ObjectiveTo further evaluate the relation between usage of proton pump inhibitor (PPI) and the risk of pancreatic cancer. MethodThe observational studies were systematically searched in the databases of PubMed, Embase, Web of Science, Cochrane Library, ClinicalTrials.gov, CNKI, Wanfang, and VIP. The combined odds ratio (OR) and 95% confidence interval (CI) of pancreatic cancer risk were estimated by the corresponding effect model according to the heterogeneous results, and the subgroup analysis, meta-regression, and sensitivity analysis were performed. In addition, the relation between the defined daily dose (DDD) and usage time of PPI and the pancreatic cancer risk were studied by using restricted cubic spline. ResultsA total of 14 studies were included, including 1 601 430 subjects. The meta-analysis result showed that usage of PPI was positively correlated with the risk of pancreatic cancer [I2=98.9%, OR (95%CI)=1.60 (1.21, 2.11), P<0.001]. The subgroup analysis results showed that usage of PPI would increase the risk of pancreatic cancer in the subgroups of literature published before 2018 [OR (95%CI)=1.88 (1.05, 3.38), P=0.034], non-Asian regions [OR (95%CI)=1.37 (1.04, 1.82), P=0.028], case-control studies [OR (95%CI)=1.59 (1.16, 2.18), P=0.004], cohort studies [OR (95%CI)=1.65 (1.13, 2.39), P=0.009], and high-quality studies [OR (95%CI)=1.62 (1.19, 2.20), P=0.002]. The dose-response curve showed that there was a nonlinear relation between the usage of PPI and the risk of pancreatic cancer (χ2linear=2.27, P=0.132; Pnonlinear=0.039). When the usage of PPI was 800 DDD or less, usage of PPI would increase the risk of pancreatic cancer, but there was no statistical significance when the usage of PPI was more than 800 DDD. The time-effect curve showed that there was a linear relation between the usage time of PPI and the risk of pancreatic cancer (χ2linear=6.92, P=0.009), and the risk of pancreatic cancer would increase by 2.3% if the usage of PPI increased by one month [OR=1.02, 95%CI (1.01, 1.04), P=0.009]. The sensitivity analysis confirmed that the results were stable by gradually eliminating each study, the OR (95%CI) of the risk of pancreatic cancer was 1.37 (1.08, 1.74) to 1.66 (1.22, 2.27), and the publication bias was not found by Egger test (P=0.594).ConclusionsFrom the results of this meta-analysis, usage of PPI will increase the risk of pancreatic cancer, and the dosage of PPI and usage time of PPI may be related to the risk of pancreatic cancer. The clinical usage of PPI should be strictly controlled, and the dosage and usage time should also be carefully considered.
To study the mechanism of p16,Cyclin D1 and CDK4 and their relationship with pancreatic carcinoma, their expressions were examined by immunchistochemistry methods. Results: overpression of Cyclin D1 and CDK4 was revealed in these samples and p16 was undertectable. There was a negitive correlation between p16 and Cyclin D1 (Ｐ＜0.05), and a positive relation between Cyclin D1 and CDK4 (Ｐ＜0.05). The results indicate that abnormality of p16, Cyclin D1 and CDK4 may be involved in the molecular mechanism of pancreatic carcinoma, p16 lower expression and Cyclin D1 over expression may coexit in the development of pancreatic carcinoma.
Objective To evaluate the effect of regiono-perfusional chemotherapy of pancreatic adenocarcinoma, and to seek the management of its complications. MethodsThirty-six patients with unresectable pancreatic adenocarcinoma received selectively intra-arterial catheterization and perfused with 5-Fu, ADM, DDP. Results Six patients had complete response, 15 partial response, and one underwent radical resection subsequently. Cmplications occurred in 14 patients with 2 patients died of complications.Conclusion Regiono-perfusional chemotherapy of pancreatic adenocarcinoma is effective, but the complications can not be neglected.
ObjectiveTo explore the values of CA19-9, CA242, CEA, and CA125 single or combined detection on clinical diagnosis and prognosis for patients with pancreatic cancer. MethodsSerum tumor markers CA199, CA242, CEA, and CA125 of 63 patients with pancreatic cancer, 33 patients with cancer of bile duct, and 27 patients with benign pancreatic disease were detected, and those patients were followed up after operation. ResultsThe levels of CA19-9, CA242, CEA, and CA125 in patients with pancreatic cancer were significantly higher than those in patients with benign pancreatic disease and cancer of bile duct (Plt;0.05). The sensitivity of CA19-9 alone was the highest in the four tumor markers for the patients with pancreatic cancer 〔79.4% (50/63)〕, but the specificity (61.9%) was lower than that of CA242 (83.3%) and CEA (80.0%). The specificity of combined detection of CA199+CA242+CEA was the highest 〔93.3% (56/60)〕. The level of CA19-9 in carcinoma of body/tail of pancreas was significantly higher than that of carcinoma of pancreas head or whole pancreas (Plt;0.05). The serum levels of CA19-9 and CA242 in patients with stage Ⅳ were significantly higher than those in stage Ⅰ or Ⅱ/Ⅲ (Plt;0.05). Fifteen patients were lost to follow up, 48 patients were followed up 2－12 months with an average 6 months. The levels of CA242 and CA199 in patients with pancreatic cancer on 0.5 month and 3 months after operation were lower than those before operation (Plt;0.05). ConclusionsSingle detection of CA19-9 can improve the diagnostic sensitivity, and combined detection of tumor markers CA199+CA242+CEA can improve the diagnostic specificity. CA19-9 or CA242 is a valuable marker for evaluating treatment effects and estimating prognosis.
Objective To explore the application of nutritional and inflammatory markers in the prognosis assessment of resectable pancreatic cancer, and to provide new ideas for the prognosis assessment of patients with pancreatic cancer. Method The recent studies on nutritional and inflammatory markers for prognosis of resectable pancreatic cancer at home and abroad were reviewed. Results Radical pancreaticoduodenectomy was the preferred treatment for patients with resectable pancreatic cancer. Poor nutritional status and severe systemic inflammatory response were closely related to postoperative tumor recurrence and other poor prognosis. Nutritional and inflammatory markers played an important role in evaluating the prognosis of resectable pancreatic cancer. Conclusion Nutritional and inflammatory markers, as simple and economical prognostic indicators, have broad clinical application prospects in the prognostic assessment of resectable pancreatic cancer.
慢性胰腺炎是一种胰腺的进展性和不可逆性炎症病变，最终将导致胰腺结构破坏和内、外分泌功能的丧失。病程通常呈反复发作性，表现为复发性腹痛或慢性无痛综合征。急性胰腺炎、慢性胰腺炎和胰腺癌这三种疾病之间存在着较复杂的关系。急性胰腺炎的发作通常先于慢性胰腺炎几年时间，而胰腺癌往往是在慢性胰腺炎明确诊断后20年左右发生，关于他们在发病上是否存在着一定的序贯性或是有其他短暂的联系，目前仍有争论。一些资料完整的临床病例随访分析提示，长期患慢性胰腺炎的患者发展为胰腺癌的危险性明显高于普通人群。
【 Abstract 】 Objective Overexpressions of epidermal growth factor (EGF) and EGF receptor have been associated with progression and invasive phenotype of pancreatic cancer. However, the underlying molecular mechanism by which EGF worked in pancreatic cancer cells has not been completely understood. In this study, effect of EGF on the invasion and metastasis of pancreatic cancer cells and its regulatory mechanism were investigated. Methods The effects of EGF on the proliferation, adhesion and invasion of pancreatic cancer cells were detected by WST-1 proliferation assay, adhesion assay and invasive assay, respectively. The activity and expression of MMP-2 and MMP-9 were examined by zymography, Western blot and RT-PCR, respectively. The activity of NF- κ B was examined by EMSA. Results EGF could significantly promote the invasiveness of pancreatic cancer cells but did not affect cell proliferation or adhesion. The expressions of NF- κ B and MMP-9 were significantly increased by EGF, but EGF did not affect the activity and expression of MMP-2. Furthermore, EGF stimulated the NF- κ B binding activity. Pretreatment with NF- κ B inhibitors, pyrrolidine dithiocarbamate (PDTC), could significantly inhibit the activity of NF- κ B induced by EGF. Meanwhile, the EGF-induced expression and activity of MMP-9, as well as cell invasiveness were also inhibited by NF- κ B inhibitor. Conclusion EGF could increase the expression and promote the invasiveness of MMP-9 via the activation of NF- κ B in pancreatic cancer cells, which implies that NF- κ B inhibitant, such as PDTC, may diminish the invasiveness of pancreatic cancer cells.