RESUMO
The new type coronavirus disease 2019 (COVID-19) is a contagious disease of severe lung inflammation induced by 2019 novel coronavirus (2019-nCoV). The World Health Organization (WHO) nomenclature of the newly discovered coronavirus was 2019-nCoV and the disease caused by 2019-nCoV was named COVID-19 on January 12, 2020. After 2019-nCoV invasion into a human body, it can stimulate the human immune system and engender a large number of cytokines, triggering a cytokine storm, resulting in severe infection, acute lung injury, multiple organ dysfunction, etc. Therefore, theoretically, the removal of over-production of cytokines can avoid the occurrence of cytokine storm and reduce the incidence of severe critical COVID-19 and serious poor prognosis. In this review, the authors systematically reviewed the past published reports related to the occurrence of cytokine storm in sepsis resulting in deterioration of disease situation, and recently they analyzed the therapeutic effects of patients with severe critical COVID-19 using endotoxin adsorption membrane for treatment in the disease course, further providing the effective clinical evidence of applying endotoxin adsorption membrane for treatment of COVID-19.
RESUMO
Objective To investigate the relationship between fasting plasma glucose (FPG) and islet α-cell and β-cell function in patients with type 2 diabetes mellitus (T2DM).Methods Four hundred and thirty-seven patients with T2DM were divided into 3 groups according to the level of FPG:F1 group:FPG ≤ 6 mmol/L (73 cases),F2 group:6 mmol/L ＜ FPG ≤ 7 mmol/L (103 cases),and F3 group:FPG ＞ 7mmol/L (261 cases),and 30 cases of healthy people were selected as control group.Oral glucose tolerance test,insulin releasing test and glucagon releasing test were performed to observe the differences of glucagon,glucagon/ insulin,the ratio of 30 min insulin and blood glucose value after glucose load (△ I30/△ G30),and the area under curve of insulin (AUC1) among the 4 groups and the correlation analysis was performed between glucagon and other indicators.Results Glycosylated hemoglobin (HbA1c),plasma glucose 120 at min after glucose load in F1,F2 and F3 group were significantly higher than those in control group,and there were statistical differences (P ＜0.05).In F1,F2,F3 group,with the increase of the HbA1c,the course of disease and plasma glucose at 120 min after glucose load showed increasing trend.The triglyceride in F2 group and F3 group was significantly higher than that in F1 group and control group,and low density lipoprotein cholesterol in F3 group was significantly higher than that in F1 group,F2 group and control group,and there were statistical differences (P ＜ 0.05).The glucagon at 60,120 min after glucose load in F1 group,30,60,120 min after glucose load in F2 group,and 30,60,120,180 min after glucose load in F3 group was significantly higher than that in control group,and there were statistical differences (P ＜ 0.05).The glucagon at 60,120,180 min after glucose load in F2 group,at fasting and 30,60,120,180 rain after glucose load in F3 group was significantly higher than that in F1 group,and there were statistical differences (P ＜ 0.05).The glucagon at fasting and 30,60,120,180 min after glucose load in F3 group was significantly higher than that in F2 group,and there were statistical differences (P ＜ 0.05).The area under curve of glucagon in control group was 9.5 ±0.3,in F1 group was 9.7 ± 0.2,in F2 group was 9.9 ± 0.2,in F3 group was 10.2 ± 0.3,and there were statistical differences among the 4 groups (P ＜ 0.05).The glucagon/insulin at fasting and 30,60 min after glucose load in F1 groups,fasting and 30,60,120 min after glucose load in F2 group,fasting and 30,60,120 min after glucose load in F3 group was significantly higher than that in control group,and there were statistical differences (P＜ 0.05).The glucagon/insulin at fasting and 60,120 min after glucose load in F2 group,fasting and 30,60,120,180 min after glucose load in F3 group was significantly higher than that in F1 group,and there were statistical differences (P ＜ 0.05).The glucagon/insulin 30,60,120,180 min after glucose load in F3 group was significantly higher than that in F2 group,and there were statistical differences (P＜ 0.05).The homeostasis model of assessment for insulin resistance index (HOMA-IR) in F2 group and F3 group was significantly higher than that in control group and F1 group,in F3 group was significantly higher than that in F2 group,and there were statistical differences (P＜ 0.05).The insulin sensitivity index (ISI) in F2 group and F3 group was significantly lower than that in control group and F1 group,in F3 group was significantly lower than that in F2 group,and there were statistical differences (P ＜ 0.05).The homeostasis model of assessment for islet β-cell function index (HOMA-β) and △I30/△G30 in F1,F2,F3 group were significantly lower than those in control group,and there were statistical differences (P ＜ 0.05).The AUC1 in F2 group was significantly lower than that in control group,and AUC1 in F3 group was significantly lower than that in control group,F1 group and F2 group,there were statistical differences (P ＜0.05).The results of Pearson correlation analysis showed there was negative correlation between glucagon and △I30/△G30,HOMA-β,body mass index,ISI,AUC1 (r =-0.229,-0.153,-0.151,-0.146,-0.136,P＜0.01 or ＜0.05),and there was positive correlation between glucagon and FPG,area under curve of glucose (AUCG),HbA1c,course of disease and HOMA-IR (r =0.545,0.476,0.273,0.193,0.189,P ＜ 0.01).The results of multiplestepwise regression analysis showed there was positive correlation between glucagon and FPG,AUCG,HbA1c,course of disease (P ＜0.01 or ＜0.05),and there was negative correlation between glucagon and △I30/△ G30 (P ＜ 0.05).Conclusions Islet β-cell function is decreased with the increasing of FPG,while islet α-cell function is increased,especially in those with higher levels of FPG.Regulation of glucagon should be concerned to make the blood glucose target easier to reach,at the same time of protecting β-cell function.