Project description:BackgroundThough the initiation of Highly Active Antiretroviral Therapy (HAART) has led to decreased HIV/AIDS related mortality, the regimen has been reported to be associated with lipid toxicities. Baseline data on such disturbances are required to induce countrywide interventional HIV/AIDS programs. The aim of this study was to determine the frequency and risks of dyslipidemia in HIV patients on HAART medication in Eritrea.MethodsA cross sectional study was conducted on HIV/AIDS patients in two national referral hospitals in Asmara, Eritrea. A structured questionnaire was used to collect demographic data and blood sample was taken for analyses of lipid profile tests. Data was analyzed using chi-square test, Post Hoc and logistic regression in SPSS software.ResultsThe study included 382 participants of whom 256(67%) were females. Their median age, CD4+ T cell count (cell/microliter) and duration of HAART (years) was 45(IQR: 38-51), 434(IQR: 294-583) & 5(IQR: 3-5) respectively. The prevalence of dyslipidemia was 331(86.6%). Increased Low Density Lipoprotein-C (LDL-C) 213(55.8%) was the predominant abnormality. Abacavir was significantly related with highest means of triglycerides (TG) (228.17 ± 193.81) and lowest means of High Density Lipoprotein (HDL-C) (46.94 ± 12.02). Females had substantially higher proportions of TG (aOR = 2.89, 95% CI: 1.65-5.05) and TC/HDL ratio (aOR = 2.33, 95% CI: 1.40-3.87) and low HDL-C (aOR = 2.16, 95% CI: 1.34-3.48). Increased age was related with increased pro-atherogenic lipid parameters. High LDL-C was more infrequent in non-smokers (aOR = 0.028, 95% CI: 0.12-0.69).ConclusionThe study showed a high prevalence of dyslipidemia in HIV-patients receiving HAART in Eritrea. Sex, age and smoking practice were among key factors associated with dyslipidemia. The necessity to assess lipid profiles and other cardiovascular risk factors before initiation of HAART treatment and continuous monitoring during therapy is mandatory.
Project description:This study evaluated the impact of 9 single nucleotide polymorphisms (SNPs) in 6 candidate genes (APOB, APOA5, APOE, APOC3, SCAP, and LDLR) over dyslipidemia in HIV-infected patients on stable antiretroviral therapy (ART) with undetectable viral loads. Blood samples were collected from 614 patients at reference services in the cities of Porto Alegre, Pelotas, and Rio Grande in Brazil. The SNPs were genotyped by conventional polymerase chain reaction (PCR) and real-time PCR. The prevalence of dyslipidemia was particularly high among the protease inhibitors-treated patients (79%). APOE (rs429358 and rs7412) genotypes and APOA5 -1131T>C (rs662799) were associated with plasma triglycerides (TG) and low-density-lipoprotein cholesterol levels (LDL-C). The APOA5 -1131T>C (rs662799) and SCAP 2386A>G (rs12487736) polymorphisms were significantly associated with high-density-lipoprotein cholesterol levels. The mean values of the total cholesterol and LDL-C levels were associated with both the APOB SP Ins/Del (rs17240441) and APOB XbaI (rs693) polymorphisms. In conclusion, our data support the importance of genetic factors in the determination of lipid levels in HIV-infected individuals. Due to the relatively high number of carriers of these risk variants, studies to verify treatment implications of genotyping before HAART initiation may be advisable to guide the selection of an appropriate antiretroviral therapy regimen.
Project description:BackgroundDiabetes mellitus (DM) is a major and increasing public health problem that may be underdiagnosed and undertreated among persons living with HIV (PLWH).ObjectiveTo describe the diagnosis, treatment and follow-up of DM among PLWH.MethodsThis study was performed inside a monocentric cohort of 1494 PLWH. DM was defined as having a FG ≥126 mg/dL twice or a HbA1c ≥6.5%, or a history of diabetes, or receiving antidiabetic treatment. The first visit mentioning a diagnosis of DM was considered as the baseline visit. Chi-Square or Fisher exact test were used to examine the association between categorical variables and DM, Wilcoxon or Student t-test were used for continuous variables.Results156 PLWH with DM were included. Compared to non-diabetic participants, they were more likely to be native of Sub Saharan Africa (31.6% vs. 22.4%, p = 0.027) and older (54.6 vs. 49.9 years, p<0.001), to have a higher BMI (> 25 for 46.1% vs. 35.3%, p = 0.020) and a poorer control of HIV (HIV RNA<50 copies/mL: 80.1% vs. 89.5%, p<0.001). The diagnosis of DM was missed in 37.8% of PLWH, and 47.2% of PLWH treated for DM did not reach a HbA1c<7%. PLWH with DM were more frequently on antihypertensive and/or lipid-lowering medications: 94.2% had a LDL-cholesterol <70 mg/dL and 60.9% had a blood pressure <140/90 mmHg.ConclusionIn a setting of HIV-control, HIV care providers should focus on metabolic issues. The management of DM and associated risk factors is mandatory to prevent cardiovascular disease in PLWH.
Project description:Type 2 diabetes mellitus (T2DM) is closely related to hepatic steatosis and fibrosis. The aim of this study was to analyze the occurrence of hepatic steatosis and fibrosis in patients with T2DM and to explore the risk factors.A total of 629 patients with T2DM were enrolled. Liver stiffness value (LSV) and controlled attenuation parameters (CAP) were measured using Fibroscan. Liver fibrosis was diagnosed when LSV was greater than 7.4?kPa, and advanced liver fibrosis was diagnosed when LSV was greater than 10.6?kPa. Hepatic steatosis diagnosis was made when CAP value was greater than 238?dB/m. Demographic information, physical examination data, and laboratory tests results were collected. The 629 patients were classified into 2 groups by the liver fibrosis and liver steatosis, and then the difference was analyzed.Among patients enrolled, 231 patients were diagnosed as liver fibrosis. The age of the patients in the fibrosis group was significantly greater than that in the non-fibrosis group, and similar trends were observed in the waist-hip ratio (WHR), systolic blood pressure, and diastolic blood pressure. The proportion of smoking and alcoholic consumption was significantly lower in patients with non-fibrosis group. A total of 426 patients were diagnosed with liver steatosis. Body mass index (BMI), WHR, systolic blood pressure, and diastolic blood pressure in patients with steatosis were significantly higher than those in non-steatosis group. We observed that the LSV (P?=?.042) and CAP value (P?<?.001) are positively correlated with metabolic syndrome components in T2DM patients. Older age (OR?=?1.099, P?=?.001), high BMI (OR?=?1.088, P?=?.003), low platelet level (OR?=?0.996, P?=?.014), and smoking (OR?=?1.653, P?=?.013) were independent risk factors of liver fibrosis among T2DM patients. High BMI (OR?=?1.369, P?<?.001), high diastolic blood pressure (OR?=?1.048, P?<?.001), and high gamma glutamyl transpeptidase (OR?=?1.018, P?=?.009) were independent risk factors for liver steatosis among T2DM patients.This study suggested risk factors screening of liver fibrosis and steatosis. Timely intervention should be taken into consideration among high risk patients to prevent progress liver diseases.
Project description:We evaluated longitudinal changes in viral replication and emergence of viral variants in the context of T cell homeostasis and gene expression in GALT of three HIV-positive patients who initiated HAART during primary HIV infection but opted to interrupt therapy thereafter. Longitudinal viral sequence analysis revealed that a stable proviral reservoir was established in GALT during primary HIV infection that persisted through early HAART and post-therapy interruption. Proviral variants in GALT and peripheral blood mononuclear cells (PBMCs) displayed low levels of genomic diversity at all times. A rapid increase in viral loads with a modest decline of CD4 T cells in peripheral blood was observed, while gut mucosal CD4 T cell loss was severe following HAART interruption. This was accompanied by increased mucosal gene expression regulating interferon (IFN)-mediated antiviral responses and immune activation, a profile similar to those found in HAART-naive HIV-infected patients.
Project description:BackgroundChronic inflammation has been associated with insulin resistance and related metabolic dysregulation, including type 2 diabetes mellitus (T2DM). Several non modifiable (i.e. genetic predisposition) and modifiable (i.e. sedentary lifestyle, energy-dense food) risk factors were suggested to explain the mechanisms involved in the development of inflammation, but are difficult to assess in clinical routine. The present study aimed to identify easy to asses clinical and biological risk factors associated with inflammation in patients with T2DM.MethodsOne hundred nine patients (51 men, 58 women), 28-60 years old, from seven primary healthcare centers in Gaza City, Palestine, took part to the cross-sectional study (November 2013-May 2014). Study participants had T2DM with no history of inflammatory diseases, cardiovascular diseases, medication and/or any health condition that might affect the inflammatory markers, interleukin 6 (IL-6) and C-reactive protein (CRP). Inflammation was defined for IL-6 ≥ 2 pg/mL and CRP ≥ 6 mg/L. Multivariable logistic regressions were used to identify the relationship between inflammation and clinical and biological risk factors.ResultsAfter adjustment for age and gender, inflammation seems to increase with increased body mass index (BMI) (OR: 1.427 [1.055-1.931]), increased fasting blood glucose (OR: 1.029 [1.007-1.052]) and decreased adiponectin values (OR: 0.571 [0.361-0.903]). There were also significant relationships between inflammation and BMI (OR: 1.432 [1.042-1.968]), fasting blood glucose (OR: 1.029 [1.006-1.052]) and adiponectin (OR: 0.569 [0.359-0.902]), after adjustment for smoking habits and physical activity.ConclusionManaging obesity and associated complications (i.e. hyperglycemia, high adiponectin levels) might help decreasing inflammation in individuals with T2DM.
Project description:Analysis of peripheral blood mononuclear cells (PBMCs) taken from 24 HIV-infected male participants before the start of highly active antiretroviral therapy (HAART). Results identify biomarkers for the identification of HIV-infected participants that progress to good versus poor CD4+ T cell recovery after 48 weeks of HAART.
Project description:To investigate the timing, incidence, clinical presentation, pharmacokinetics and pharmacogenetic predictors for antiretroviral and anti-tuberculosis drug induced liver injury (DILI) in HIV patients with or without TB co-infection.A total of 473 treatment naïve HIV patients (253 HIV only and 220 with HIV-TB co-infection) were enrolled prospectively. Plasma efavirenz concentration and CYP2B6*6, CYP3A5*3, *6 and *7, ABCB1 3435C/T and SLCO1B1 genotypes were determined. Demographic, clinical and laboratory data were collected at baseline and up to 48 weeks of antiretroviral therapy. DILI case definition was according to Council for International Organizations of Medical Sciences (CIOMS). Incidence of DILI and identification of predictors was evaluated using Cox Proportional Hazards Model. The overall incidence of DILI was 7.8% (8.3 per 1000 person-week), being non-significantly higher among patients receiving concomitant anti-TB and HAART (10.0%, 10.7 per 1000 person-week) than those receiving HAART alone (5.9%, 6.3 per 1000 person-week). Frequency of CYP2B6*6 allele (p = 0.03) and CYP2B6*6/*6 genotype (p = 0.06) was significantly higher in patients with DILI than those without. Multivariate cox regression model indicated that CYP2B6*6/*6 genotype and anti-HCV IgG antibody positive as significant predictors of DILI. Median time to DILI was 2 weeks after HAART initiation and no DILI onset was observed after 12 weeks. No severe DILI was seen and the gain in CD4 was similar in patients with or without DILI.Antiretroviral and anti-tuberculosis DILI does occur in our setting, presenting early following HAART initiation. DILI seen is mild, transient and may not require treatment interruption. There is good tolerance to HAART and anti-TB with similar immunological outcomes. Genetic make-up mainly CYP2B6 genotype influences the development of efavirenz based HAART liver injury in Tanzanians.
Project description:ObjectiveThe aim of this study was to determine the prevalence of diabetes mellitus and its associated factors among human immunodeficiency virus-infected patients on anti-retroviral therapy in Northeast Ethiopia.ResultsA facility based cross-sectional study was conducted among 408 HIV-infected adults (≥ 18 years old) attending an ART clinic in Northeast Ethiopia from January to March 30, 2018. The mean (± SD) age of studied patients was 37 ± 10.3 years, and 273 (66.9%) were female. Of the total participants, 36 (8.8%, 95% CI 6.4% to 11.8%) had diabetes and 61 (15.0%, 95% CI 11.5% to 18.6%) had impaired fasting glucose level (111-125 mg/dl). Only fourteen (3.4%) participants knew their diabetes status during data collection. In the multivariate analysis, older age (age > 45 years; AOR = 3.51, 95% CI 1.52-8.10, P = 0.003), a family history of diabetes (AOR = 6.46, 95% CI 3.36-21.29, P < 0.001), duration of ART (AOR = 2.67, 95% CI 1.16-6.17, P = 0.021), and hypertension (AOR = 2.62, 95% CI 1.20-5.72, P = 0.016) were independently associated with increased odds of diabetes. These results highlight the need for regular diabetes screening among HIV-infected patients on ART in order to prevent or reduce disease-related outcomes of these patients in this study setting.
Project description:We evaluated longitudinal changes in viral replication and emergence of viral variants in the context of T cell homeostasis and gene expression in GALT of three HIV-positive patients who initiated HAART during primary HIV infection but opted to interrupt therapy thereafter. Longitudinal viral sequence analysis revealed that a stable proviral reservoir was established in GALT during primary HIV infection that persisted through early HAART and post-therapy interruption. Proviral variants in GALT and peripheral blood mononuclear cells (PBMCs) displayed low levels of genomic diversity at all times. A rapid increase in viral loads with a modest decline of CD4 T cells in peripheral blood was observed, while gut mucosal CD4 T cell loss was severe following HAART interruption. This was accompanied by increased mucosal gene expression regulating interferon (IFN)-mediated antiviral responses and immune activation, a profile similar to those found in HAART-naive HIV-infected patients. Gut mucosal responses to HAART interruption were evaluated with Affymetrix arrays