Objective To determine the incidence of vitamin B1 deficiency in critically ill patients, to compare vitamin B1 levels between septic and non-septic patients, and to explore the relationship between vitamin B1 levels and lactate levels. Methods Using a retrospective study method, critically ill patients admitted to the Department of Intensive Care of Nanjing Drum Tower Hospital from February 2022 to November 2022 were included in the study, and the patients were divided into sepsis and non-sepsis groups according to the admission diagnosis, and the differences in the vitamin B1 levels of the patients between the two groups were analyzed, as well as the correlation between the vitamin B1 levels and the lactic acid levels. Results There was a significant difference in serum vitamin B1 levels between the sepsis patients and the non-sepsis patients [(1.6±0.3)ng/mL vs. (2.1±0.2)ng/mL, P=0. 009]. For all patients, there was no correlation between vitamin B1 levels and lactate levels. But when the patient was in a hyperlactate state (lactate level ≥2 mmol/L), vitamin B1 levels were significantly negatively correlated with lactate levels (r=–0. 229, P=0. 004). Conclusions Vitamin B1 deficiency is prevalent in critically ill patients and is strongly correlated with whether or not the patient is septic. Vitamin B1 levels are significantly and negatively correlated with lactate levels when the patient's lactate level is ≥2 mmol/L.
ObjectiveTo explore the effect of continuous renal replacement therapy (CRRT) to treat sepsis associated acute kidney injury (AKI) in patients aged over 80.MethodsForty-one patients diagnosed with sepsis and AKI were enrolled in geriatric RICU department of Huadong Hospital from January 2013 to July 2018, 38 patients were male and 3 were female. All patients were treated with anti-infection and fluid resuscitation therapy. After comprehensive judgment of the indication of renal replacement, they were divided into two groups by the choices of using CRRT. There were 20 patients in CRRT group and 21 in control group. Clinical data such as age, body mass index, previous diseases, 28-day mortality rate, blood cells, APACHEⅡ as well as SOFA scores were compared between two groups. Blood renal function and inflammatory markers at the first day were also compared to those after 3-day treatment of initial time.ResultsNo statistical difference was observed in sex ratio, age, body mass index and previous diseases between two groups (all P>0.05). There was also no difference in APACHEⅡ score, SOFA score, blood cells, hemoglobin and survival time. The 28-day mortality rate in CRRT group was lower than that in control group (P<0.05). The levels of serum UA and C reactive protein (CRP) in CRRT group decreased after 3-day treatment compared with those at the onset, and the differences were statistically significant (all P<0.05). The level of serum blood urea nitrogen (BUN), creatinine (Cr), uric acid (UA) and cystain C in control group increased after 3 days compared with those at the onset, and the difference were statistically significant (all P<0.05). There was no significant difference in serum BUN, Cr, UA, cystain C, CRP and procalcitonin (PCT) between two groups at the onset (all P>0.05). After 3 days of CRRT, the levels of serum PCT, BUN, Cr and UA in CRRT group were lower than those in the control group (all P<0.05).ConclusionCRRT can improve hyperuricemia, control deterioration of renal function, reduce early systemic inflammatory response and 28-day mortality rate in aged patients with sepsis and AKI.
Objective To investigate the pathological characteristics of hepatic energy metabolism changes due to biliary sepsis. Methods The hepatic mitochondrial respiratory function and content of ATP was dynamically measured in the self controlled rabbit model of biliary sepsis.Results The mitochondrial S3, respiration control rate (RCR) and phosphorus/oxygen (P/O) were significantly dropping in the infective hepatic lobe 12 hrs after operation with S4 increasing markedly, and the oxidative phosphorylation was uncoupled from 48 hrs after operation onward. The hepatic mitochondrial RCR showed early ascending and then dropping in the non-infective hepatic lobe. The content of ATP and mitochondrial respiratory activity decreased synchronously in both hepatic lobes. Conclusion The hepatic energy metabolic failure was induced in the early stage by biliary sepsis. This is probably the pathological basis of biliary sepsis that is highly critical and always lead to MOF following acute liver function failure.
Objective To investigate the effects of ulinastatin on Treg/Th17 and immune status in patients with severe sepsis.Methods A total of 80 patients with severe sepsis, who were hospitalized in ICU during October 2011 to July 2012, were randomly divided into a routine group and a ulinastatin group. The patients in the ulinastatin group were intravenously administered 30mg ulinastatin three times per day for 5 days in addition to routine bundle treatment. The expression of Treg, Th17 and HLA-DR were detected on the first day in ICU and 5 days after treatment. 20 healthy individuals served as controls. Results Compared with the control group, the severe sepsis group had overexpression of Treg and Th17 ( P lt;0. 01) , higher ratio of Treg/Th17( P lt;0. 01) , and decreased HLA-DR expression of CD14 monocyte ( P lt; 0. 01) . In the severe sepsis patients, ulinastatin injection reduced the abnormal expression of Treg and Th17 ( P lt; 0. 01) , decreased the ratio of Treg/Th17( P lt; 0. 01) , and improved the expression of HLA-DR ( P lt; 0. 01) more effectively compared with the routine treatment. Ulinastatin also lowered 28-day mortality of the patients with sepsis, but the difference between the ulinastatin group and the routine group was not significant. Conclusions In severe sepsis patients, there were abnormal overexpression of Treg and Th17, imbalance of Treg/Th17, and underexpression of HLA-DR which imply an immune suppression. Ulinastatin can decrease the expression of Treg and Th17, inverses the ratio of Treg/Th17, and improve the expression of HLA-DR, so as to improve the prognosis of severe sepsis patients.
Sepsis-associated acute kidney injury (SAKI) is a common complication of patients in intensive care unit, and also an independent risk factor leading to high mortality of sepsis patients. SAKI leads to an extended hospital stay for patients, resulting in a huge medical burden. The pathogenesis of SAKI is complex, and systemic inflammatory response plays an important role in it. At present, blood adsorption is the main method for treating SAKI in intensive care units, but there is no consensus on the relevant treatment strategies. This article summarizes new perspectives and research conclusions on the application of blood adsorption technology in the treatment of SAKI, aiming to provide new references for the blood adsorption treatment strategies of SAKI.
ObjectiveTo systematically review the efficacy of antibiotic treatment in sepsis patients under the guidance of procalcitonin. MethodsDatabases including PubMed, The Cochrane Library (Issue 9, 2016), EMbase, Web of Science, CBM, WanFang Data, VIP and CNKI were electronically searched from inception to September 2016 to collect randomized controlled trials (RCTs) about antibiotic treatment in sepsis under the guidance of procalcitonin. Two reviewers independently screened literature, extracted data and assessed the risk bias of included studies, and then meta-analysis was performed by RevMan 5.3 software. ResultsA total of 15 RCTs involving 3 328 sepsis patients were included. Among them, 1 649 were in the procalcitionin group and 1 679 patients in the control group. The results of meta-analysis showed that:the PCT group could significantly reduce the using time of antibiotics (MD=-2.37, 95%CI -2.96 to -1.78, P<0.000 01), the ICU length of stay (MD=-0.26, 95%CI -0.46 to -0.07, P=0.007), the hospital length of stay (MD=-2.78, 95%CI -4.53 to -1.04, P=0.002), as well as the 28-day mortality (MD=0.78, 95%CI 0.66 to 0.93, P=0.005). There were no significant differences between the two groups in ICU mortality, in-hospital mortality and clinical cure rate. ConclusionUsing the procalcitontin to guide the antibiotic treatment in sepsis can reduce the patients' use of antibiotics, ICU length of stay, in-hospital length of stay and 28-day mortality, but can not reduce the patients' ICU mortality, in-hospital mortality and clinical cure rate. Due to the limited quality and quantity of included studies, the current conclusions are needed more studies to validate.
Objective To investigate the effect of non-coding RNA activated by DNA damage (NORAD) on acute lung injury (ALI) in septic rats by regulating the miR-155-5p/TLR6 molecular axis. Methods The rats were randomly divided into control group, model group, low NORAD expression no-load group (LV-sh-NC), low NORAD expression group (LV-sh-NORAD), low NORAD expression +miR-155-5p low expression no-load group (LV-sh-NORAD+NC antagomir), NORAD low expression +miR-155-5p low expression group (LV-sh-NORAD+miR-155-5p antagomir). ELISA kits were applied to detect interleukin (IL)-8, IL-1β, and tumor necrosis factor-α (TNF-α) levels; quantitative real-time polymerase chain reaction was applied to detect the expression of NORAD, miR-155-5p, and Toll-like receptor 6 (TLR6) genes in lung tissue of rats in each group. The ratio of wet weight to dry weight (W/D) of lung tissue was measured. The pathological changes of lung tissue were observed by hematoxylin-eosin staining, and apoptosis in lung tissue cells was detected by terminal deoxynucleotidyl transferase dUTP nick end labeling. Western blot was applied to detect the expressions of TLR6, Bax, Bcl-2, and cleaved cysteinyl aspartate specific proteinase 3 caspase-3) proteins in cells. Dual luciferase reporter gene experiment was applied to verify the relationship between miR-155-5p and NORAD and TLR6. Results Compared with the control group, the lung tissue of rats in the model group and LV-sh-NC group was obviously damaged, the levels of serum IL-1β, TNF-α, IL-8, expression of NORAD and TLR6 mRNA in lung tissue, W/D ratio, apoptosis rate, expression of TLR6, Bax, and Cleaved-caspase-3 proteins were obviously increased, the expression of miR-155-5p and Bcl-2 proteins in lung tissue was obviously reduced (P<0.05). Down-regulation of NORAD expression could reduce lung tissue injury, serum IL-1β, TNF-α, IL-8 levels, mRNA expression of NORAD and TLR6 in lung tissue, W/D ratio, apoptosis rate, TLR6, Bax, Cleaved caspase-3 protein expression, and cleaved caspase-3 protein expression. The expression of miR-155-5p and Bcl-2 protein in lung tissue were significantly increased (P<0.05). Down-regulating the expression of miR-155-5p could reduce the improvement effect of negatively regulated NORAD on sepsis ALI rats (P<0.05). Conclusion Interference with NORAD can alleviate lung injury in ALI rats by regulating the miR-155-5p/TLR6 molecular axis.
Sepsis 已经成为危重症医学中较为常见的一种综合征，它定义为因病原体感染而引起的全身性炎症反应综合征。严重Sepsis患者预后不佳，治疗上也较为困难，特别是合并Septic Shock和多器官功能不全综合征（MODS）的患者，死亡率仍然较高，因此近年来在临床及研究上均已引起明显的重视。为了能促进Sepsis的研究及治疗，国际上多个医学专科分会联合发起“拯救Sepsis运动（Surviving Sepsis Campaign, SSC）”，并于2004年首次发表了相应的指南，即Surviving Sepsis Campaign Guideline for Management of Severe Sepsis and Septic Shock。今年初SSC再次发表了新版的指南，主要是结合近年的研究成果而在原版的基础上进行适当的补充和更新，以指导临床上严重Sepsis的抢救及治疗。