BACKGROUND Obesity and diabetes are associated with high levels of oxidative stress.In Romanian patients with obesity and(or)diabetes,this association has not been sufficiently explored.AIM To evaluate oxidative stres...BACKGROUND Obesity and diabetes are associated with high levels of oxidative stress.In Romanian patients with obesity and(or)diabetes,this association has not been sufficiently explored.AIM To evaluate oxidative stress in obese and(or)diabetic subjects and to investigate the possible correlations between oxidative stress and anthropometric/biochemical parameters.METHODS Oxidative stress was evaluated from a single drop of capillary blood.Reactive oxygen species(ROS)were evaluated using the free oxygen radical test(FORT).The free oxygen radical defence(FORD)assay was used to measure antioxidant levels.RESULTS FORT levels were higher in obese subjects(3.04±0.36 mmol/L H2O2)vs controls(2.03±0.14 mmol/L H2O2)(P<0.0001).FORD levels were lower in obese subjects(1.27±0.13 mmol/L Trolox)vs controls(1.87±1.20 mmol/L Trolox)(P=0.0072).Obese diabetic subjects had higher FORT values(3.16±0.39 mmol/L H2O2)vs non-diabetic counterparts(2.99±0.33 mmol/L H2O2)(P=0.0233).In obese subjects,FORT values correlated positively with body mass index(BMI)(r=0.48,P=0.0000),waist circumference(WC)(r=0.31,P=0.0018),fasting plasma glucose(FPG)(r=0.31,P=0.0017),total cholesterol(TC)(r=0.27,P=0.0068)and uric acid(r=0.36,P=0.0001).FORD values correlated negatively with BMI(r=-0.43,P=0.00001),WC(r=-0.28,P=0.0049),FPG(r=-0.25,P=0.0130),TC(r=-0.23,P=0.0198)and uric acid(r=-0.35,P=0.0002).In obese diabetic subjects,FORT values correlated positively with BMI(r=0.49,P=0.0034)and TC(r=0.54,P=0.0217).FORD values were negatively associated with BMI(r=-0.54,P=0.0217)and TC(r=-0.58,P=0.0121).CONCLUSION Oxidative stress levels,as measured by the FORT and FORD assays,were higher in obese subjects vs controls.ROS levels were elevated in diabetic obese patients vs obese non-diabetic patients and controls.展开更多
Myeloproliferative neoplasms(MPNs)are defined as clonal disorders of the hematopoietic stem cell in which an exaggerated production of terminally differentiated myeloid cells occurs.Classical,Philadelphia-negative MPN...Myeloproliferative neoplasms(MPNs)are defined as clonal disorders of the hematopoietic stem cell in which an exaggerated production of terminally differentiated myeloid cells occurs.Classical,Philadelphia-negative MPNs,i.e.,polycythemia vera,essential thrombocythemia and primary myelofibrosis,exhibit a propensity towards the development of thrombotic complications that can occur in unusual sites,e.g.,portal,splanchnic or hepatic veins,the placenta or cerebral sinuses.The pathogenesis of thrombotic events in MPNs is complex and requires an intricate mechanism involving endothelial injury,stasis,elevated leukocyte adhesion,integrins,neutrophil extracellular traps,somatic mutations(e.g.,the V617F point mutation in the JAK2 gene),microparticles,circulating endothelial cells,and other factors,to name a few.Herein,we review the available data on Budd-Chiari syndrome in Philadelphia-negative MPNs,with a particular focus on its epidemiology,pathogenesis,histopathology,risk factors,classification,clinical presentation,diagnosis,and management.展开更多
Myeloproliferative neoplasms(MPNs)are a heterogeneous group of hematologic malignancies characterized by an abnormal proliferation of cells of the myeloid lineage.Affected individuals are at increased risk for cardiov...Myeloproliferative neoplasms(MPNs)are a heterogeneous group of hematologic malignancies characterized by an abnormal proliferation of cells of the myeloid lineage.Affected individuals are at increased risk for cardiovascular and thrombotic events.Myocardial infarction(MI)may be one of the earliest clinical manifestations of MPNs or may be a thrombotic complication that develops during the natural course of the disease.In the present review,we examine the epidemiology,pathogenesis,clinical presentation,and management of MI in MPNs based on the available literature.Moreover,we review potential biomarkers that could mediate the MI-MPNs crosstalk,from classical biochemical tests,e.g.,lactate dehydrogenase,creatine kinase and troponins,to pro-inflammatory cytokines,oxidative stress markers,and clonal hematopoiesis.展开更多
文摘BACKGROUND Obesity and diabetes are associated with high levels of oxidative stress.In Romanian patients with obesity and(or)diabetes,this association has not been sufficiently explored.AIM To evaluate oxidative stress in obese and(or)diabetic subjects and to investigate the possible correlations between oxidative stress and anthropometric/biochemical parameters.METHODS Oxidative stress was evaluated from a single drop of capillary blood.Reactive oxygen species(ROS)were evaluated using the free oxygen radical test(FORT).The free oxygen radical defence(FORD)assay was used to measure antioxidant levels.RESULTS FORT levels were higher in obese subjects(3.04±0.36 mmol/L H2O2)vs controls(2.03±0.14 mmol/L H2O2)(P<0.0001).FORD levels were lower in obese subjects(1.27±0.13 mmol/L Trolox)vs controls(1.87±1.20 mmol/L Trolox)(P=0.0072).Obese diabetic subjects had higher FORT values(3.16±0.39 mmol/L H2O2)vs non-diabetic counterparts(2.99±0.33 mmol/L H2O2)(P=0.0233).In obese subjects,FORT values correlated positively with body mass index(BMI)(r=0.48,P=0.0000),waist circumference(WC)(r=0.31,P=0.0018),fasting plasma glucose(FPG)(r=0.31,P=0.0017),total cholesterol(TC)(r=0.27,P=0.0068)and uric acid(r=0.36,P=0.0001).FORD values correlated negatively with BMI(r=-0.43,P=0.00001),WC(r=-0.28,P=0.0049),FPG(r=-0.25,P=0.0130),TC(r=-0.23,P=0.0198)and uric acid(r=-0.35,P=0.0002).In obese diabetic subjects,FORT values correlated positively with BMI(r=0.49,P=0.0034)and TC(r=0.54,P=0.0217).FORD values were negatively associated with BMI(r=-0.54,P=0.0217)and TC(r=-0.58,P=0.0121).CONCLUSION Oxidative stress levels,as measured by the FORT and FORD assays,were higher in obese subjects vs controls.ROS levels were elevated in diabetic obese patients vs obese non-diabetic patients and controls.
文摘Myeloproliferative neoplasms(MPNs)are defined as clonal disorders of the hematopoietic stem cell in which an exaggerated production of terminally differentiated myeloid cells occurs.Classical,Philadelphia-negative MPNs,i.e.,polycythemia vera,essential thrombocythemia and primary myelofibrosis,exhibit a propensity towards the development of thrombotic complications that can occur in unusual sites,e.g.,portal,splanchnic or hepatic veins,the placenta or cerebral sinuses.The pathogenesis of thrombotic events in MPNs is complex and requires an intricate mechanism involving endothelial injury,stasis,elevated leukocyte adhesion,integrins,neutrophil extracellular traps,somatic mutations(e.g.,the V617F point mutation in the JAK2 gene),microparticles,circulating endothelial cells,and other factors,to name a few.Herein,we review the available data on Budd-Chiari syndrome in Philadelphia-negative MPNs,with a particular focus on its epidemiology,pathogenesis,histopathology,risk factors,classification,clinical presentation,diagnosis,and management.
文摘Myeloproliferative neoplasms(MPNs)are a heterogeneous group of hematologic malignancies characterized by an abnormal proliferation of cells of the myeloid lineage.Affected individuals are at increased risk for cardiovascular and thrombotic events.Myocardial infarction(MI)may be one of the earliest clinical manifestations of MPNs or may be a thrombotic complication that develops during the natural course of the disease.In the present review,we examine the epidemiology,pathogenesis,clinical presentation,and management of MI in MPNs based on the available literature.Moreover,we review potential biomarkers that could mediate the MI-MPNs crosstalk,from classical biochemical tests,e.g.,lactate dehydrogenase,creatine kinase and troponins,to pro-inflammatory cytokines,oxidative stress markers,and clonal hematopoiesis.
