The present study aims to describe the clinical and paraclinical profile of patients infected by viral hepatitis B and C and follow-up. The clinical and paraclinical data used in this description are from patients inf...The present study aims to describe the clinical and paraclinical profile of patients infected by viral hepatitis B and C and follow-up. The clinical and paraclinical data used in this description are from patients infected by viral hepatitis B and C of the HOSCO Hepato-Gastroenterological Department from May 15, 2021 to July 23, 2021. The informed consent was provided to each patient included in this study. “Univariate analyses were evaluated using Pearson’s Chi2 test” using R software version 4.0.2. During the study period, we identified 149 patients with viral hepatitis B and/or C who met our inclusion criteria. The sex ratio was 0.83 at the rate of 68 men for 81 women with the average age at 37.17 years ± 12.21 years. The most represented age group was 30 - 44 years (49.7%). The most incriminated risk factors were medical care by injection (62.58%), excision (31.90%), blood transfusion (4.29%) and scarification (1.23%). HBV infection was the majority with a frequency of 95.97%. The HBV viral load was measured in 91.95% of patients, 77.18% of whom had a detectable DNA viral load ≤ 2000 IU/mL. The clinical and biological course was good in patients after therapeutic initiation. HBV-HCV-HIV co-infection was 0.67%. Abdominal ultrasound was normal in 87.92% of patients. Fibrosis was minimal and moderate in 58.39% and 19.46% of patients. Among patients, 52.35% were on Tenofovir therapy, 2.68% on Sofosbuvir/Velpatasvir, 0.67% on ARVs and 44.29% did not require treatment. Viral hepatitis B and C are common, and both affect sex. Thus, new screening strategies need to be implemented to improve the diagnosis of hepatitis B and C. Effective strategies against viral hepatitis B and C must be developed, subsequently.展开更多
Knowledge of the clinical and biological profile of patients infected with HIV and hepatitis B and/or C is essential in order to identify and implement effective management strategies. Methods: This was a retrospectiv...Knowledge of the clinical and biological profile of patients infected with HIV and hepatitis B and/or C is essential in order to identify and implement effective management strategies. Methods: This was a retrospective descriptive study from January 01, 2016 to June 01, 2021. Adult patients aged at least 18 years infected with HIV type 1 and/or 2, na?ve to ARV treatment. Univariate analyses were assessed using Pearson’s Chi2 test. The Student Newman test was used for comparison between groups using R software version 4.0.2. Objective: To draw up the epidemiological, clinical, paraclinical and evolutionary profiles of HIV-treated-patients in relation to HIV/HBV and HIV/HCV co-infections in order to allow the identification and the implementation of effective management strategies. Results: Of the 379 patients included 280 (73.88%) were women. At treatment initiation, the mean age was 40.14 ± 11.84 years. The majority of patients consulted at WHO stage III (51.45%). Clinical suspicion was the most frequent screening circumstance (51.71%). The pathologies frequently reported at the first consultation were diarrhea (28%) and shingles (16%). Body mass index was normal in 50.5% of patients. HIV1 infection was the majority (91.03%). A total of 270 had a CD4 count at treatment initiation. The mean CD4 cell count was 304.17 ± 242.06 cells/μL, and 116 (42.59%) of them had a CD4 ≤ 200 cells/μL. Viral load at treatment initiation was documented in 62 patients (16.35%) and 70.97% of them had a detectable viral load (greater than 1000 copies/mL). The clinical and biological evolution was relatively good in patients after therapeutic initiation. HIV-HBV co-infection was 24.11% and HIV-HCV co-infection was 2.26%. The mortality rate was 3.69%. Conclusion: These results reflect a significant delay in HIV infection diagnosis. Furthermore, hepatitis B and/or C is co-infections that increasingly affect people living with HIV. It also appears that COVID 19 disease has had a strong impact on patient management. Thus, new screen展开更多
Background: The World Health Organization (WHO) has set a goal to eradicate or at least significantly reduce the prevalence the human immunodeficiency virus (HIV), hepatitis B Virus (HBV) and Hepatitis C Virus (HCV) b...Background: The World Health Organization (WHO) has set a goal to eradicate or at least significantly reduce the prevalence the human immunodeficiency virus (HIV), hepatitis B Virus (HBV) and Hepatitis C Virus (HCV) by 2030. The main objective was to provide an evolving overview of the prevalence of HIV, HBV and HCV infection between 2003 and 2022 in Burkina Faso. Methods: It was a retrospective cross-sectional study based on data from 2003 to 2022. The data were collected using information available in the databases of the HOSCO and CERBA laboratories and included all individuals who underwent HIV and/or HBV and/or HCV testing. Data analysis was performed using SPSS version 20.0, EpiInfo 7, and R version 4.1.0. Results were considered statistically significant if p Results: The study recorded 7432 samples and the mean age of the subjects was 27.98 ± 8.50 years. During this period, the respective prevalence of HIV, HBV, and HCV were 4.66% (346/7432), 8.77% (582/6636) and 5.54% (322/5816). However, from 2003 to 2022, there was a significant decrease (P y=−1.75x+12.59;y=−0.24x+10.01and y=−0.11x+6.02, with “y” corresponding to prevalence and “x” to the years. Conclusion: Burkina Faso needs to rigorously apply prevention and control strategies recommended by the WHO by 2030.展开更多
Hepatocellular carcinoma(HCC)represents a global health problem.Infections with hepatitis B or C virus,non-alcoholic steatohepatitis disease,alcohol abuse,or dietary exposure to aflatoxin are the major risk factors to...Hepatocellular carcinoma(HCC)represents a global health problem.Infections with hepatitis B or C virus,non-alcoholic steatohepatitis disease,alcohol abuse,or dietary exposure to aflatoxin are the major risk factors to the development of this tumor.Regardless of the carcinogenic insult,HCC usually develops in a context of cirrhosis due to chronic inflammation and advanced fibrosis.Galectins are a family of evolutionarily-conserved proteins defined by at least one carbohydrate recognition domain with affinity forβ-galactosides and conserved sequence motifs.Here,we summarize the current literature implicating galectins in the pathogenesis of HCC.Expression of"proto-type"galectin-1,"chimera-type"galectin-3 and"tandem repeat-type"galectin-4 is up-regulated in HCC cells compared to their normal counterparts.On the other hand,the"tandemrepeat-type"lectins galectin-8 and galectin-9 are downregulated in tumor hepatocytes.The abnormal expression of these galectins correlates with tumor growth,HCC cell migration and invasion,tumor aggressiveness,metastasis,postoperative recurrence and poor prognosis.Moreover,these galectins have important roles in other pathological conditions of the liver,where chronic inflammation and/or fibrosis take place.Galectin-based therapies have been proposed to attenuate liver pathologies.Further functional studies are required to delineate the precise molecular mechanisms through which galectins contribute to HCC.展开更多
AIM:To evaluate steatosis,insulin resistance(IR)and patatin-like phospholipase domain-containing 3(PNPLA3) and their relation to disease progression in hepatitis B and C viruses(HCV-HBV) coinfected patients.METHODS:Th...AIM:To evaluate steatosis,insulin resistance(IR)and patatin-like phospholipase domain-containing 3(PNPLA3) and their relation to disease progression in hepatitis B and C viruses(HCV-HBV) coinfected patients.METHODS:Three hundred and thirty patients with biopsy proven chronic hepatitis were enrolled:66 had HBV-HCV,66 HBV and 198 HCV infection.Prevalence of steatosis,IR and PNPLA3 polymorphisms and their relation to anthropometric,biochemical,virological and histological parameters were evaluated.RESULTS:Prevalence of steatosis in group HBV-HCV was similar to that in HCV(47.0% vs 49.5%,respec-tively);group HBV showed the lowest steatosis(33.3%).Group HBV-HCV had a lesser degree of steatosis than HCV(P = 0.016),lower HCV RNA levels(P = 0.025) and lower prevalence and degree of IR(P = 0.01).PNPLA3 polymorphisms were associated with steatosis.Group HBV-HCV showed higher levels of liver fibrosis than group HCV(P = 0.001),but similar to that ob-served in HBV group.In HBV-HCV group,liver fibrosis was not associated with steatosis,IR or PNPLA3.HBV infection was the independent predictor of advanced liver fibrosis.CONCLUSION:HBV-HCV co-infected patients have lower degree of hepatic steatosis,IR and HCV RNA than HCV mono-infected;co-infected patients showed a more rapid liver fibrosis progression that seems to be due to the double infection and/or HBV dominance.展开更多
目的:研究肝细胞中乙型肝炎病毒(hepatitis B virus,HBV)复制对分化抑制因子(inhibitor of differentiation,Id)家族表达的影响。方法:利用q RT-PCR、Western blot检测分析Id家族在HBV瞬时或稳定复制的肝癌细胞中表达水平的变化,并在HB...目的:研究肝细胞中乙型肝炎病毒(hepatitis B virus,HBV)复制对分化抑制因子(inhibitor of differentiation,Id)家族表达的影响。方法:利用q RT-PCR、Western blot检测分析Id家族在HBV瞬时或稳定复制的肝癌细胞中表达水平的变化,并在HBV复制质粒PCH9-HBV1.1转染的正常肝细胞和HBV转基因小鼠肝组织细胞模型中进一步验证。将乙型肝炎病毒S蛋白(hepatitis B virus S protein,HBs)、乙型肝炎病毒核心蛋白(hepatitis B virus core protein,HBc)、乙型肝炎病毒DNA聚合酶(hepatitis B virus DNA polymerase,HBp)、乙型肝炎病毒X蛋白(hepatitis B virus X protein,HBx)的过表达质粒转染HepG2细胞,检测各组与载体对照组细胞中Id家族表达水平的变化,分析比较乙肝病毒编码的4种蛋白对Id家族的调控作用。利用荧光素酶报告基因检测病毒各组分蛋白对Id蛋白启动子活性的影响。结果:瞬时转染HBV表达质粒的HepG2细胞较对照组细胞,Id1、Id3的mRNA和蛋白表达水平均降低(mRNA:t=3.952、3.189,P=0.017、0.033;蛋白:t=10.532、4.155,P=0.000、0.014);HepG2.2.15中Id1、Id3 mRNA和蛋白的表达水平较HepG2对照组均下降(m RNA:t=5.553、7.211,P=0.005、0.002;蛋白:t=4.193、3.849,P=0.014、0.018);HepAD38(Tet-)中Id1、Id3蛋白的表达量较HepAD38(Tet+)组均降低(t=3.052、3.712,P=0.038、0.021)。同时,HBV的复制可以抑制LO2细胞及小鼠肝组织中Id1、Id3的表达(mRNA:t=14.564、3.281、3.489、3.495,P=0.000、0.030、0.025、0.025;蛋白:t=5.651、5.336、4.948、5.149,P=0.005、0.006、0.008、0.007)。转染HBV病毒各编码蛋白质粒的HepG2细胞中,HBc组Id1、Id3较载体对照组的mRNA表达水平降低最明显(77.7%、76.2%,F=9.945、37.528,t=6.481、10.915,P=0.000、0.000),Western blot结果显示HBx组Id1、Id3蛋白表达量下降最明显(86.2%、68.4%,F=38.225、7.159,t=12.550、5.295,P=0.000、0.001)。双荧光素酶报告基因检测结果表明,HBc组Id1、Id3启动子活性较对照组降幅最大(62.2%、56.3%,F=16展开更多
文摘The present study aims to describe the clinical and paraclinical profile of patients infected by viral hepatitis B and C and follow-up. The clinical and paraclinical data used in this description are from patients infected by viral hepatitis B and C of the HOSCO Hepato-Gastroenterological Department from May 15, 2021 to July 23, 2021. The informed consent was provided to each patient included in this study. “Univariate analyses were evaluated using Pearson’s Chi2 test” using R software version 4.0.2. During the study period, we identified 149 patients with viral hepatitis B and/or C who met our inclusion criteria. The sex ratio was 0.83 at the rate of 68 men for 81 women with the average age at 37.17 years ± 12.21 years. The most represented age group was 30 - 44 years (49.7%). The most incriminated risk factors were medical care by injection (62.58%), excision (31.90%), blood transfusion (4.29%) and scarification (1.23%). HBV infection was the majority with a frequency of 95.97%. The HBV viral load was measured in 91.95% of patients, 77.18% of whom had a detectable DNA viral load ≤ 2000 IU/mL. The clinical and biological course was good in patients after therapeutic initiation. HBV-HCV-HIV co-infection was 0.67%. Abdominal ultrasound was normal in 87.92% of patients. Fibrosis was minimal and moderate in 58.39% and 19.46% of patients. Among patients, 52.35% were on Tenofovir therapy, 2.68% on Sofosbuvir/Velpatasvir, 0.67% on ARVs and 44.29% did not require treatment. Viral hepatitis B and C are common, and both affect sex. Thus, new screening strategies need to be implemented to improve the diagnosis of hepatitis B and C. Effective strategies against viral hepatitis B and C must be developed, subsequently.
文摘Knowledge of the clinical and biological profile of patients infected with HIV and hepatitis B and/or C is essential in order to identify and implement effective management strategies. Methods: This was a retrospective descriptive study from January 01, 2016 to June 01, 2021. Adult patients aged at least 18 years infected with HIV type 1 and/or 2, na?ve to ARV treatment. Univariate analyses were assessed using Pearson’s Chi2 test. The Student Newman test was used for comparison between groups using R software version 4.0.2. Objective: To draw up the epidemiological, clinical, paraclinical and evolutionary profiles of HIV-treated-patients in relation to HIV/HBV and HIV/HCV co-infections in order to allow the identification and the implementation of effective management strategies. Results: Of the 379 patients included 280 (73.88%) were women. At treatment initiation, the mean age was 40.14 ± 11.84 years. The majority of patients consulted at WHO stage III (51.45%). Clinical suspicion was the most frequent screening circumstance (51.71%). The pathologies frequently reported at the first consultation were diarrhea (28%) and shingles (16%). Body mass index was normal in 50.5% of patients. HIV1 infection was the majority (91.03%). A total of 270 had a CD4 count at treatment initiation. The mean CD4 cell count was 304.17 ± 242.06 cells/μL, and 116 (42.59%) of them had a CD4 ≤ 200 cells/μL. Viral load at treatment initiation was documented in 62 patients (16.35%) and 70.97% of them had a detectable viral load (greater than 1000 copies/mL). The clinical and biological evolution was relatively good in patients after therapeutic initiation. HIV-HBV co-infection was 24.11% and HIV-HCV co-infection was 2.26%. The mortality rate was 3.69%. Conclusion: These results reflect a significant delay in HIV infection diagnosis. Furthermore, hepatitis B and/or C is co-infections that increasingly affect people living with HIV. It also appears that COVID 19 disease has had a strong impact on patient management. Thus, new screen
文摘Background: The World Health Organization (WHO) has set a goal to eradicate or at least significantly reduce the prevalence the human immunodeficiency virus (HIV), hepatitis B Virus (HBV) and Hepatitis C Virus (HCV) by 2030. The main objective was to provide an evolving overview of the prevalence of HIV, HBV and HCV infection between 2003 and 2022 in Burkina Faso. Methods: It was a retrospective cross-sectional study based on data from 2003 to 2022. The data were collected using information available in the databases of the HOSCO and CERBA laboratories and included all individuals who underwent HIV and/or HBV and/or HCV testing. Data analysis was performed using SPSS version 20.0, EpiInfo 7, and R version 4.1.0. Results were considered statistically significant if p Results: The study recorded 7432 samples and the mean age of the subjects was 27.98 ± 8.50 years. During this period, the respective prevalence of HIV, HBV, and HCV were 4.66% (346/7432), 8.77% (582/6636) and 5.54% (322/5816). However, from 2003 to 2022, there was a significant decrease (P y=−1.75x+12.59;y=−0.24x+10.01and y=−0.11x+6.02, with “y” corresponding to prevalence and “x” to the years. Conclusion: Burkina Faso needs to rigorously apply prevention and control strategies recommended by the WHO by 2030.
文摘Hepatocellular carcinoma(HCC)represents a global health problem.Infections with hepatitis B or C virus,non-alcoholic steatohepatitis disease,alcohol abuse,or dietary exposure to aflatoxin are the major risk factors to the development of this tumor.Regardless of the carcinogenic insult,HCC usually develops in a context of cirrhosis due to chronic inflammation and advanced fibrosis.Galectins are a family of evolutionarily-conserved proteins defined by at least one carbohydrate recognition domain with affinity forβ-galactosides and conserved sequence motifs.Here,we summarize the current literature implicating galectins in the pathogenesis of HCC.Expression of"proto-type"galectin-1,"chimera-type"galectin-3 and"tandem repeat-type"galectin-4 is up-regulated in HCC cells compared to their normal counterparts.On the other hand,the"tandemrepeat-type"lectins galectin-8 and galectin-9 are downregulated in tumor hepatocytes.The abnormal expression of these galectins correlates with tumor growth,HCC cell migration and invasion,tumor aggressiveness,metastasis,postoperative recurrence and poor prognosis.Moreover,these galectins have important roles in other pathological conditions of the liver,where chronic inflammation and/or fibrosis take place.Galectin-based therapies have been proposed to attenuate liver pathologies.Further functional studies are required to delineate the precise molecular mechanisms through which galectins contribute to HCC.
文摘AIM:To evaluate steatosis,insulin resistance(IR)and patatin-like phospholipase domain-containing 3(PNPLA3) and their relation to disease progression in hepatitis B and C viruses(HCV-HBV) coinfected patients.METHODS:Three hundred and thirty patients with biopsy proven chronic hepatitis were enrolled:66 had HBV-HCV,66 HBV and 198 HCV infection.Prevalence of steatosis,IR and PNPLA3 polymorphisms and their relation to anthropometric,biochemical,virological and histological parameters were evaluated.RESULTS:Prevalence of steatosis in group HBV-HCV was similar to that in HCV(47.0% vs 49.5%,respec-tively);group HBV showed the lowest steatosis(33.3%).Group HBV-HCV had a lesser degree of steatosis than HCV(P = 0.016),lower HCV RNA levels(P = 0.025) and lower prevalence and degree of IR(P = 0.01).PNPLA3 polymorphisms were associated with steatosis.Group HBV-HCV showed higher levels of liver fibrosis than group HCV(P = 0.001),but similar to that ob-served in HBV group.In HBV-HCV group,liver fibrosis was not associated with steatosis,IR or PNPLA3.HBV infection was the independent predictor of advanced liver fibrosis.CONCLUSION:HBV-HCV co-infected patients have lower degree of hepatic steatosis,IR and HCV RNA than HCV mono-infected;co-infected patients showed a more rapid liver fibrosis progression that seems to be due to the double infection and/or HBV dominance.
文摘目的:研究肝细胞中乙型肝炎病毒(hepatitis B virus,HBV)复制对分化抑制因子(inhibitor of differentiation,Id)家族表达的影响。方法:利用q RT-PCR、Western blot检测分析Id家族在HBV瞬时或稳定复制的肝癌细胞中表达水平的变化,并在HBV复制质粒PCH9-HBV1.1转染的正常肝细胞和HBV转基因小鼠肝组织细胞模型中进一步验证。将乙型肝炎病毒S蛋白(hepatitis B virus S protein,HBs)、乙型肝炎病毒核心蛋白(hepatitis B virus core protein,HBc)、乙型肝炎病毒DNA聚合酶(hepatitis B virus DNA polymerase,HBp)、乙型肝炎病毒X蛋白(hepatitis B virus X protein,HBx)的过表达质粒转染HepG2细胞,检测各组与载体对照组细胞中Id家族表达水平的变化,分析比较乙肝病毒编码的4种蛋白对Id家族的调控作用。利用荧光素酶报告基因检测病毒各组分蛋白对Id蛋白启动子活性的影响。结果:瞬时转染HBV表达质粒的HepG2细胞较对照组细胞,Id1、Id3的mRNA和蛋白表达水平均降低(mRNA:t=3.952、3.189,P=0.017、0.033;蛋白:t=10.532、4.155,P=0.000、0.014);HepG2.2.15中Id1、Id3 mRNA和蛋白的表达水平较HepG2对照组均下降(m RNA:t=5.553、7.211,P=0.005、0.002;蛋白:t=4.193、3.849,P=0.014、0.018);HepAD38(Tet-)中Id1、Id3蛋白的表达量较HepAD38(Tet+)组均降低(t=3.052、3.712,P=0.038、0.021)。同时,HBV的复制可以抑制LO2细胞及小鼠肝组织中Id1、Id3的表达(mRNA:t=14.564、3.281、3.489、3.495,P=0.000、0.030、0.025、0.025;蛋白:t=5.651、5.336、4.948、5.149,P=0.005、0.006、0.008、0.007)。转染HBV病毒各编码蛋白质粒的HepG2细胞中,HBc组Id1、Id3较载体对照组的mRNA表达水平降低最明显(77.7%、76.2%,F=9.945、37.528,t=6.481、10.915,P=0.000、0.000),Western blot结果显示HBx组Id1、Id3蛋白表达量下降最明显(86.2%、68.4%,F=38.225、7.159,t=12.550、5.295,P=0.000、0.001)。双荧光素酶报告基因检测结果表明,HBc组Id1、Id3启动子活性较对照组降幅最大(62.2%、56.3%,F=16
