Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0021051 (immunodeficiency)
 71,517 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Abnormalities of glucose regulation, including impaired glucose tolerance and insulin resistance, are often seen among human immunodeficiency virus (HIV)-infected patients receiving highly active antiretroviral therapy. Insulin resistance in this population may result from antiviral medication directly impairing glucose uptake in the muscle, effects of HIV per se, or indirect effects, such as fat redistribution. Insulin resistance may increase the risk of coronary heart disease among this population of patients, in part by inhibiting normal thrombolysis. The optimal treatment for insulin resistance and impaired glucose intolerance in HIV-infected patients is not known, but preliminary studies have suggested that metformin, an insulin sensitizing agent, improves insulin sensitivity, blood pressure, and waist circumference. Initial studies of thiazolidinediones also suggest the potential utility of such agents to improve insulin sensitivity, decrease hepatic steatosis, and increase subcutaneous fat. Further studies are needed to determine the optimal treatment strategy for insulin resistance in this population.
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PMID:Mechanisms and strategies for insulin resistance in acquired immune deficiency syndrome. 1294 79

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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PMID:Management of protease inhibitor-associated hyperlipidemia. 1472 85

This report reviews current data pertaining to the development of dyslipidemia during treatment with protease inhibitors and the associated risk for cardiovascular disease in patients who have the human immunodeficiency virus. Most protease inhibitors used to manage the human immunodeficiency virus and the acquired immunodeficiency syndrome are associated with prompt, marked, and sustained increases in serum lipid levels that are consistent with an increased 10-year risk for coronary heart disease as determined in the Framingham Heart Study. Management of lipid elevations in patients who use protease inhibitors is discussed. Novel protease inhibitors, which have minimal effects on lipid profiles, may have a role in the long-term management of the human immunodeficiency virus.
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PMID:Long-term cardiovascular risk with protease inhibitors and management of the dyslipidemia. 1546 73

Endothelial dysfunction is a critical initial step of atherogenesis that subsequently contributes to the progression and clinical manifestations of atherosclerosis. The use of human immunodeficiency virus type 1 (HIV-1) protease inhibitor (PI) agents has been associated with increased cardiovascular events and worsening of multiple coronary heart disease risk factors including dys-lipidemia, insulin resistance, and endothelial dysfunction. Endothelial dysfunction may be caused by HIV infection itself as well as treatment-related effects of the antiretroviral agents used to treat HIV. The available evidence suggests that PIs may induce endothelial dysfunction via their effects on both lipid and glucose metabolism. Studies in healthy subjects confirm a role for reduced endothelial nitric oxide production in the endothelial dysfunction associated with the PI indinavir. Further work is needed to determine the relative tendencies of other antiretroviral agents to induce endothelial dysfunction, the physiologic mechanisms involved, and the contribution of the metabolic and body shape changes associated with HIV treatment-related lipodystrophy, and to establish effective interventions for endothelial dysfunction in HIV-infected patients.
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PMID:Clinical aspects of endothelial dysfunction associated with human immunodeficiency virus infection and antiretroviral agents. 1547 Feb 73

There has been increasing interest in the research of flavonoids from dietary sources, due to growing evidence of the versatile health benefits of flavonoids through epidemiological studies. As occurrence of flavonoids is directly associated with human daily dietary intake of antioxidants, it is important to evaluate flavonoid sources in food. Fruits and vegetables are the main dietary sources of flavonoids for humans, along with tea and wine. However, there is still difficulty in accurately measuring the daily intake of flavonoids because of the complexity of existence of flavonoids from various food sources, the diversity of dietary culture, and the occurrence of a large amount of flavonoids itself in nature. Nevertheless, research on the health aspects of flavonoids for humans is expanding rapidly. Many flavonoids are shown to have antioxidative activity, free-radical scavenging capacity, coronary heart disease prevention, and anticancer activity, while some flavonoids exhibit potential for anti-human immunodeficiency virus functions. As such research progresses. further achievements will undoubtedly lead to a new era of flavonoids in either foods or pharmaceutical supplements. Accordingly, an appropriate model for a precise assessment of intake of flavonoids needs to be developed. Most recent research has focused on the health aspects of flavonoids from food sources for humans. This paper reviews the current advances in flavonoids in food, with emphasis on health aspects on the basis of the published literature, which may provide some guidance for researchers in further investigations and for industries in developing practical health agents.
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PMID:Flavonoids in food and their health benefits. 1567 17

Dyslipidemia and coronary heart disease (CHD) are of increasing concern in persons with human immunodeficiency virus (HIV) infection who are living longer because of the benefits of highly active antiretroviral therapy (HAART). All classes of drugs used in HAART have been associated with atherogenic changes in lipid profiles. The management of HIV-infected persons with dyslipidemia and/or CHD currently emphasizes the importance of monitoring and optimizing lipid levels through lifestyle changes, switching antiretrovirals (ARVs), and lipid-lowering treatments utilizing guidelines developed for persons without HIV infection. In HIV-infected persons, the use of lipid-lowering drugs may result in pharmacokinetic interactions with ARVs, complicating the management of patients. Recent advances in our understanding of the differential effects of specific ARVs on lipids is beginning to alter the clinical approach to management. In the absence of randomized clinical trials, clinicians should aggressively treat atherogenic dyslipidemia by primarily utilizing or switching to ARVs with the lowest potential to induce CHD or, when this is not possible or is ineffective, secondarily by the addition of lipid-lowering therapy. The current optimal management of HIV infection requires careful selection of ARVs with consideration given to the potential development of CHD and an understanding of how to manage dyslipidemia.
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PMID:Coronary heart disease risk, dyslipidemia, and management in HIV-infected persons. 1568 55

Thanks to antiretroviral therapy, people with human immunodeficiency virus (HIV) infection are living longer, but as they do, non-HIV medical problems become more relevant. In particular, dyslipidemia, an important reversible risk factor for cardiovascular disease, has been linked to HIV infection and its treatment. Although controversy remains as to whether people with HIV infections will develop premature coronary heart disease, it seems prudent to manage dyslipidemia in these patients just as we do in our HIV-negative patients. Interactions between lipid-lowering drugs and antiretroviral drugs require special attention.
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PMID:Dyslipidemia in HIV patients. 1639 25

We assessed myocardial perfusion (blinded interpretation of a single-photon emission computed tomography) and known risk factors for atherosclerosis in 105 randomly selected human immunodeficiency virus (HIV)-infected patients in a clinic in Mexico City and in a community sample of 105 age and gender-matched infection-free subjects. An abnormal scan was obtained in 4.8% of the infected and in 7.6% of the non-infected subjects. Severity of scintigraphic abnormalities was similar in both groups. In these Mexican HIV-infected patients, despite a long time of infection and of exposure to combined antiretroviral therapy and to other classical risk factors for atherosclerosis, there was no evidence of increased risk for abnormal myocardial perfusion. Dissimilar magnitude in the hazard of coronary heart disease may occur among infected populations with different frequencies of traditional predisposing factors for cardiovascular illness.
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PMID:Human immunodeficiency virus-infected subjects have no altered myocardial perfusion. 1725 26

The introduction of highly active antiretroviral therapy (HAART) has dramatically improved the long-term prognosis of human immunodeficiency virus (HIV)-infected patients, but several abnormalities of lipid and glucose metabolism have recently been reported with increasing frequency in patients receiving potent new antiretroviral combinations. Although a rare occurrence before the HAART era, insulin resistance has now been described as an important component of the lipodystrophy syndrome, including body fat redistribution, hypertriglyceridemia, hypercholesterolemia, hyperinsulinemia, and hyperglycemia. The etiology of such abnormalities remains unclear; but protease inhibitors and, to a lesser extent, nucleoside reverse transcriptase inhibitors are believed to contribute to the pathogenetic mechanism. The potential clinico-pathological consequences of glucose metabolism dysregulation, such as atherosclerosis and coronary heart disease, all make the management of insulin resistance and diabetes mellitus a challenge in the management of HIV-infected patients. Because of similarities to pathogenesis and clinical presentation of type 2 diabetes mellitus, treatment of HAART-associated hyperinsulinemia and hyperglycemia could follow the recommendations of the American Diabetes Association, but the most effective and safe management of these metabolic alterations is still unknown. The present review evaluated the most recently published data about incidence, risk factors, pathogenesis, clinical complications, and management of glucose disorders associated with antiretroviral therapy.
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PMID:Insulin Resistance and Diabetes Mellitus in HIV-Infected Patients Receiving Antiretroviral Therapy. 1837 Jun 93

Cardiovascular disease has been frequent in HIV-infected patients both before and after the advent of antiretroviral therapy (HAART). The pathogenic basis for the increase of cardiovascular disease, in particular myocardial lesions, may involve HIV-1 itself or other mechanisms including endothelial dysfunction, activation of proinflammatory cytokines, and changes in platelets, which lead to atherosclerotic lesions of blood vessels. In the last decade, among the proinflammatory cytokines, interleukin 18 seems to play a central role in the inflammatory cascade, leading to development of atherosclerotic disease and the occurrence of ischemic heart disease in uninfected HIV-1 people. Increased levels of interleukin 18 were observed in HIV-1 infected patients. This review attempts to evaluate the role of interleukin 18 in cardiovascular disease, especially in myocardial infarction, in HIV-1 infection, as well as the relationship between interleukin 18 and atherosclerotic plaque formation. Two other characteristic aspects in HIV-1 infection, metabolic syndrome and lipodystrophy, will be evaluated in light of activity of interleukin 18. Moreover, the role of platelets and interleukin 18 as an important linkage between chronic inflammation, endothelial dysfunction, and atherogenesis will be highlighted. Finally, experimental an animal model of rhesus macaques infected with simian immunodeficiency virus clearly demonstrates the involvement of interleukin 18 in myocardial lesions, and that circulating levels of interleukin 18 are important predictors of coronary heart disease. In conclusion, interleukin 18 may be considered a partner in crime with other factors, including endothelial dysfunction, increased expression and production of adhesion molecules and proinflammatory cytokines in determining cardiovascular disease.
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PMID:Interleukin 18 and cardiovascular disease in HIV-1 infection: a partner in crime? 2021 8


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