中西医结合治疗慢性盆腔炎98例

目的观察中西医结合用药,治疗慢性盆腔炎的疗效。方法采用替硝唑等腹腔灌注,薏苡附子败酱散加减治疗本病98例。同时设对照组98例,单纯用替硝唑等腹腔灌注。结果治疗组总有效率为96%,明显高于对照组总有效率82%(P<0.05)。结论替硝唑等腹腔灌注配合中药治疗慢性盆腔炎,中西药有协同作用,安全可靠,容易掌握,经济有效。

失眠症的研究与治疗

目的:总结和评价近年来失眠症发病机制、临床诊断和治疗的研究进展,以期对进一步的研究有所启示。资料来源:应用计算机检索PubMed和ScienceDirectOnline数据库1990-01/2005-10的相关文献,检索词“Insomnia,Etiology,Diagnoses,Therapy”,限定文章语言种类为英文。同时计算机检索中国期刊全文数据库、维普数据库1990-01/2005-10的相关文献,检索词“失眠症、病因学、诊断、治疗”,限定文章语言种类为中文。资料选择:对资料进行初审,选取与失眠症的病因学、诊断和治疗相关的文献,通过摘要开始查找全文,以是否与失眠症及其治疗相关作为纳入标准。数据提炼:共收集到51篇与失眠症的病因学、诊断、治疗有关的论文,排除24篇重复研究或与本文主题联系不够密切的论文。资料综合:失眠症的病因极其复杂,与自身的易感素质和外界的特定条件有关;失眠的发病机制与睡眠-觉醒周期有关;失眠的诊断主要依靠患者自述的病史;失眠的治疗首先要建立在对患者全面的评估和准确诊断之上,通过消除导致失眠的各种因素,达到改善睡眠质量的目的。目前常用的治疗手段有厌恶治疗、物理治疗、心理治疗以及中医治疗等。结论:由于失眠的病因复杂多样,发病机制与睡眠-觉醒周期密切相关,其诊断主要依靠患者自述的病史和临床诊断资料等原因,对失眠症的治疗应采用综合治疗手段。

失语症的康复治疗:研究与应用

目的:探讨失语症的言语语言治疗、药物治疗和影响治疗效果的因素。资料来源:应用计算机检索Pubmed数据库2000-01/2006-01期间的有关失语症方面的文献。检索词为“aphasia,anomia,treat,treatment,therapy,cure,heal”,并限定文章语言种类为English。同时计算机检索CNKI2000-01/2006-01期间的有关失语症方面的文献。检索词为“失语,治疗”,并限定文章语言种类为中文。资料选择:共检索300余篇文献进行筛选。以近3年内研究内容相关且发表在权威杂志上的文章优先,选择了以失语症治疗为主要研究内容的文献24篇。资料提炼:将资料进行分类,其中19篇是关于言语语言治疗的文献,5篇是关于药物治疗的文献。资料综合:言语语言治疗和药物治疗是治疗失语症的主要方法。言语语言治疗主要包括刺激法、阻断去除法、认知心理学的方法、计算机辅助治疗和小组治疗等。但言语语言治疗的有效性尚有争议。药物治疗主要有溴隐停、右苯丙胺、吡拉西坦和中药治疗等。药物治疗虽对失语的恢复有帮助,但治疗机制还不确切。影响失语症恢复的因素很多,发病时失语的严重程度是最主要的因素,失语症的类型,患者的职业,受教育程度,及社会支持等都对言语的恢复有影响。结论:①失语症的治疗强度与其康复效果有关系。要选择合理的治疗方法还需进一步的研究。②药物治疗的效果虽已被证明有效,但适用范围广、副作用小的药物开发还有待于进一步的研究。③治疗时需要综合考虑可能影响康复效果的各种因素来制定个性化的治疗方案。

慢性阻塞性肺疾病夜间低氧血症患者氧疗方式的初步研究

【目的】研究慢性阻塞性肺疾病(COPD)患者夜间低氧的发生情况并探讨鼻导管及无创通气Bi-PAP方式吸氧对夜间低氧的疗效。【方法】220例稳定期COPD患者采用便携式初筛诊断仪进行睡眠监测,对存在夜间低氧患者行鼻导管及无创通气BiPAP方式进行氧疗下重复睡眠监测。【结果】夜间低氧血症的发生率为41.8%(92/220),夜间低氧与日间血氧饱和度(SaO2)相关;其中64%(59/92)患者经鼻导管氧疗效果好,而36%(33/92)患者改为无创通气BiPAP方式进行氧疗夜间低氧得以改善。【结论】COPD患者夜间睡眠时出现低氧或低氧血症加重,COPD与阻塞性睡眠呼吸暂停低通气综合征(OSAHS)并存可加重夜间低氧血症,部分患者需要无创通气进行氧疗才能改善夜间低氧血症。

磁控胶囊内镜在合并慢性疾病且有胃镜检查相对禁忌证的老年患者中的应用

【目的】分析磁控胶囊内镜(magnetic capsule endoscopy,MCE)在合并慢性疾病且有胃镜检查相对禁忌证的老年(>65岁)患者应用中的安全性及耐受性。【方法】选取中南大学湘雅二医院2015年11月至2017年7月因上消化道症状需行胃镜检查明确诊断的54例有普通胃镜检查相对禁忌证的老年患者为研究对象.观察患者检查前、检查中和检查后生命体征的变化、不良反应事件发生率及舒适感程度。【结果】患者检查前、中和检查后心率、呼吸、收缩压及舒张压等生命体征无明显变化.其差异无统计学意义(P>0.05);受检者末端指血氧饱和度前后变化无统计学意义(P>0.05)。不良反应发生率低,仅2例(3.7%)出现轻微恶心,1例(1.9%)出现气促。2例(3.7%)感觉轻度不适.54例患者(100%)均表示愿意再接受此检查。【结论】MCE在有普通胃镜检查相对禁忌证的老年患者应用中是安全、可行的,患者舒适度高。

胃灵冲剂对慢性萎缩性胃炎大鼠胃黏膜影响的实验研究

目的:探讨胃灵冲剂对慢性萎缩性胃炎(CAG)大鼠胃黏膜保护作用的机理。方法:将120只Wis-tar雄性大鼠随机分为5组:正常组,模型组,维酶素对照组,胃灵冲剂大、小剂量组。除正常组外其余各组采用综合方法造模。5组大鼠施加相关因素1个月后处死,检测胃黏膜组织中PGE2、氨基己糖水平并观察胃黏膜组织学方面的改变。结果:模型大鼠胃黏膜组织PGE2及氨基己糖水平明显低于正常组,病理改变明显,经胃灵冲剂治疗后,PGE2与氨基己糖水平恢复正常,胃黏膜病理组织学改善明显。结论:胃灵冲剂可能是通过调节胃肠道激素水平从而起到保护和修复胃黏膜的作用。

认知行为疗法在住院老年慢性病合并抑郁症状中的应用

目的观察认知行为疗法对老年慢性躯体疾病合并抑郁患者的疗效和生活质量的影响。方法在正常治疗和常规护理基础上,实验组介入认知行为疗法,并对实验组和对照组进行汉密尔顿抑郁量表(HAMD)、Spitzer生活指数评分表(QLI)的测评。结果 HAMD量表总分实验组比对照组明显下降,实验组生活质量提高比对照组更明显,两组间比较差异有统计学意义。结论认知行为疗法在老年慢性躯体疾病合并抑郁患者的临床应用,可有效改善患者症状,使患者躯体症状明显改善,生活自理能力提高。

Overexpression of lentivirus-mediated glial cell line-derived neurotrophic factor in bone marrow stromal cells and its neuroprotection for the PC12 cells damaged by lactacystin

Objective To construct recombinant lentiviral vectors for gene delivery of the glial cell line-derived neurotropnic factor （GDNF）, and evaluate the neuroprotective effect of GDNF on lactacystin-damaged PC12 cells by transfecting it into bone marrow stromal cells （BMSCs）. Methods pLenti6/V5-GDNF plasmid was set up by double restriction enzyme digestion and ligation, and then the plasmid was transformed into Top10 cells. Purified pLenti6/V5-GDNF plasmids from the positive clones and the packaging mixture were cotransfected to the 293FT packaging cell line by Lipofectamine2000 to produce lentivirus, then the concentrated virus was transduced to BMSCs. Overexpression of GDNF in BMSCs was tested by RT-PCR, ELISA and immunocytochemistry, and its neuroprotection for lactacystin-damaged PC12 cells was evaluated by MTT assay. Results Virus stock of GDNF was harvested with the titer of 5.6×10^5 TU/mL. After tmnsduction, GDNF-BMSCs successfully secreted GDNF to supematant with nigher concentration （800 pg/mL） than BMSCs did （less than 100 pg/mL）. The supematant of GDNF-BMSCs could significantly alleviate the damage of PC12 cells induced by lactacystin （10 μmol/L）. Conclusion Overexpression of lentivirus-mediated GDNF in the BMSCs cells can effectively protect PC12 cells from the injury by the proteasome inhibitor.

Etiopathogenesis of inflammatory bowel diseases

Theories explaining the etiopathogenesis of inflammatory bowel disease （IBD） have been proposed ever since Crohn＇s disease （CD） and ulcerative colitis （UC） were recognized as the two major forms of the disease. Although the exact cause（s） and mechanisms of tissue damage in CD and UC have yet to be completely understood, enough progress has occurred to accept the following hypothesis as valid： IBD is an inappropriate immune response that occurs in genetically susceptible individuals as the result of a complex interaction among environmental factors, microbial factors, and the intestinal immune system. Among an almost endless list of environmental factors, smoking has been identified as a risk factor for CD and a protective factor for UC. Among microbial factors, no convincing evidence indicates that classical infectious agents cause IBD, while mounting evidence points to an abnormal immune response against the normal enteric flora as being of central importance. Gut inflammation is mediated by cells of the innate as well as adaptive immune systems, with the additional contribution of non-immune cells, such as epithelial, mesenchymal and endothelial cells, and platelets.

Survival and prognostic factors in hepatitis B virus-related acute-on-chronic liver failure

AIM:To investigate the survival rates and prognostic factors in patients with hepatitis B virus-related acuteon-chronic liver failure(HBV-ACLF).METHODS:Clinical data in hospitalized patients with HBV-ACLF admitted from 2006 to 2009 were retrospectively analyzed.Their general conditions and survival were analyzed by survival analysis and Cox regression analysis.RESULTS:A total of 190 patients were included in this study.The overall 1-year survival rate was 57.6%.Patients not treated with antiviral drugs had a significantly higher mortality[relative risk(RR)=0.609,P=0.014].The highest risk of death in patients with ACLF was associated with hepatorenal syndrome(HRS)(RR=2.084,P=0.026),while other significant factors were electrolyte disturbances(RR=2.062,P=0.010),and hepatic encephalopathy(HE)(RR=1.879,P<0.001).CONCLUSION:Antiviral therapy has a strong effect on the prognosis of the patients with HBV-ACLF by improving their 1-year survival rate.HRS,electrolyte disturbances,and HE also affect patient survival.

Why do young people with chronic kidney disease die early?

Cardiovascular disease poses the greatest risk of premature death seen among patients with chronic kidney disease(CKD).Up to 50% of mortality risk in the dialysis population is attributable to cardiovascular disease and the largest relative excess mortality is observed in younger patients.In early CKD,occlusive thrombotic coronary disease is common,but those who survive to reach end-stage renal failure requiring dialysis are more prone to sudden death attributable mostly to sudden arrhythmic events and heart failure related to left ventricular hypertrophy,coronary vascular calcification and electrolyte disturbances.In this review,we discuss the basis of the interaction of traditional risk factors for cardiovascular disease with various pathological processes such as endothelial dysfunction,oxidative stress,low grade chronic inflammation,neurohormonal changes and vascular calcification and stiffness which account for the structural and functional cardiac changes that predispose to excess morbidity and mortality in young people with CKD.

Management of hepatorenal syndrome

Hepatorenal syndrome （HRS） is defned as development of renal dysfunction in patients with chronic liver diseases due to decreased effective arterial blood volume. It is the most severe complication of cirrhosis because of its very poor prognosis. In spite of several hypotheses and research, the pathogenesis of HRS is still poorly understood. The onset of HRS is a progressive process rather than a suddenly arising phenomenon. Since there are no specifc tests for HRS diagnosis, it is diagnosed by the exclusion of other causes of acute kidney injury in cirrhotic patients. There are two types of HRS with different characteristics and prognostics. Type 1 HRS is characterized by a sudden onset acute renal failure and a rapid deterioration ofother organ functions. It may develop spontaneously or be due to some precipitating factors. Type 2 HRS is characterized by slow and progressive worsening of renal functions due to cirrhosis and portal hypertension and it is accompanied by refractory ascites. The only definitive treatment for both Type 1 and Type 2 HRS is liver transplantation. The most suitable bridge treatment or treatment for patients who are not eligible for transplantation is a combination of terlipressin and albumin. For the same purpose, it is possible to try hemodialysis or renal replacement therapies in the form of continuous veno-venous hemofiltration. Artificial hepatic support systems are important for patients who do not respond to medical treatment.Transjugular intrahepatic portosystemic shunt may be considered as a treatment modality for unresponsive patients to medical treatment. The main goal of clinical surveillance in a cirrhotic patient is prevention of HRS before it develops. The aim of this article is to provide an updated review about the physiopathology of HRS and its treatment.

Chronic kidney disease in acute coronary syndromes

Chronic kidney disease(CKD) is associated with a high burden of coronary artery disease. In patients with acute coronary syndromes(ACS), CKD is highly prevalent and associated with poor short- and long-term outcomes. Management of patients with CKD presenting with ACS is more complex than in the general population because of the lack of well-designed randomized trials assessing therapeutic strategies in such patients. The almost uniform exclusion of patients with CKD from randomized studies evaluating new targeted therapies for ACS, coupled with concerns about further deterioration of renal function and therapy-related toxic effects, may explain the less frequent use of proven medical therapies in this subgroup of high-risk patients. However, these patients potentially have much to gain from conventional revascularization strategies used in the general population. The objective of this review is to summarize the current evidence regarding the epidemiology and the clinical and prognostic relevance of CKD in ACS patients, in particular with respect to unresolved issues and uncertainties regarding recommended medical therapies and coronary revascularization strategies.

Type 2 diabetes mellitus and CA 19-9 levels

AIM： To prospectively investigate serum CA 19-9 levels in type 2 diabetic patients in comparison with age and gender-matched control subjects.METHODS： We recorded duration of diabetes and examined fasting glucose levels, HbAlc levels and serum CA 19-9 levels in 76 type 2 diabetic patients and 76 controls. Abdominal CT was performed in order to eliminate abdominal malignancy in the diabetic and control groups.RESULTS： The average CA 19-9 level was 46.0 ± 22.4 U/mL for diabetic patients whereas it was 9.97± 7.1 U/mL for the control group （P 〈 0.001 ）. Regression analysis showed a positive correlation between diabetes and CA 19-9 independent from age, gender, glucose level and HbAlc level （t = 8.8, P 〈 001 ）. Two of the diabetic patients were excluded from the study because of abdominal malignancy shown by CT at the initial evaluation. For all patients, abdominal CT showed no pancreatic abnormalities. CONCLUSION： CA 19-9 is a tumor-associated antigen, which is elevated in pancreatic, upper gastrointestinal tract, ovarian hepatocellular, and colorectal cancers, as well as in inflammatory conditions of the hepatobiliary system, biliary obstruction and in thyroid diseases. Diabetes has been claimed to be a risk factor for pancreatic cancer, which is increasing its incidence and has one of the lowest survival rates of all cancers. CA 19-9 is used in the diagnosis of pancreatic cancer but is also a marker of pancreatic tissue damage that might be caused by diabetes. We propose that a higher cutoff value of CA 19-9 should be used in diabetics to differentiate benign and malignant pancreatic disease, and subtle elevations of CA 19-9 in diabetics should be considered as the indication of exocrine pancreatic dysfunction.

Role of different imaging modalities of vascular calcification in predicting outcomes in chronic kidney disease

Vascular calcification(VC) is common among patientswith chronic kidney disease(CKD).The severity of VC is associated with increased risk of cardiovascular events and mortality.Risk factors for VC include traditional cardiovascular risk factors as well as CKD-related risk factors such as increased calcium and phosphate load.VC is observed in arteries of all sizes from small arterioles to aorta,both in the intima and the media of arterial wall.Several imaging techniques have been utilized in the evaluation of the extent and the severity of VC.Plain radiographs are simple and readily available but with the limitation of decreased sensitivity and subjective and semi-quantitative quantification methods.Mammography,especially useful among women,offers a unique way to study breast arterial calcification,which is largely a medial-type calcification.Ultrasonography is suitable for calcification in superficial arteries.Analyses of wall thickness and lumen size are also possible.Computed tomography(CT) scan,the gold standard,is the most sensitive technique for evaluation of VC.CT scan of coronary artery calcification is not only useful for cardiovascular risk stratification but also offers an accurate and an objective analysis of the severity and progression.

Treatment of dyslipidemia in chronic kidney disease: Effectiveness and safety of statins

Several cardiovascular(CV)risk factors may explain the high rate of CV death among patients with chronic kidney disease(CKD).Among them both traditional and uremia-related risk factors are implicated and,moreover,the presence of kidney disease represents"per se"a multiplier of CV risk.Plasma lipid and lipoprotein profiles are changed in quantitative,but above all in qualitative,structural,and functional ways,and lipoprotein metabolism is influenced by the progressive loss of renal function.Statin therapy significantly reduces cholesterol synthesis and both CV morbidity and mortality either directly,by reducing the lipid profile,or via pleiotropic effects;it is supposed to be able to reduce both the progression of CKD and also proteinuria.These observations derive from a post-hoc analysis of large trials conducted in the general population,but not in CKD patients.However,the recently published SHARP trial,including over 9200 patients,either on dialysis or pre-dialysis,showed that simvastatin plus ezetimibe,compared with placebo,was associated with a significant low-density lipoprotein cholesterol reduction and a 17%reduction in major atherosclerotic events.However,no benefit was observed in overall survival nor in preserving renal function in patients treated.These re-cent data reinforce the conviction among nephrologists to consider their patients at high CV risk and that lipid lowering drugs such as statins may represent an important tool in reducing atheromatous coronary disease which,however,represents only a third of CV deaths in patients with CKD.Therefore,statins have no protective effect among the remaining two-thirds of patients who suffer from sudden cardiac death due to arrhythmia or heart failure,prevalent among CKD patients.The safety of statins is demonstrated in CKD by several trials and recently confirmed by the largest SHARP trial,in terms of no increase in cancer incidence,muscle pain,creatine kinase levels,severe rhabdomyolysis,hepatitis,gallstones and pancreatitis;thus confirming the handiness of statins in CKD patients.Here we will review the latest data available concerning the effectiveness and safety of statin therapy in CKD patients.

Vascular calcification in chronic kidney disease: Pathogenesis and clinical implication

Cardiovascular disease is the leading cause of deathamong patients with chronic kidney disease （CKD）.Vascular calcification （VC） is one of the independentrisk factors associated with cardiovascular disease andcardiovascular mortality in both the general populationand CKD patients. Earlier evidence revealed substan-tially higher prevalence of VC in young adults on chron-ic hemodialysis compared to the general population inthe same age range, indicating the infuence of CKD-related risk factors on the development of VC. Patho-genesis of VC involves an active, highly organized cel-lular transformation of vascular smooth muscle cells tobone forming cells evidenced by the presence of bonematrix proteins in the calcifed arterial wall. VC occursin both the intima and the media of arterial wall withmedial calcification being more prevalent in CKD. Inaddition to traditional cardiovascular risks, risk factorsspecific to CKD such as phosphate retention, excessof calcium, history of dialysis, active vitamin D therapy in high doses and deficiency of calcification inhibitors play important roles in promoting the development of VC. Non-contrast multi-slice computed tomography has often been used to detect coronary artery calcif-cation. Simple plain radiographs of the lateral lumbar spine and pelvis can also detect VC in the abdominal aorta and femoral and iliac arteries. Currently, there is no specifc therapy to reverse VC. Reduction of calcium load, lowering phosphate retention using non-calcium containing phosphate binders, and moderate doses of active vitamin D may attenuate progression. Parenteral sodium thiosulfate has also been shown to delay VC progression.

Chronic Epstein-Barr virus-related hepatitis in immunocompetent patients

AIM: To investigate reactivated Epstein-Barr virus (EBV) infection as a cause for chronic hepatitis. METHODS: Patients with occasionally established elevated serum aminotransferases were studied. HIV, HBV and HCV-infections were excluded as well as any other immunosuppressive factors, metabolic or toxic disorders. EBV viral capsid antigen (VCA) IgG and IgM, EA-R and EA-D IgG and Epstein-Barr nuclear antigen (EBNA) were measured using IFA kits. Immunophenotyping of whole blood was performed by multicolor flow cytometry. CD8+ T cell responses to EBV and PHA were determined according to the intracellular expression of IFN-γ. RESULTS: The mean alanine aminotransferase (ALT) and gamma glutamyl transpeptidase (GGTP) values exceeded twice the upper normal limit, AST/ALT ratio < 1. Serology tests showed reactivated EBV infection in all patients. Absolute number and percentages of T, B and NK cells were within the reference ranges. Fine subset analysis, in comparison to EBV+ healthy carriers, revealed a significant decrease of naive T cells (P < 0.001), accompanied by increased percentage of CD45RA- (P < 0.0001), and terminally differentiated CD28-CD27- CD8+ T cells (P < 0.01). Moderately elevated numbers of CD38 molecules on CD8+ T cells (P < 0.05) proposed a low viral burden. A significantly increased percentage of CD8+ T cells expressing IFN-γ in response to EBV and PHA stimulation was registered in patients, as compared to controls (P < 0.05). Liver biopsy specimens from 5 patients revealed nonspecific features of low-grade hepatitis.CONCLUSION: Chronic hepatitis might be a manifestation of chronic EBV infection in the lack of detectable immune deficiency; the expansion of CD28- CD27- and increase of functional EBV-specific CD8+ T cells being the only surrogate markers of viral activity.

Psychological impact of chronic hepatitis C:Comparison with other stressful life events and chronic diseases

AIM： To examine the psychological impact of chronic hepatitis C （CHC） diagnosis in a large cohort of CHC patients as compared with other stressful life events and chronic diseases carrying a risk of life-threatening complications. METHODS： One hundred and eighty-five outpatients with compensated CHC were asked to self-grade, using a 100-mm visual analogue scale （VAS）, the degree of stress caused by the learning of CHC diagnosis and the perceived severity of their disease. Diagnosis-related stress was compared to four other stressful life events and perceived CHC severity was compared to four other common chronic diseases. RESULTS： Learning of CHC diagnosis was considered a major stressful event （mean ± SD scores： 72±25）, significantly less than death of a loved-one （89±13, P〈0.0001） and divorce （78 ± 23, P〈0.007）, but more than job dismissal （68 ± 30, P〈 0.04） and home removal （26±24, P〈 0.0001）. CHC was considered a severe disease （74± 19）, after AIDS （94±08, P〈 0.001） and cancer （91± 11, P〈 0.001）, but before diabetes （66±23, P〈0.001） and hypertension （62±20, P〈0.001）. Perceived CHC severity was not related to the actual severity of liver disease, assessed according to Metavir fibrosis score. In multivariate analysis, diagnosisrelated stress was related to perceived disease severity （P〈0.001）, trait anxiety （P〈 0.001） and infection through blood transfusion （P〈 0.001）. CONCLUSION： Our results show the considerable psychological and emotional burden that a diagnosis of CHC represents, even in the absence of significant liver disease. They should be taken into account when announcing a diagnosis of CHC in order to reduce its negative effects.