Acute pancreatitis (AP) is a life-threatening inflammatory condition of the pancreas. Gentianine (GTN), derived from Gentiana scabra, has been demonstrated to suppress inflammation in various diseases. Nonetheless, the specific effects and related pathways through which GTN influences AP progression remain unclear. Herein, we aimed to elucidate the regulatory effects of GTN on AP. Our results confirmed that the reduction in cell proliferation induced by caerulein could be reversed after GTN treatment (25 mu M, 50 mu M and 100 mu M). Moreover, while caerulein treatment increased cell apoptosis, subsequent GTN treatment reduced this effect, as well as the inflammation provoked by caerulein. Furthermore, activation of the Toll-like receptor 4 (TLR4)/nucleotide-binding oligomerization domain, leucine-rich repeat and pyrin domain-containing 3 (NLRP3) pathway induced by caerulein was counteracted by GTN administration. In summary, this research revealed for the first time that GTN promotes cell proliferation and reduces inflammation and oxidative stress in AR42J cells in a caerulein-induced AP cell model, suggesting that GTN holds promise as an effective therapeutic agent for AP.

Objective:Delirium is a common complication of acute pancreatitis. Receptor-interacting protein kinase 3 (RIP3) is an activator of programmed cell necrosis. This study aimed to determine its ability to predict delirium after acute pancreatitis. Methods:In total, 297 patients with acute pancreatitis were prospectively enrolled in this study. Patients were divided into two subgroups (study and validation groups: 197 and 100 cases, respectively). Serum RIP3 levels were measured in all patients and in 100 healthy controls. Acute Physiology and Chronic Health Evaluation (APACHE) II, Ranson, and sequential organ failure assessment (SOFA) scores were used for the severity assessment. In-hospital delirium was observed as an outcome variable. Multifactorial analyses were performed to discern severity correlations and outcome associations. Results:Serum RIP3 levels were significantly higher in the patients than in the controls. Serum RIP3 levels had linear relationships under the restricted cubic spline and were independently correlated with APACHE II, Ranson, and SOFA scores. Serum RIP3 levels were linearly correlated with the likelihood of developing in-hospital delirium and exhibited a strong discrimination efficiency under the receiver operating characteristic curve. Serum RIP3 levels, coupled with APACHE II scores, Ranson scores, and SOFA scores, were the four independent predictors of in-hospital delirium. No interactions were revealed regarding its relevance to sex, age, or body mass index in subgroup analysis. These were integrated to form a model graphically represented by a nomogram that showed effective stability, clinical fit, and predictive ability for in-hospital delirium. The model was verified in the validation group. Conclusion:An incremental trend in serum RIP3 levels was notable after acute pancreatitis. Serum RIP3 levels are independently related to illness severity and occurrence of in-hospital delirium, indicating that serum RIP3 may be a potential biomarker of acute pancreatitis.

Tauroursodeoxycholic acid (TUDCA) can activate farnesoid X receptor (FXR) to involve in the formation of gallstones. Here, this study aimed to probe the potential mechanism of TUDCA-FXR network in the formation of bile duct stone. The levels of TUDCA, FXR and NCK1 were decreased, while the level of miR-107 was increased in the serum of bile duct stone patients. FXR expression was positively correlated with TUDCA or NCK1 expression in patients, moreover, TUDCA pretreatment in biliary epithelial cells increased the levels of FXR and NCK1, and rescued the decrease of NCK1 caused by FXR knockdown in cells. Then functional analysis showed FXR knockdown caused apoptosis and endoplasmic reticulum stress (ERS) as well as suppressed proliferation in biliary epithelial cells in vitro, which were attenuated by TUDCA pretreatment or NCK1 overexpression Mechanistically, NCK1 was a target of miR-107, which was up-regulated by FXR silencing, and FXR knockdown-induced decrease of NCK1 was rescued by miR-107 inhibition. Additionally, miR-107 expression was negatively correlated with TUDCA expression in bile duct stone patients, and TUDCA pretreatment in biliary epithelial cells decreased miR-107 expression by FXR. Functionally, the pretreatment of TUDCA or FXR agonist suppressed miR-107-evoked apoptosis and ERS in biliary epithelial cells. In conclusion, TUDCA up-regulates FXR expression to activate NCK1 through absorbing miR-107, thus suppressing the apoptosis and ERS in biliary epithelial cells, these results provided a theoretical basis for elucidating the mechanism of bile duct stone formation.

目的 探讨腹腔镜胆总管切开取石术(LCBDE)联合改良T管安置法治疗胆囊结石合并胆总管结石(CBDS)的疗效.方法 回顾性研究 2022年 1月到 2022 年 12 月本院接诊的 92 例胆囊结石合并CBDS患者的病历,依据治疗方法的不同,分为观察组和对照组各 46 例,对照组患者采用 LCBDE+常规 T管安置治疗,观察组采用LCBDE联合改良T管安置法治疗.记录两组患者的手术时间、术中出血量、术后胆管引流时间、胃肠功能恢复时间、术后下床活动时间、住院时间,并比较两组患者治疗前、治疗后的生活质量量表(SF-36)评分的变化,并记录术后并发症的发生情况.结果 观察组的临床指标均优于对照组(P＜0.05);观察组治疗后的生活质量各项评分均高于对照组(P＜0.05);两组并发症发生率比较,差异无统计学意义(P＞0.05).结论 LCBDE联合改良T管安置法治疗胆囊结石合并CBDS的临床效果明显,可提高患者的生活质量,值得在临床中进行推广应用.

Purpose: To examine the effect of abietic acid (AA) in the treatment of acute pancreatitis (AP) in mice.Methods: C57BL/6J mice were randomly assigned to 4 groups: sham, AP, AP + 20 mg/kg AA, and AP + 40 mg/kg AA groups. To induce AP mouse model, the mice received intraperitoneal (IP) injections of cerulein. The extent of pancreatic tissue damage was evaluated by histological examination. Serum ALT, lipase, and amylase levels were determined by commercial kits while TUNEL assay was used to assess the apoptosis of pancreatic cells. The contents of Bax, Caspase-3, Bcl-2, p-ERK/ERK, p-JNK/JNK, and p-P38/P38 in pancreatic tissues were evaluated by western blot while the contents of IL-6, TNF-α, IL-1β, nitrite, MDA, and GSH in the tissues were evaluated by enzyme-linked immunosorbent assay (ELISA) kits.Results: AA relieved pancreatic damage and reduced ALT, lipase, and amylase levels in ceruleintreated AP mouse (p < 0.001). AA repressed apoptosis of pancreatic cells in cerulein-induced AP mouse, and inhibited oxidative stress and inflammatory response in the mice by reducing IL-6, TNF-α, IL-1β, nitrite, and MDA contents; it also enhanced the levels of GSH in the tissues (p < 0.001). In addition, AA inhibited MAPK pathway activity in the mice (p < 0.001).Conclusion: AA ameliorates pancreatic damage, pancreatic cell apoptosis, oxidative stress, and inflammation in cerulein-induced AP mouse by inhibiting MAPK pathway. This study offers a new potential drug for the management of AP and expands the relevant molecular regulatory mechanisms.

Hepatocellular carcinoma (HCC) is a common liver cancer that accounts for 90% of cases. Doxorubicin exhibits a broad spectrum of antitumor activity and is one of the most active agents in HCC. WW domain-containing protein 2 (WWP2) is highly expressed in HCC tissues and activates protein kinase B (AKT) signaling pathway to enhance tumor metastasis. However, the role of WWP2 in the glycolysis and antitumor effects of doxorubicin and the epigenetic alterations of WWP2 in HCC remain to be elucidated. The levels of WWP2 and N6-methyladenosine methyltransferase-like 3 (METTL3) in clinical samples and cells were investigated. WWP2 were silenced or overexpressed to study the role of WWP2 in regulating cell proliferation, colony formation, and glycolysis. RNA immunoprecipitation was performed to test m6 A levels. Quantitative reverse-transcription polymerase chain reaction (RT-PCR) and Western blot were used to measure mRNA and protein, respectively. WWP2 silencing inhibits cell proliferation, colony formation, and glycolysis, while WWP2 overexpression has the inverse effects via the AKT signaling pathway. Silencing WWP2 enhances doxorubicin's antitumor effect, while WWP2 overexpression suppresses doxorubicin's antitumor effect. Data also support that METTL3 mediates WWP2 m6A modification, and m6A reader, IGF2BP2, binds to the methylated WWP2 to promote the stability of WWP2, leading to upregulation of WWP2. METTL3 mediates WWP2 m6A modification, which can be recognized and bound by IGF2BP2 to increase the stability of WWP2, leading to WWP2 overexpression which inhibits the antitumor effects of doxorubicin through METTL3/WWP2/AKT/glycolysis axis.

多原发癌(multiple primary cancers,MPCs)也称重复癌或多中心癌,指同时或先后发生于患者同一或不同器官的2种或2种以上经组织病理学证实的原发性恶性肿瘤[1].一般认为,两个肿瘤间隔时间<6个月为同时性多原发癌,>6个月为异时性多原发癌.患者同一次就诊时发现两种癌症的情况较为罕见,定义为即时性双原发癌[2].现对丽水市人民医院收治的一例即时性双原发癌诊治过程进行分析,希望对今后的临床工作有一定的参考作用.

目的 探讨WWP的E3泛素连接酶2(ww domain-containing protein 2,WWP2)沉默对肝癌细胞系黏附、侵袭和迁移的影响作用.方法 通过RNA沉默技术降低肝癌细胞系的WWP2水平,用Transwell法检测细胞迁移和侵袭,CCK-8法检测细胞的增殖情况,Western blot法检测caspase7、caspase8、Bcl-2、Bax、PTEN、p-Akt及Akt的蛋白水平.结果 沉默WWP2后,肝癌细胞BEL-7404和Huh7的WWP2mRNA和蛋白的表达水平明显下降(P<0.001),BEL-7404细胞和Huh7细胞的凋亡相关标志物caspase7、caspase8及Bax的蛋白水平表达都显著升高(P<0.01)、PTEN的蛋白水平升高(P<0.01),Bcl-2、p-Akt的蛋白水平显著下降(P<0.01),肝癌细胞BEL-7404和Huh7的细胞活力、黏附能力、侵袭能力和迁移能力都明显减弱(P<0.001).结论 沉默WWP2可抑制肝癌BEL-7404细胞和Huh7细胞增殖、黏附、侵袭和迁移,并促进细胞凋亡,其作用机制可能与PTEN/Akt信号通路相关.

One of the most prominent characteristics of hepatic ischemia-reperfusion injury (HI/R) is an intense inflammatory reaction, which plays a key role in inflammatory injury induced by ischemia-reperfusion. Nucleotide-binding oligomerization domain-containing protein (NOD-), leucine-rich repeat (LRR), and pyrin domains-containing protein 3 (NLRP3) are involved in the inflammatory injury of ischemia-reperfusion as an important pattern recognition receptor for innate immunity. G protein-coupled receptor 30 (GPR30) is a newly identified as 7-transmembrane G protein-coupled receptor and can be activated by many stimulations including estrogen. The current study aims to explore whether GPR30 agonist (G1) can alleviate hepatic ischemia-reperfusion injury HI/R by inhibiting NLRP3. An induced HI/R rat model was generated, blood and liver samples were gathered and subjected to histological examination, biochemical assays, Western blot assays, and qRT-PCR. Our results indicated GPR30 agonist (G1) pretreatment or NLRP3 silencing significantly decreased the serum levels of Interleukin 1 beta (IL-1 beta), alanine aminotransferase (ALT) and aspartate aminotransferase, improved histological alterations and hepatocyte apoptosis. Moreover, G1 pretreatment or NLRP3 silencing downregulated the protein level of Caspase-1 and pro-Interleukin 1 beta (pro-IL-1 beta) while G1 pretreatment upregulated the expression of GPR30 (p < 0.05). In conclusion, the salutary effects of GPR30 agonists on HI/R are mediated at least in part through downregulating NLRP3 expression. GPR30 may be used as a therapy target of HI/R.

背景 miR-145-3p在头颈癌、肺癌和胃癌等肿瘤可发挥抑癌的作用,而其在肝癌中的表达和作用并不清楚.目的 探讨miR-145-3p在肝癌中的表达及其对肝癌细胞的增殖与凋亡的调控作用.方法 用RT-qPCR法检测肝癌组织、癌旁组织、肝细胞株(Hep3B、Huh-7、HepG2和SMMC-7721)与正常肝细胞株L-02中miR-145-3p的表达水平;将miR-145-3p mimic或miR-145-3p inhibitor转入Hep3B细胞,用CCK-8法、流式细胞术、TUNEL法和Western blot法分别检测细胞活力、细胞周期、细胞凋亡和4型黏蛋白(mucin4,MUC4)表达.用荧光素酶报告基因实验鉴定miR-145-3p的靶基因.将pcDNA-MUC4转入已转染miR-145-3p mimic的细胞,用CCK-8法和TUNEL法分别检测细胞活力与细胞凋亡.结果 miR-145-3p在肝癌组织和细胞中呈低表达.过表达miR-145-3p能抑制细胞增值和G0/G1期到S期转换,促进凋亡和降低MUC4表达;而敲减miR-145-3p则作用相反.MUC4是miR-145-3p的靶基因.过表达MUC4能逆转miR-145-3p mimic对细胞存活的抑制作用.结论 miR-145-3p在肝癌低表达,且其表达与T分期呈负相关.过表达miR-145-3p可抑制肝癌细胞存活与生长,而敲减miR-145-3p能促进肝癌细胞存活与生长.

目的:探讨GPER激动剂G-1在大鼠肝脏缺血再灌注损伤中的作用.方法:采用Pringle's法制作肝脏缺血再灌注损伤模型,选取健康清洁级雄性SD大鼠54只,随机分成假手术组(PO组)、肝缺血再灌注组(IR组)和G-1预处理+肝缺血再灌注组(GIR组)三组,每组18只.各组分别在缺血再灌注6h、12h和24h共3个时间点的血液及肝组织标本,检测血清谷丙转氨酶(ALT)浓度,TUNEL法观察肝细胞的凋亡情况及ELISA法测定白细胞介素1β(IL-1β)水平.结果:GIR、IR组与PO组比较,血清ALT、白细胞介素1β(IL-1β)水平升高(P<0.01),但GIR组明显低于IR组(P<0.05);GIR、IR组肝细胞的凋亡率明显高于PO组(P<0.05),但GIR组明显低于IR组(P<0.01).结论:GPER激动剂G-1预处理能降低IL-1β水平,抑制IL-1β产生来减轻肝脏缺血再灌注损伤.

目的 探讨肝癌患者护理中采用情境体验式健康教育的临床疗效.方法 选取2017年9月～2018年9月于我院就诊的肝癌患者74例,以"双盲法"为原则进行分组,分别是常规组(n=37)和研究组(n=37),常规组应用常规护理,研究组采用情境体验式健康教育,比较两组护理干预后的心理状态、生活质量、健康教育认知水平、依从性情况.结果 干预前两组心理状态指标SAS、SDS评分均处于同一水平,干预后两组上述指标评分均明显降低,且研究组SAS、SDS评分降低程度比常规组更显著(P<0.05);与常规组相比,研究组生活质量各指标身体功能、角色功能、情绪功能、社会功能、总体生活质量评分更高(P<0.05);研究组健康教育知识掌握程度明显比常规组更好(P<0.05);研究组、常规组患者依从率分别为91.89％、70.27％,研究组明显更好(P<0.05).结论 肝癌患者护理中采用情境体验式健康教育,可有效改善患者的不良心理情绪,增强认知水平,进而提高生活质量,值得临床广泛推广.

BackgroundAvitinib is one type of the third‐generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) for the treatment of non‐small cell lung cancer (NSCLC) with EGFR mutations. The purpose of this study was to investigate the effect of avitinib on the pharmacokinetics of osimertinib, one FDA approved third‐generation TIKI, both in vitro and in vivo.MethodsThe in vitro metabolic stability and inhibitory effect of avitinib on osimertinib were assessed with rat liver microsomes (RLM) to determine its IC50 values. For the in vivo study, 18 Sprague‐Dawley rats were randomly divided into three groups: the avitinib multiple dose group (30 mg/kg avitinib once daily for seven days), the avitinib single dose group (PEG200 once daily for six days and a dose of 30 mg/kg avitinib in PEG200 on day 7) and the control group (equal amounts of PEG200 once daily for seven days). Next, all rats were given osimertinib at a dosage of 10 mg/kg. UPLC/MS‐MS was used for the determination of the concentration of osimertinib in plasma.ResultsIn vitro analysis revealed that the IC50 value of osimertinib in rat liver microsomes was 27.6 μM. When rats were pretreated with avitinib, the values of AUC and MRT of the osimertinib were increased, and its Cmax and Tmax were significantly extended, whereas the values of CLz/F were significantly decreased (P < 0.05).ConclusionsBoth in vitro and in vivo results demonstrated that a drug‐drug interaction between avitinib and osimertinib occurred and more attention should be paid when avitinib and osimertinib are synchronously administered in clinic.Key pointsSignificant findings of the studyOsimertinib is the only market available third‐generation EGFR‐TKI and it has been reported that some drugs could have drug‐drug interactions with it.What this study addsFor the first time, we systematically investigated the effect of avitinib, one newly developed third‐generation EGFR‐TKI, on the pharmacokinetics of osimertinib both in vitro and in vivo using a rat model.

目的 探讨合并肝内胆管结石的肝内胆管细胞癌(ICC)临床病理特征及肝内胆管结石对ICC术后生存效果的影响.方法 回顾性分析丽水市人民医院2013年1月至2018年12月118例首次行根治性手术治疗的ICC患者临床资料,按有无合并肝内胆管结石分为两组,其中合并肝内胆管结石的ICC(结石阳性组)58例,无合并肝内胆管结石的ICC(结石阴性组)60例,对两组患者的临床病理特点以及术后无瘤生存率和总生存率进行对比分析.结果 与结石阴性组相比,结石阳性组在肿瘤大小、CA199、CEA、碱性磷酸酶及γ-谷氨酰胺转肽酶水平明显较高,差异有统计学意义(P<0.001),且结石阳性组肿瘤更容易出现周围神经侵犯、血管侵犯、区域内淋巴结转移及肿瘤分期晚等病理特征(P<0.001).结石阳性组患者1、3、5年无瘤生存率分别为31.9％、10.7％、3.5％,明显低于结石阴性组56.67％、33.3％、16.67％(χ2=46.61,P<0.001);结石阳性组患者1、3、5年总生存率分别为57.1％、21.8％、10.7％,也明显低于结石阴性组76.7％、43.3％、23.3％(χ2=26.60,P<0.001).结论 合并肝内胆管结石的肝内胆管细胞癌患者更易发生淋巴结转移、血管侵犯,肿瘤分期晚,术后生存效果较差.

Hepatocellular carcinoma (HCC), the most common aggressive malignancy of liver, is the third leading cause of cancer death across the world. Laminin gamma 1 (Lamc1), encodes laminin-γ1, an extracellular matrix protein involved in various progresses such as tumor cell proliferation and metabolism. In the present study, high expression of Lamc1 and PKM2 was observed in tumor tissues of HCC patients. In vitro, down-regulation of Lamc1 inhibited proliferation of HCC cells by promoting cell death, reduced glucose consumption and lactate production, accompanied by a decrease in the expression of glucose transporter 1 (GLUT1) and lactate dehydrogenase A (LDHA), and PTEN increased, as well as PTEN S380 and AKT S473/T308 phosphorylation decreased, while Lamc1 up-regulation had the opposite effect. The effects of PKM2 were similar to that of Lamc1 and markedly counteracted the effects of Lamc1 down-regulation. In addition, Lamc1-induced increase in PKM2 expression was strongly attenuated by a PI3K inhibitor, LY294002 or a si-p110 PI3K, with a significant decrease in GLUT1 and LDHA expression, as well as decreased AKT T308 phosphorylation. Thus, we speculated that Lamc1 was implicated in the progression of HCC probably by regulating PKM2 expression through PTEN/AKT pathway.

Objective To compare the clinical efficacy of laparoscopic choledochoscope combined with U100plus laser and ERCP in the treatment of incarcerated stones of the lower common bile duct. Methods The clinical data of 54 patients with incarcerated stones of the lower common bile duct admitted to our hospital from Jan. 2014 to Dec. 2017 were retrospectively analyzed. The patients were divided into laparoscopic choledochoscope combined with U100plus laser lithotripsy group,ERCP group.Success rate of stone extraction,rate of complications and recurrence rate of stone were compared among the 2 groups. Results The difference in the success rate of stone extraction and rate of complications between the two groups was statistically significant(P<0.05).There was no significant difference in the recurrence rate of stone between the two groups(P>0.05). Conclusion Laparoscopic choledochoscope combined with U100plus laser lithotripsy in the treatment of incarcerated stones of the lower common bile duct is safe and effective. Laparoscopic choledochoscope combined with U100plus laser lithotripsy has higher success rate and fewer complications than ERCP in the treatment of incarcerated stones of the lower common bile duct.

目的 探讨应用腹腔镜治疗结石相关性肝内胆管细胞癌的可行性和治疗效果.方法 收集笔者医院2013年1月～2017年12月经筛选符合纳入标准的60例患者资料,30例行腹腔镜肝切除术(腹腔镜组),30例采用开腹肝切除术(开腹组);两组患者的手术方式包括左半肝切除术、肝门部区域淋巴结清扫术、胆囊切除、胆总管切开取石、胆管镜检查取石、胆管镜下激光碎石、T管引流术等,分析和对比两组手术时间、术中出血量、术中并发症、术后疼痛、术后镇痛药物应用、术后住院时间、术后切口美容效果、下床活动时间、恢复饮食时间、术后并发症、结石清除率以及肿瘤复发率等指标.结果 腹腔镜组手术时间长于开腹组(P＜0.01),其术后住院时间、术中出血量与开腹组比较,差异有统计学意义(P＜0.01),其术后止痛药使用率、术后切口美容效果、术后切口疼痛及术后并发症的发生率与开腹组比较,差异有统计学意义(P＜0.01),比开腹组更早地恢复下床活动和进食(P＜0.01),两组结石清除率及术后半年肿瘤复发率比较,差异无统计学意义(P＞0.05),且均无围术期死亡病例.结论 对于符合入选标准的病例,腹腔镜手术是安全可行的,可以达到与开腹手术同样的效果,它具有切口小、痛苦轻、恢复快、并发症少等微创手术的优势.

目的 比较腹腔镜根治术与开腹根治术治疗早期胆囊癌的临床疗效.方法 回顾性分析丽水市人民医院于2014年1月至2017年12月期间收治的52例早期胆囊癌(T1b～T2期)患者的临床资料,根据根治术式不同分为腹腔镜组(23例)和开腹组(29例).比较两组患者的手术时间、术中出血量、术后胃肠功能恢复时间、术后住院时间、术后并发症发生率及肿瘤复发率.结果 两组患者的手术时间、术中出血量、术后并发症发生率及肿瘤复发率比较差异均无统计学意义(P>0.05).与开腹组比,腹腔镜组患者的术后胃肠功能恢复时间[(19.70±5.59)h vs(28.90±8.21)h,P<0.01]、术后住院时间更短[(9.30±2.77)d vs(12.59±3.13)d,P<0.01],差异有统计学意义.结论 腹腔镜胆囊癌根治术治疗早期胆囊癌安全、有效,且恢复快.

Objective To investigate the effect of laparoscopic cholecystectomy(LC)combined with percutaneous transhepatic gallbladder puncture(PTGD)on acute cholecystitis with surgical contraindications and postoperative concurrent effects. Methods Using retrospective analysis, 168 patients with acute cholecystitis with severe heart/lung/renal dysfunction who were diagnosed and treated in our hospital from April 2014 to April 2017 were studied and divided into single LC according to different treatment methods. The time of operation,the amount of blood loss,and the number of intraoperative conversion to open surgery postoperative visual analogue pain(VAS)score,first postoperative anal ejection time,and hospitalization time body temperature,white blood cell count,changes in serum alkaline phosphatase,total bilirubin,and incidence of postoperative complications before and 72 hours after surgery of single LC group(emergency LC surgery) and combination group(PTGD combined with LC)were observed. Results The operation time and the laparotomy rate were higher in the combined group than in the single LC group,but the VAS score, first postoperative anal venting time,and postoperative LC hospital stay were all lower or earlier than the single LC group. The body temperature,white blood cell count,serum alkaline phosphatase and total bilirubin improvement were better than single LC group,and the incidence of postoperative complications and mortality rate were lower than that of single LC group. The above differences were statistically significant(P<0.05). Conclusion For patients with acute cholecystitis with severe heart/lung/renal function cancer,PTGD combined with LC has higher safety and clinical efficacy,and is more conducive to the recovery of postoperative patients.

目的 探讨晚期原发性肝癌患者应用肝动脉化疗栓塞术联合深部热疗治疗的临床效果.方法 将2015年10月～2017年10月来我院接受治疗的82例晚期原发性肝癌患者选为观察对象,依照随机数字表法分为对照组(n=41)和试验组(n=41).对照组患者给予肝动脉化疗栓塞术治疗,试验组患者在对照组基础上给予深部热疗治疗,对两组患者临床疗效、甲胎蛋白(AFP)水平、Kamofsky(KPS)评分及不良反应发生率进行统计比较.结果 试验组患者临床总有效率明显高于对照组,分别为70.7％、41.5％,差异有统计学意义(P＜0.05).两组患者治疗后AFP水平明显降低,与治疗前相比,差异有统计学意义(P＜0.05),且试验组患者明显低于对照组,差异有统计学意义(P＜0.05).两组患者治疗后KPS评分明显升高,与治疗前相比,差异有统计学意义(P＜0.05),且试验组患者明显高于对照组,差异有统计学意义(P＜0.05).两组患者胃肠道反应、肝功能损害、发热、白细胞下降发生率比较,差异无统计学意义(P＞0.05).结论 晚期原发性肝癌患者应用肝动脉化疗栓塞术联合深部热疗治疗的临床效果更加确切,不仅可以缩小肿瘤,还可以提高生活质量,是一种值得临床推广与应用的治疗方案.