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)

The relationship between oral and general health has been increasingly recognised during the past two decades. Several epidemiological studies have linked poor oral health with cardiovascular disease, poor glycaemic control in diabetics, low birth-weight pre-term babies, and a number of other conditions, including rheumatoid arthritis and osteoporosis. Oral infections are also recognised as a problem for individuals suffering from a range of chronic conditions, including cancer and infection with human immunodeficiency virus, as well as patients with ventilator-associated pneumonia. This review considers the systemic consequences of odontogenic infections and the possible mechanisms by which oral infection and inflammation can contribute to cardiovascular disease, as well as the oral conditions associated with medically compromised patients. A large number of clinical studies have established the clinical efficacy of topical antimicrobial agents, e.g., chlorhexidine and triclosan, in the prevention and control of oral disease, especially gingivitis and dental plaque. The possible risks of antimicrobial resistance are a concern, and the benefits of long-term use of triclosan require further evaluation. Oral infections have become an increasingly common risk-factor for systemic disease, which clinicians should take into account. Clinicians should increase their knowledge of oral diseases, and dentists must strengthen their understanding of general medicine, in order to avoid unnecessary risks for infection that originate in the mouth.
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PMID:Oral infections and systemic disease--an emerging problem in medicine. 1771 25

In this paper, we report 21 cases of Campylobacter fetus bloodstream infection observed in our institution over a 9-year period. The median age of the patients was 78 years. Most of them (62%) had a significant underlying disease, such as diabetes, immunodeficiency or cardiovascular disease. The main clinical features were fever with (62% of cases) or without (38%) extra-intestinal symptoms. These included mycotic aneurysm of the abdominal aorta (24%) and cellulitis (19%). Antibiotic treatment was mainly based on amoxicilline-clavulanate (57%) or imipenem (21%), for a median duration of 28 days. A favourable outcome was observed in 72% of cases. Death directly attributable to infection was observed for three patients, due to the rupture of an infected aneurysm or relapsing bloodstream infection with septic shock. All patients initially treated with imipenem had a favourable outcome. This report adds evidence that C. fetus bloodstream infection should be suspected in elderly patients with fever, immunodeficiency and cardiovascular damages. Imipenem seems to be the most active drug, especially in severe cases.
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PMID:Campylobacter fetus bloodstream infection: risk factors and clinical features. 1799 95

Many innovative and effective smoking-cessation treatments, both behavioral and pharmacologic, have been developed over the past several decades. However, these treatments traditionally have been developed for use with populations of healthy smokers. Despite the disease management implications, efforts to design and evaluate cessation interventions targeting smokers diagnosed with chronic diseases are reported infrequently in the literature. The purpose of this paper is to provide a brief overview of the evidence linking continued smoking to disease progression and adverse treatment outcomes across a range of common chronic diseases: cardiovascular disease (CVD), chronic obstructive pulmonary disease (COPD), diabetes, asthma, cancer, and human immunodeficiency virus/acquired immunodeficiency syndrome (HIV/AIDS). Where studies are available, the efficacy of smoking-cessation interventions specifically developed or applied to these patient populations is reviewed. Finally, limitations and gaps in smoking research and treatment with chronically ill patients are discussed, and future research priorities are recommended.
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PMID:Smoking cessation a critical component of medical management in chronic disease populations. 1802 17

Although cardiotoxic effects of highly active antiretroviral therapy (HAART) are a growing concern, there is a lack of prospective studies of subclinical involvement of the heart in human immunodeficiency virus (HIV)-infected patients. This study evaluated noninvasively cardiac morphologic characteristics and function in HIV-positive (HIV(+)) men receiving HAART for > or =2 years with no clinical evidence of cardiovascular disease. Echocardiography at rest, including tissue Doppler imaging and exercise testing, were performed in 30 HIV(+) men (age 42.1 +/- 4.7 years, duration of HIV infection 10.4 +/- 4.7 years, duration of HAART 5.3 +/- 2.1 years) and 26 age-matched healthy controls. At rest, HIV(+) patients had similar left ventricular (LV) mass indexed to height(2.7) (40.6 +/- 9.5 vs 37.5 +/- 9.3 g/m; p >0.05), but a higher prevalence of LV diastolic dysfunction (abnormal relaxation or pseudonormal filling pattern in 64% of patients vs 12% of controls; p <0.001). LV systolic function indexes were significantly lower (ejection fraction 60.4 +/- 8.7% vs 66.9 +/- 6.9%; p <0.01, and tissue Doppler imaging peak systolic velocity 11.4 +/- 1.6 vs 13.5 +/- 2.2 cm/s; p <0.001). Pulmonary artery pressure was higher in patients compared with controls (32.1 +/- 5.4 vs 26.1 +/- 6.5 mm Hg; p <0.001). Exercise testing showed decreased exercise tolerance in HIV(+) patients, with no case of myocardial ischemia. In conclusion, subclinical cardiac abnormalities are frequently observed in HIV(+) patients on HAART. The usefulness of systematic noninvasive screening in this population should be considered. GECEM study no. 30: National Agency for AIDS Research (ANRS).
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PMID:Subclinical cardiac abnormalities in human immunodeficiency virus-infected men receiving antiretroviral therapy. 1863 12

The relationship between human immunodeficiency virus (HIV) infection and cardiovascular disease is still under debate, but it appears that the risk of myocardial infarction in those with HIV infection who are receiving highly active antiretroviral therapy (HAART) is increased. There has been less focus, however, on the effect of HIV and HAART on left ventricular function. Evidence from the past 20 years in both Westernized and developing countries has indicated that subclinical left ventricular dysfunction in HIV-infected individuals with and without well-controlled HIV infection is prevalent and may represent emerging cardiac disease. The specific roles of HIV infection and HAART are unclear, but they may exert independent direct and indirect effects on the myocardium. These effects may include chronic inflammation, metabolic complications (ie, insulin resistance, lipotoxicity, dyslipidemia), and mitochondrial toxicity. The objective of this article is to review the evidence for HIV- and HAART-related left ventricular dysfunction in persons infected with HIV.
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PMID:Left ventricular dysfunction in human immunodeficiency virus infection. 1845 7

In the era of highly active antiretroviral therapy (HAART), human immunodeficiency virus (HIV) infection has become a chronic disease in which patients may develop significant metabolic complications and risk factors for cardiovascular disease (CVD), including insulin resistance, visceral fat deposition, and increases in atherogenic cholesterol and triglyceride levels. Epidemiologic studies have found that persons infected with HIV are likely to be at higher risk for premature CVD compared with the general population, and clinical studies examining endothelial function in HIV-infected cohorts have supported such conclusions. The mechanisms underlying the regulation of endothelial function in HIV-infected persons appear to be multifactorial, including direct effects of HIV on the endothelium, indirect effects of HIV on lipids and inflammatory cytokines, HAART-related effects, and traditional/host factors. Better understanding of these processes can lead to improved strategies for the long-term management of HIV infection.
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PMID:Determinants of endothelial function in human immunodeficiency virus infection: a complex interplay among therapy, disease, and host factors. 1845 8

Highly active antiretroviral therapy has greatly reduced mortality among human immunodeficiency virus (HIV)-infected patients by delaying, and possibly preventing, progression to AIDS. The risk of cardiovascular disease (CVD) is now an important consideration in these patients and may increase as they live longer. Risk factors for CVD, the inflammatory effects of HIV, and the metabolic complications of antiretroviral therapy may accelerate the onset of CVD. Death from myocardial infarction, however, is still rare compared with death from progression of HIV disease, and the benefits of antiretroviral therapy clearly outweigh any associated risk of CVD. In this review, the authors describe the risk of accelerated CVD in HIV-infected individuals, the proposed viral and therapy-related mechanisms of CVD, the clinical features of CVD in these patients, and monitoring and management guidelines to reduce CVD risk. Identifying, monitoring, and treating CVD risk factors in HIV-positive patients is vital to improving their lives and should become standard practice.
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PMID:Accelerated cardiovascular disease and myocardial infarction risk in patients with the human immunodeficiency virus. 1845 9

Human immunodeficiency virus (HIV)-infected patients have a higher incidence of oxidative stress, endothelial dysfunction, and cardiovascular disease than uninfected individuals. Recent reports have demonstrated that viral proteins upregulate reactive oxygen species, which may contribute to elevated cardiovascular risk in HIV-1 patients. In this study we employed an HIV-1 transgenic rat model to investigate the physiological effects of viral protein expression on the vasculature. Markers of oxidative stress in wild-type and HIV-1 transgenic rats were measured using electron spin resonance, fluorescence microscopy, and various molecular techniques. Relaxation studies were completed on isolated aortic rings, and mRNA and protein were collected to measure changes in expression of nitric oxide (NO) and superoxide sources. HIV-1 transgenic rats displayed significantly less NO-hemoglobin, serum nitrite, serum S-nitrosothiols, aortic tissue NO, and impaired endothelium-dependent vasorelaxation than wild-type rats. NO reduction was not attributed to differences in endothelial NO synthase (eNOS) protein expression, eNOS-Ser1177 phosphorylation, or tetrahydrobiopterin availability. Aortas from HIV-1 transgenic rats had higher levels of superoxide and 3-nitrotyrosine but did not differ in expression of superoxide-generating sources NADPH oxidase or xanthine oxidase. However, transgenic aortas displayed decreased superoxide dismutase and glutathione. Administering the glutathione precursor procysteine decreased superoxide, restored aortic NO levels and NO-hemoglobin, and improved endothelium-dependent relaxation in HIV-1 transgenic rats. These results show that HIV-1 protein expression decreases NO and causes endothelial dysfunction. Diminished antioxidant capacity increases vascular superoxide levels, which reduce NO bioavailability and promote peroxynitrite generation. Restoring glutathione levels reverses HIV-1 protein-mediated effects on superoxide, NO, and vasorelaxation.
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PMID:Vascular oxidative stress and nitric oxide depletion in HIV-1 transgenic rats are reversed by glutathione restoration. 1845 25

Statin drugs are widely prescribed to achieve aggressive low-density lipoprotein lowering in order to decrease cardiovascular disease. Although some of the immunomodulatory effects of statins may stabilize atherosclerotic plaque, they may be harmful in certain segments of the population. Recently, statins have been shown to increase the concentration of regulatory T cells (Tregs), in vivo. There is evidence that this increases the risk of many cancers, particularly in the elderly. Furthermore, a statin induced increase in Tregs may be detrimental in neurodegenerative disorders, such as amyotrophic lateral sclerosis; and a myriad of infectious diseases. These include, but are not limited to, human immunodeficiency virus, hepatitis B virus, hepatitis C virus, and varicella zoster virus. These issues need our attention, and call for a heightened state of vigilance among those prescribing statins.
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PMID:The double-edged sword of statin immunomodulation. 1857 Dec 56

Since the emergence of highly active antiretroviral therapy (HAART), human immunodeficiency virus-1 (HIV-1)-infected patients have demonstrated dramatic decreases in viral burden and opportunistic infections, and an overall increase in life expectancy. Despite these positive HAART-associated outcomes, it has become increasingly clear that HIV-1 patients have an enhanced risk of developing cardiovascular disease over time. Clinical studies are instrumental in our understanding of vascular dysfunction in the context of HIV-1 infection. However, most clinical studies often do not distinguish whether HIV-1 proteins, HAART, or a combination of these 2 factors cause cardiovascular complications. This review seeks to address the roles of both HIV-1 proteins and antiretroviral drugs in the development of endothelial dysfunction because endothelial dysfunction is the hallmark initial step of many cardiovascular diseases. We analyze recent in vitro and in vivo studies examining endothelial toxicity in response to HIV-1 proteins or in response to the various classes of antiretroviral drugs. Furthermore, we discuss the multiple mechanisms by which HIV-1 proteins and HAART injure the vascular endothelium in HIV-1 patients. By understanding the molecular mechanisms of HIV-1 protein- and antiretroviral-induced cardiovascular disease, we may ultimately improve the quality of life of HIV-1 patients through better drug design and the discovery of new pharmacological targets.
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PMID:The roles of HIV-1 proteins and antiretroviral drug therapy in HIV-1-associated endothelial dysfunction. 1852 51


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