慢性萎缩性胃炎伴肠化生是一种常见的消化系统疾病,被世界卫生组织称作胃癌前病变.西医治疗本病难以逆转肠化,临床疗效不佳.陆敏教授临证二十余年,治疗慢性萎缩性胃炎伴肠化生经验颇丰,疗效显著.他认为脾胃虚弱是本病的发病基础,痰湿瘀结是发病关键,治疗时以健脾补中为主,理气散结为辅,标本兼顾,扶正与祛邪同用,同时需注意三因制宜,随证加减,调养后天.

Hypertrophic scar (HS) is a condition characterized by excessive synthesis and deposition of collagen. There are many clinical methods to alleviate HS, but most of them are accompanied by many complications. To investigate the effects of β-Elemene, extracted from the ginger family plant Wenyujin, on human hypertrophic scar fibroblast (hHSFs). Cultured hHSFs and human normal fibroblasts, observed the effect of β-Elemene on apoptosis, extracellular matrix, and endoplasmic reticulum stress (ERS) by western blot, Real Time-Polymerase Chain Reaction (RT-PCR), and flow cytometry. Based on our findings, it is clear that β-Elemene could inhibit the expression of α-smooth muscle actin (α-SMA), collagen I, and fibronectin, reduced collagen deposition. Further studies had found that β-Elemene could increase the expression of ERS-related proteins CHOP and Calnexin in a dose-dependent manner, thereby promoting the aggregation of cleaved-caspase-3 and inducing hHSFs to undergo poptosis. This process may depend on the regulation of P53. The results of our study indicates that β-Elemene induced hHSFs to undergo apoptosis though ERS pathway in a P53-dependent manner, which means that our research provided a new strategy for the development of drugs for the treatment of HS.

目的:探讨直肠癌新辅助治疗中盆腔骨髓保护调强放疗与病理反应的相关性.方法:回顾性分析2017年01月至2020年12月于我院接受新辅助放化疗及根治性手术的192例Ⅱ、Ⅲ期直肠癌患者的临床病理资料,其中95例为接受盆腔骨髓保护调强放疗的患者(淋巴细胞保护组),余97例患者来源于本单位回顾性数据库(对照组).比较两组患者淋巴细胞绝对计数最低值、淋巴细胞下降程度及肿瘤病理反应率差异,分析直肠癌新辅助治疗中盆腔骨髓保护调强放疗与病理反应的相关性.结果:淋巴细胞保护组患者放化疗期间最低淋巴细胞计数、放化疗后淋巴细胞计数及病理反应率均高于对照组,差异有统计学意义.淋巴细胞保护组3-4级淋巴细胞减少症发生率为38.9％,低于对照组的56.8％(P=0.034).多因素Logistic回归分析结果显示3-4级淋巴细胞减少症、淋巴细胞保护、临床分期及等待手术期间化疗是肿瘤病理反应状态的独立影响因素.结论:直肠癌患者新辅助放化疗期间3-4级淋巴细胞减少症与治疗后肿瘤病理反应状态密切相关,通过盆腔骨髓保护调强放疗可有效保护患者的淋巴细胞,减轻3-4级淋巴细胞减少症发生率,提高肿瘤病理反应.

The excessive deposition of extracellular matrix (ECM) is the main characteristic of liver fibrosis, and hepatic stellate cells (HSCs) are the main source of ECM. The removal of activated HSCs has a reversal effect on liver fibrosis. Western blot and MTT analysis indicated that curcumol could relieve hepatic fibrosis by promoting HSCs receptor-interacting protein kinase 1/3 (RIP1/RIP3)-dependent necroptosis. Importantly, autophagy flow was monitored by constructing the mRFP-GFP-LC3 plasmid, and it was found that curcumol cleared activated HSCs in a necroptosis manner that was dependent on autophagy. Our study suggested that the activation of necrosome formed by RIP1 and RIP3 depended on Atg5, and that autophagosomes were also necessary for curcumol-induced necroptosis. Furthermore, microscale thermophoresis and co-immunoprecipitation assay results proved that curcumol could target Sirt1 to regulate autophagy by reducing the acetylation level of Atg5. The HSCs-specific silencing of Sirt1 exacerbated CCl4 -induced liver fibrosis in mice. The deacetylation of Atg5 not only accelerated the accumulation of autophagosomes but also enhanced the interaction between Atg5 and RIP1/RIP3 to induce necroptosis. Overall, our study indicated that curcumol could activate Sirt1 to promote Atg5 deacetylation and enhanced its protein-protein interaction function, thereby inducing autophagy and promoting the necroptosis of HSCs to reduce liver fibrosis.

Background and Aims:Recognition of excessive activation of hepatic stellate cells (HSCs) in liver fibrosis prompted us to investigate the regulatory mechanisms of HSCs. We aimed to examine the role of O-GlcNAcylation modification of alanine, serine, cysteine transporter 2 (ASCT2) in HSCs and liver fibrosis.Methods:The expression of O-GlcNAcylation modification in fibrotic mice livers and activated HSCs was analyzed by western blotting. Immunoprecipitation was used to assess the interaction of ASCT2 and O-GlcNAc transferase (OGT). In addition, ASCT2 protein stability was assayed after cycloheximide (CHX) treatment. The O-GlcNAcylation site of ASCT2 was predicted and mutated by site-directed mutagenesis. Real-time PCR, immunofluorescence, kit determinations and Seahorse assays were used to clarify the effect of ASCT2 O-GlcNAcylation on HSC glutaminolysis and HSC activation. Western blotting, immunochemistry, and immunohistofluorescence were used to analyze the effect of ASCT2 O-GlcNAcylation in vivo.Results:We observed significantly increased O-GlcNAcylation modification of ASCT2. ASCT2 was found to interact with OGT to regulate ASCT2 stability. We predicted and confirmed that O-GlcNAcylation of ASCT2 at Thr122 site resulted in HSCs activation. We found Thr122 O-GlcNAcylation of ASCT2 mediated membrane trafficking of glutamine transport and attenuated HSC glutaminolysis. Finally, we validated the expression and function of ASCT2 O-GlcNAcylation after injection of AAV8-ASCT2 shRNA in CCl4-induced liver fibrosis mice in vivo.Conclusions:Thr122 O-GlcNAcylation regulation of ASCT2 resulted in stability and membrane trafficking-mediated glutaminolysis in HSCs and liver fibrosis. Further studies are required to assess its role as a putative therapeutic target.

Background: Triple-negative breast carcinomas (TNBCs) are a breast carcinoma with the most aggressive form, which is demonstrated as enhanced invasion and recurrence. Britannin is extracted mainly from the traditional Chinese herb Inula japonica Thunb, and few studies have focused on its effect on TNBC. Moreover, there is still no report concerning the role of Britannin in degrading the transcripts of Zinc finger E-box-binding homeobox 1 (ZEB1) proteins. Purpose: To explore the potential effect of Britannin on invasion and stemness of TNBCs and its underlying mechanism. Methods: Cellular activity was measured using MTT, and cell cycle was measured using flow cytometry (FCM). The effect of Britannin on the migrating and invading abilities of MDA-MB-231 and 4T1 cells were measured using the wound healing and transwell assays. The sizes and number of breast carcinoma cells were measured by tumor formation assay and in vitro limiting-dilution assay. CD44 expression in tumor spheroids was tested by immunofluorescence assay. Nextly, the expressions of epithelial-mesenchymal transition (EMT) markers and ZEB1 protein expressional level were detected by western blot . ZEB1 mRNA expressional level was analyzed using RT-qPCR. Drug affinity-responsive target stability (DARTS) method was used to detect the binding activity between Britannin and ZEB1. Co-immunoprecipitation (Co-IP) analysis was applied to test the ubiquitination of ZEB1. The mouse models for experimental lung metastasis of 4T1 cells were established to detect the anti-metastasis effect of Britannin in vivo, and the expressional levels of EMT markers in lung metastases were detected by immunohistochemistry. Results: Britannin could inhibit cell growth and G2/M arrest in TNBC cells. Britannin could inhibit the migrating and invading ability without inducing severe apoptosis of MDA-MB-231 and 4T1 cells. Meanwhile, Britannin reduced the size and number of spheroids formed in these two cells, and decreased the expressional level of stem cells biomarker CD44 in tumor spheroids. Mechanism research showed that Britannin specifically bound to ZEB1 and induced its ubiquitination in MDA-MB-231 cells. Afterwards, Britannin disturbed protein stability and promoted ZEB1 protein degradation. Importantly, Britannin could not inhibit cell invasion and spheroid formation after ZEB1 expression was knocked down. Finally, Britannin inhibition of 4T1 cell metastasis was confirmed through establishing mouse models for the experimental lung metastasis. It was proved that both Britannin and paclitaxel could decrease the lung metastases, and Britannin could also down-regulate the protein expressional levels of ZEB1, MMP9 and CD44. Conclusion: This study reveals that Britannin suppresses the invasion and metastasis of TNBC cells through degrading ZEB1, which suggests that Britannin can be used to prevent tumor metastasis and recurrence via degrading ZEB1 proteins.

目的 比较直肠癌患者新辅助放疗两种盆腔骨髓勾画方法的剂量学参数及骨髓抑制(HT)差异,为临床盆腔骨髓勾画方法提供参考.方法 前瞻性入组60例南京中医药大学附属医院2016-03-01-2018-08-31收治的Ⅱ、Ⅲ期新辅助放化疗的直肠癌患者,采用分层区组随机化方法分为MRI识别盆腔骨髓勾画法组(MRI组)及CT图像勾画骨髓腔法组(CT组),每组各30例.比较两组患者盆腔骨髓及PTV剂量学参数、2级及以上骨髓抑制(HT2+)发生率差异,分析盆腔骨髓剂量学参数与HT2+关系.结果 MRI组患者盆腔骨髓平均体积(t=7.34,P=0.002)、Vs(t=5.759,P=0.003)、V10(t=6.665,P=0.002)、V20 (t=9.864,P=0.000)及HT2+(x2=5.554,P=0.018)明显低于CT组.MRI组盆腔骨髓V20(B=0.901,SE=0.338,Wald=7.085,OR=2.462,95％CI:1.268～4.780,P=0.008)与急性HT2+显著相关,当盆腔骨髓V20 ＞70.4％时,HT2+发生率更高.结论 相较于CT图像勾画盆腔骨髓腔法,MRI法能够减少盆腔骨髓低剂量受照体积,限制盆腔活性骨髓V20≤70.4％,可降低Ⅱ、Ⅲ期直肠癌患者新辅助放疗HT2+发生率.

Background To evaluate the value of pretreatment inflammatory-nutritional biomarkers in predicting responses to neoadjuvant chemoradiotherapy (nCRT) and survival in patients with locally advanced rectal cancer (LARC). Methods Patients with LARC who underwent nCRT and subsequent surgery between October 2012 and December 2019 were considered for inclusion. Neutrophil to lymphocyte ratio (NLR), platelet to lymphocyte ratio (PLR), lymphocyte to monocyte ratio (LMR), and prognostic nutritional index (PNI) were calculated from according to routine laboratory data within 1 week prior to nCRT. The correlations between baseline inflammatory-nutritional biomarkers and responses were analyzed using Chi-square test or Fisher’s exact test, and multivariate logistic regression analysis was performed to identify the independent predictors of pathological responses to nCRT. Univariate and multivariate Cox proportional hazard models were used to assess the correlations of predictors with disease-free survival (DFS) and overall survival (OS). Results A total of 273 patients with LARC were enrolled in this study. Higher LMR and PNI were observed in the good-response group, meanwhile higher NLR and PLR were observed in the poor-response group. Multivariate logistic regression analysis results revealed that PLR and PNI independently predicted responses to nCRT. Multivariable Cox regression analysis determined that PNI was an independent predictor of DFS and OS in patients with LARC. The value of pretreatment PNI in predicting responses and survival was continuously superior to those of NLR, PLR, and LMR. The optimal cutoff value of the PNI was approximate 45. Subgroup analyses indicated that the pathological responses and survival in the high PNI group (≥ 45) were significantly better than those in the low PNI group (< 45), especially in patients with clinical stage III rectal cancer. Conclusion The pretreatment PNI can serve as a promising predictor of response to nCRT and survival in patients with LACR, which is superior to NLR, PLR, and LMR, and the patients with clinical stage III rectal cancer who have a higher PNI are more likely to benefit from nCRT.

目的:探讨尼妥珠单抗联合放疗对老年食管鳞癌患者治疗的有效性和安全性.方法:选取2015年5月至2016年4月我院收治的27例病理确诊为食管鳞癌、年龄＞70岁的患者为研究对象.患者不适合或拒绝手术及化疗而予尼妥珠单抗联合单纯放疗.患者行调强放疗同期使用尼妥珠单抗200 mg·周-1.评估临床疗效、毒副作用及远期生存情况.结果:27例患者均完成治疗计划.中位生存期及中位无进展生存期分别为17.0个月和16.0个月;2年和3年的总生存率分别为49.6％和37.2％,无疾病进展率分别为45.6％和21.4％.患者疗程中均出现1～2度放射性食管炎,无3度以上食管炎及血液学毒性发生.结论:尼妥珠单抗联合单纯放疗对老年食管鳞癌患者安全有效,但仍需扩大样本量进一步研究证实.

Relevant researches have recognized the vital role of inducing ferroptosis in the treatment of tumor. The latest findings indicate that PEBP1/15-LO can play an essential role in the process of cell death. However, its role in regulating ferroptosis in hepatocellular carcinoma (simplified by HCC) remains unclear. The previous research of our team has proved that DHA can induce ferroptosis of hepatic stellate cells. In this study, we found that DHA could also induce ferroptosis in HCC cells. Interestingly, DHA induced ferroptosis by promoting the formation of PEBP1/15-LO and promoting cell membrane lipid peroxidation. In addition, we also found that DHA had no obvious regulatory effect on 15-LO, but it could promote PEBP1 protein expression. Importantly, we discovered the upregulation of PEBP1 induced by DHA was related to the inhibition of its ubiquitination degradation. In vivo experiments have also obtained consistent results that DHA can inhibit tumor growth and affect the expression of ferroptosis markers in tumor tissues, which would be partially offset by interference with PEBP1.

目的:分析不同的炎症及营养相关指标与直肠癌新辅助放化疗后肿瘤病理反应状态及患者预后的相关性,探讨其临床应用价值.方法:回顾性分析2012年10月至2019年2月在南京中医药大学附属医院接受新辅助放化疗及根治性手术的211例Ⅱ、Ⅲ期直肠癌患者的临床病理资料,依据患者放化疗前1周内血常规和肝肾功能检查结果,计算基线中性粒细胞/淋巴细胞之值(NLR)、血小板/淋巴细胞之值(PLR)、淋巴细胞/单核细胞之值(LMR)及预后营养指数(PNI).根据患者术后病理结果,基于肿瘤消退分级(TRG)标准评价肿瘤病理反应状态.采用Logistic模型、Kaplan-Meier法、Cox回归模型分析各炎症及营养相关指标与直肠癌新辅助放化疗肿瘤病理反应状态及患者预后的相关性.结果:新辅助放化疗后病理反应(TRG 0～1级)患者共135例(64.0％),非病理反应(TRG 2～3级)患者76例(36.0％).多因素Logistic回归分析结果显示,基线PNI(OR=1.245,95％CI 1.123～1.380,P<0.001)及癌胚抗原(OR=0.500,95％CI 0.255～0.979,P=0.043)是病理反应状态的独立影响因素.多因素预后分析显示性别、淋巴(ypN)分期、基线NLR及PNI是无病生存期(DFS)的独立影响因素;性别、ypN分期及基线PNI是总生存期(OS)的独立影响因素.分层分析显示ypN阳性患者中高PNI组(PNI>45)5年DFS和OS显著长于低PNI组(无病生存率63.6％vs.48.0％,P=0.002;总生存率69.2％vs.51.9％,P=0.005),而ypN阴性患者中高PNI组与低PNI组预后差异无统计学意义(无病生存率83.2％vs.79.5％,P=0.252;总生存率89.2％vs.85.1％,P=0.299).结论:基线PNI水平与Ⅱ、Ⅲ期直肠癌新辅助放化疗后肿瘤病理反应状态及患者预后相关,其疗效预测价值优于NLR、PLR及LMR.PNI简单无创、经济有效,可作为临床预后预测指标的补充,值得进一步研究.

目的:探讨固定铅门调强计划(fj-IMRT)相对于常规分野调强计划(sf-IMRT)在胸中段食管癌放疗中的潜在剂量学优势.方法:选择10例接受根治性放疗的胸中段食管癌患者,分别制定sf-IMRT和fj-IMRT计划,统计靶区适形度指数、均匀性指数、靶区和危及器官的剂量体积参数、总射野数和机器跳数,各指标差异采用配对t检验.结果:sf-IMRT计划靶区D2％低于fj-IMRT计划(P=0.025).双肺平均剂量(Dmean)、V5、V10、V20,左肺Dmean、V5、V10、V20、V30、V40,右肺Dmean、V5、V10,心脏Dmean和V40,靶区外身体Dmean、V5、V10、V20有显著差异(P<0.05),fj-IMRT优于sf-IMRT计划.两计划射野总数相同,fj-IMRT计划和sf-IMRT计划机器跳数分别为(1081.98±241.32)MU和(997.12±209.73)MU,sf-IMRT计划显著低于fj-IMRT计划(P=0.013).结论:对于胸中段食管癌,fj-IMRT相较sf-IMRT能够显著降低肺、心脏和全身的低剂量照射,同时保证相似的靶区剂量覆盖和治疗实施效率.

目的 探讨采用MRI识别盆腔内造血活性骨髓,优化老年直肠癌患者调强放疗(IMRT)计划的临床价值.方法 对Ⅱ、Ⅲ期接受新辅助放化疗的老年直肠癌患者分别采用依据MRI识别盆腔活性骨髓法(MRI法)及CT图像骨窗下勾画骨髓腔法(CT法)两种方法勾画盆腔骨髓,并设计MRI-IMRT及CT-IMRT两种治疗计划.比较两种方法定义的骨髓体积及IMRT计划的骨髓及靶区、其他危及器官(小肠、膀胱及股骨头)的剂量学参数差异.结果 MRI法勾画的盆腔骨髓平均体积为(374.42±138.58)cm3,CT法为(1142.56±118.72)cm3,MRI法勾画的盆腔骨髓平均体积明显小于CT法,两组间差异有统计学意义(P<0.05).MRI-IMRT计划的盆腔骨髓各剂量体积受量均低于CT-IMRT计划,两种计划间盆腔骨髓V5、V10及V20差异有统计学意义(P<0.05).两种IMRT计划的靶区覆盖率及其他危及器官各剂量学参数差异均无统计学意义(P>0.05).结论 在Ⅱ、Ⅲ期老年直肠癌新辅助IMRT中,采用MRI能较清晰的识别盆腔造血活性骨髓范围,相较于传统的CT图像勾画骨髓腔方式,可明显缩小骨髓体积,利于IMRT计划实施.MRI-IMRT计划在保证靶区覆盖率,且不增加周围危及器官受量的前提下,可有效降低盆腔活性骨髓低剂量辐射剂量体积(V5、V10及V20).

目的 探讨食管造影在食管癌同期放化疗中的检查应用及疗效评估.方法 选取2017年3月至2019年3月我院收治的经放化疗、X线食管造影、资料完整的食管癌患者57例为研究对象,回顾性分析食管癌放化疗治疗后行食管造影的检查应用、X线表现及疗效评估.结果 本组57例患者,食管造影X线显示,病灶范围、长度、充盈缺损、黏膜皱襞破坏、管腔改变及食管动力学变化均优于治疗前,差异显著,放化疗治疗总有效率为89.47％ (51/57).结论 食管癌放化疗,疗效显著、肯定,通过X线食管造影检查,对疗效评估及并发症的防治得以明确及诊断.

目的:对MRI诊断强直性脊柱炎骶骼关节病变的应用价值进行分析和观察.方法:本次研究中共计选取分析了2016年1月到2020年4月期间在我院采取了强直性脊柱炎骶骼关节病变治疗的186例患者资料,分别对所有患者进行MRI检查以及CT检查,以患者皋病理诊断结果为准,对比两种检查方式在强直性脊柱炎骶骼关节病变疾病的诊断效果.结果:MRI检查方式中患者的诊断准确率、特异度以及敏感度均高于CT检查方式,两种检查方式中数据对比差异存在意义(P＜0.05).两种不同检查方式中,在Ⅳ级病变当中的检出概率对比差异不存在统计学意义(P＞0.05),在0级患至Ⅲ级病变当中,MRI检查方式的检出概率高于CT检查方式,两种检查方式中数据对比差异存在意义(P＜0.05).MRI检查方式在骨质异常情况之中的检出概率高于CT检查方式.两种检查方式中数据对比差异存在意义(P＜0.05).结论:在诊断强直性脊柱炎骶骼关节病变患者时,使用MRI检查方式具有显著效果,尤其在早期的骶骼关节病变当中,具有比较好的优势,值得在临床进行推广.

目的 分析局限期食管小细胞癌(SCEC)患者接受放化疗后的疗效及预后影响因素.方法 回顾性分析2000年1月至2016年12月江苏省中医院和浙江丽水市中心医院行放化疗治疗的38例局限期SCEC患者的临床资料,患者均行调强或三维适形放疗,放疗总剂量50～66 Gy,每日剂量1.8～2.0 Gy.放疗同步化疗(顺铂和依托泊苷)2周期以及序贯2周期.随访3年并分析患者中位生存时间、1年和3年生存率、治疗期间不良反应,利用Cox回归模型分析患者预后的影响因素.结果 38例患者平均随访时间(30.4±4.6)个月,中位生存时间25.2个月(9～41个月),1年和3年生存率分别为75.12％和32.31％.其中18例(47.37％)患者出现3～4级粒细胞减少,16例(42.11％)患者出现3～4级血小板减少,12例(31.58％)患者出现3级贫血.Cox回归模型结果显示,纵隔或胃周淋巴结转移为影响SCEC预后的危险因素.结论 根治性放化疗对局限期SCEC患者的疗效可期,有无纵隔或胃周淋巴结转移是其预后影响因素之一.

目的:探讨宫颈癌盆腔外照射治疗中OPS系统应用价值.方法:选取61例宫颈癌患者,随机分为实验组、对照组,实验组使用OPS辅助CBCT验证,对照组仅使用CBCT验证.CBCT采集治疗前图像信息,匹配实时摆位图像与定位图像,分析比较两组X、Y、Z三轴误差数据,对放疗中及放疗后所致不良反应及疗效进行临床比较分析.结果:实验组摆位误差X(2.9±0.8)mm、Y(3.9±1.1)mm、Z(2.0±0.9)mm小于对照组误差X(4.3±1.4)mm、Y(5.9±1.7)mm、Z(3.2±1.5)mm.实验组骨髓抑制、急性肠道症状等可观测不良反应大于Ⅰ级的患者数明显少于对照组.实验组在X、Y、Z三个方向上的值分别是4.03 mm、5.45 mm、3.65 mm;对照组在X、Y、Z三个方向上值分别是6.51 mm、8.38 mm、5.49 mm(P<0.05).结论:在宫颈癌放疗摆位中引入OPS可有效提高摆位精确度,降低摆位误差;在不降低治疗疗效情况下,有效减轻了放疗期间不良反应.

Abstract The purpose of this study was to investigate the potential advantages of the fixed‐jaw technique (FJT) over the conventional split‐field technique (SFT) for cervical and upper thoracic esophageal cancer (EC) patients treated with intensity‐modulated radiotherapy. The SFT and FJT plans were generated for 15 patients with cervical and upper thoracic EC. Dosimetric parameters and delivery efficiency were compared. An area ratio (AR) of the jaw opening to multileaf collimator (MLC) aperture weighted by the number of monitor units (MUs) was defined to evaluate the impact of the transmission through the MLC on the dose gradient outside the PTV50.4, and the correlation between the gradient index (GI) and AR was analyzed. The FJT plans achieved a better GI and AR (P < 0.001). There was a positive correlation between the GI and AR in the FJT (r = 0.883, P < 0.001) and SFT plans (r = 0.836, P < 0.001), respectively. Moreover, the mean dose (Dmean), V5Gy–V40Gy for the lungs and the Dmean, V5Gy–V50Gy for the body‐PTV50.4 in the FJT plans were lower than those in the SFT plans (P < 0.05). The FJT plans demonstrated a reduction trend in the doses to the spinal cord PRV and heart, but only the difference in the heart Dmean reached statistical significance (P < 0.05). The FJT plans reduced the number of MUs and subfields by 5.5% and 17.9% and slightly shortened the delivery time by 0.23 min (P < 0.05). The gamma‐index passing rates were above 95% for both plans. The FJT combined with target splitting can provide superior organs at risk sparing and similar target coverage without compromising delivery efficiency and should be a preferred intensity‐modulated radiotherapy planning method for cervical and upper thoracic EC patients.

目的:观察八珍汤防治局部晚期宫颈癌患者同步放化疗骨髓抑制的临床疗效.方法:将80例局部晚期宫颈癌患者随机分为治疗组和对照组,每组40例.所有患者均住院行盆腔外照射,外照射结束后于门诊行内照射治疗.自接受外照射治疗开始当日起采用紫杉醇加顺铂方案(TP方案)行静脉同步全身化疗,28d为1个周期,连续化疗4个周期.治疗组从放化疗开始(研究起点)同时加服以八珍汤为主方的中药,直至全部放化疗结束后1个月(研究终点).观察并比较2组患者骨髓抑制情况、重组人粒细胞集落刺激因子(rhG-CSF)、悬浮红细胞及重组人白介素-11(IL-11)使用量以及生活质量和免疫功能等.结果:治疗组Ⅲ—Ⅳ级骨髓抑制发生率明显低于对照组(P<0.05),重组人粒细胞集落刺激因子(rhG-CSF)使用剂量及悬浮红细胞输注剂量明显低于对照组(P<0.05).研究终点时治疗组KPS评分分值及稳定率均显著高于对照组(P<0.05).研究终点时治疗组CD3+、CD4+细胞水平及CD4+/CD8+比值高于本组研究起点及同期对照组,差异有统计学意义(P<0.05).结论:八珍汤能够显著减少局部晚期宫颈癌同步放化疗患者骨髓抑制发生率,延缓患者KPS评分下降趋势,改善患者免疫功能,提高患者治疗耐受度及生活质量,具有积极治疗作用.

目的 观察益髓健脾汤防治直肠癌患者新辅助同期放化疗骨髓抑制的临床疗效.方法 2015年10月至2017年10月共入组直肠癌新辅助同期放化疗患者60例,随机分为治疗组及对照组各30例,均行盆腔调强放疗(处方剂量:95％PTV=50Gy/25次,5次/周,周一至周五),联合同期化疗(卡培他滨片,825 mg/m2,口服,每日2次,放疗日),共5周.治疗组从放化疗开始(研究起点)同时加服益髓健脾汤,疗程至放疗结束后30天(研究终点);对照组仅行同期放化疗.观察2组患者骨髓抑制发生、中医证候和生活质量等情况.结果 治疗组Ⅲ～Ⅳ级骨髓抑制发生率明显低于对照组(P＜0.05);重组人粒细胞集落刺激因子(rhG-CSF)使用剂量明显低于对照组(P＜0.01);治疗组平均住院时间短于对照组(P＜0.05).2组患者均无Ⅳ级泌尿、消化系统不良反应发生.与对照组相比,研究组的中医证候积分降低(P＜0.05);研究终点时治疗组KPS评分稳定率为83.33％,高于对照组(56.67％),P＜0.05.结论 益髓健脾汤能显著减少直肠癌新辅助同期放化疗患者骨髓抑制发生率,改善患者治疗后相关中医临床症状,延缓KPS评分下降趋势,提高患者治疗耐受度及生活质量.