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Testing a biobehavioral model of irritable bowel syndrome.

机译:测试肠易激综合症的生物行为模型。

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OBJECTIVE: The pathogenesis of irritable bowel syndrome (IBS) is probably multifactorial with dysfunction at different levels of the brain-gut axis. The aim of this study was to evaluate an existing biobehavioral model of IBS symptom generation in a large group of patients. MATERIAL AND METHODS: In 104 IBS patients, we assessed symptom severity by a symptom diary, visceral hypersensitivity using a barostat, autonomic function by measuring arterial baroreflex sensitivity and psychological functioning using questionnaires. Structural equation modeling was used to calculate the reciprocal and chronological relationships between the model variables. RESULTS: Analysis of the adjusted original model indicated poor fit [Satorra-Bentler chi=28.47; degrees of freedom (df)=11, P<0.01; comparative fit index (CFI)=0.78], which was caused by omission of two paths (illness behavior-IBS symptoms and trauma-IBS symptoms). The revised model yielded a reasonable fit (chi=13.88, df=9, P=0.13; CFI=0.94). The model explained 18.7% of the variance in IBS symptoms. Illness behavior completely mediated the effect of cognitions on IBS symptoms and partly mediated the effect of trauma on IBS symptoms. The fit of this alternative model was good (chi=9.85, df=8, P=0.28; CFI=0.98). The alternative model explained 20.0% of the variance in IBS symptoms. CONCLUSION: The proposed biobehavioral model could not be validated. Although visceral hypersensitivity and IBS symptom severity significantly correlate, autonomic function and IBS symptoms do not. Cognitive-behavioral aspects are important in the clinical expression of IBS, with illness behavior playing an intermediate and central role.
机译:目的:肠易激综合症(IBS)的发病机制可能是多因素的,在脑肠轴的不同水平上功能障碍。这项研究的目的是评估一大群患者中现有的IBS症状发生的生物行为模型。材料与方法:在104名IBS患者中,我们通过症状日记,使用气压调节器的内脏超敏性,通过测量动脉压力反射敏感性的自主功能和问卷调查的心理功能来评估症状严重程度。结构方程建模用于计算模型变量之间的倒数和时间关系。结果:调整后的原始模型的分析表明拟合度较差[Satorra-Bentler chi = 28.47;自由度(df)= 11,P <0.01;比较拟合指数(CFI)= 0.78],这是由于省略了两种路径(疾病行为-IBS症状和创伤-IBS症状)引起的。修改后的模型产生了合理的拟合度(chi = 13.88,df = 9,P = 0.13; CFI = 0.94)。该模型解释了IBS症状差异的18.7%。疾病行为完全介导了认知对IBS症状的影响,部分介导了创伤对IBS症状的影响。该替代模型的拟合良好(chi = 9.85,df = 8,P = 0.28; CFI = 0.98)。替代模型解释了IBS症状变化的20.0%。结论:所提出的生物行为模型无法得到验证。尽管内脏超敏反应和IBS症状严重程度显着相关,但自主神经功能和IBS症状却不相关。认知行为方面在IBS的临床表达中很重要,疾病行为起着中间和重要的作用。

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