老年多浆膜腔积液156例临床分析

目的:探讨老年多浆膜腔积液的临床特点及其常见病因,以提高临床诊断率。方法:对经X放射线、超声波或CT检查确诊的老年多浆膜腔积液156例患者的临床资料进行回顾性分析。结果:老年多浆膜腔积液最常见病因为恶性肿瘤(32.7%),其次为心功能不全、结缔组织疾病、结核病、肝硬化、肾功能不全、甲状腺功能减退症等;老年多浆膜腔积液的病因与积液部位、积液性质等有一定关系。结论:老年多浆膜腔积液病因复杂,鉴别诊断应注意恶性肿瘤、甲状腺功能减退症,临床上应结合病史、症状体征、积液性质及特殊检查综合诊断。     

多浆膜腔积液241例临床分析

目的：探讨多浆膜腔积液的临床特点及其与常见病因之间的关系。方法：回顾性分析北京协和医院诊断为多浆膜腔积液241例患者的临床资料。结果：多浆膜腔积液最常见病因为恶性肿瘤(31．3％)，其次为结缔组织疾病、结核、肝硬化、心功能不全等；结核的发病率较单部位积液者低。多浆膜腔积液的病因与积液部位、积液性质、性状及下肢水肿等有一定关系。结论：多浆膜腔积液病因复杂，鉴别诊断比较困难，特别是结核性积液与恶性积液在症状、体征、积液的各种性状上有重叠，因此，临床的综合判断对诊断至关重要。     

恶性浆膜腔积液脱落细胞中P21 ras蛋白表达状况及其意义

目的:检测浆膜腔积液脱落细胞P21 ras蛋白表达状况,探讨其对恶性浆膜腔积液的诊断价值.方法:将新鲜浆膜腔积液离心后收集脱落细胞,取部分细胞涂片进行常规细胞学诊断,据此将积液分为良性与恶性两组.对余下脱落细胞作"标准化"处理,包括去除红细胞、多聚甲醛固定、调整细胞浓度、制备细胞涂片,然后进行P21 ras蛋白免疫化学染色(SP法).结果:共108例浆膜腔积液,恶性53例,良性55例.39例恶性积液P21 fas蛋白免疫化学染色阳性(73.6%),且多为强阳性或阳性;12例良性积液P21 ras蛋白染色阳性(21.8%),且多为弱阳性或阳性,两组间阳性率(χ2=29.02,P＜0.001)及阳性强度(Uc=6.786,P＜0.001)的差异均有显著性统计学意义.P21 ras蛋白免疫化学染色诊断恶性积液的敏感度为73.6%,特异度为78.2%,诊断符合率达75.9%.结论:浆膜腔积液中脱落细胞P21 ras蛋白免疫化学染色在肿瘤细胞多为阳性,良性细胞多为阴性,对恶性体腔积液的诊断有较大的价值.     

85例血性心包积液的病因及诊断方法分析

目的:总结分析血性心包积液的病因及其诊断方法,为诊断和鉴别诊断提供指导性资料。方法:对85例血性心包积液患者的临床表现、影像学检查、实验室检查结果进行回顾分析。结果:85例血性心包积液的病因中,肿瘤性41例(48.23%)、结核性27例(31.76%)、其他各种原因引起者17例(20.01%)。肿瘤性心包积液中癌胚抗原的平均值173μg/L,显著高于结核性心包积液的平均值0.62μg/L;结核性心包积液腺苷脱氢酶平均值44.5U/L,显著高于癌性心包积液平均值15U/L;结核性心包积液患者中心包积液和血液抗结核抗体(kjhkt)检测阳性率分别为62.5%和75%,显著高于肿瘤性心包积液患者(均为阴性)。结论:恶性肿瘤和结核是血性心包积液的主要病因。心包积液的脱落细胞学检查和腺苷脱氢酶、癌胚抗原、kjhkt等项实验室检查为血性心包积液病因诊断和鉴别诊断的主要手段,联合应用可提高诊断的准确性。     

贝伐珠单抗治疗恶性浆膜腔积液的研究进展

传统的治疗方法对恶性浆膜腔积液的控制效果有限,因此需要寻求有效的药物治疗恶性浆膜腔积液,以控制疾病进展、提高患者生活质量。贝伐珠单抗的出现为治疗恶性浆膜腔积液带来了新的希望。本文系统回顾了贝伐珠单抗单药或联合治疗恶性胸腔积液、恶性腹腔积液和恶性心包积液的疗效和安全性,并阐述了恶性浆膜腔积液形成机制和血管内皮生长因子的作用。总结发现,贝伐珠单抗作为靶向血管内皮生长因子的药物,在恶性胸腔、腹腔和心包积液的治疗中表现出良好的疗效,不仅能提高患者生活质量,还不增加化疗药物的不良反应,但仍存在一些不足之处,如缺乏大型临床研究、贝伐珠单抗治疗恶性腹腔积液与恶性心包积液仍缺乏统一标准、贝伐珠单抗应用于恶性心包积液的研究较少等。     

p16、RAR-β和APC基因甲基化联合检测对恶性浆膜腔积液的诊断价值

目的:探讨浆膜腔积液沉渣细胞的肿瘤抑制蛋白(p16)、视黄酸受体β(RAR-β)和结肠腺瘤性息肉病(APC)基因甲基化状态检测在良、恶性浆膜腔积液中的鉴别诊断价值。方法:选取太和医院的患者浆膜腔积液患者65例,其中良性浆膜腔积液27例,恶性浆膜腔积液38例。运用甲基化特异性PCR技术对p16、RAR-β和APC基因启动子区域进行甲基化检测。结果:p16基因和RAR-β基因的甲基化频率2组比较差异无统计学意义;APC基因甲基化频率良性组为7.4%,恶性组为28.9%,2组比较差异有统计学意义(P0.05);p16、RAR-β和APC基因甲基化检测的阳性率恶性组为84.2%,84.2%,76.3%,良性组为33.3%,44.4%,14.8%,2组比较差异有统计学意义(P0.05)。结论:浆膜腔积液p16、RAR-β和APC基因甲基化检查对恶性肿瘤的早期诊断具有非常重要的诊断价值。     

血性心包积液病因分析

目的探讨血性心包积液的病因分布特点。方法选自2002年1月至2012年7月北京军区总医院东区64例和2013年4月至2014年4月北京朝阳急诊抢救中心4例,行心包穿刺明确诊断为血性心包积液患者68例。其中男性28例,女性40例,年龄范围19~87岁。按年龄将患者分为2组,老年组33例(≥60岁)和中青年组35例(18~59岁)。按性别分男性组(28例)和女性组(40例)。收集所有患者临床资料,分析血性心包积液病因分布。结果患者常见病因为恶性肿瘤(55.9%)、结核(26.4%)及非特异性心包积液(7.4%)。其他病因分别为心力衰竭、主动脉夹层及先心病等。老年组与中青年组的常见病因分布比例比较,差异无统计学意义(P均0.05)。男性组和女性组血性心包积液的常见病因分别为肿瘤和结核,男性与女性病因分布比例比较,差异无统计学意义(P均0.05)。肿瘤致血性心包积液,肺肿瘤占60.5%,妇科肿瘤13.2%,消化道肿瘤10.5%,心包间皮瘤5.3%,肾及肾上腺肿瘤5.3%,皮肤及颈部淋巴瘤各2.6%。结论肿瘤和结核为血性心包积液的主要致病因素,与年龄和性别无明显相关。     

浆膜腔积液脱落细胞端粒酶逆转录酶mRNA检测及其意义

恶性浆膜腔积液已成为恶性肿瘤转移的一个突出表现，本研究采用核酸原位杂交技术对浆膜腔积液脱落细胞端粒酶逆转录酶(hTERT)mRNA进行分析，旨在明确积液中各种脱落细胞hTERT mRNA的表达状况，探讨其在恶性浆膜腔积液中的诊断价值。     

细胞块技术应用质量控制方法对恶性浆膜腔积液诊断效能探讨

目的探讨细胞块病理技术在恶性浆膜腔积液细胞学诊断应用中的价值、存在的问题及质控方法,以进一步提高细胞块病理诊断的准确性。方法选择2016-02～2018-02该院276例恶性浆膜腔积液,均进行传统细胞学涂片(conventional smear,CS)和质控前常规细胞块技术(routine cell block,RCB)操作流程,对RCB切片诊断中可疑或阴性病例按预设5项主要质量控制指标再行质控后细胞块制备技术(quality control in cell block technology,QCCB)切片检查,将三者诊断结果进行对比分析,比较三者结果的准确性,分析各自存在的问题。结果 276例恶性浆膜腔积液中用CS确诊恶性肿瘤218例(78.99%),其中确诊恶性且肿瘤分类明确199例(72.10%)。RCB确诊恶性肿瘤233例(84.42%),其中确诊恶性且肿瘤分类明确225例(81.52%)。QCCB确诊恶性肿瘤272例(98.55%),其中确诊恶性且肿瘤分类明确270例(97.83%),无误诊或漏诊病例。RCB相对于CS能提高恶性肿瘤诊断率5.43%,提高分型诊断准确率9.42%,但两者差异无统计学意义(P0.05)。QCCB相对于CS和RCB,在提高确诊恶性肿瘤和分型诊断准确率方面差异均有统计学意义(P 0.05)。结论细胞块技术在恶性浆膜腔积液细胞学病理诊断中显著优于传统细胞学,加强细胞块病理技术各环节质量控制有利于减少不确定诊断,并有助于避免误诊和漏诊。     

169例胸腔积液病因分布和临床特点

目的探讨胸腔积液的病因分布和临床特征。方法分析我院所有收治并且资料完整的胸腔积液患的临床资料。结果 169例胸腔积液患者的病因依次为:结核性胸膜炎89例(52.66%)、恶性肿瘤35例(20.71%)、心功能不全18例(10.65%)、肺炎或肺部感染17例(10.06%),其他10例。结核性胸腔积液以40岁以下患者占48.3%,老年病人在增加,腺苷脱氨酶的敏感率为79.78%;恶性胸腔积液以60岁以上患者居多(65.7%),40岁以下极少(5.7%)。恶性胸腔积液查到肿瘤细胞者26例,阳性率为73%。结论胸腔积液主要病因是结核和肿瘤,结核患者以青年居多,恶性肿瘤以老年患者居多。临床综合分析是判断病因的关键。     

Tumormarker im Perikarderguss bei malignen und nichtmalignen Perikarderg��ssen

Background

The differential diagnosis of pericardial effusion is often challenging because different etiologies can be discussed. Of particular therapeutic and prognostic importance is the definitive differentiation of malignant pericardial effusion from benign effusions. The definitive diagnosis of malignant pericardial effusion is established by a positive cytological examination of the pericardial fluid. However, pericardial fluid cytology, although specific has variable sensitivity. Tumor markers are often investigated after pericardiocentesis but their utility as an aid for the diagnosis of malignant pericardial effusion is not well established. The aim of this study was to measure the concentrations of the tumor markers CEA, CA?19-9, CA?72-4, SCC and NSE in malignant and non-malignant pericardial effusions and to assess their diagnostic utility in differentiating malignant from benign pericardial effusion.

Methods

We investigated the pericardial fluid of 29?patients with proven malignant pericardial effusion and 25?patients with non-malignant pericardial effusion. The etiology of the pericardial effusion was defined by pericardial cytology, epicardial histology and PCR for cardiotropic viruses from pericardial and epicardial tissue acquired by pericardioscopy. The group with non-malignant pericardial effusion comprised 15?patients with autoreactive effusion and 10?patients with viral pericardial effusion. We analyzed the following tumor markers in the pericardial fluid: carcinoembryonic antigen (CEA), carbohydrate antigen (CA)?19-9, carbohydrate antigen (CA)?72-4, squamous cell carcinoma (SCC) antigen and neuron-specific enolase (NSE).

Results

Of the tumor markers tested the mean concentrations of the CEA, CA?72-4 and CA?19-9 were significantly higher in malignant pericardial effusions than in non-malignant effusions (CEA 450.66 ±1620.58???g/l vs. 0.72 ±1.49???g/l, p<0.001; CA?19-9 1331.31 ±3420.87?kU/l vs. 58.85 ±17.53?kU/l, p=0.04; CA?72-4 707.90 ±2397.55?kU/l vs. 0.48 ±2.40?kU/l, p<0.001). ROC curve analysis showed that pericardial fluid CA?72-4 yielded an area under the curve (AUC) of 0.85 (95% confidence interval 0.74?C0.95), followed by CEA with 0.80 (95% confidence interval 0.68?C0.92). Pericardial fluid CA?72-4 levels >1.0?kU/l had 72% sensitivity (95% confidence interval 53%?C87%) and 96% specificity (95% confidence interval 80%?C99.9%) and CA?72-4 levels >2.5?kU/l had 69% sensitivity (95% confidence interval 49%?C85%) and 96% specificity (95% confidence interval 80%?C99.9%) in differentiating malignant pericardial effusions from effusions due to benign conditions.

Conclusion

Malignant pericardial effusions are associated with significantly higher pericardial concentrations of the tumor markers CEA, CA?72-4 and CA?19-9. Of the tested tumor markers, measurement of CA?72-4 levels in pericardial fluid offered the best diagnostic accuracy. Based on our data evaluation of every patient with unexplained pericardial effusion and negative pericardial fluid cytology should include the measurement of pericardial fluid CA?72-4 levels. Under these circumstances the elevation of pericardial fluid CA?72-4 levels should include malignancy as a probable diagnosis.     

Cytokine activation in pericardial fluids in different forms of pericarditis

There are many causes of pericardial effusion and it is useful to classify them etiologically, since this disorder is the most common pathologic process involving the pericardium. This report details our experience with pericardioscopy and epicardial biopsy in 101 patients with pericardial effusions in whom pericardioscopy was performed. By means of clinical data and polymerase chain reaction we tried to elucidate the etiology of the pericardial effusion which were classified as follows: we found 41 effusions to be induced by primary malignant tumors or tumors metastatic to the pericardium. Specific diagnosis of viral and bacterial pericarditis was established in 17 patients by examination of the pericardial effusion with PCR, where we found 3 patients positive for adenovirus, 5 patients positive for cytomegalovirus, 2 patients positive for enterovirus-RNA and 5 patients positive for borrelia Burgdorferi-DNA. Additionally, idiopathic effusions (lymphocytic and autoreactive) were seen in 35 patients. In summary immunological and molecular biology investigations seem to provide an additional tool in the diagnostic of pericardial effusion with unknown etiology. If we focus on the ELISA results, there is some evidence, that the demonstration [table: see text] of activation markers and soluble mediators of inflammation such as Il-6, Il-8 and IFN-gamma in pericardial effusion and the simultaneously lack of these mediators in sera of the patients first may be helpful in the discrimination of autoreactive and lymphocytic effusion. Second, this cytokine pattern or distribution indicates a possible local inflammatory process, where these cytokines were all released from activated T lymphocytes present in lymphocytic effusion. In the future, this may have therapeutic implications.     

Echocardiographic findings of pericardial involvement in patients with malignant pleural mesothelioma with a history of environmental exposure to asbestos and erionite

OBJECTIVE: The aim of the present study was to evaluate the pericardial involvement in patients with malignant mesothelioma caused by exposure to different minerals. METHODOLOGY: Forty-two patients (mean age of 52 +/- 12 years) with malignant mesothelioma were examined with transthoracic echocardiography. Thirty-three (78.9%) patients had a history of environmental exposure to asbestos and nine (21.4%) had a history of environmental exposure to erionite. RESULTS: In 19 (45.2%) patients with malignant pericardial mesothelioma, pericardial involvement was determined by echocardiography. The other 23 (54.8%) patients had no pericardial involvement. Pericardial effusion was detected in nine (64.3%) patients and pericardial effusion was small in six (14.3%) patients, moderate in one (2.4%) patient and large in two patients. Thickening of the pericardium was observed in eight (19%) patients. In another two (7.1%) patients pericardial calcification was observed. Among the 33 patients who had been exposed to asbestos, 15 (45.5%) had pericardial involvement, and among the nine patients with a history of exposure to erionite, four (44.4%) had pericardial involvement. There was no difference in terms of pericardial involvement in different stages of the tumour (P > 0.05). CONCLUSIONS: Pericardial involvement is commonly seen in patients with malignant mesothelioma. Among patients exposed to asbestos or zeolite there was no difference in terms of pericardial involvement. Furthermore, pericardial involvement was not related with the stage of the tumour.     

Enlarged left atrium causing possible false positive echocardiographic diagnosis of pericardial effusion.

Echocardiographic examination in a patient with IHSS, mitral insufficiency, and cardiomegaly suggested the possibility of a pericardial effusion. Echocardiographic M-mode scanning documented the continuity of the space posterior to the pericardium with an enlarged left atrium. Subsequent cineangiographic studies confirmed an enlarged left atrium and the absence of pericardial effusion. Left atrial enlargement may cause a false positive echocardiographic diagnosis of pericardial effusion.     

Tamponnade tardive : quatre cas de complication rare du traumatisme fermé du thorax

Delayed post-traumatic pericardial effusion is a rare condition after blunt trauma. The diagnosis of the effusion can be made by the clinical signs, which is not very specific and the cardiac echography. The etiological diagnosis remains difficult because it requires the elimination of the other causes of pericarditis. Their treatment consists in evacuating the pericardial effusion. The evolution thereafter is simple. We report four cases of patients with pericardial effusion late after a thoracic injury. Imaging the blood test, the examination of the pericardial fluid and the anatomopathological examination of the pericardium, eliminates the other etiologies.     

Effusive-constrictive hemodynamic pattern due to neoplastic involvement of the pericardium

Eight patients with metastatic malignancy of the pericardium who demonstrated the hemodynamics of subacute effusive-constrictive pericarditis were studied. All patients had clinical evidence of cardiac tamponade due to malignant pericardial effusion and were referred for therapeutic pericardiocentesis. In six in whom pericardiocentesis was successfully performed, right atrial pressure remained elevated after pericardiocentesis and return of the intrapericardial pressure to zero; in these patients, hemodynamic data were initially compatible with tamponade but suggested constriction after removal of the pericardial fluid. In the remaining two patients, echocardiography revealed pericardial fluid, but attempted pericardiocentesis was unsuccessful. In these two patients, the hemodynamic data suggested pericardial constriction; subsequent pathologic examination revealed neoplastic involvement of the visceral pericardium. Thus, subacute effusive-constrictive pericarditis, previously recognized as a complication of tuberculosis or mediastinal radiation, may also be due to metastatic malignancy. The syndrome can readily be demonstrated when right heart catheterization is performed in conjunction with pericardiocentesis.     

Pericardioscopy as adjunct to pericardial window

A technique for pericardioscopy at the time of subxiphoid pericardial window was evaluated in 17 patients undergoing surgery for clinically suspected malignant pericardial effusion. Best results were obtained using a rigid mediastinoscope for inspection of the posterior and lateral pericardial surfaces. No complications ensued, although many patients experienced cardiac arrythmias which always resolved with removal of the scope. Pericardioscopy revealed cancer transgressing the pericardium near the pulmonary veins in one patient, and this would have been missed without pericardioscopy. Pericardioscopy confirmed palpable metastatic deposits on the inferior pericardial surface in two other patients. In 14 patients, pericardioscopy did not reveal malignancy, although four of these patients had both positive fluid cytologic findings and malignant infiltration of the pericardial biopsy. In one patient a palpable but not visible nodule was proved to be an extrinsic hepatic metastasis. Pericardioscopy is a safe intervention chiefly applicable in patients with central tumors and pericardial effusion in whom subxiphoid pericardial window is not clearly diagnostic at the time of surgery.     

Malignant pericardial diseases: diagnosis and treatment

Pericardial involvement in malignant disease is fairly common. Usually the various clinical presentations--effusion, tamponade, constriction--occur in patients with known malignancy. Primary malignancy of the pericardium is rare, whereas secondary tumor involvement of the pericardium is more frequently observed. The common secondary solid tumors involving the pericardium are from lung and breast carcinomas; of the nonhematologic malignancies, lymphomas and leukemias are most frequent. A high index of suspicion in patients with malignancy, along with a history, physical examination, x-ray films, ECG, and echocardiography, will often make the diagnosis in a hemodynamically compromised patient. Occasionally, cardiac catheterization and pericardial biopsy are necessary to differentiate malignant pericardial disease from radiation pericarditis and restrictive heart disease. Therapy is dependent on the underlying condition and includes pericardiectomy, chemotherapy to obliterate the pericardial space, and external beam radiotherapy. These therapies are all palliative, but provide months of hemodynamic relief. The underlying prognosis of malignant pericardial disease remains grave.     

Neoplastic pericarditis--the role of different diagnostic procedures

The aim of the study was to assess the role of different diagnostic procedures in the recognition of malignant pericarditis. Consecutive medical records of the patients with pericardial effusion treated with pericardiocentesis or pericardioscopy in the period of 1982-2002 were analyzed retrospectively. Criteria of neoplastic pericarditis were: positive result of pericardial fluid cytology and/or neoplastic infiltration found in pericardial biopsy specimen. Criteria of non-neoplastic pericarditis were: negative result of pericardial fluid cytology and pericardial biopsy specimen, no neoplastic disease diagnosed at presentation and during 3-years of follow up. Malignant pericarditis was diagnosed in 47 patients (pts), nonmalignant in 51. Echocardiographic signs of cardiac tamponade were found in 80% of pts with neoplastic pericarditis and 40% of pts with non-malignant disease (p = 0.0001). Chest CT scan revealed the presence of enlarged mediastinal lymph nodes in 94% of pts with malignant pericarditis and only 11% of pts with non-malignant disease (p = 0.00001). Pericardial thickness on CT scan exceeded 8 mm in 75% of the pts with malignant pericarditis and 8% of pts with nonmalignant disease (p = 0.0003). Pericardial fluid (pf) CEA concentration was significantly higher in the patients with neoplastic pericarditis than in the pts with non-malignant process. CEA > 5 ng/ml and Cyfra 21-1>50 ng/ml were found in 43% of the pts with malignant pericarditis and none of the pts with benign pericarditis. Thus we recommend chest CT scan and pericardial fluid tumor markers (CEA and Cyfra 21-1) assessment as the procedures helpful in the recognition of malignant pericarditis.