初发Graves病^131I治疗早期血清CXCL10、IL-6的变化及意义

目的观察初发Graves病（GD）患者131I治疗早期血清CXC趋化因子配体10（CXCL10）、IL-6的变化及意义。方法应用ELISA法检测43例初发GD患者（观察组）131I治疗前及治疗后1周、2周、2个月血清CXCL10、IL-6水平,并与30例正常健康体检者（对照组）进行对照。结果观察组131I治疗前血清CXCL10、IL-6水平显著高于对照组（P均〈0.01）。与治疗前比较,131I治疗后1周CXCL10水平升高（P〈0.01）,2周时无统计学差异（P〉0.05）,2个月时显著降低（P〈0.01）;血清IL-6在治疗后2周（P〉0.05）、2个月时变化趋势与CXCL10相同（P〈0.01）。CXCL10与FT3、FT4、TSH无相关性,与TPOAb具有相关性（r=0.50,P〈0.01）;IL-6与以上指标均无相关性。结论血清CXCL10、IL-6参与了GD患者131I治疗早期炎性反应。     

丙基硫氧嘧啶与甲巯咪唑对Graves病患者细胞因子的影响

将64例Graves病(GD)患者分为甲巯咪唑组(MMI,n=30)和丙基硫氧嘧啶组(PTU,n=34),20名健康志愿者作为对照组.采集各组患者治疗前、治疗后3、6个月血清,分别用酶标记免疫吸附法检测血浆白细胞介素(IL)-2、IL-6及促甲状腺素受体抗体(TRAb)的水平.结果显示,2组治疗前一般情况比较差异无统计学意义.2组用药后6个月IL-2、IL-6水平较治疗前差异均有明显统计学意义(P＜0.05),随时间延长IL-2逐渐升高,IL-6逐渐降低;用药6个月后MMI组IL-6水平较PTU组明显降低(P＜0.05).2组治疗前TRAb水平无显著差异,2组治疗后3和6个月TRAb差异均有统计学意义(均P＜0.01),随时问增加逐渐下降.IL-2/IL-6比值在同一组治疗3、6个月后均较治疗前明显升高(P＜0.05).治疗6个月后MMI组较PTU组更高(P＜0.05).GD治疗前血清中IL-6水平与FT3、FT4呈正相关,IL-2水平与FT3、FT4和TRAb呈负相关;治疗3、6个月后,IL-2、IL-6与FT3、FT4无明显相关性;MMI组治疗前后IL-2、IL-6水平均与TRAb相关.这些结果提示,MMI较PTU更具有改善GD患者自身免疫的作用.     

Graves病患者甲状腺激素水平正常后sTSH长期抑制机制的探讨

目的 探讨临床上部分Graves病(GD)患者经抗甲状腺药物(ATD)治疗后甲状腺激素水平达到正常,但促甲状腺素(TSH)仍长期处于被抑制状态的机制.方法 入选初发122例GD甲亢患者,予以初始等效剂量的ATD治疗,每月随访时根据甲状腺功能测定的结果酌情减量,并适时添加左旋甲状腺素(L-T4).当甲状腺激素(FT3、FT4)水平持续正常3个月即达随访标准,复查FT3、FT4、sTSH、TSH受体抗体(TRAb),并根据TRAb是否阳性分组比较.结果 122例GD甲亢患者经(7.1±1.1)个月的ATD治疗后,甲状腺激素水平均已经达到正常3个月.随访时,58例TRAb转为阴性,64例TRAb持续阳性.两组甲状腺激素水平无差异, TRAb阳性组的sTSH水平明显低于阴性组[0.044 mIU/L(0.001～4.163 mIU/L) vs 1.749 mIU/L(0.079～4.646 mIU/L),P＜0.01];血清sTSH水平与TRAb呈明显负相关(r=-0.539,P＜0.01),与FT3、FT4、年龄、病程、治疗时间、L-T4剂量、L-T4添加时间等均无相关性.结论 药物治疗过程中,甲状腺激素水平正常的GD患者,其TSH水平长期受抑制的原因与高水平TRAb相关,可能由于TRAb直接与垂体内TSH受体结合,通过超短环反馈抑制TSH的分泌所致.     

Graves 病患者血清 Th1／Th2细胞因子水平变化及意义

目的：观察Graves病（ GD）患者血清Th1/Th2细胞因子水平变化,并分析其意义。方法选择52例GD患者（ GD组）及60例同期健康体检者（对照组）,以ELISA法检测血清Th1细胞因子肿瘤坏死因子α（ TNF-α）、γ-干扰素（ IFN-γ）及Th2细胞因子IL-4、IL-10水平,以化学发光法检测甲状腺功能指标游离三碘甲状腺氨酸（ FT3）、游离甲状腺素（ FT4）、促甲状腺素（ TSH）水平,Pearson相关分析法分析上述两类指标间的关系。结果 GD组血清细胞因子水平均高于对照组,TNF-α/IL-4、TNF-α/IL-10、IFN-γ/IL-4和IFN-γ/IL-10均低于对照组（P均＜0．05）;GD组血清IL-4、IL-10与FT3、FT4均呈明显正相关,与TSH呈明显负相关（P均＜0．05）。结论 GD患者存在血清Th1/Th2细胞因子平衡紊乱,Th2细胞因子介导的体液免疫可能在其发病中具有重要作用。     

脑梗死病人血清FT3、TSH水平与病情严重程度的关系探讨

目的探讨脑梗死病人血清游离三碘甲状腺原氨酸(FT3)、促甲状腺激素(TSH)水平与病情严重程度的关系。方法选取2017年1月—2018年12月辽宁省人民医院收治的100例急性脑梗死病人,根据病人美国国立卫生研究院卒中量表(NIHSS)评分分为轻度组(41例)、中度组(33例)、重度组(26例);另筛选同期在本院行健康体检的健康志愿者30名作为对照组。应用化学发光法检测各组血清FT3、TSH水平,Spearman相关性分析法分析血清FT3、TSH水平与病情严重程度的关系。结果脑梗死组血清FT3明显低于对照组,TSH明显高于对照组,差异均有统计学意义(P0.05);不同疾病严重程度的脑梗死病人血清FT3、TSH比较差异有统计学意义(P0.05),血清FT3水平:轻度组中度组高度组;血清TSH:轻度组中度组重度组,组间比较差异均有统计学意义(P0.05);Spearman相关性分析显示,血清FT3与病情严重程度呈负相关(r=-0.564,P0.01),血清TSH与病情严重程度呈正相关(r=0.567,P0.01)。结论脑梗死病人血清FT3、TSH水平与病情严重程度明显相关。     

甲亢患者β_2-微球蛋白与甲状腺激素相关性研究

目的探讨甲亢患者β2-微球蛋白含量与甲状腺激素间的关系及其可能具有的临床价值。方法 40例甲亢患者作为观察组,40例健康体检人群为对照组。对比分析不同组间和不同疗效间各项实验室指标的差异,并进行血清和尿β2-微球蛋白与FT3、FT4、TSH的相关性分析。结果治疗前,甲亢患者FT3、FT4、TSH及血清和尿β2-微球蛋白含量与对照组比较均有统计学差异（P〈0.01）,治疗后,无统计学差异（P〉0.05）;治愈组患者血清和尿β2-微球蛋白、FT3、FT4、TSH含量与好转组及无效组间的差异均有统计学意义（P〈0.01）;治疗前,血清和尿β2-微球蛋白与FT3、FT4呈正相关,与TSH呈负相关。结论甲亢患者β2-微球蛋白含量与甲状腺激素关系密切,可作为判断病情变化和疗效观察的重要指标。     

趋化因子CXCL12/CXCR4轴与lgr5基因在结直肠癌组织中的表达

目的 探讨人结直肠癌组织中趋化因子CXCL12/CXCR4轴、干细胞标志物lgr5基因的表达变化及与临床病理特征间的关系.方法 采用SYBR Green实时定量PCR检测27例结直肠癌组织、27例匹配的远端切缘正常组织中CXCL12、CXCR4及lgr5 mRNA表达.结果 结直肠癌组织中CXCR4、lgr5 mRNA表达明显高于匹配正常组织(P＜0.01),CXCL12 mRNA表达水平低于正常组织(P＜0.01).结直肠癌组织CXCL12、CX-CR4及lgr5mRNA在不同性别、年龄、肿瘤原发部位、大小、组织学类型组间表达差异均无统计学意义(均P＞0.05).但有淋巴结转移组CXCR4及lgr5 mRNA表达高于无淋巴结转移组,且有淋巴结转移组CXCL12 mRNA表达下降更显著(P＜0.05).结论 CXCL12基因表达下调、CXCR4、lgr5基因表达上调参与了结直肠癌组织生长及转移,CXCL12/CXCR4生物轴、lgr5有望成为抗肿瘤治疗的新靶点.     

Graves病患者131I治愈前后尿微量蛋白的变化观察

目的：探讨Graves病（简称GD）患者131 I治愈前后尿微量蛋白变化的影响因素。方法选择GD患者20例（GD组）,根据131I治愈前后分成治疗前的GD组、治愈3个月R3M组、治愈12个月R12M组,并设正常对照组20例。采用全自动化学免疫发光法检测血清游离甲功3项[包括游离三碘甲状腺原氨酸（ FT3）、游离甲状腺素（ FT4）、促甲状腺素（ TSH）]、促甲状腺受体抗体（ TRAb）、尿微量白蛋白（ Alb）、尿免疫球蛋白（IgG）、尿微球蛋白（β2-MG）含量。采用散射比浊法检测血清中超敏C反应蛋白（hs-CRP）。全自动血凝仪测定血清D-二聚体（ D-D）。 SPECT计算总肾小球滤过率（ TRGFR）。结果 GD组游离甲功3项与各组比较差异有统计学意义（ P＜0.01）。 GD组、R3M组的TRAb、Alb、IgG与其余组比较差异有统计学意义（ P＜0.01）。直线相关分析显示,FT3与Alb、IgG呈显著正相关（ r分别为0.64、0.72, P均＜0.01）, TRAb与Alb、IgG呈显著正相关（ r分别为0.66、0.56,P均＜0.01）。结论 GD肾损害的部位在肾小球,与免疫紊乱关系密切;GD相关抗体的消失可作为判断GD肾损害的恢复及治疗效果的参考指标。     

脑梗死后抑郁与甲状腺激素水平相关性的研究

目的探讨急性脑梗死后抑郁患者甲状腺激素水平的变化。方法对120例急性脑梗死患者进行分组,脑梗死后无抑郁组(60例)和脑梗死后抑郁组(60例),各组中轻、中、重度抑郁各20例。60例正常健康体检者为对照组。收集脑梗死组发病第2天及第14天的血清及对照组血清待测。测定所有血清游离三碘甲状腺原氨酸(FT3)、游离甲状腺素(FT4)及促甲状腺素(TSH)水平,比较脑梗死后抑郁与脑梗死后无抑郁及脑梗死后不同程度抑郁甲状腺激素水平的变化情况。结果脑梗死后无抑郁组及脑梗死后抑郁组发病第2天时血清FT3水平低于对照组,FT4水平高于对照组,差异有统计学意义(P0.05),且脑梗死后抑郁组较脑梗死后无抑郁组变化更显著,(P0.05);脑梗死后无抑郁组血清促甲状腺素(TSH)较对照组增高(P0.05),而脑梗死后抑郁组TSH水平与对照组相比差异无统计学意义。发病第14天脑梗死后无抑郁组FT3、FT4基本恢复,与对照组比较差异无统计学意义;而脑梗死后抑郁组FT3、FT4水平恢复不明显,与对照组相比差异有统计学意义(P0.05)。3组的TSH水平差异不明显;脑梗死后抑郁患者TSH的改变量与HAMD评分密切相关(P0.05),而血FT3、FT4与HAMD评分无相关关系(P0.05)。结论急性脑梗死患者抑郁症状可能与甲状腺激素水平变化有关,血清FT3、FT4和TSH可作为评价急性脑梗死患者抑郁症状及程度的客观指标。     

Graves病患者血清氨基端-脑钠肽前体水平的变化

目的 研究Graves病(GD)甲亢患者血清氨基端.脑钠肽前体(NT-proBNP)的变化特点及临床意义.方法 入选GD患者269例,其中初发患者90例.测定血清甲状腺激素、促甲状腺素受体抗体(TRAb)和NT-proBNP水平.结果 血清NT-pmBNP与FT3(r=0.260,P<0.01)、FT4(r=0.297,P<0.01)和心率正相关(r=0.251,P<0.05);与超敏TSH(sTSH)负相关(r=-0.157,P<0.01).校正年龄、性别和体重指数(BMI)后,血清NT-pmBNP仍与FT3、FT4和TRAb正相关(均P<0.01).校正血清FT3,FT4、sTSH、TRAb、年龄、性别、BMI后,初发组和治疗组的血清NT-proBNP差异仍有统计学意义(P<0.01),血清FT4对NT-pwBNP有显著影响(P<0.01),NT-proBNP水平的升高在甲亢已经控制的患者中同样存在.结论 GD患者血清NT-pwBNP水平随着FT4的升高而明显上升,不受性别、年龄和BMI的影响.监测血清NT-pmBNP有助于了解GD患者的血管僵硬度和容量变化,为早期防治甲亢引起的心血管疾病提供依据.     

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。     

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.     

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.     

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.     

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.     

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.     

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。     

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.     

Prevalence of Coronary Artery Disease in Patients with Valvular Heart Disease

ABSTRACT. To evaluate the usefulness of preoperative coronary angiography in patients undergoing preoperative investigation because of valvular heart disease, we performed coronary angiography in a consecutive series of 329 patients. The prevalence of significant coronary artery disease was 32%. Asymptomatic coronary artery disease was present in 13%. Angina pectoris proved to be a poor predictor of coronary artery disease in aortic valve disease. In mitral valve disease, however, the specificity was high. A cost-benefit calculation was carried out in order to assess what advantage routine coronary angiography might have. According to this, coronary angiography should be performed in all patients suffering from valvular heart disease with angina pectoris, whereas it can be omitted in younger patients without angina. A cut-off point of 60 years seems appropriate for aortic valve disease and 65 years for mitral valve disease.