Disease In HIV-infected Patients Research Articles

The difficulties of classifying renal disease in HIV-infected patients*

The difficulties of classifying renal disease in HIV-infected patients*

Neurological opportunistic diseases in HIV infected patients in a western hospital of Venezuela, 2007 -2009

Neurological opportunistic diseases in HIV infected patients in a western hospital of Venezuela, 2007 -2009

Cholesterol, vitamin D and cardiovascular prevention in HIV patients treated with antiretroviral therapy

It is widely believed that dyslipidaemia related to the duration of highly active antiretroviral therapy (HAART) contributes most to an increased predicted risk of cardiovascular disease (CVD) among patients with HIV. Consequently, it is increasingly suggested that hypercholesterolemia should be actively managed with the use of lipid-lowering drugs. However, when studying the impact of individual antiretroviral drugs on the risk of coronary heart disease in HIV-infected patients, it has been shown that the risk of myocardial infarction is only partly mediated by an effect of HAART on lipid metabolism [ [1] Lang S. Mary-Krause M. Cotte L. Clinical Epidemiology Group of the French Hospital Database on HIV et al. Impact of individual antiretroviral drugs on the risk of myocardial infarction in human immunodeficiency virus-infected patients: a case–control study nested within the French Hospital Database on HIV ANRS cohort CO4. Arch Intern Med. 2010; 170: 1228-1238 Crossref PubMed Scopus (264) Google Scholar ]. Furthermore, in this setting, hypercholesterolemia may represent a blessing in disguise.

Recruiting and Baseline of the HIV-HEART Study: A Prospective, Multicenter Trial to Analyze Cardiac Diseases in HIV-Infected Patients

Background: An increased life span and the amount of cardiovascular risk factors necessitate a closer look on cardiac diseases in the population of human immunodeficiency virus (HIV) – infected subjects. Therefore, we launched a cardiology driven study analyzing HIV-associated diseases supported by the federal ministry of research.

Recruiting and Baseline of the HIV-HEART Study: A Prospective, Multicenter Trial to Analyze Cardiac Diseases in HIV-Infected Patients

Recruiting and Baseline of the HIV-HEART Study: A Prospective, Multicenter Trial to Analyze Cardiac Diseases in HIV-Infected Patients

Primary spinal hydatid cyst in a patient with acquired immunodeficiency syndrome

Spinal hydatid cyst is a serious and unusual infectious disease. There is little information on infections caused by cestodes in patients with human immunodeficiency virus (HIV) infection. Although infrequent, infections by cestodes constitute a cause of disease in HIV-infected patients, especially in endemic areas. This report presents, for the first time in the literature, primary spinal cyst hydatid in a patient with acquired immunodeficiency syndrome.

Predicting the risk of cardiovascular disease in HIV-infected patients: the Data collection on Adverse Effects of Anti-HIV Drugs Study

HIV-infected patients receiving combination antiretroviral therapy may experience metabolic complications, potentially increasing their risk of cardiovascular diseases (CVDs). Furthermore, exposures to some antiretroviral drugs seem to be independently associated with increased CVD risk. We aimed to develop cardiovascular risk-assessment models tailored to HIV-infected patients. Prospective multinational cohort study. The data set included 22,625 HIV-infected patients from 20 countries in Europe and Australia who were free of CVD at entry into the Data collection on Adverse Effects of Anti-HIV Drugs Study. Using cross-validation methods, separate models were developed to predict the risk of myocardial infarction, coronary heart disease, and a composite CVD endpoint. Model performance was compared with the Framingham score. The models included age, sex, systolic blood pressure, smoking status, family history of CVD, diabetes, total cholesterol, HDL cholesterol and indinavir, lopinavir/r and abacavir exposure. The models performed well with area under the receiver operator curve statistics of 0.783 (range 0.642-0.820) for myocardial infarction, 0.776 (0.670-0.818) for coronary heart disease and 0.769 (0.695-0.824) for CVD. The models estimated more accurately the outcomes in the subgroups than the Framingham score. Risk equations developed from a population of HIV-infected patients, incorporating routinely collected cardiovascular risk parameters and exposure to individual antiretroviral therapy drugs, might be more useful in estimating CVD risks in HIV-infected persons than conventional risk prediction models.

Prevalence of Cardiac Manifestations in HIV-Infected Patients in Iran

Prevalence of Cardiac Manifestations in HIV-Infected Patients in Iran

Prevalence and Risk Factors for Abnormal Liver Stiffness in HIV-infected Patients without Viral Hepatitis Coinfection: Role of Didanosine

Unexpected cases of severe liver disease in HIV-infected patients have been reported and an association with didanosine (ddI) has been suggested. Transient elastography (TE) might detect patients harbouring such a condition. Our objective was to search for the presence of abnormal liver stiffness (LS) in a cohort of HIV-infected patients without HBV or HCV coinfection and to assess the related factors. A cross-sectional prospective study was conducted. LS was assessed by TE in 258 HIV-infected patients without HBV or HCV coinfection and with no evidence of acute hepatotoxicity or other origins of liver disease. LS values > or =7.2 kPa were considered abnormal. Multivariate analyses were performed to identify factors associated with abnormal LS. Abnormal LS was observed in 29 (11.2%) patients. A total of 18 (16.4%) patients previously treated with ddI and 11 (7.4%) of those who never received ddI had LS values > or =7.2 kPa (P=0.02). The prevalence of abnormal LS was higher in patients previously treated with abacavir than in those who had never received abacavir (15 [21.7%] versus 14 [7.4%]; P=0.001). After multivariate analyses, age (adjusted odds ratio [AOR] 1.05, 95% confidence interval [CI] 1.002-1.1; P=0.004) alcohol intake >50 g/day (AOR 7.2, 95% CI 2.6-19.7; P<0.0001), CD4(+) T-cell count <200 cells/ml (AOR 3.4, 95% CI 1.06-11.007; P=0.03), time on ddI treatment (AOR 1.31, 95% CI 1.12-1.52; P=0.001) and previous abacavir exposure (AOR 3.01, 95% CI 1.18-7.67; P=0.02) were independently associated with abnormal LS. The prevalence of abnormal LS in HIV-infected patients without HBV or HCV coinfection is substantial. Long-term exposure to ddI is a major cause of liver damage in these patients.

Diagnóstico, tratamiento y prevención de las alteraciones renales en pacientes con infección por el virus de la inmunodeficiencia humana. Recomendaciones del Grupo de Estudio del Sida/Plan Nacional sobre el Sida

The incidence of opportunistic infections and tumours in HIV-infected patients has sharply declined in the HAART era. At the same time there has been a growing increase of other diseases not directly linked to immunodeficiency. Renal diseases are an increasing cause of morbidity and mortality among HIV-infected patients. In the general population, chronic renal failure has considerable multiorgan repercussions that have particular implications in patients with HIV infection. The detection of occult or subclinical chronic kidney disease is crucial since effective measures for delaying progression exist. Furthermore, the deterioration in glomerular filtration should prompt clinicians to adjust doses of some antiretroviral agents and other drugs used for treating associated comorbidities. Suppression of viral replication, strict control of blood pressure, dyslipidemia and diabetes mellitus, and avoidance of nephrotoxic drugs in certain patients are fundamental components of programs aimed to prevent renal damage and delaying progression of chronic kidney disease in patients with HIV. Renal transplantation and dialysis have also special implications in HIV-infected patients. In this article, we summarise the updated clinical practice guidelines for the evaluation, management and prevention of renal diseases in HIV-infected patients from a panel of experts in HIV and nephrologists on behalf of the Spanish AIDS Study Group (GESIDA) and the National AIDS Plan.

Silicone in HIV-1-infected patients: a cause of misdiagnosed granulomatous disease

Granulomatous diseases are common in HIV-infected patients and are usually related to opportunistic infectious or tumoral conditions. We report three cases of uncommon granulomatous disease in HIV-infected patients who had previously received silicone and for which diagnostic investigations remained negative.

Enfermedad cardiovascular en el paciente infectado por el virus de la inmunodeficiencia humana

With the introduction of effective antiretroviral therapy (ART), cardiovascular disease has gained importance as a cause of morbidity and mortality in HIV-infected persons. Herein, we will study the risk of cardiovascular disease in HIV-infected persons compared to the non-infected population. The relative contributions regarding the host, HIV infection and antiretroviral therapy will be presented in the light of current knowledge. The absolute risk of developing cardiovascular disease in HIV-infected patients receiving antiretroviral therapy is low. However, this risk is increasing compared to the risk in uninfected persons. This fact is substantially due to a higher prevalence of underlying traditional cardiovascular risk factors that are mostly host-dependent. HIV infection may contribute both directly through immune activation and inflammation and indirectly through immunodeficiency. The type of antiretroviral treatment, also to a lesser degree than HIV infection, may also contribute through its impact on metabolic effects and also because of the changes produced in body fat parameters. Prevention of cardiovascular disease in HIV-infected patients should be standard care. The traditional risk factors should be investigated and aggressively treated whenever possible, since they play a major role in the development of cardiovascular disease. Antiretroviral therapy should be initiated earlier in patients with high cardiovascular risk. From a purely cardiovascular perspective, the benefits of ART, regardless of the drugs used, clearly outweigh any potential risk.

HIV Infection: An Independent Risk Factor of Peripheral Arterial Disease

HIV Infection: An Independent Risk Factor of Peripheral Arterial Disease

Anticoagulant therapy for nodular regenerative hyperplasia in a HIV-infected patient

BackgroundNodular regenerative hyperplasia (NRH) has been recently recognized as an emergent cause of liver disease in HIV-infected patients. NRH may cause non-cirrhotic portal hypertension with potentially severe consequences such as refractory ascites, variceal bleeding and hypersplenism. Obliteration of the small intrahepatic portal veins in association with prothrombotic disorders linked to HIV infection itself or anti-retroviral therapy seem to be the causes of NRH and thus the term HIV-associated obliterative portopathy has been proposed.Case PresentationHere we describe a case of a HIV-infected patient with biopsy-proven NRH and listed for liver transplantation (LT) because of refractory ascites and repeated upper gastrointestinal bleedings. A transjugular intrahepatic portosystemic shunt was placed as a bridge to LT and did not improve liver function. However, anticoagulant therapy with low-molecular-weight heparin (LMWH) was associated with rapid improvement in the liver condition and allowed to avoid LT in this patient.ConclusionsThus, this case underscores the relation between thrombophilia and HIV-associated NRH and emphasizes anticoagulant therapy as possible treatment.

Renal disease in AIDS: it is not always HIVAN

Human immunodeficiency virus (HIV) infection can cause a broad spectrum of clinical manifestations, ranging from an asymptomatic carrier state to severe immunodeficiency. The most common renal lesion, HIV-associated nephropathy (HIVAN), is a sclerosing glomerulopathy. However, potentially reversible causes of renal disease in HIV-infected patients should also be considered. We describe two cases of patients with acquired immune-deficiency syndrome (AIDS) who presented with rapidly progressive renal failure but were found to have reversible etiologies. The first case was found to have syphilis and the second, disseminated histoplasmosis; their renal injury resolved after initiation of a third-generation cephalosporin antibiotic and amphotericin B, respectively.

Increased prevalence of subclinical coronary atherosclerosis detected by coronary computed tomography angiography in HIV-infected men

The degree of subclinical coronary atherosclerosis in HIV-infected patients is unknown. We investigated the degree of subclinical atherosclerosis and the relationship of traditional and nontraditional risk factors to early atherosclerotic disease using coronary computed tomography angiography. Seventy-eight HIV-infected men (age 46.5 +/- 6.5 years and duration of HIV 13.5 +/- 6.1 years, CD4 T lymphocytes 523 +/- 282; 81% undetectable viral load), and 32 HIV-negative men (age 45.4 +/- 7.2 years) with similar demographic and coronary artery disease (CAD) risk factors, without history or symptoms of CAD, were prospectively recruited. 64-slice multidetector row computed tomography coronary angiography was performed to determine prevalence of coronary atherosclerosis, coronary stenosis, and quantitative plaque burden. RESULTS HIV-infected men demonstrated higher prevalence of coronary atherosclerosis than non-HIV-infected men (59 vs. 34%; P = 0.02), higher coronary plaque volume [55.9 (0-207.7); median (IQR) vs. 0 (0-80.5) microl; P = 0.02], greater number of coronary segments with plaque [1 (0-3) vs. 0 (0-1) segments; P = 0.03], and higher prevalence of Agatston calcium score more than 0 (46 vs. 25%, P = 0.04), despite similar Framingham 10-year risk for myocardial infarction, family history of CAD, and smoking status. Among HIV-infected patients, Framingham score, total cholesterol, low-density lipoprotein, CD4/CD8 ratio, and monocyte chemoattractant protein 1 were significantly associated with plaque burden. Duration of HIV infection was significantly associated with plaque volume (P = 0.002) and segments with plaque (P = 0.0009) and these relationships remained significant after adjustment for age, traditional risk factors, or duration of antiretroviral therapy. A total of 6.5% (95% confidence interval 2-15%) of our study population demonstrated angiographic evidence of obstructive CAD (>70% luminal narrowing) as compared with 0% in controls. Young, asymptomatic, HIV-infected men with long-standing HIV disease demonstrate an increased prevalence and degree of coronary atherosclerosis compared with non-HIV-infected patients. Both traditional and nontraditional risk factors contribute to atherosclerotic disease in HIV-infected patients.

Risk of cardiovascular disease in HIV-infected patients

The life expectancy of people living with HIV infection has improved dramatically since the use of highly active antiretroviral therapy (HAART). Now that patients with HIV infection are living longer, the focus of its treatment should shift to long-term management spanning decades. Diseases of ageing, including cardiovascular disease (CVD), have now become more important. The evidence of cardiovascular risk associated with HIV infection and antiretroviral therapy is explored and discussed in this article.

Regional Gene Expression of LOX-1, VCAM-1, and ICAM-1 in Aorta of HIV-1 Transgenic Rats

BackgroundIncreased prevalence of atherosclerotic cardiovascular disease in HIV-infected patients has been observed. The cause of this accelerated atherosclerosis is a matter of controversy. As clinical studies are complicated by a multiplicity of risk-factors and a low incidence of hard endpoints, studies in animal models could be attractive alternatives.Methodology/Principal FindingsWe evaluated gene expression of lectin-like oxidized-low-density-lipoprotein receptor-1 (LOX-1), vascular cell adhesion molecule-1 (VCAM-1), and intercellular adhesion molecule-1 (ICAM-1) in HIV-1 transgenic (HIV-1Tg) rats; these genes are all thought to play important roles in early atherogenesis. Furthermore, the plasma level of sICAM-1 was measured. We found that gene expressions of LOX-1 and VCAM-1 were higher in the aortic arch of HIV-1Tg rats compared to controls. Also, the level of sICAM-1 was elevated in the HIV-1Tg rats compared to controls, but the ICAM-1 gene expression profile did not show any differences between the groups.Conclusions/SignificanceHIV-1Tg rats have gene expression patterns indicating endothelial dysfunction and accelerated atherosclerosis in aorta, suggesting that HIV-infection per se may cause atherosclerosis. This transgenic rat model may be a very promising model for further studies of the pathophysiology behind HIV-associated cardiovascular disease.

P27 Prevalence and pattern of rheumatic diseases in HIV infected patients in South India

P27 Prevalence and pattern of rheumatic diseases in HIV infected patients in South India

Esophageal Variceal Bleed in a HIV Patient Secondary to Non-Cirrhotic Portal Hypertension After Didanosine Use

Purpose: We present a case of a HIV patient presenting with hematemesis secondary to esophageal varices, who was subsequently found to have noncirrhotic portal hypertension (NCPH) likely secondary to previous didanosine use. A 59 year old male with a history of HIV on ART since 1985, presented to our hospital with an episode of large volume hematemesis, and pre-syncopal symptoms. He was first diagnosed with HIV in 1985. He was initially started on monotherapy with zidovudine. In 1988, he entered a study for didanosine (ddI) and remained on this monotherapy till 1999. He then received stavudine monotherapy from 1999 until 2001, and then switched to his current therapy of abacavir, lamivudine, and efavirenz. With treatment he has had an undetectable viral load and CD4 count above 400. On presentation he had a Hct drop from 40 to 32. Emergent EGD demonstrated 3 large cords of esophageal varices with stigmata of recent bleeding. Banding ligation was performed with no further bleeding. He had no prior history of liver disease or ETOH abuse. His hepatitis serologies, BMI, LFT's, albumin, PT/INR were all normal. He had a mild thrombocytopenia. Abdominal US demonstrated patent hepatic and portal vasculature, normal appearing liver, and mild splenomegaly with small ascites. Transjugular liver biopsy was performed demonstrating a normal hepatic venous pressure gradient of 4 mmHg. Liver biopsy showed hepatocellular disarray, portal fibrosis, hepatoportal sclersosis with no steatosis, bridging fibrosis or cirrhosis. These findings are consistent with non-cirrhotic portal hypertension likely secondary from his previous prolonged exposure to didanosine. Chronic liver disease in HIV infected patients is increasing in occurrence, often secondary to co-infection with hepatitis B/C, alcohol abuse, fatty liver disease, or medication-induced hepatotoxicity. Non-cirrhotic portal hypertension can be due to portal vein thrombosis, nodular regenerative hyperplasia, incomplete septal cirrhosis, vasculitides, schistosomiasis, or idiopathic (hepatoportal sclerosis). Recent case series and case control studies have shown an association between HIV patients on ART and NCPH. Suspected causes in these patients include medication affect specifically long term ddI therapy versus direct affect from HIV. In HIV patients presenting with upper GI bleed, esophageal varices needs to be considered even in the absence of cirrhosis as NCPH is a potential complication of the ART treatment or HIV itself.