目的建立预测胰十二指肠切除(PD)术后发生切口疝的风险列线图模型,为切口疝的早期干预提供依据。 方法回顾性分析2009年1月至2017年1月于邯郸市中心医院行PD术的926患者的临床资料,随访发生切口疝的患者24例(切口疝组),未发生切口疝的按照1∶5的比例随机抽取120例为非切口疝组。分别使用单因素和Logistic回归多因素分析术后切口疝的独立危险因素,并建立相关列线图预测模型。 结果年龄≥60岁(OR=5.800,95% CI 1.530~21.984)、BMI≥24 kg/m2(OR=4.165,95% CI 1.187~14.613)、糖尿病(OR=5.321,95% CI 1.548~18.285)、呼吸系统疾病(OR=4.565,95% CI 1.225~17.007)、切口感染(OR=6.803,95% CI 1.573~29.419)及手术时间≥6 h(OR=6.934,95% CI 1.938~24.813)是PD术后发生切口疝的独立危险因素(P<0.05)。基于以上6项独立危险因素建立列线图模型,并对该模型进行验证,预测值同实测值基本一致,C-index 0.890(95% CI 0.854~0.926),说明本研究列线图模型具有良好的精准度和区分度。 结论年龄≥60岁、BMI≥24 kg/m2、糖尿病、呼吸系统疾病、切口感染及手术时间≥6 h是PD术后发生切口疝的独立危险因素,本研究建立的列线图预测模型具有良好的精准性和区分度,有利于临床筛查PD术后发生切口疝的高风险人群和制定针对性规避措施。 相似文献
Primary antibody deficiencies (PAD) are the most common subtype of primary immunodeficiencies, characterized by increased susceptibility to infections and autoimmunity, allergy, or malignancy predisposition. PAD syndromes comprise of immune system genes highlighted the key role of B cell activation, proliferation, migration, somatic hypermutation, or isotype switching have a wide spectrum from agammaglobulinemia to selective Ig deficiency. In this study, we describe the molecular and the clinical aspects of fifty-two PAD patients. The most common symptoms of our cohort were upper and lower respiratory infections, bronchiectasis, diarrhea, and recurrent fever. Almost all patients (98%) had at least one of the symptoms like autoimmunity, lymphoproliferation, allergy, or gastrointestinal disease. A custom-made next-generation sequencing (NGS) panel, which contains 24 genes, was designed to identify well-known disease-causing variants in our cohort. We identified eight variants (15.4%) among 52 PAD patients. The variants mapped to BTK (n?=?4), CD40L (n?=?1), ICOS (n?=?1), IGHM (n?=?1), and TCF3 (n?=?1) genes. Three novel variants were described in the BTK (p.G414W), ICOS (p.G60*), and IGHM (p.S19*) genes. We performed Sanger sequencing to validate pathogenic variants and check for allelic segregation in the family. Targeted NGS panel sequencing can be beneficial as a suitable diagnostic modality for diagnosing well-known monogenic PAD diseases (only 2–10% of PADs); however, screening only the coding regions of the genome may not be adequately powered to solve the pathogenesis of PAD in all cases. Deciphering the regulatory regions of the genome and better understanding the epigenetic modifications will elucidate the molecular basis of complex PADs.