, have been found to decrease mortality and improve quality of life in patients with HIV infection. However, these drugs have been associated with a syndrome of fat redistribution, insulin resistance, and hyperlipidemia. Elevations in serum total cholesterol and triglyceride levels, along with dyslipidemia that typically occurs in patients with HIV infection, may predispose patients to complications such as premature atherosclerosis and pancreatitis. It has been estimated that hypercholesterolemia and hypertriglyceridemia occur in greater than 50% of protease inhibitor recipients after 2 years of therapy, and that the risk of developing hyperlipidemia increases with the duration of treatment with protease inhibitors. In general, treatment of hyperlipidemia should follow National Cholesterol Education Program guidelines; efforts should be made to modify/control coronary heart disease risk factors (i.e. smoking; hypertension; diabetes mellitus) and maximize lifestyle modifications, primarily dietary intervention and exercise, in these patients. Where indicated, treatment usually consists of either pravastatin or atorvastatin for patients with elevated serum levels of LDL-C and/or total cholesterol. Atorvastatin is more potent in lowering serum total cholesterol and triglycerides compared with other hydroxymethylglutaryl coenzyme A (HMG-CoA) reductase inhibitors, but it is also associated with more drug interactions compared with pravastatin. Simvastatin and lovastatin are significantly metabolized by cytochrome P450 enzymes (CYP3A4) and are therefore not recommended for coadministration with protease inhibitors. A fibric acid derivative (gemfibrozil or fenofibrate) should be used in patients with primary hypertriglyceridemia. However, it must be kept in mind that protease inhibitors, such as nelfinavir and ritonavir, induce enzymes involved in the metabolism of the fibric acid derivatives and may, therefore, reduce the lipid-lowering activity of coadministered gemfibrozil or fenofibrate. In certain patients HMG-CoA reductase inhibitors may be used in combination with fibric acid derivatives but patients should be carefully monitored for liver and skeletal muscle toxicity. Select patients may experience improvements in serum lipid levels when their offending protease inhibitor(s) is/are exchanged for efavirenz, nevirapine, or abacavir; however each patient's virologic and immunologic status must be taken closely into consideration.

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Section: Therapeutic Intervention Datamentioning

confidence: 60%

Section: Therapeutic Intervention Datamentioning

confidence: 99%

Management of Protease Inhibitor-Associated Hyperlipidemia

Penzak

Chuck

2002

American Journal of Cardiovascular Drugs

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“…Several case reports by Thomas et al [96] and de Luis et al demonstrated initial TG-lowering activity of fenofibrate in HIV-infected patients [97]. Subsequently, Calza et al [85] and Caramelli et al [98] demonstrated further efficacy of fenofibrate in larger case series.…”

Section: Targeting Elevated Tgs In Hiv-infected Patientsmentioning

confidence: 99%

Management of dyslipidemia in HIV-infected patients

Malvestutto

Aberg

2011

Clinical Lipidology

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Antiretroviral therapy has dramatically increased survival for HIV-infected individuals. As this population lives longer, coronary heart disease has become an important comorbid condition. Dyslipidemia in HIV-infected individuals is a complex condition, with multiple contributing factors including the HIV virus itself, individual genetic characteristics and antiretroviral therapy-induced metabolic changes. Effective management of dyslipidemia in this population is essential to reduce cardiovascular risk but presents multiple challenges due to interactions between antiretroviral therapy agents and lipid-lowering medications.

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“…Studies evaluating the relationship between vitamin D status and CD4 counts have been conflicting. 2,4,[29][30][31][32][33][34] Thus, plasma concentrations of LL-37 may be a more direct link to CD4 counts than circulating concentrations of 25(OH)D.…”

Section: Discussionmentioning

confidence: 99%

LL-37 Concentrations and the Relationship to Vitamin D, Immune Status, and Inflammation in HIV-Infected Children and Young Adults

Tangpricha

Judd

Ziegler

et al. 2014

AIDS Research and Human Retroviruses

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Antimicrobial peptide LL-37 is produced in response to active vitamin D to exert immunomodulatory effects and inhibits HIV replication in vitro. To date, no studies have investigated LL-37 in HIV-infected patients. This study sought to investigate LL-37 and the relationship to 25-hydroxyvitamin D [25(OH)D] and HIV-related variables in this population. HIV-infected subjects and healthy controls ages 1-25 years old were prospectively enrolled in this cross-sectional study. Fasting plasma LL-37 and 25(OH)D concentrations were measured in duplicate with ELISA. HIV + subjects (36 antiretroviral therapy (ART)-experienced subjects; 27 ART-naïve subjects) and 31 healthy controls were enrolled. Overall, 93% were black and the median age was 20 years. There was no difference in median (interquartile range) LL-37 between the HIV-infected group and controls [58.3 (46.4,69.5) vs. 51.3 (40.8,98.2) ng/ml, respectively; p = 0.57]; however, the ART-experienced group had higher concentrations than the ART-naive group [66.2 (55.4,77.0) vs. 48.9 (38.9,57.9) ng/ml, respectively; p < 0.001]. LL-37 was positively correlated with 25(OH)D in controls, but not in HIV-infected groups, and was positively correlated with current CD4 and DCD4 (current-nadir) in the ART-experienced group. After adjustment for age, race, sex, and HIV duration, the association between LL-37 and CD4 remained significant. These findings suggest that HIV and/or HIV-related variables may alter the expected positive relationship between vitamin D and LL-37 and should be further investigated.

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Fenofibrate in hyperlipidaemia secondary to HIV protease inhibitors

Cited by 15 publications

References 8 publications

Management of Protease Inhibitor-Associated Hyperlipidemia

Management of Protease Inhibitor-Associated Hyperlipidemia

Management of dyslipidemia in HIV-infected patients

LL-37 Concentrations and the Relationship to Vitamin D, Immune Status, and Inflammation in HIV-Infected Children and Young Adults

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