Differentiation between tuberculosis and leukemia in abdominal and pelvic lymph nodes: evaluation with contrast-enhanced multidetector computed tomography

PURPOSE:

To compare the characteristics of tubercular vs. leukemic involvement of abdominopelvic lymph nodes using multidetector computed tomography (CT).

MATERIALS AND METHODS:

We retrospectively reviewed multidetector computed tomography features including lymph node size, shape, enhancement patterns, and anatomical distribution, in 106 consecutive patients with newly diagnosed, untreated tuberculosis (55 patients; 52%) or leukemia (51 patients; 48%). In patients with leukemia, 32 (62.7%) had chronic lymphocytic leukemia, and 19 (37.3%) had acute leukemias; of these, 10 (19.6%) had acute myeloid leukemia, and 9 (17.6%) had acute lymphocytic leukemia.

RESULTS:

The lower para-aortic (30.9% for tuberculosis, 63.2% for acute leukemias and 87.5% for chronic lymphocytic leukemia) and inguinal (9.1% for tuberculosis, 57.9% for acute leukemias and 53.1% for chronic lymphocytic leukemia) lymph nodes were involved more frequently in the three types of leukemia than in tuberculosis (both with p <0.017). Tuberculosis showed peripheral enhancement, frequently with a multilocular appearance, in 43 (78.2%) patients, whereas patients with leukemia (78.9% for acute myeloid leukemia and acute lymphocytic leukemia, 87.5% for chronic lymphocytic leukemia) demonstrated predominantly homogeneous enhancement (both with p <0.017). For the diagnosis of tuberculosis, the analysis showed that a peripheral enhancement pattern had a sensitivity of 78.2%, a specificity of 100%, and an accuracy of 88.7%. For the diagnosis of leukemia, the analysis showed that a homogeneous enhancement pattern was associated with a sensitivity of 84.3%, a specificity of 94.5%, and an accuracy of 89.6%.

CONCLUSION:

Our findings indicate that the anatomical distribution and enhancement patterns of lymphadenopathy seen on multidetector computed tomography are useful for differentiating between untreated tuberculosis and leukemia of the abdominopelvic lymph nodes.     

miR-181a在急性淋巴细胞白血病患儿中的表达及其功能研究

目的 检测microRNA-181a(miR-181a)在急性淋巴细胞白血病(ALL)患儿中的表达水平,并研究其在ALL细胞株CCRF-CEM细胞及耐药株CEM-C1细胞中的功能.方法 采用实时荧光定量PCR方法检测ALL患儿骨髓样本、ALL细胞株CCRF-CEM细胞及其耐药株CEM-C1细胞中miR-181a的表达水平.采用电穿孔转染的方法抑制耐药株CEM-C1细胞并上调非耐药株CCRF-CEM细胞中miR-181a的表达,予不同浓度梯度(终浓度分别为0.01、0.1、1、10、100、1 000 ng/ml)喜树碱处理后,采用CCK-8法观察各浓度梯度喜树碱处理后细胞的存活情况,绘制细胞增殖抑制曲线并计算半数抑制浓度(IC50).结果 初诊-复发组患儿初诊及复发骨髓样本miR-181a相对表达水平(4.84±2.71及6.53±2.20)均高于对照组(1.41±0.53)(P=0.017、0.001),初诊-完全缓解组患儿初诊骨髓样本miR-181a水平(7.58±2.50)较对照组明显升高(P=0.000),而完全缓解后miR-181a水平下降至1.35±0.35,与对照组比较差异无统计学意义(P=0.863).CEM-C1细胞miR-181a相对表达水平(-4.39±0.08)较CCRF-CEM细胞(-2.32±0.03)明显升高(P=0.000).转染miR-181a抑制剂CEM-C1细胞较转染阴性对照组增殖抑制率明显升高(P＜0.05),IC50分别为30.61、2 255.00 ng/ml,耐药指数(RI) =73.67.miR-181a过表达CCRF-CEM细胞较阴性对照组增殖抑制率明显降低(P＜0.05),IC50分别为126.60、1.34 ng/ml,RI=94.26.结论 ALL患儿骨髓及CEM-C1细胞中miR-181a异常高表达,抑制CEM-C1细胞中miR-181a的表达可明显增加CEM-C1细胞的药物敏感性,在CCRF-CEM细胞中上凋miR-181a的表达能明显增加CCRF-CEM细胞的耐药性.     

继发性肺淋巴瘤43例CT分析

目的探讨继发性肺淋巴瘤(SPL)的CT表现。方法回顾性分析经穿刺活检、手术病理证实诊断为SPL的43例患者的临床和CT资料。结果 43例病理类型中31例非霍奇金淋巴瘤(NHL),12例霍奇金淋巴瘤(HL);胸部CT示肺内结节影8例,其中多发实性结节影4例,单发实性结节影2例,多发浅淡磨玻璃样结节1例;大片实变19例,单发实变9例,其余10例均为多发片状实变影;团块影16例,单发团块4例,多发团块影12例,其中2例伴不规则空洞性团块。43例中7例接受增强检查,大部病灶呈不均匀轻中度强化,3例病灶内见坏死无强化区,1例伴不规则空洞,1例病灶内可见穿行血管。伴随其它CT表现包括10例伴有单侧胸腔大量积液,3例伴有单侧少量积液,1例伴有肋骨破坏及胸壁肿块影,7例纵隔、腋下淋巴结肿大,4例病例发现肺以外器官的侵犯。结论 SPL可表现为结节影、实变影及团块影,可单发、多发,掌握其CT影像特点,能够为临床诊疗提供帮助。     

Microparticle bearing tissue factor: A link between promyelocytic cells and hypercoagulable state

Patients with hematological malignancies have a 28-fold increased risk of venous thromboembolism (VTE). Among patients with acute myelogenous leukemia (AML), the 2-year cumulative incidence of VTE is 5.2%. Several studies suggest that microvesicles (MVs) harboring TF may play a role in VTE and disseminated intravascular coagulation (DIC) in acute promyelocytic leukemia (APL).     

Glucocorticoid and proteasome inhibitor impact on the leukemic lymphoblast: multiple, diverse signals converging on a few key downstream regulators

Twenty years ago a proteasome inhibitor was suggested as therapy for glucocorticoid-resistant multiple myeloma, a disease that involves terminally differentiated B cells. Since then, research has proven that it has utility on a number of tumors resistant to chemotherapy. Hematologic malignancy, however, often involves lesser differentiated cells, which have a high potential to modulate their intrinsic machinery and thereby activate alternative rescue pathways. A corresponding multiplicity of therapies is not always practical. One approach to conditions with heterogeneous physiology is to identify key biochemical mediators, thereby reducing the number of treatment targets. Results from several ongoing studies indicate convergence of genomically diverse signal pathways to a limited number of key downstream regulators of apoptosis. Convergence of pathways can be exploited to address the problem of genetic heterogeneity in acute leukemia: this would mean treating multiple molecular aberrations with fewer drugs and enhanced therapeutic benefit.     

异基因外周血干细胞移植治疗白血病的临床观察

目的:观察同胞供者异基因外周血干细胞移植(allo-PBSCT)治疗白血病的疗效及并发症.方法:分析11例白血病患者行同胞供者HLA相合allo-PBSCT治疗的临床资料.供者干细胞动员用粒细胞集落刺激因子(G-CSF),用CS-3000血细胞分离机采集外周血干细胞.患者用改良马利兰加环磷酰胺(Bu/CY)为预处理方案,用环孢菌素A(CSA)+短程甲氨蝶呤(MTX)+霉酚酸酯(MMF)方案预防移植物抗宿主病(GVHD),用前列腺素E1(凯时)+低分子肝素预防肝静脉闭塞病(HVOD),用美司钠预防出血性膀胱炎(HC).结果:获得单个核细胞数(MNC)的中位数为8.3(4.5～13.0)×108/kg;CD34+细胞计数的中位数为6.2(2.4～12.4)×106/kg.10例患者获得造血重建,白细胞和血小板植活的中位数时间均为15(13 ～ 18)d;1例患者干细胞未植入.并发症:发生感染11例,GVHD 8例,HVOD 3例,HC 1例.中位随访15.5(1 ～39)个月,生存率为63.6％(7例),无病存活率为54.5％(6例);4例死亡.结论:同胞供者allo-PBSCT是治疗白血病一种有效手段,移植相关并发症主要为感染、GVHD、HVOD.     

白血病抑制因子与支气管哮喘

在支气管哮喘(简称哮喘)的发病过程中,机体神经、免疫与内分泌系统均参与其中,它是一个多步骤的过程,涉及到大量的细胞因子、炎症介质和神经递质.白血病抑制因子(leukemia inhibitory factor,LIF)是连接神经-免疫-内分泌系统网络的桥梁,LIF通过调节多种炎症细胞,如嗜酸粒细胞、淋巴细胞和肥大细胞等,促进炎性介质的释放;促进气道感觉神经末梢释放P物质等神经肽,上调气道上皮细胞神经激肽-1受体(neurokinin-1 receptor,NK-1R)的表达,诱发气道神经源性炎症;此外,LIF还可下调糖皮质激素受体的表达,导致糖皮质激素抵抗.因此LIF水平在哮喘患者血清、痰液、支气管肺泡灌洗液、支气管黏膜中均可有所升高.本文就LIF的生物学特征以及与哮喘发病的关系作一综述,旨在为探讨哮喘的发病机制和临床治疗提供理论依据.     

丙戊酸联合伏立诺他增强阿糖胞苷对人Dami白血病细胞株杀伤作用的机制研究

目的探讨丙戊酸(VPA)联合伏立诺他(SAHA)增强阿糖胞苷(Ara-c)对人Dami白血病细胞株的杀伤作用,并探讨其分子学机制。方法设空白对照组、Ara-c组、VPA组、SAHA组、VPA+Ara-c组、SAHA+Ara-c组,VPA+SAHA+Ara-c组,分别作用于对数生长期的Dami白血病细胞,MTT比色法检测药物对细胞的生长抑制作用;用PI法通过流式细胞仪检测细胞周期;RT-PCR方法检测转录因子GATA-1、胞苷脱氨酶(CDA)及脱氧胞苷激酶(DCK)mRNA水平的变化。结果 VPA和SAHA共同联合Ara-c用药组细胞生长抑制率明显高于VPA联合Ara-c组及SAHA联合Ara-c组,各组间相比,具有显著性差异。Dami细胞经过VPA和SAHA处理后均出现细胞周期阻滞现象,主要阻滞在G1期,与对照组相比差异有显著性(P0.05);VPA和SAHA联合用药组G1期细胞所占比例高于SAHA组(P0.05),与VPA组差异无显著性(P0.05)。VPA组、SAHA组、VPA和SAHA联合用药组GATA-1和CDA mRNA表达水平均低于对照组(P0.05),各组间差异无显著性(P0.05);VPA组DCK mRNA表达水平高对照组(P0.05)、SAHA组与对照组比较差异无显著性(P0.05)、VPA和SAHA联合用药组DCK mRNA表达水平高于VPA组和SAHA组(P0.05)。结论 VPA联合SAHA可增强阿糖胞苷对Dami白血病细胞的杀伤作用,可能是通过增加DCK的表达,从而增加阿糖胞苷体内活性代谢产物所致。     

亚砷酸联合维甲酸化疗治疗急性早幼粒细胞白血病疗效观察

目的：：研究急性早幼粒细胞白血病行亚砷酸和维甲酸、化疗联合治疗效果。方法：资料取本院2008年4月至2015年4月急性早幼粒细胞白血病90例患者予回顾分析,按治疗方案分成两组,对照组行维甲酸与化疗,观察组联合亚砷酸,对比两组疗效。结果：观察组早幼粒细胞比例与总白细胞数改善效果比对照组优( P<0.05)。结论：急性早幼粒细胞白血病患者行亚砷酸和维甲酸、化疗联合治疗效果满意。