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Slow transit constipation has been traditionally considered and classified as a functional disorder. However, clinical and manometric evidence has been accumulating that suggests how most of the motility alterations in STC might be considered of neuropathic type.In addition, further investigations showed that subtle alterations of the enteric nervous system, not evident to conventional histological examination, may be present in these patients. In the present article we will discuss these evidences, and will try to put them in relation with the abnormal motor function of the large bowel documented in this pathological condition.  相似文献   

3.
糖尿病自主神经病变是糖尿病常见的并发症之一,是糖尿病神经并发症的一部分。目前关于糖尿病自主神经病变的发病机制尚不十分明确,有报道患病率为17%~40%。本病可广泛累及心血管、胃肠、泌尿和生殖等多个器官系统,具有起病隐匿,病情逐渐进显示,糖尿病心脏自主神经病变作为糖尿病的并发症是临床常见病,严重影响糖尿病患者的生活质量,可使糖尿病患者出现心动过速、体位性低血压等不适症状。  相似文献   

4.
Cardiac and vascular changes in cirrhosis: Pathogenic mechanisms   总被引:17,自引:2,他引:15  
Cardiovascular abnormalities accompany both portal hy-pertension and cirrhosis.These consist of hyperdynamiccirculation,defined as reduced mean arterial pressureand systemic vascular resistance,and increased cardiacoutput.Despite the baseline increased cardiac output,ventricular inotropic and chronotropic responses tostimuli are blunted,a condition known as cirrhotic car-diomyopathy.Both conditions may play an initiating oraggravating pathogenic role in many of the complicationsof liver failure or portal hypertension including ascites,variceal bleeding,hepatorenal syndrome and increasedpostoperative mortality after major surgery or livertransplantation.This review briefly examines the majormechanisms that may underlie these cardiovascular ab-normalities,concentrating on nitric oxide,endogenouscannabinoids,central neural activation and adrenergicreceptor changes.Future work should address the com-plex interrelationships between these systems.  相似文献   

5.
The possible relationship between diabetes mellitus (DM) and colorectal cancer (CRC), concerning pathophysiological and molecular mechanisms is highlighted in this review. The most recent and complete articles and developments in this particular field were thoroughly reviewed. Common risk factors, such as obesity, sedentary lifestyle, and Western diet between DM and CRC, led to the theory that DM might be a causal agent for CRC development. Various studies have connected type 2 DM and CRC, either proximal o...  相似文献   

6.
胰性脑病的病理、病因、发病机制和防治   总被引:5,自引:2,他引:3  
巫协宁 《胰腺病学》2003,3(1):49-50
胰性脑病是重症胰腺炎(急性坏死性胰腺炎)的严重并发症之一,由于对重症胰腺炎的处理欠当或过早进食,仍偶有发生。 一、胰性脑病的病理 胰性脑病的病变首先是由Rothermich与von Haan在  相似文献   

7.
Drug-induced liver injury is a significant and still unresolved clinical problem. Limitations to knowledge about the mechanisms of toxicity render incomplete the detection of hepatotoxic potential during preclinical development. Several xenobiotics are lipophilic substances and their transformation into hydrophilic compounds by the cytochrome P-450 system results in production of toxic metabolites. Aging, preexisting liver disease, enzyme induction or inhibition, genetic variances, local O_2 supply and, above all, the intrinsic molecular properties of the drug may affect this process. Necrotic death follows antioxidant consumption and oxidation of intracellular proteins, which determine increased permeability of mitochondrial membranes, loss of potential, decreased ATP synthesis, inhibition of Ca~(2+)-dependent ATPase, reduced capability to sequester Ca~(2+) within mitochondria, and membrane bleb formation. Conversely, activation of nucleases and energetic participation of mitochondria are the main intracellular mechanisms that lead to apoptosis. Non-parenchymal hepatic cells are inducers of hepatocellular injury and targets for damage. Activation of the immune system promotes idiosyncratic reactions that result in hepatic necrosis or cholestasis, in which different HLA genotypes might play a major role. This review focuses on current knowledge of the mechanisms of drug-induced liver injury and recent advances on newly discovered mechanisms of liver damage. Future perspectives including new frontiers for research are discussed.  相似文献   

8.
糖尿病性神经病变的发病机制与治疗   总被引:6,自引:0,他引:6  
李红专  翟秀华 《山东医药》2002,42(12):57-57
糖尿病性神经病变 (DNP)是糖尿病常见并发症之一。神经病变可累及感觉神经、运动神经及植物神经 ,产生剧烈疼痛、麻木、运动障碍 ,甚至引起下肢坏疽而截肢。本文就其发病机制及治疗综述如下。1  DNP的发病机制1.1 微血管病变学说 与 DNP发生关系较密切的是微血管病变 [1 ]。特别是小动脉和毛细血管的基底膜增厚 ,血管内皮细胞增生 ,血管壁内有脂肪和多糖类沉积 ,以致血管管腔狭窄 ;同时血液粘滞度增高 ,神经内滋养血管易被纤维蛋白和血小板聚集而堵塞 ,从而导致神经缺血缺氧。表现为糖尿病性周围神经病变患者周围神经再生障碍。1.2 …  相似文献   

9.
A 60-years old male was admitted to our department for investigation of constipation and hypogastric discomfort intensified during defecation of a few weeks duration. The cause proved to be a rectal carcinosarcoma that was treated by abdominoperineal resection and postoperative chemo-radiotherapy. The patient died 6 months later due to hepatic failure, showing evidence of disseminated disease. In general colonic carcinosarcomas constitute a rare category of malignant neoplasms whose nature is still incompletely understood. No specific treatment guidelines exist. Surgery is the mainstay of treatment and regardless of the addition of adjuvant therapy the prognosis is very poor. Systematic genetic analysis may be the clue for understanding the pathogenesis of these mysterious tumors.  相似文献   

10.
黄海  宋成运  李运田 《心脏杂志》2013,25(2):246-249
越来越多的证据表明,氧化应激是糖尿病性心肌病(DCM)的统一发病机制。本文就氧化应激引起DCM的病理生理机制进行了综述,提示DCM患者使用胰岛素泵强化治疗后氧化应激水平明显降低。  相似文献   

11.
《Primary Care Diabetes》2022,16(6):797-803
AimsTo determine the rates and predictors of the regression to normoglycemia and progression to diabetes among subjects with pre-diabetes.MethodsA 10-year longitudinal population-based study was conducted among 1329 participants with pre-diabetes in the Tehran Lipid and Glucose Study. Pre-diabetes was divided into isolated IFG (iIFG), isolated IGT (iIGT), and combined IFG/IGT. Univariate and stepwise multivariable Cox regression was used to evaluate predictors of glycemic conversions.ResultsThe cumulative incidences of normoglycemia and diabetes were 43.7% (95%CI 40.9–46.4) and 40.1% (37.3–42.7), respectively. Isolated IGT returned to normoglycemia more than iIFG (HR:1.26, 1.05–1.51), but there was no difference in how quickly they progressed to diabetes. Regression to normoglycemia was associated with younger age, female sex, lower BMI, no familial history of diabetes, higher HDL-C, and ex-smoking. Older age, higher BMI, diastolic blood pressure, total cholesterol, lower HDL-C, and familial history for diabetes were associated with progression to diabetes. The influence of BMI on glycemic status conversions diminished with age. At approximately above 60 years old, the hazards of BMI for any conversions faded out.ConclusionsThe modifiable predictors of regression to normoglycemia and progression to diabetes are roughly the same. The importance of BMI attenuates in elderly subjects.  相似文献   

12.
深圳市DM、IGT患病率与性别、年龄和文化程度的关系   总被引:13,自引:0,他引:13  
目的 探讨深圳市糖尿病(DM),糖耐量减低(IGT)患病率与性别,年龄及文化程度的关系。方法 对20岁以上的8200例行糖尿病流行病学调查。  相似文献   

13.
糖尿病及糖调节受损的诊断标准及其变迁   总被引:9,自引:0,他引:9  
回顾了糖尿病诊断标准的产生背景、修改过程及依据,介绍了空腹血糖受损及糖耐量减低概念的提出及诊断切点的调整变化及这种变化所带来的益处。同时,比较了美国糖尿病学会与世界卫生组织糖尿病诊断标准的不同之处,指出目前糖尿病诊断中的不足之处。另外,糖化血红蛋白A1c可能成为糖尿病筛查和诊断的可靠指标。  相似文献   

14.
目的探讨空腹血糖受损(IFG)、糖耐量受损(IGT)人群发生糖尿病的危险性及其影响因素.方法对1999年7月~12月包钢集团公司2万余人糖尿病普查中IFG、IGT患者730人于2001年9~11月进行随访调查.测量身高、体重、腰围、血压,作过夜空腹75 g葡萄糖耐量试验,同时测定空腹胰岛素(FINS)及服糖后2 h胰岛素(PINS),血总胆固醇(TC),甘油三酯(TG),高密度脂蛋白胆固醇(HDL-C).结果随访的656人中138人发生糖尿病.其中孤立性IFG(I-IFG)糖尿病年转变率为5.1%,孤立性(I-IGT)为11.5%,IGT为14.0%,IFG/IGT为20.2%.I-IGT、IGT及IFG/IGT糖尿病年转变率明显高于I-IFG(均P<0.001).与I-IFG比较,I-IGT发生糖尿病的危险比为2.65,IFG/IGT为5.96.I-IFG转归为糖尿病的危险因素主要是年龄(OR 1.05)和BMI(OR 1.03).I-IGT是2h血糖(OR 2.02)、家族史(OR 2.19)及腰围(OR 1.08).各项临床指标2年的变化结果转归为I-IFG、I-IGT者2年前后的年龄、体重、腰围、BMI、血压、TC均值及其肥胖、腹型肥胖、血脂代谢紊乱、高血压的患病率均比NGT转归组高;I-IFG与I-IGT比较差异无显著性.结论 I-IGT发生糖尿病的危险性明显高于I-IFG,主要危险因素为腰围、餐后血糖、家族史.I-IFG发生糖尿病的危险因素则是年龄、BMI.故对IGT应给予积极的干预治疗,而对于IFG应定期随访.  相似文献   

15.
Aims/hypothesis  The value of diagnostic categories of glucose intolerance for predicting type 2 diabetes is much debated. We therefore sought to estimate relative and population-attributable risk of different definitions based on fasting (impaired fasting glucose [IFG]) or 2 h plasma glucose concentrations (impaired glucose tolerance [IGT]) and to describe the associated clinical phenotypes. Methods  We prospectively observed a population-based cohort of 1,963 non-diabetic participants (mean age 47 years), in whom an OGTT was performed at baseline and 7 years later. Results  IGT was fivefold more prevalent (13.5%) than IFG. In both categories, participants were older, heavier, hyperinsulinaemic, hyperproinsulinaemic and dyslipidaemic compared with participants with normal glucose tolerance. Relative risk of incident diabetes was similar for IFG and IGT categories (3.73 [95% CI: 2.18–6.39] and 4.01 [95% CI: 3.12–5.14], respectively), but the population-attributable risk was fivefold higher for IGT (29% [95% CI: 26–32]) than for IFG (6% [95% CI: 5–7]). Isolated IFG carried no increase in risk. Lowering the threshold to 5.6 mmol/l raised the population-attributable risk of IFG to 23% (95% CI: 20–25); its contribution to diabetes progression, however, was largely due to co-existent IGT. In multivariate analysis adjusting for sex, age, familial diabetes and BMI, fasting and 2 h glucose were independent predictors. Conclusions/interpretation  Fasting and 2 h glucose values are independent predictors of incident diabetes. Isolated IFG is not a high-risk condition; lowering the diagnostic threshold increases the population-attributable risk of IFG fourfold, but performing an OGTT captures additional diabetes progressors compared with the number identified by IFG.  相似文献   

16.
Diabetic neuropathy is the most common complication of diabetes, affecting 50% of diabetic patients. Currently, the only treatment for diabetic neuropathy is glucose control and careful foot care. In this review, we discuss the idea that excess glucose overloads the electron transport chain, leading to the production of superoxides and subsequent mitochondrial and cytosolic oxidative stress. Defects in metabolic and vascular pathways intersect with oxidative stress to produce the onset and progression of nerve injury present in diabetic neuropathy. These pathways include the production of advanced glycation end products, alterations in the sorbitol, hexosamine and protein kinase C pathways and activation of poly-ADP ribose polymerase. New bioinformatics approaches can augment current research and lead to new discoveries to understand the pathogenesis of diabetic neuropathy and to identify more effective molecular therapeutic targets.  相似文献   

17.

Background

The aim of this study was to explore the correlation between obstructive sleep apnea (OSA) and diabetic neuropathy.

Materials and methods

After working out searching strategy, literatures were screened from the electronic databases: PubMed, Embase, and the Cochrane library. R 3.12 was utilized to perform meta-analysis, and odds ratio (OR) and its 95% confidence interval (CI) were used to present effect size. Heterogeneity was assessed by χ2-based Q test and I2 statistics. Publication bias was estimated by Egger’s test and sensitivity was evaluated by leave one out methods.

Results

According to the criteria, a total of 11 studies with 1842 patients were enrolled in this study. With a significant heterogeneity (Q = 31.83, I2 = 68.60%), the random effects model was utilized to assess the effect size of pooled data. A remarkable correlation was identified OSA and diabetic neuropathy (OR = 1.84, 95% CI: 1.18–2.87) without publication bias (t = 1.68, P = 0.13). Meanwhile, the result of leave one out performed a well sensitivity. Moreover, the subgroup analyses presented that OSA was significantly correlated with type 1 diabetic neuropathy (OR = 1.97, 95% CI: 1.19–3.25), but no remarkable correlation was identified between OSA and type 1 (OR = 1.84, 95% CI: 0.86–3.93) or 1 + 2 (OR = 1.30, 95% CI: 0.43–3.92) diabetic neuropathy.

Conclusion

OSA was significantly correlated with neuropathy in type 1 diabetes, but not in type 2 and type 1 + 2 diabetes.  相似文献   

18.
空腹血糖受损诊断标准下调的合理性分析   总被引:16,自引:3,他引:16  
目的 探讨空腹血糖受损 (IFG)诊断点从 6.1mmol/L下调至 5 .6mmol/L的合理性。方法对1986年入选的 468名非糖尿病人群〔3 41例正常糖耐量 (NGT) ,12 7例糖耐量受损 (IGT)〕在 1988年 ,1990年和 1992年分别进行OGTT复查 ,测定空腹血糖 (FPG)及 2h血糖 (2hPG)。以COX模型分析不同基线血糖水平增加糖尿病的风险。结果  (1) 10 9例 6年后发生糖尿病。COX成比例风险模型分析校正年龄、性别、体重指数 (BMI)影响后发现FPG与 2型糖尿病发病显著相关 (P =0 .0 0 0 1)。基线FPG 5 .6~ 6.0mmol/L组糖尿病发病危险性比FPG <5 .6mmol/L组已显著增加 ,RR为 3 .3 (95 %CI 2 .0~ 5 .3 ,P =0 .0 0 0 1)。 (2 )受试者工作特征 (ROC)曲线分析FPG预测糖尿病发病的最佳阈值是 5 .6mmol/L ,以FPG 5 .6mmol/L为诊断点IFG预报糖尿病发病的灵敏度、特异度、阳性预测值分别为 45 .0 % ,92 .8%和 65 .3 %。 (3 )NGT个体中COX成比例风险模型校正年龄、性别、BMI后显示 ,FPG分组 (5 .0~ 6.0mmol/L与 <5 .0mmol/L)与糖调节受损 (IGR ,包括IFG或IGT)发生显著正相关 (P =0 .0 0 7)。ROC曲线显示 ,FPG预测糖耐量恶化而进展为DM或IGR的最佳阈值为 5 .3mmol/L。结论  (1)本组非糖尿病人群中FPG预测糖尿病发病的最佳阈值为 5 .6mmol/L  相似文献   

19.
空腹血糖受损诊断标准下调对糖调节受损人群检出率的影响   总被引:12,自引:0,他引:12  
目的 分析空腹血糖受损(IFG)的空腹血糖(FPG)诊断标准下调对糖调节受损(IGR)人群检出率的影响,并探讨区分糖调节正常与受损的FPG理想截定点。方法 对2882例无2型糖尿病(T2DM)史的受试者进行口服葡萄糖耐量试验。采用1997年和2003年美国糖尿病学会分类诊断标准进行比较。结果 (1)IFG诊断标准下调后,单纯IFG者增加367例,IFG者由424例增加到1032例,其中包含的糖耐量受损(IGT)者由243例增加到484例;709例IGT者,包括在IFG者中的比例由34%上升到68%。(2)与糖耐量正常(NGT)人群相比,新增单纯IFG人群体质指数、FPG、2hPG、糖化血红蛋白、甘油三酯、胆固醇均升高(均P<0.01),超重(52.6 vs 39.7%,χ^2=6.79,P〈0.01)和高甘油三酯血症发生率(32.2% vs 24.9%,;χ^2=3.98,P〈0.05)明显增高。(3)非T2DM人群中诊断IGR(7.8≤2hPG<11.1mmol/L)的FPG理想截定点为5.6mmol/L。结论 IFG诊断标准下调后,IFG、IFG+IGT检出率明显增加;新增单纯IFG人群已经出现糖、脂代谢异常;非T2DM人群中诊断IGR的FPG理想截定点为5.6mmol/L。  相似文献   

20.
震动感觉阈值检查在糖尿病神经病变诊断中的应用   总被引:11,自引:0,他引:11  
震动感觉阈值检查(VPT)用于诊断糖尿病神经病变简便、无创、重复性好、患者顺应性好。其敏感性优于其他依赖临床症状、体征的方法和尼龙单丝检查。本文介绍VPT及其与其他临床常用诊断糖尿病神经病变方法的比较,简述了VPT检查时需要注意的问题,如年龄、探头的压力、检查者的经验和患者对于检查的理解等。  相似文献   

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