Consenso multidisciplinar para el manejo de la tromboembolia de pulmón

We have updated recommendations on 12 controversial topics that were published in the 2013 National Consensus on the diagnosis, risk stratification and treatment of patients with pulmonary embolism (PE). A comprehensive review of the literature was performed for each topic, and each recommendation was evaluated in two teleconferences. For diagnosis, we recommend against using the Pulmonary Embolism Rule Out Criteria (PERC) rule as the only test to rule out PE, and we recommend using a D-dimer cutoff adjusted to age to rule out PE. We suggest using computed tomography pulmonary angiogram as the imaging test of choice for the majority of patients with suspected PE. We recommend using direct oral anticoagulants (over vitamin K antagonists) for the vast majority of patients with acute PE, and we suggest using anticoagulation for patients with isolated subsegmental PE. We recommend against inserting an inferior cava filter for the majority of patients with PE, and we recommend using full-dose systemic thrombolytic therapy for PE patients requiring reperfusion. The decision to stop anticoagulants at 3 months or to treat indefinitely mainly depends on the presence (or absence) and type of risk factor for venous thromboembolism, and we recommend against thrombophilia testing to decide duration of anticoagulation. Finally, we suggest against extensive screening for occult cancer in patients with PE.     

嘌呤能受体X1与肺腺癌预后及免疫细胞浸润的相关性研究

目的：探索嘌呤能受体X1(purinergic receptor，P2RX1)与肺腺癌(LUAD)患者预后及免疫细胞浸润的相关性。方法：利用生物信息学技术分析非小细胞肺癌中P2RX1的表达及其甲基化与患者预后的关系，对P2RX1共表达基因进行富集分析并筛选核心基因。利用TIMER 2.0数据库、R软件等分析P2RX1与免疫细胞、免疫检查点、免疫基质评分等的相关性。结果：P2RX1在LUAD中表达下调，低表达P2RX1的患者预后较差(P<0.05)，且P2RX1与肿瘤纯度、分期等临床病理因素有关(P<0.05)。P2RX1的表达与肺鳞癌患者预后无明显相关。Cg06475633等P2RX1 CpG位点甲基化与患者预后相关。P2RX1共表达基因主要富集于免疫细胞活化、分化等通路和生物学进程，核心基因主要包括BTK、IKZF1等。P2RX1的表达与B细胞浸润、免疫/基质评分、PD-1、CTLA-4等多个免疫检查点显著相关(P<0.05)。结论：P2RX1有望成为LUAD诊断和免疫治疗的新靶点。     

Diagnosing pulmonary thromboembolism: Concerns and controversies

Pulmonary thromboembolism (PTE) is an important cause of mortality/morbidity even today despite advancement in clinical understanding as well as diagnostic facilities. Clinical diagnosis of PTE is often challenging because of nonspecific sign/symptoms. Adherence to clinical decision-making protocols and appropriate use of diagnostic modalities like computed tomography pulmonary angiography can resolve the diagnostic dilemma in most cases and help in the overall management of PTE. This article deals with various concerns as well as controversies surrounding accurate diagnosis of PTE as on date.     

Solid‐type poorly differentiated adenocarcinoma of the stomach: Deficiency of mismatch repair and SWI/SNF complex

ARID1A, one of the subunits in SWI/SNF chromatin remodeling complex, is frequently mutated in gastric cancers with microsatellite instability (MSI). The most frequent MSI in solid‐type poorly differentiated adenocarcinoma (PDA) has been reported, but the SWI/SNF complex status in solid‐type PDA is still largely unknown. We retrospectively analyzed 54 cases of solid‐type PDA for the expressions of mismatch repair (MMR) proteins (MLH1, PMS2, MSH2, and MSH6), SWI/SNF complex subunits (ARID1A, INI1, BRG1, BRM, BAF155, and BAF170) and EBER, and mutations in KRAS and BRAF. We analyzed 40 cases of another histological type of gastric cancer as a control group. The solid‐type PDAs showed coexisting glandular components (76%), MMR deficiency (39%), and complete/partial loss of ARID1A (31%/7%), INI1 (4%/4%), BRG1 (48%/30%), BRM (33%/33%), BAF155 (13%/41%), and BAF170 (6%/2%), EBER positivity (4%), KRAS mutation (2%), and BRAF mutation (2%). Compared to the control group, MMR deficiency and losses of ARID1A, BRG1, BRM, and BAF155 were significantly frequent in solid‐type PDAs. Mismatch repair deficiency was associated with the losses of ARID1A, BRG1, and BAF155 in solid‐type PDAs. In the MMR‐deficient group, solid components showed significantly more frequent losses of ARID1A, BRG1, BRM, and BAF155 compared to glandular components (P = .0268, P = .0181, P = .0224, and P = .0071, respectively). In the MMR‐proficient group, solid components showed significantly more frequent loss of BRG1 compared to glandular components (P = .012). In conclusion, solid‐type PDAs showed frequent losses of MMR proteins and the SWI/SNF complex. We suggest that loss of the SWI/SNF complex could induce a morphological shift from differentiated‐type adenocarcinoma to solid‐type PDA.     

SARIMA模型在苏州市肺结核发病预测中的应用

目的 建立苏州市肺结核发病的SARIMA模型并预测发病,为苏州市肺结核防控提供参考。方法 收集结核病信息管理系统（新）中苏州市2010年1月—2018年12月肺结核月发病数,通过时间序列分析建立SARIMA模型并预测苏州市2019年肺结核的发病情况。结果 苏州市肺结核发病数具有明显的季节周期性,每年的发病最高峰为5月,发病最低谷为2月。苏州市肺结核发病数的最佳拟合模型为SARIMA (0,1,1)×(0,1,1)₁₂,AIC=9.590,SBC=9.644,模型参数均具有统计学意义,模型残差为白噪声序列,模型的预测值与实际值平均绝对百分比误差MAPE=7.943%,模型预测精度较高。预测苏州市2019年肺结核发病数为3 467例,月发病数平均值为289例,发病水平较2018年略有下降。结论 SARIMA(0,1,1)×(0,1,1)₁₂模型能较好拟合出苏州市肺结核发病数的时间变化趋势,可应用于苏州市肺结核月发病数的短期预测。     

不伴红细胞增多的慢性阻塞性肺疾病患者并发肺栓塞的影响因素研究

背景　慢性阻塞性肺疾病（COPD）患者肺栓塞（PE）发生率显著高于常人，但目前不伴红细胞增多的COPD患者并发PE的机制尚不明确。目的　探讨不伴红细胞增多的COPD患者并发PE的影响因素。方法　本研究为回顾性病例对照研究。收集2017年1-12月在新疆医科大学第一附属医院呼吸与呼吸危重症中心住院治疗的血红蛋白（Hb）≤140 g/L的COPD患者。依据肺多层螺旋CT肺血管成像（CTPA）检查结果将患者分为并发PE组和单纯COPD组。记录患者的年龄、性别、合并症、服用抗血小板或抗凝药物史。采用倾向性评分匹配（PSM）方法，通过二元Logistic回归分析估计倾向性评分值，采用1∶1最邻近原则匹配，卡钳值为0.05，筛选出基线相同的两组病例。记录患者的D-二聚体、血常规检查结果，比较两组间差异；分析不伴红细胞增多的COPD患者并发PE的影响因素，红细胞分布宽度（RDW）与中性粒细胞/淋巴细胞比值（NLR）的相关性。结果　共纳入病例339例，其中单纯COPD组289例，并发PE组50例。采用PSM方法筛选两组患者，最终得到单纯COPD组、并发PE组各50例进行后续研究。并发PE组患者D-二聚体、中性粒细胞计数（N）、RDW、NLR高于单纯COPD组，淋巴细胞计数（L）低于单纯COPD组（P<0.05）。二元Logistic回归分析结果显示，RDW是不伴红细胞增多的COPD患者并发PE的影响因素〔OR=1.561，95%CI（1.096，2.225），P<0.05〕。Spearman秩相关分析结果显示，不伴红细胞增多的COPD患者RDW与NLR呈正相关（rs=0.225，P<0.05）。结论　RDW升高是Hb≤140 g/L的COPD患者并发PE的危险因素，且RDW与NLR呈正相关。