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Query: UMLS:C0019693 (HIV)
 170,526 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

With the advent of more effective therapies for human immunodeficiency virus (HIV) infection, HIV-infected patients are living longer and cardiovascular disease is becoming more obvious in this population. Patients with HIV infection represent one of the most rapidly developing groups with cardiovascular disease globally. Cardiovascular disease complicating HIV infection is likely to contribute to burgeoning healthcare costs. Pericarditis, myocarditis, cardiomyopathy, atherosclerotic coronary vasculopathy, arterial aneurysms, pulmonary hypertension, and endocarditis occur with increased frequency in these patients. Pericardial tamponade, dilated cardiomyopathy, endocarditis, and vasculopathy can lead to fatal outcomes in this population. The advent of cardiomyopathy heralds a very poor prognosis in patients infected with HIV. Coronary vasculopathy without obvious risk factors can lead to myocardial ischemia in young patients infected with the virus. Moreover, the protease inhibitors used to treat HIV infection induce a syndrome of lipodystrophy and dyslipidemia that may be associated with accelerated atherosclerosis as well as insulin resistance. All these factors contribute to increased cardiovascular morbidity and mortality in the HIV-infected population. HIV infection, opportunistic infections, secreted viral proteins such as gp120 (envelope protein) or Tat (transactivator of viral transcription), and cytokines elaborated during the course of HIV infection of the immune system all contribute to pathogenesis of these disorders. Further basic and clinical studies are required to understand the pathogenesis of cardiovascular complications and develop appropriate management strategies for these patients.
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PMID:The cardiovascular and metabolic complications of HIV infection. 1117 4

We examine here several diseases that are associated with inappropriate activation of the chemokine network. Detailed comment has been restricted to pathological states for which there are compelling data either from clinical observations or animal models. These include cardiovascular disease, allergic inflammatory disease, transplantation, neuroinflammation, cancer and HIV-associated disease. Discussion focuses on therapeutic directions in which the rapidly evolving chemokine field appears to be headed.
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PMID:Chemokines and disease. 1117 2

Endothelial dysfunction and/or injury is pivotal to the development of cardiovascular and inflammatory pathology. Endothelial dysfunction and/or injury has been described in Human Immunodeficiency Virus (HIV) infection. Elaboration of circulating markers of endothelial activation, such as soluble adhesion molecules and procoagulant proteins, occurs in HIV infection. Certain endothelial cells, such as those lining liver sinusoids, human umbilical vein endothelial cells, bone marrow stromal endothelial cells or brain microvascular endothelial cells, have been shown to be variably permissive for HIV infection. Entry of virus into endothelial cells may occur via CD4 antigen or galactosyl-ceramide receptors. Other mechanisms of entry including chemokine receptors have been proposed. Nevertheless, endothelial activation may also occur in HIV infection either by cytokines secreted in response to mononuclear or adventitial cell activation by virus or else by the effects of the secreted HIV-associated proteins, gp 120 (envelope glycoprotein) and Tat (transactivator of viral replication) on endothelium. Enhanced adhesiveness of endothelial cells, endothelial cell proliferation and apoptosis as well as activation of cytokine secretion have all been demonstrated. Synergy between select inflammatory cytokines and viral proteins in inducing endothelial injury has been shown. In HIV infection, dysfunctional or injured endothelial cells potentiate tissue injury, inflammation and remodeling, and accelerate the development of cardiovascular disease.
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PMID:The effects of HIV infection on endothelial function. 1120 21

Periodontitis is a chronic bacterial infection of the supporting structures of the teeth. The host response to infection is an important factor in determining the extent and severity of periodontal disease. Systemic factors modify periodontitis principally through their effects on the normal immune and inflammatory mechanisms. Several conditions may give rise to an increased prevalence, incidence or severity of gingivitis and periodontitis. The effects of a significant number of systemic diseases upon periodontitis are unclear and often it is difficult to causally link such diseases to periodontitis. In many cases the literature is insufficient to make definite statements on links between certain systemic factors and periodontitis and for several conditions only case reports exist whereas in other areas an extensive literature is present. A reduction in number or function of polymorphonuclear leukocytes (PMNs) can result in an increased rate and severity of periodontal destruction. Medications such as phenytoin, nifedipine, and cyclosporin predispose to gingival overgrowth in response to plaque and changes in hormone levels may increase severity of plaque-induced gingival inflammation. Immuno-suppressive drug therapy and any disease resulting in suppression of the normal inflammatory and immune mechanisms (such as HIV infection) may predispose the individual to periodontal destruction. There is convincing evidence that smoking has a detrimental effect on periodontal health. The histiocytoses diseases may present as necrotizing ulcerative periodontitis and numerous genetic polymorphisms relevant to inflammatory and immune processes are being evaluated as modifying factors in periodontal disease. Periodontitis severity and prevalence are increased in diabetics and worse in poorly controlled diabetics. Periodontitis may exacerbate diabetes by decreasing glycaemic control. This indicates a degree of synergism between the two diseases. The relative risk of cardiovascular disease is doubled in subjects with periodontal disease. Periodontal and cardiovascular disease share many common risk and socio-economic factors, particularly smoking, which is a powerful risk factor for both diseases. The actual underlying aetiology of both diseases is complex as are the potential mechanisms whereby the diseases may be causally linked. It is thought that the chronic inflammatory and microbial burden in periodontal disease may predispose to cardiovascular disease in ways proposed for other infections such as with Chlamydia pneumoniae. To move from the current association status of both diseases to causality requires much additional evidence. Determining the role a systemic disease plays in the pathogenesis of periodontal disease is very difficult as several obstacles affect the design of the necessary studies. Control groups need to be carefully matched in respect of age, gender, oral hygiene and socio-economic status. Many studies, particularly before the aetiological importance of dental plaque was recognised, failed to include such controls. Longitudinal studies spanning several years are preferable in individuals both with and without systemic disease, due to the time period in which periodontitis will develop.
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PMID:Periodontal manifestations of systemic disease. 1135 36

Garlic has been used for hundreds of years to treat fungal, parasitic, and viral infections, and has anti-inflammatory properties that show promise for prevention of cardiovascular disease. Researchers are focusing on an extract of garlic called ajoene which also appears to protect CD+ cells from attack by HIV early in the viral life cycle. At low concentrations, the drug appears to have little toxicity, and its anti-HIV activity is 45 times more powerful than the drug dextran sulfate. Ajoene is found only in fresh garlic and is not readily available. One researcher found that garlic impairs the activity of the liver enzymes that process protease inhibitors and raises the protease inhibitor levels.
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PMID:Garlic extract for HIV? 1136 38

A case study of a 41-year-old man who tested positive for HIV, but who has no symptoms of HIV disease, is provided. Two physician responses regarding when to initiate antiretroviral therapy in an asymptomatic patient with intermediate-stage HIV infection are detailed. Among other factors, treatment initiation depends upon patient acceptance, probability of adherence, and prognosis, defined by CD4 cell count and viral load test results. The patient's risk for cardiovascular disease without the use of PIs and his concerns about initiating antiretroviral treatment are also addressed by both physicians.
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PMID:When to start? 1136 3

There is growing concern that the metabolic complications associated with HIV and antiretroviral therapy may lead to accelerated coronary artery disease (CAD). Traditional cardiovascular risk factors, such as hypertension, hyperlipidemia, diabetes mellitus, and visceral fat accumulation, are increasingly seen in HIV patients receiving HAART. These factors are in addition to nonreversible risk factors, such as male sex, age greater than 40 years, and family history of premature CAD. Patients may also be smokers and may have a sedentary lifestyle, both of which predispose to significant CAD. In older patients and those with other risk factors, there may be an accentuation of these risk factors by HAART, although these factors also occur in young patients with no other risk factors. It is still unknown whether the factors predispose HIV patients to accelerated cardiovascular disease. Short-term studies, including 2 large cross-sectional studies, do not show an increased risk of cardiovascular complications or cardiac death, but longer follow-up is needed to answer such questions effectively. Even if patients are not at increased risk for cardiovascular disease, they are at least at the same risk as HIV-negative, age-matched persons with similar risk factors. It is, therefore, pertinent to identify and effectively manage those risk factors that can be modified.
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PMID:HIV and cardiovascular risk factors. 1159 42

Insulin resistance is increasingly recognized among HIV-infected patients with fat redistribution (lipodystrophy) who are receiving highly active antiretroviral therapy. The mechanisms of insulin resistance in this population remain unknown, but could relate to a decrease in glucose transport caused by the direct effects of certain antiretroviral agents, such as the protease inhibitors, or to the effects of severe fat redistribution, including subcutaneous fat loss and increased visceral adiposity. Insulin resistance in patients with HIV lipodystrophy is associated with hyperlipidemia and impaired fibrinolysis, and might increase the risk of cardiovascular disease (CVD). Furthermore, insulin-sensitizing agents might improve insulin resistance and reduce the risk of CVD in this population.
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PMID:Insulin resistance in the HIV-lipodystrophy syndrome. 1159 44

Mesenchymal tumors of the appendix are very rare, and specific stromal tumors (i.e., gastrointestinal stromal tumors, GISTs) have not been reported in this location to date. Four GISTs were identified in the review of primary mesenchymal tumors of the appendix from the files of the Armed Forces Institute of Pathology from 1970 to 1998. There were also one benign schwannoma, one diffuse neurofibroma with neurofibromatosis 1, one leiomyosarcoma in a child with HIV infection, and one inflammatory fibroid polyp. The four appendiceal GISTs occurred in adult males 56-72 years of age (mean 63 years). Two tumors occurred in patients who had surgery for appendicitis-like symptoms: one was an incidental finding during surgery for a malignant gastric epithelioid GIST and one was an incidental autopsy finding. Only one of the two appendices operated for symptoms had acute inflammation, and a polypoid GIST projected outward from the proximal part of appendix. Three tumors were partially obliterating nodules, eccentrically expanding the appendiceal wall. All four were spindle cell tumors, and three of them contained extracellular collagen globules (skeinoid fibers); none had atypia or mitotic activity (<1/50 high power fields). Immunohistochemically, two tumors studied were positive for CD117 (KIT), and two were positive for CD34. The tumors were negative for alpha-smooth muscle actin and S-100 protein. Follow-up revealed death from cardiovascular disease in one case (4 years after appendectomy) and liver failure because of malignant gastric epithelioid GIST metastatic to liver in another case 15 years after the appendectomy. This report documents the rare occurrence of CD117-positive GISTs as primary appendiceal tumors.
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PMID:Gastrointestinal stromal tumors in the appendix: a clinicopathologic and immunohistochemical study of four cases. 1622 28

Persons with human immunodeficiency virus (HIV) infection might be at risk for ischemic cardiovascular disease (CVD). We reviewed the records of 16 HIV-infected persons with proven CVD (8 cases of angina and 8 cases of myocardial infarctions). This represents 1.7% of HIV-infected persons seen at our institution from 1 April 1999 through 25 April 2000. In comparison with 32 HIV-infected age- and sex-matched controls, case patients had more risk factors for CVD (median number of risk factors for CVD, 3 versus 1; P<.001), lower nadir CD4+ lymphocyte counts (median, 101 cells/mm3 versus 278 cells/mm3; P=.02), and a longer duration of prior exposure to nucleoside analogs (median, 190 weeks versus 130 weeks; P=.02). There was no difference in the duration of exposure to protease inhibitors. Ischemic CVD occurs in HIV-infected persons and appears to be most closely associated with traditional risk factors for coronary artery disease (for example, hypertension and hypercholesterolemia). Lower CD4+ lymphocyte counts and duration of HIV infection might also be risk factors or markers for the development of ischemic CVD.
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PMID:Ischemic cardiovascular disease in persons with human immunodeficiency virus infection. 1217 41


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