Effect of iron deficiency without anaemia on days alive and out of hospital in patients undergoing valvular heart surgery

Comprehensive evidence regarding the treatment of non-anaemic iron deficiency in patients undergoing valvular heart surgery is lacking. This study aimed to investigate the association between non-anaemic iron deficiency and postoperative outcomes in these patients. We retrospectively analysed 321 patients of which 180 (56%) had iron deficiency (defined as serum ferritin < 100 ng.ml^-1 or < 300 ng.ml^-1 with transferrin saturation < 20%). While the iron-deficient group had lower pre-operative haemoglobin levels than the non-iron deficient group (median (IQR [range]) 134 (127–141 [120–172]) g.l^-1, 143 (133–150 [120–179]) g.l^-1, p = 0.001), there was no between-group difference in allogeneic red blood cell transfusion. Median (IQR [range]) days alive and out of hospital at postoperative day 90 was 1 day shorter in the iron-deficient group (80 (77–82 [9–85]) days vs. 81 (79–83 [0–85]) days, p = 0.026). In multivariable analysis, only cardiopulmonary bypass duration (p = 0.032) and intra-operative allogeneic red blood cell transfusion (p = 0.011) were significantly associated with reduced days alive and out of hospital at postoperative day 90. Iron deficiency did not exert any adverse influence on secondary outcomes except length of hospital stay. Our findings indicate that non-anaemic iron deficiency alone is not associated with adverse effects in patients undergoing valvular heart surgery when it does not translate into an increased risk of allogeneic transfusion.     

基于DTI评价急性缺血性脑卒中运动功能缺损程度与肾虚髓亏证的相关性研究＊

目的 运用核磁共振弥散张量成像技术（DTI），从皮质脊髓束损伤程度评价的角度，探讨肾虚髓亏证与急性缺血性脑卒中运动功能缺损程度相关性，丰富中风病病机及证候诊断，拓宽缺血性脑卒中的中医药防治思路，为急性缺血性脑卒中肾虚髓亏证患者运动功能损伤程度提供临床依据，强调肾虚髓亏证在急性缺血性脑卒中运动功能损伤中的重要意义。方法 纳入符合诊断标准的90例病例，根据证候分别归入肾虚髓亏组和非肾虚髓亏组，每组各45例。每组患者均给予常规西药治疗。对两组患者入院后行弥散张量成像检测，同时分别于治疗前及治疗后14天，记录两组患者NIHSS评分、改良Barthel指数量表及简化Fugl-Meyer运动功能评分量表评分，比较两组病例发病时的轻重程度及治疗前后两组病例组间的恢复差异。结果 研究显示，治疗前肾虚髓亏组在NIHSS评分方面高于非肾虚髓亏组（P<0.05）；治疗前肾虚髓亏组在改良Barthel指数量表及简化Fugl-Meyer运动功能评分方面低于非肾虚髓亏组（P<0.05）。治疗前后NIHSS评分、改良Barthel指数评分及简化Fugl-Meyer运动功能评分改善情况，非肾虚髓亏组要优于肾虚髓亏组（P<0.05）。治疗前两组患者在健侧内囊后肢及大脑脚外侧处FA值及ADC值无明显差异；肾虚髓亏组在患侧内囊后肢及大脑脚外侧处FA值及ADC值均低于非肾虚髓亏组（P<0.05）。相关性分析得出，两组患者患侧内囊后肢FA值与患者治疗前NIHSS评分呈负相关；两组患者患侧内囊后肢FA值与患者改良Barthel指数评分及简化Fugl-Meyer运动功能评分呈正相关；肾虚髓亏组患者患侧内囊后肢FA值与肾虚髓亏证中医证候评分呈负相关。结论 肾虚髓亏是急性缺血性脑卒中运动功能障碍的重要病机。研究结果显示，两组皮质脊髓束损伤程度与神经功能及运动功能损伤存在相关性，且肾虚髓亏组在皮质脊髓束的损伤程度方面与其中医证候评分呈负相关。     

血清胱抑素C和尿微量白蛋白联合检测在人类免疫缺陷病毒感染者肾功能损伤检测中的应用价值

目的评估血肌酐和尿常规的常规检测基础上联合血清胱抑素C和尿微量白蛋白检测在人类免疫缺陷病毒（HIV）感染者肾功能损伤检测中的应用价值。 方法以2019年2～5月于首都医科大学附属北京地坛医院感染一科住院的169例HIV感染者为研究对象，完善其尿常规、尿微量白蛋白、血肌酐、血清胱抑素C检测；分析尿蛋白及尿微量白蛋白的阳性检出率及其差异，血肌酐升高及血清胱抑素C升高的比例及其差异。计算应用替诺福韦酯（TDF）及合并丙型肝炎、高血压、糖尿病、肿瘤的肾功能损伤的相对危险度。 结果169例HIV感染者中尿常规示尿蛋白阳性者5例（3.0%），尿微量白蛋白升高者17例（10.1%），两者阳性检出率差异具有统计学意义（χ² = 5.9、P = 0.007）。血肌酐升高者10例（5.9%），血清胱抑素C升高者20例（11.8%），两者阳性检出率差异具有统计学意义（χ² = 3.0、P = 0.042）。在尿常规和血肌酐检测的基础上联合检测尿微量白蛋白和血清胱抑素C的总体阳性检出率为49例（30.0%）。CD4⁺ T淋巴细胞计数< 200个/μl与≥ 200个/μl组患者血清胱抑素C水平分别为0.94（0.83，1.05）mg/L、0.85（0.77，0.95）mg/L，差异具有统计学意义（Z =-3.02、P = 0.003）。应用TDF及合并丙型肝炎、高血压、糖尿病、肿瘤的肾功能损伤的相对危险度分别为1.1、1.5、1.9、2.2和1.4。 结论HIV感染者中，单纯以尿常规为依据评估有无蛋白尿，以血肌酐水平为依据评估肾小球滤过功能会低估肾功能损伤的患病率。在常规检测血肌酐和尿常规的基础上联合检测血清胱抑素C和尿微量白蛋白在提高HIV感染者肾功能损伤检出率方面具有重要的应用价值。低CD4⁺ T淋巴细胞计数、应用TDF及合并丙型肝炎、高血压、糖尿病、肿瘤均为肾功能损伤的危险因素。     

早期十全大补汤联合肠内营养乳剂治疗胃癌术后(气血两虚证)喂养不耐受临床评价

目的探讨早期使用十全大补汤联合肠内营养乳剂(TP)治疗胃癌术后(气血两虚证)发生喂养不耐受(FI)的影响因素及对营养指标、中医证候积分的影响。方法回顾性分析术后早期行十全大补汤联合TP治疗的80例胃癌术后(气血两虚)患者的病历资料,根据是否出现FI分为耐受组(34例)和不耐受组(46例)。FI的相关影响因素进行单因素及多因素分析,并观察FI对患者营养指标、中医证候积分的影响。结果单因素分析显示,患者术后第1天下床活动时间、开始肠内营养(EN)的时间、使用营养泵、早期灌肠与FI的发生密切相关(P <0. 05);多因素Logistic回归分析显示,患者第1天下床活动时间≥2 h[OR=0. 022,P=0. 001,95%CI(0. 002,0. 223)]、使用营养泵[OR=0. 021,P=0. 000,95%CI(0. 003,0. 162)]是FI发生的独立危险因素;术后10 d,耐受组患者白蛋白(ALB)、血红蛋白(Hb)升高水平优于不耐受组(P <0. 05),中医证候积分显著低于不耐受组(P <0. 05)。结论胃癌术后(气血两虚证)患者早期给予十全大补汤联合TP治疗开始后,患者第1天下床活动时间不短于2 h、使用营养泵能有效减少FI的发生,并改善了患者的营养状态,减轻了中医临床症状。     

益气通脉饮联合西药治疗气虚血瘀型冠心病心绞痛90例临床疗效观察

目的:探讨益气通脉饮治疗气虚血瘀型冠心病心绞痛的临床疗效。方法:选取2017年10月—2019年2月烟台业达医院收治的气虚血瘀型冠心病心绞痛的患者90例作为研究对象,根据随机数字表法将所选患者均分为两组,每组各45例,两组的一般资料经统计学方法,差异无统计学意义(P>0.05),因此具有可比性。对照组给予常规西药进行治疗,观察组在对照组治疗基础上给予益气通脉饮治疗,1个月后比较两组临床的疗效,评估治疗前后中医证候、心绞痛症状分级和血脂水平。临床检测的数据通过统计产品与服务解决方案(Statistical Product and Service Solutions,SPSS) 19.0软件进行分析和处理,计量的数据使用平均数±标准差(x±s)表示,采用双侧t检验,计数的数据采用χ~2检验,以%表示,以P<0.05为差异有统计学意义。结果:治疗后,对照组和观察组都有一定疗效,但观察组的改善中医证候总有效率95.56%(43/45),高于对照组的82.22%(37/45),两组比较具有统计学意义(P<0.05);心绞痛的症状总有效率观察组为93.33%(42/45),对照组为77.78%(35/45),两组比较差异有统计学意义(P<0.05);与治疗前相比较,两组治疗后的三酰甘油(Triglyceride,TG)、血清总胆固醇(Serum Total Cholesterol,TC)、高密度脂蛋白胆固醇(High Density Liptein Cholesterol,HDL-C)水平均降低(P<0.05),且观察组治疗后低于对照组(P<0.05),两组治疗后的HDL-C升高(P<0.05),组间比较,差异无统计学意义(P>0.05)。结论:益气通脉饮治疗气虚血瘀型冠心病心绞痛的疗效显著,值得临床进一步研究与推广应用。     

Lack of ceramide synthase 2 suppresses the development of experimental autoimmune encephalomyelitis by impairing the migratory capacity of neutrophils

Ceramide synthases (CerS) synthesise ceramides of defined acyl chain lengths, which are thought to mediate cellular processes in a chain length-dependent manner. In experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis (MS), we observed a significant elevation of CerS2 and its products, C24-ceramides, in CD11b⁺ cells (monocytes and neutrophils) isolated from blood. This result correlates with the clinical finding that CerS2 mRNA expression and C24-ceramide levels were significantly increased by 2.2- and 1.5-fold, respectively, in white blood cells of MS patients. The increased CerS2 mRNA/C24-ceramide expression in neutrophils/monocytes seems to mediate pro-inflammatory effects, since a specific genetic deletion of CerS2 in blood cells or a total genetic deletion of CerS2 significantly delayed the onset of clinical symptoms, due to a reduced infiltration of immune cells, in particular neutrophils, into the central nervous system. CXCR2 chemokine receptors, expressed on neutrophils, promote the migration of neutrophils into the central nervous system, which is a prerequisite for the recruitment of further immune cells and the inflammatory process that leads to the development of MS. Interestingly, neutrophils isolated from CerS2 null EAE mice, as opposed to WT EAE mice, were characterised by significantly lower CXCR2 receptor mRNA expression resulting in their reduced migratory capacity towards CXCL2. Most importantly, G-CSF-induced CXCR2 expression was significantly reduced in CerS2 null neutrophils and their migratory capacity was significantly impaired. In conclusion, our data strongly indicate that G-CSF-induced CXCR2 expression is regulated in a CerS2-dependent manner and that CerS2 thereby promotes the migration of neutrophils, thus, contributing to inflammation and the development of EAE and MS.