Outcomes of people living with HIV (PLWH) developing non-AIDS events (NAEs) remain poorly defined. We aimed to classify NAEs according to severity, and to describe clinical outcomes and prognostic factors after NAE occurrence using data from CoRIS, a large Spanish HIV cohort from 2004 to 2013.Prospective multicenter cohort study.Using a multistate approach we estimated 3 transition probabilities: from alive and NAE-free to alive and NAE-experienced ("NAE development"); from alive and NAE-experienced to death ("Death after NAE"); and from alive and NAE-free to death ("Death without NAE"). We analyzed the effect of different covariates, including demographic, immunologic and virologic data, on death or NAE development, based on estimates of hazard ratios (HR). We focused on the transition "Death after NAE".8,789 PLWH were followed-up until death, cohort censoring or loss to follow-up. 792 first incident NAEs occurred in 9.01% PLWH (incidence rate 28.76; 95% confidence interval [CI], 26.80-30.84, per 1000 patient-years). 112 (14.14%) NAE-experienced PLWH and 240 (2.73%) NAE-free PLWH died. Adjusted HR for the transition "Death after NAE" was 12.1 (95%CI, 4.90-29.89). There was a graded increase in the adjusted HRs for mortality according to NAE severity category: HR (95%CI), 4.02 (2.45-6.57) for intermediate-severity; and 9.85 (5.45-17.81) for serious NAEs compared to low-severity NAEs. Male sex (HR 2.04; 95% CI, 1.11-3.84), age>50 years (1.78, 1.08-2.94), hepatitis C-coinfection (2.52, 1.38-4.61), lower CD4 cell count at cohort entry (HR 2.49; 95%CI 1.20-5.14 for CD4 cell count below 200 and HR 2.16; 95%CI 1.01-4.66 for CD4 cell count between 200-350, both compared to CD4 cell count higher than 500) and concomitant CD4<200 cells/mL (2.22, 1.42-3.44) were associated with death after NAE. CD4 count and HIV-1 RNA at engagement, previous AIDS and hepatitis C-coinfection predicted mortality in NAE-free persons.NAEs, including low-severity events, increase prominently the risk for mortality in PLWH. Prognostic factors differ between NAE-experienced and NAE-free persons. These findings should be taken into account in the clinical management of PLWH developing NAEs and may permit more targeted prevention efforts.
Background Data supporting a link between body-fat distribution changes and cardiovascular disease risk in HIV- infected patients are scarce and contradictory. We evaluated endothelial dysfunction, an early event in the development of atherosclerosis, and pro- atherosclerotic plasma biomarkers in HIV-infected patients with lipodystrophy. Methods HIV-infected patients with and without lipodystrophy were prospectively enrolled. Endothelial function was measured through flow-mediated dilatation (FMD) of the brachial artery. Plasma levels of several biomarkers of inflammation, endothelial activation and coagulation associated with adipose tissue and endothelial dysfunction were determined. Results The study included 110 patients, 55 of them with lipodystrophy. FMD was significantly lower in patients with lipodystrophy than in those without lipodystrophy (median [IQR] 3.1% [0.4–8.9] versus 6.3% [3.3–10.7]; P=0.004). Patients with isolated lipoatrophy exhibited the lowest FMD (2.6% [0–6.6]; P Kruskal–Wallis =0.02). Lipodystrophy was associated with significantly higher plasma levels of interleukin 6 (IL-6) and plasminogen activator inhibitor 1 (PAI-1) and lower levels of adiponectin; severe lipodystrophy was associated with higher concentrations of vascular cell adhesion molecule 1 (sVCAM-1). There was an inverse correlation between FMD and IL-6 (Spearman's rho =-0.26; P=0.007). In a multivariate regression model with the lowest quartile of FMD as the dependent variable and lipodystrophy, traditional cardiovascular risk factors, 10-year Framingham risk score, pro- atherosclerotic biomarkers and HIV-related variables as predictors, the only independent predictor of endothelial dysfunction was lipodystrophy (odds ratio 5.22, 95% confidence interval 1.76–15.46; P=0.003). Conclusions Lipodystrophy is associated with endothelial dysfunction, independently of the presence of traditional cardiovascular risk factors. This finding and the accompanying profile of pro-atherosclerotic biomarkers support an increased cardiovascular risk in HIV-infected patients with lipodystrophy.
Both low and high ankle–brachial index are considered as indicators of systemic atherosclerosis in older HIV-negative adults. Whether those ankle–brachial index values are predictors of atherosclerosis in HIV-positive subjects remains unknown. We measured ankle–brachial index in 139 HIV-infected patients and compared the results obtained with carotid intima-media thickness, a well established marker of subclinic atherosclerosis. Ankle–brachial index was associated with carotid intima-media thickness. Patients with low ankle–brachial index, but not those with high ankle–brachial index, had high carotid intima-media thickness.
All cases of avascular necrosis of the bone (AVN) diagnosed in HIV-infected patients from 1990 to 2000 in two Spanish provinces were examined. The frequency of AVN has increased since 1996, reaching a high of 1.19 cases per 1000 HIV-infected patients in the year 2000. AVN was predominantly seen in patients with advanced HIV disease and 86% had at least one risk factor previously associated with AVN. Ninety-one percent had had previous exposure to antiretroviral drugs and 70% had been given HAART before developing AVN. Avascular necrosis of the bone (AVN), which is also referred to as osteonecrosis, is being increasingly reported in HIV-infected patients [1–8]. Whether AVN is an HIV-related complication, an adverse effect of antiretroviral therapy or is caused by another HIV-associated condition or therapy is unknown. Recent reports have associated AVN with metabolic complications of protease inhibitor (PI) therapy (i.e. hyperlipidaemia) [4,9,10] and with immunological and virological improvements resulting from highly active antiretroviral therapy (HAART) [5]. A link between AVN of the hip and the use of megestrol acetate has also been suggested [11]. Many of the previous studies on this issue have consisted of case reports or small series of cases in patients receiving HAART, and very few have provided data regarding frequency and patient characteristics. This study aims to describe the frequency and associated factors of AVN in a large Spanish cohort of HIV-infected patients before and after the HAART era. We reviewed all cases of AVN diagnosed in HIV-infected patients from 1990 to 2000 in the Valencian–Murcian HIV clinical cohort. This clinical cohort consists of clinical and demographic data from 19 HIV clinics in two provinces in south-eastern Spain. These clinics have provided medical care for a population of more than 10 000 HIV-infected patients since the beginning of the AIDS epidemic. Cases were identified from the records of HIV clinics by physicians caring for HIV-infected patients. A case was defined as having AVN when there was both a clinical and a radiographic diagnosis. A retrospective chart review was performed, and data were extracted using a standardized data collection sheet. The potential risk factors previously associated with AVN evaluated in this study included: a previous history of local trauma; the use of corticosteroids; alcohol abuse; the presence of anticardiolipin or antiphospholipid antibodies; a previous diagnosis of deep venous thrombosis or other hypercoagulable state; hyperlipaemia; and the use of megestrol acetate. To estimate trends in frequency, the annual incidence rates of AVN in AIDS patients were obtained from 1993 to 2000 using the total number of AIDS cases reported from all clinics to the Spanish National Registry of AIDS as the denominator. Incidence rates of AVN in HIV-infected patients were obtained for the years 1996, 1998, and 2000 in the Valencian community using the total number of HIV cases cared for in the clinics of this province (1996: 5705 patients; 1998: 6028 patients; 2000: 7572 patients) as the denominator. From 1990 to 2000, a total of 23 symptomatic cases of AVN were identified. There was a constant increase in the number of cases throughout the study period. Only four cases were diagnosed before 1996, nine additional cases from 1997 to 1999 and 10 cases in 2000. There was a marked increase in the annual incidence of AVN in AIDS patients since 1997 (1993: 3.7/1000 patients; 1994: 0/1000 patients; 1995: 1.6/1000 patients; 1996: 1.6/1000 patients; 1997: 4.1/1000 patients; 1998: 7.9/1000 patients; 1999: 12.9/1000 patients; 2000: 57.8/1000 patients). The frequency of AVN increased from 1.6 per 1000 AIDS patients during 1993–1996 to 14 per 1000 patients in 1997–2000 (P < 0.001 by chi-squared test). There was also a notable increase in the incidence of AVN in HIV-infected patients in the Valencian community from 0.18 per 1000 HIV-infected patients in 1996 to 1.19 per 1000 patients in 2000 (P = 0.0023 by chi-squared test). Demographic characteristics are shown in Table 1. Twenty-one of the 23 cases (91%) had had previous exposure to antiretroviral drugs. Sixteen out of 23 patients (70%) had been given HAART before developing AVN. At the time of diagnosis, 19 patients (83%) were receiving antiretroviral therapy with nucleoside analogue reverse transcriptase inhibitors, 13 (56%) were on treatment with PI, and three patients (13%) were on treatment with non-nucleoside analogue reverse transcriptase inhibitors as part of HAART regimens. Seven of the 23 patients (30%) had never received either PI or non-nucleoside analogue reverse transcriptase inhibitors before developing AVN. The median time from initiation of antiretroviral therapy to the diagnosis of AVN was 24 months (range 4 months to 8.5 years).Table 1: Demographic characteristics of 23 HIV-infected patients with avascular necrosis. Three patients (13%) had cholesterol levels higher than 240 mg/dl, and five had triglyceride levels greater than 200 mg/dl, but only one case had a cholesterol level greater than 300 mg/dl and another had a fasting triglyceride level higher than 300 mg/dl. Only two patients had clinical features consistent with lipodystrophy at diagnosis of AVN. Twenty out of 23 cases (86%) had at least one identifiable risk factor previously associated with AVN in HIV-negative individuals, and in 13 cases (57%) there were more than one of these predisposing factors (Table 1). Three out of 23 patients (14%) did not have any potential risk factor for developing AVN. All were on HAART and had a plasma HIV viral load below 500 copies/ml at diagnosis of AVN. This study confirmed that AVN is an emerging complication of HIV infection. In the year 2000, the incidence reached a high of 1.19 cases per 1000 patients, which is 29-fold higher than the population-based incidence [12]. An increasing trend in the incidence of new cases of AVN in HIV-infected patients has also been observed in some institutions in the USA [7,8], and a staggeringly high prevalence of asymptomatic AVN of the hip has recently been reported [13]. In the present study, the sharp increase in the frequency of AVN was observed since 1997, soon after PI were released in Spain and HAART became the standard of care for HIV-infected patients. However, HAART can not be the only explanation for AVN because 30% of our cases had not received HAART. Furthermore, our series do not suggest that either hyperlipidaemia or lipodystrophy are linked to AVN. In fact, only two of our patients had concurrent lipodystrophy, and although seven others had mild hypercholesterolaemia or hypertriglyceridaemia, none of them had marked hyperlipidaemia. Félix Gutiérreza Sergio Padillaa Enrique Ortegab J. Adolfo Garcíac Juan Floresd Carlos Galerae Esperanza Merinof Mar Masiáa Pablo Roigg Vicente Boixf Joaquín Portillaf José M. Cuadradog Joan Gregorih José Lopezi
Abstract Background Switching from boosted PIs to dolutegravir in people living with HIV (PLWH) with high cardiovascular risk improved plasma lipids at 48 weeks in the NEAT022 trial. Whether this strategy may have an impact on cardiovascular biomarkers is unknown. Methods We assessed 48 week changes in biomarkers associated with inflammation, endothelial dysfunction, monocyte immune activation, oxidation, insulin resistance, hypercoagulability, heart failure, myocardial injury, and glomerular and tubular kidney injury. Results Of 415 PLWH randomized in the NEAT022 study, 313 (75.4%) remained on allocated therapy and had paired samples available. Soluble CD14 (–11%, P < 0.001) and adiponectin (–11%, P < 0.001) significantly declined and high-sensitive C-reactive protein (–13%, P = 0.069) and oxidized LDL (–13%, P = 0.084) tended to decrease with dolutegravir. Switching to dolutegravir remained significantly associated with soluble CD14 and adiponectin reductions after adjustment for baseline variables. There were inverse correlations between soluble CD14 and CD4 count changes (P = 0.05), and between adiponectin and BMI changes (P < 0.001). Conclusions Switching from boosted PIs to dolutegravir in PLWH with high cardiovascular risk led to soluble CD14 and adiponectin reductions at 48 weeks. While decreasing soluble CD14 may entail favourable health effects in PLWH, adiponectin reduction may reflect less insulin sensitivity associated with weight gain.
Background: HIV-infected children have abnormal cerebral metabolites, measured by proton MR spectroscopy (1H-MRS), but how these abnormalities relate to brain function is unclear. Methods: Metabolite concentrations in five brain regions of 20 HIV-infected and 13 control children were measured, and these findings were correlated with age, log10 plasma viral load, CD4 count, and neuropsychological scores. Results: Compared with control subjects, HIV patients had decreased choline concentration [Cho] in left frontal white matter (LFW) (−12%; p = 0.04); those with high viral load (>5,000 HIV RNA copies/mL) had decreased right basal ganglia (RBG) [Cho] (−15%; p = 0.005), and [Cr] (−13%; p = 0.02). Patients with high viral load also had higher [Cho] in the midfrontal gray matter (MFG) (+25%; p = 0.002) and lower myo-inositol [Ins] in the RBG (−18%; p = 0.04) than patients with low HIV viral load. N-Acetyl aspartate concentration ([NAA]) correlated with age in right frontal white matter (RFW) (r = 0.59, p = 0.04), LFW (r = 0.66, p = 0.02), and right hippocampus (RHIP) (r = 0.69, p = 0.02) only in control subjects. In contrast, [Ins] correlated with age in both RFW and LFW (r = 0.71, p = 0.0006; r = 0.65, p = 0.006) only in the HIV patients. Log10 plasma viral load correlated positively with [Ins] in RFW (r = 0.54, p = 0.02) and [Cho] in MFG (r = 0.49, p = 0.04). Compared with control subjects, HIV patients had poorer spatial memory (p = 0.045) and delayed spatial memory correlated with [Cho] in RHIP (r = 0.68, p = 0.02). Conclusions: These data suggest that normal brain development may be affected in children infected with HIV at birth, particularly evidenced by the lack of age-related increases in the neuronal marker [NAA]. Early, aggressive treatment of infants with HIV before development of encephalopathy is warranted.
ObjectivesTo evaluate the 5 year effects of an intensive intervention versus the standard-of-care intervention on cardiovascular risk factors in HIV-infected patients on antiretroviral therapy (ART).
Se estudió la presencia de enfermedades en 34 enjambres de abejas africanizadas, recientemente establecidos en diferentes zonas de Costa Rica. De cada enjambre, se colectaron aproximadamente 100 abejas adultas de la cámara de cría (interior), en un frasco plástico de boca ancha. A cada muestra se le adicionó alcohol al 70 %, de manera que las abejas quedaran cubiertas, con la finalidad de conservarlas para su posterior análisis. Las muestras de abejas se analizaron en el Laboratorio de Patología Apícola del Centro de Investigaciones Apícolas Tropicales (CINAT-UNA), donde se realizó diagnóstico de varroosis, nosemiasis y acariosis. Con base en el estudio realizado, se debe indicar la presencia de varroosis y nosemiasis en enjambres de abejas africanizadas recién constituidos, así como la ausencia de acariosis. En el 41.0 % de las muestras positivas a Varroa, se detectó un nivel de infestación leve, con un promedio de 2.0 ± 0.05 (ácaros/100 abejas); mientras que solamente en un 6.0 % de las muestras positivas el nivel de infestación fue fuerte. Por otro lado, en el 26.0 % de las muestras positivas a Nosema spp., se determinó un nivel de infección muy leve, mientras que el 18.0 % mostró uno leve. No se detectaron niveles de infección moderados ni fuertes de Nosema spp. Por lo anterior y debido a que la mayoría de los productores captura e introduce los enjambres directamente al apiario, se recomienda cuarentenar y realizar diagnóstico de laboratorio, para conocer la situación sanitaria. Lo dicho permitirá tomar acciones inmediatas relacionadas con el control de enfermedades y, de esta manera, prevenir el contagio de colmenas sanas en el apiario.
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