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)

Thanks to a worldwide collaborative effort among health care providers, academia, governments, and industry, our knowledge base about infection caused by the human immunodeficiency virus (HIV) has expanded exponentially. During the past 2 decades, we have learned about its pathogenesis, virology, immunology, epidemiology and treatment. In the developed world, the approach to persons with HIV disease has evolved from palliative disease care to use of a chronic disease model, where survival is measured by decades, not months or years. More and more, clinical decision-making for HIV-infected patients is driven by comorbidities, including cardiothoracic disease. Thus, our clinically stable HIV population is increasingly accessing those health care services required by any maturing population, including the usual services of cardiothoracic surgeons. In this article, we review the basic facts of HIV disease, with an emphasis on occupational risks and infection control procedures.
Semin Thorac Cardiovasc Surg 2000 Apr
PMID:An overview of HIV infection and AIDS: etiology, pathogenesis, diagnosis, epidemiology, and occupational exposure. 1080 35

The immunocompromised state is a major risk factor for the development of malignant tumors. Individuals with human immunodeficiency virus (HIV), and acquired immunodeficiency syndrome (AIDS) represent a large segment of the immunocompromised group of patients. Kaposi's sarcoma, B-cell non-Hodgkin's lymphoma, primary central nervous system lymphoma, and invasive cervical carcinoma are malignant tumors that are all AIDS-defining illnesses. Lung cancer is also seen with a higher frequency in AIDS patients. Malignant tumors are more aggressive in this group of patients as compared with the general population. Prognosis is poor, although with the improved survivals seen with new treatment in these patients, aggressive therapy is still warranted.
Semin Thorac Cardiovasc Surg 2000 Apr
PMID:Thoracic malignancies associated with AIDS. 1080 38

Enteric loss of protein with the sequelae of edema, immunodeficiency, and hypercoagulability is being diagnosed with increasing frequency after Fontan procedure. The precise pathophysiological mechanism is unknown; however, protein-losing enteropathy (PLE) after Fontan procedure is likely related to a hemodynamic derangement that is not easily detectable via standard hemodynamic measures presently obtainable in the cardiac catheterization laboratory. Treatment options include (1) symptomatic relief via diuretics, supplemental albumin infusion, and dietary change to high protein/high medium-chain triglyceride intake, (2) hemodynamic improvement via afterload reduction (angiotensin-converting enzyme inhibitors), repair of branch pulmonary artery stenoses, or coil embolization of aortopulmonary collaterals, (3) intestinal cell membrane stabilization via high-dose steroids or heparin infusion, and (4) attempt at alteration of the primary hemodynamic derangement via fenestration of the systemic venous baffle or via heart transplantation. Further understanding of the cause of PLE after Fontan procedure is needed before more effective treatment options can be used. Copyright 1998 by W.B. Saunders Company
Semin Thorac Cardiovasc Surg Pediatr Card Surg Annu 1998
PMID:Management of protein-losing enteropathy after the Fontan procedure. 1148 3

While cardiac myocytes are not generally considered conventional cellular targets of retroviral infection with HIV-1, the increasing recognition of AIDS related cardiomyopathy has raised important questions as to the viral pathogenesis. Our laboratory has explored the role of simian immunodeficiency viral (SIV) infection in non-human primates as a suitable large-animal model to examine cardiac involvement. Our data suggest that in the presence of inflammatory myocarditis, SIV is localized to CD4 bearing inflammatory cells and not cardiac myocytes, suggesting that the heart may be an innocent bystander in AIDS cardiomyopathy.
Trends Cardiovasc Med 2001 Aug
PMID:SIV cardiomyopathy in non-human primates. 1167 55

The incidence of myocardial infarction in patients who have the aquired immunodeficiency syndrome (AIDS) is increasing. However, no effective therapeutic agents have been discovered to reduce myocardial ischemia-reperfusion (I/R) injury in pathologies associated with AIDS. The aim of this study was to determine if infarct size is increased in murine AIDS after I/R injury and if I/R injury could be attenuated with vitamin E supplementation. Three groups of mice were studied: control, murine AIDS, and murine AIDS with vitamin E supplementation. Anesthetized mice were subjected to 30 min of left anterior descending coronary artery occlusion and 120 min of reperfusion. The hearts in mice that had murine AIDS had a larger infarct size compared to controls after I/R injury. Vitamin E supplementation significantly reduced infarct size and inhibited polymorphonuclear neutrophil (PMN) CD11b expression (p < 0.05). However, vitamin E supplementation did not affect PMN reactive oxygen species (ROS) production and platelet CD62p expression. These results suggest that the reduction of myocardial I/R injury with vitamin E supplementation may be the result of the inhibition of PMN CD11b expression. Vitamin E may be a promising prophylactic agent for the reduction of the severity of myocardial I/R injury in patients who have AIDS.
Cardiovasc Toxicol 2002
PMID:Vitamin E attenuates myocardial ischemia-reperfusion injury in murine AIDS. 1227 Nov 55

Vascular complications in the course of human immunodeficiency virus (HIV) infection are multifactorial and may be caused by the virus itself or by the related opportunistic infections and neoplasms. Highly active antiretroviral therapy (HAART), which dramatically modifies the natural history of HIV disease, causes in a high proportion of patients a metabolic syndrome that includes body fat redistribution, hypercholesterolaemia, hypertriglyceridaemia and insulin resistance. These effects are particularly evident in patients treated with protease inhibitors (PIs). However, studies on the cardiovascular risk among HIV-infected individuals receiving PIs have not shown a consistent association. The pathogenesis of the HAART-associated metabolic syndrome has not been completely elucidated, but there is growing evidence that a synergistic effect between PIs and nucleoside reverse transcriptase inhibitors might play a significant role. All HIV-infected patients candidate to antiretroviral therapy and patients already under treatment should undergo an assessment that includes the evaluation of the cardiovascular risk with the available guidelines.
J Cardiovasc Risk 2002 Oct
PMID:HIV infection, antiretroviral therapy and cardiovascular risk. 1239 24

Infection of people with human immunodeficiency virus (HIV) as well as LP-BM5 infection in mice results in progressive deterioration of the immune system in the majority of untreated hosts. Peptide immunotherapy has been shown to be effective in the stimulation or immunoregulation of T-helper 1 (T(H)1) and T-helper 2 (T(H) 2) response subsets. In murine acquired immunodeficiency syndrome (AIDS), T(H)1 deficiency enables the host to be susceptible to coxsackievirus infection, inducing cardiopathology in a short period. T-cell receptor (TCR) Vbeta8.1 peptide, a 16-mer peptide containing the entire CDR1 segment and part of the FR2 region of human Vbeta8, showed both an immunoregulating and immunostimulating effect in murine AIDS. TCR Vbeta8.1 peptide acts on T cells promoting interleukin-2 production and therefore enhancing a cell-mediated immune response. It retarded development of cardiopathology due to coxsackievirus infection. Retrovirus-infected mice treated with the peptide showed a longer life span than the nontreated, retrovirus-infected animals.
J Cardiovasc Pharmacol 2003 Mar
PMID:T-cell receptor V beta 8.1 peptide reduces coxsackievirus-induced cardiopathology during murine acquired immunodeficiency syndrome. 1260 29

Human immunodeficiency virus protease inhibitors are associated with metabolic abnormalities that may increase risk of atherosclerotic vascular disease, including dyslipidemia, insulin resistance, and central obesity. Dyslipidemia, characterized by hypercholesterolemia and hypertriglyceridemia, small low- and high-density lipoprotein particles, and in some cases lipoprotein(a) excess, can be severe and has been associated with endothelial dysfunction and carotid atherosclerosis. The mechanisms underlying protease inhibitor-associated dyslipidemia have not been elucidated completely, but appear to involve hepatic overproduction of very low-density lipoproteins and to a lesser extent, impaired clearance. Insulin resistance appears to mediate part of the adverse lipoprotein changes observed in patients taking protease inhibitors. Ongoing epidemiological and surrogate endpoint studies are investigating the atherogenicity of these medications. Until the risk associated with use of protease inhibitors is better understood, identifying patients at high risk for adverse vascular events such as heart attacks, cardiac death, and stroke is a high priority. This article reviews the lipid and lipoprotein abnormalities associated with use of protease inhibitors, possible mechanisms for protease inhibitor-associated dyslipidemia, its potential atherogenicity, and use of the National Cholesterol Education Program Adult Treatment Panel III Guidelines for the management of patients with dyslipidemia.
Prog Cardiovasc Dis
PMID:Dyslipidemia in the era of HIV protease inhibitors. 1263 93

The heart is an organ frequently affected in patients with acquired immune deficiency syndrome (AIDS). Since the introduction of highly active antiretroviral therapy (HAART), a sharp decline in mortality and morbidity has been observed in human immunodeficiency virus (HIV)-infected patients. However, numerous reports of myocardial infarcts in young HIV-infected patients have raised concerns of premature coronary artery disease in this population. New risk factors for coronary heart disease such as increased insulin resistance, dyslipidemia, and lipodystrophy syndrome, which are associated with HAART, may accelerate underlying arteriosclerosis in HIV-infected patients. Data on the incidence of coronary heart disease are limited to case reports and retrospective studies. Results from ongoing, large, prospective studies will provide information on whether or not HAART may increase the incidence of myocardial infarcts and whether a drastic change in HIV therapy is warranted.
Prog Cardiovasc Dis
PMID:Epidemiology of HIV cardiac disease. 1263 95

During the past several years, many articles have described how human embryonic stem (ES) cells and adult hematopoietic stem cells (HSCs) can differentiate into cardiac muscle, blood vessels, and various other types of cells. The articles raised the expectation that these stem cells may become useful for the treatment of a variety of diseases, including cardiovascular diseases. Genetic manipulation of ES cells and HSCs would be important for such future applications of the cells. Until now, retroviral vectors have been used primarily for stable expression of transgenes in murine ES cells and HSCs. Because murine models may not predict reliably the biology of ES cells and HSCs in humans, we have utilized primate ES cells and HSCs as targets of gene transfer. We have shown that primate ES cells and HSCs can be transduced efficiently with lentiviral vectors derived from the simian immunodeficiency virus, and that the high transgene expression persists without transcriptional silencing. This highly efficient gene transfer method allows for safe and faithful gene delivery to primate ES cells and HSCs to test potential research and therapeutic applications.
Trends Cardiovasc Med 2003 Apr
PMID:Genetic manipulation of primate embryonic and hematopoietic stem cells with simian lentivirus vectors. 1269 74


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