动态血压监测评价高血压患者靶器官损害246例分析

目的探讨动态血压监测对评价高血压患者靶器官损害的价值。方法对246例高血压患者进行24h动态血压监测,其中单纯血压升高118例为原发性高血压组,伴靶器官损害128例为伴靶器官损害组,进行统计学分析。结果(1)伴靶器官损害组24h收缩压、白昼舒张压、夜间舒张压低于原发性高血压组(P<0.01);(2)靶器官损害数目累及3个器官组与累及1个器官组相比,24h平均收缩压、夜间平均舒张压、血压波动的昼夜节律异常和血压负荷参数,差异有统计学意义。结论血压波动的昼夜节律异常、24h平均收缩压、夜间平均舒张压和血压负荷越高,靶器官损害数目越多。     

动态血压与高血压患者靶器官损害的相关性研究

目的 探讨动态血压与高血压患者靶器官损害的相关性.方法 将120例进行动态血压监测的原发性高血压病患者分为两组,其中62例存在靶器官损害患者作为A组,无靶器官损害的单纯原发性高血压病患者为B组.结果 两组24h平均收缩压、脉压、血压昼夜节律、夜间平均舒张压之间差异有统计学意义(P＜0.01).结论 24h平均收缩压、脉压、血压昼夜节律、夜间平均舒张压与高血压患者靶器官损害密切相关,平稳降压有利于减少靶器官损害.     

老年代谢综合征患者动态脉压、心率变异性与靶器官损害的关系

目的探讨老年代谢综合征（MS）患者24 h脉压、心率变异性与靶器官损害的关系。方法对单纯MS患者86例,MS伴靶器官损害患者118例,对比分析24 h动态血压监测及心率变异性各指标。结果伴靶器官损害组与单纯MS组比较:24 h平均舒张压、日间舒张压、夜间舒张压降低,日间收缩压、夜间收缩压、24 h脉压、日间脉压、夜间脉压升高,心率变异性各指标（SDNN、SDANN、SD、rMSSD、PNN50）降低,两组比较有显著性差异（P<0.01或P<0.05）。结论动态脉压及心率变异性的变化可反映MS病变程度,     

老年代谢综合征患者动态血压监测分析

目的探讨老年代谢综合征(MS)患者24h动态血压、24h脉压与其靶器官损害的关系。方法将92例单纯老年高血压患者、88例单纯老年MS患者和117例伴靶器官损害的老年MS患者24h动态血压监测指标进行分析比较。结果老年MS组与单纯老年高血压组比较:MS组的夜间平均收缩压(nMSP)、24h平均脉压高于单纯高血压组(P0.01或P0.05),昼夜收缩压和舒张压差值低于单纯高血压组(P0.01)。伴靶器官损害MS组与单纯MS组比较:伴靶器官损害MS组白昼平均收缩压(dMSP)、nMSP、24h平均脉压较单纯MS组增高(P0.05或P0.01),24hMDP、dMDP、nMDP较单纯MS组降低(P0.05)。结论血压的昼夜差值与MS,脉压与MS及靶器官损害程度关系密切。     

老年原发性高血压动态血压及脉压的特点

目的：探讨老年原发性高血压动态血压及脉压的特点。方法：采用随机对照研究,回顾分析65例老年原发性高血压患者和32例中青年原发性高血压患者的动态血压表现。结果：老年原发性高血压组24h平均脉压（24hAPP）、白天平均脉压（dPP）、夜间平均脉压（nPP）,夜间平均收缩压（nSBP）显著高于中青年组（P均〈0．01）,24h平均舒张压（24hADBP）、白天平均舒张压（dDBP）、夜间平均舒张压（nDBP）显著低于中青年组（P均〈0．05）。结论：较之中青年高血压,老年原发性高血压患者的动态收缩压显著升高,动态舒张压显著降低,动态脉压明显增大。     

老年高血压病患者动态血压特点及临床分析

目的探讨老年高血压病患者血压昼夜节律变化特点。方法对我院老年病科2008年2月～7月住院的100例老年人行24h动态血压监测，将血压正常的定为对照组（42例），将高血压病患者定为观察组（58例）。分析观察血压水平、靶器官损害发生率、血压昼夜节律等指标进行分析。结果观察组的24h平均收缩压、舒张压，白天平均收缩压、舒张压，夜间平均收缩压、舒张压，昼夜下降比和靶器官损害发生率明显高于对照组（P〈0.05）。结论老年高血压病患者血压昼夜节律消失更容易损害靶器官，夜间舒张压越高，靶器官损害越重。     

原发性高血压患者心肌、动脉结构改变与动态血压参数关系的研究

目的 探讨高血压患者心肌、颈动脉结构改变与动态血压参数的相关性。方法 检测78例原发性高血压（EH）病人的左室心肌重量指数（LVMI），相对室壁厚度（RWT），颈动脉内膜-中层厚度（IMT），并进行24h无创性动态血压监测（ABPM）。结果 左室肥厚组与左室正常构型组比较，颈动脉内膜-中层增厚组与非颈动脉内膜冲层增厚组比较：24h平均收缩压、24h平均舒张压、白昼平均收缩压、白昼甲均舒张压、白昼收缩压和舒张压负荷值，差异有统计学意义（P〈0．05）；夜间平均收缩压、夜间平均舒张、夜间收缩压和舒张压负荷、24h收缩压和舒张压变异系数、血压昼夜节律异常，差异显著（P〈0．01）。结论 高血压患者靶器官损伤与血压昼夜节律及血压变异的幅度相关。     

老年原发性高血压患者动态脉压与左室质量指数的相关性

目的研究老年原发性高血压患者动态脉压与左室质量指数（LVMI）的相关性。方法选择153例老年原发性高血压患者,均行24h动态血压监测,根据平均脉压（ABPP）分为≥60mmHg组和〈60mmHg组,采用多普勒超声心动图测量室间隔厚度、左室后壁厚度及左室舒张末内径,并计算LVMI,将两组的临床资料进行分析。结果≥60mmHg组24h平均收缩压、日间平均收缩压、夜间平均收缩压、日间平均收缩压负荷值、夜间平均收缩压负荷值、24h平均收缩压负荷值及LVMI明显高于ABPP〈60mmHg组;24hABPP增大,与LVMI呈显著正相关（r=0．949,P=0．00）。结论脉压增大与LVMI呈显著正相关,治疗老年原发性高血压时,不仅要控制血压在理想水平,还要尽可能缩小脉压。     

高血压患者24h动态血压的昼夜规律及变异性研究

目的 探讨原发性高血压（EH）患者血压昼夜规律及血压波动程度即变异性的临床意义.方法 回顾分析65例EH患者24 h动态血压（24 h ABPM）监测报告.将65例EH患者分为两组：一组为高血压伴左心室肥大（LVH）30例,另一组为高血压不伴左心室肥大35例.选择同期健康体检者30名为正常血压对照组.对下列参数进行分析：①24 h平均收缩压（24 h SBP）与舒张压（24 h DBP）;②白昼平均收缩压（dSBP）与舒张压（dDBP）;③夜间平均收缩压（nSBP）与舒张压（nDBP）;④24 h收缩压标准差（24 h SSD）与舒张压标准差（24 h DSD）;⑤白昼收缩压标准差（dSSD）与舒张压标准差（dDSD）;⑥夜间收缩压标准差（nSSD）和舒张压标准差（nDSD）;⑦夜间/白昼平均收缩压比值（nSBP/dSBP）与舒张压比值（nDBP/dDBP）.结果 高血压伴LVH组与正常对照组或高血压无LVH组比较,24 h各时间段的血压均值及血压变异性差异有统计学意义（P＜0.01）,血压昼夜（清醒/睡眠）规律性不明显,nSBP/dSBP比值显著高于对照组（P＜0.01）.高血压无LVH组与正常对照组比较,血压均值差异有统计学意义（P＜0.01）,血压大多有较明显昼夜（清醒/睡眠）变化规律,血压变异性比较除白昼收缩压变异性有明显差异外,其余差异无统计学意义.结论 高血压不合并靶器官损害时,血压的变异性不显著,有明显昼夜规律性;高血压合并靶器官损害时,血压的变异性增大,无明显昼夜规律性,nSBP/dSBP比值明显增高.利用这些指标可评估高血压患者是否有靶器官损害,以便更有效地控制血压,减少并发症.     

原发性高血压24小时动态血压分析

目的：分析原发性高血压24小时动态血压变化。方法：应用美国产动态血压监测仪观察40例原发性高血压24小时动态血压并与96例血压正常进行比较。结果：单纯高血压患白天,夜间,平均收缩压,平均舒张压及24小时血压负荷值均比血压正常组高（P＜0．01）,高血压靶器官损害各组收缩压和舒张压又比单纯高压患高（P＜0．01）,结论：24小时动态血压与高血压靶器官损害有关,血压越高,靶器官损害越多,多脏器损害血压最高,脑,肾损害血压次之。     

Concerted action of wild-type and mutant TNF receptors enhances inflammation in TNF receptor 1-associated periodic fever syndrome

TNF, acting through p55 tumor necrosis factor receptor 1 (TNFR1), contributes to the pathogenesis of many inflammatory diseases. TNFR-associated periodic syndrome (TRAPS, OMIM 142680) is an autosomal dominant autoinflammatory disorder characterized by prolonged attacks of fevers, peritonitis, and soft tissue inflammation. TRAPS is caused by missense mutations in the extracellular domain of TNFR1 that affect receptor folding and trafficking. These mutations lead to loss of normal function rather than gain of function, and thus the pathogenesis of TRAPS is an enigma. Here we show that mutant TNFR1 accumulates intracellularly in peripheral blood mononuclear cells of TRAPS patients and in multiple cell types from two independent lines of knockin mice harboring TRAPS-associated TNFR1 mutations. Mutant TNFR1 did not function as a surface receptor for TNF but rather enhanced activation of MAPKs and secretion of proinflammatory cytokines upon stimulation with LPS. Enhanced inflammation depended on autocrine TNF secretion and WT TNFR1 in mouse and human myeloid cells but not in fibroblasts. Heterozygous TNFR1-mutant mice were hypersensitive to LPS-induced septic shock, whereas homozygous TNFR1-mutant mice resembled TNFR1-deficient mice and were resistant to septic shock. Thus WT and mutant TNFR1 act in concert from distinct cellular locations to potentiate inflammation in TRAPS. These findings establish a mechanism of pathogenesis in autosomal dominant diseases where full expression of the disease phenotype depends on functional cooperation between WT and mutant proteins and also may explain partial responses of TRAPS patients to TNF blockade.     

鞍钢职工心脑血管疾病现状与发病趋势

目的分析鞍钢职工大样本人群心脑血管疾病的发病率及易患因素分布情况。方法通过对鞍钢集团95 912例职工的心脑血管疾病既往史、吸烟、血压、糖尿病、血清总胆固醇、高密度脂蛋白、体重指数、总胆固醇与高密度脂蛋白胆固醇的比值等数据的分析,前瞻性分析受检人群心脑血管疾病发病的危险分层。结果冠心病1 910例(2.00%),脑血管病607例(0.63%),吸烟19 453例(20.28%),糖尿病788例(0.82%),高血压31 698例(33.05%),高脂血症8 347例(8.70%),体重超重55 462例(57.83%),总胆固醇(TC)/高密度脂蛋白胆固醇(HDL-C)≥3.5的10 487例(10.93%);缺血性心血管病发病概率多分布于极低危(68.14%)和低危(5.75%),中危(0.865%)占很小的比例,颈动脉粥样硬化斑块发生概率多分布于高危(44.23%)、中危(23.21%)和极高危(10.51%),无低危和极低危。结论目前鞍钢职工的健康状况不容乐观,应进一步加大健康知识宣教力度。     

Chronic liver inflammation: Clinical implications beyond alcoholic liver disease

Chronic alcohol exposure can lead to alcoholic liver disease, including hepatitis, cirrhosis and hepatocellular carcinoma, and chronic inflammation can simultaneously cause systemic medical illness. Recent evidence suggests that alcoholic liver disease is a predictor for liver-related diseases, cardiovascular disease, immunologic disease, and bone disease. Chronic inflammation in alcoholic liver disease is mediated by a direct inflammatory cascade from the alcohol detoxification process and an indirect inflammatory cascade in response to gut microflora-derived lipopolysaccharides (LPS). The pathophysiology of alcoholic liver disease and its related systemic illness is characterized by oxidative stress, activation of the immune cascade, and gut-liver interactions. Integrative therapeutic strategies for alcoholic liver disease include abstaining from alcohol consumption; general anti-inflammatories such as glucocorticoid, pentoxifylline, and tumour necrosis factor-α antagonist; antioxidants such as N- acetylcysteine; gut microflora and LPS modulators such as rifaximin and/or probiotics. This review focuses on the impact of chronic liver inflammation on systemic health problems and several potential therapeutic targets.     

Celiac Disease: A Disorder Emerging from Antiquity,Its Evolving Classification and Risk,and Potential New Treatment Paradigms

Celiac disease is a chronic genetically based gluten-sensitive immune-mediated enteropathic process primarily affecting the small intestinal mucosa. The disorder classically presents with diarrhea and weight loss; however, more recently, it has been characterized by subclinical occult or latent disease associated with few or no intestinal symptoms. Diagnosis depends on the detection of typical histopathological biopsy changes followed by a gluten-free diet response. A broad range of clinical disorders may mimic celiac disease, along with a wide range of drugs and other therapeutic agents. Recent and intriguing archeological data, largely from the Gobleki Tepe region of the Fertile Crescent, indicate that celiac disease probably emerged as humans transitioned from hunter-gatherer groups to societies dependent on agriculture to secure a stable food supply. Longitudinal studies performed over several decades have suggested that changes in the prevalence of the disease, even apparent epidemic disease, may be due to superimposed or novel environmental factors that may precipitate its appearance. Recent therapeutic approaches are being explored that may supplement, rather than replace, gluten-free diet therapy and permit more nutritional options for future management.     

Paediatric aspects of coeliac disease: old challenges and new ones…

The concept of coeliac disease has expanded from a gastrointestinal disease with malabsorption to a systemic immunological disease with a genetic basis. Epidemiological studies indicate that environmental factors, like the infant feeding pattern, affect the clinical presentation while population-screening studies indicate that the prevalence, at least in Caucasian populations, is similar. Secondary complications, like malignancies, osteopenia - osteoporosis, gynaecological and obstetrical problems and autoimmune diseases, are common. The risk is reduced or prevented by treatment with a gluten-free diet. The basis for such a secondary prevention is: 1. early case-finding by a) knowledge about different presentations of the disease and factors affecting that, b) generous serological testing in patients with vague symptoms, c) screening of risk groups, and, 2. support for children and adolescents with coeliac disease to comply with the gluten-free diet.     

Graves病患者血清中TSH抗体检测及其免疫学意义

利用~(125)I标记的人TSH(~(125)I-hTSH)作为放射性示踪配体,对29例正常人和58例Graves病患者血清中抗hTSH自身抗体(TSHab)进行了检测。正常人TSHab指数(TSHabJ)为0.85±0.22;而32例初发患者和26例接受抗甲状腺药物治疗患者的TSHabJ分别为1.47±0.35(P<0.001)和1.19±0.37(P>0.05)。SPA菌体结合沉淀试验表明:这种与hTSH结合的抗体属于IgG成分。TSHab的存在提示Graves病的免疫学发病已涉及到独特型-抗独特型反应机理。     

Canadian Digestive Health Foundation Public Impact Series 4: celiac disease in Canada. Incidence, prevalence, and direct and indirect economic impact

The Canadian Digestive Health Foundation initiated a scientific program to assess the incidence, prevalence, mortality and economic impact of digestive disorders across Canada in 2009. The current article presents the updated findings from the study concerning celiac disease.     

Simultaneous operation of concomitant diseases in the esophagus and lung

The aim of this study was to retrospectively review our experience of performing simultaneous operations on concomitant diseases in the esophagus and lungs. From January 1998 to July 2009, simultaneous operations were performed on 13 patients with concomitant esophageal and pulmonary diseases, using coordinated surgical approaches. Among the 13 patients, six had primary cancers in the esophagus and lungs, five had primary esophageal cancer accompanied by a benign pulmonary disease, one had benign diseases in both esophagus and lung, and one had primary esophageal cancer with metastasis to the left lower lung. All patients survived the operations. Two major complications occurred postoperatively. One complication was bronchopleural fistula and the other was intrathoracic gastric laceration. Both patients recovered after additional treatments. Simultaneous operation of concomitant diseases in the esophagus and lungs is feasible and safe in selected patients who have received careful preoperative assessment, well‐designed surgical approach, and proper perioperative management.