Subclinical Inflammation and Endothelial Dysfunction in Patients with Chronic Pancreatitis and Newly Diagnosed Pancreatic Cancer.
Subclinical Inflammation and Endothelial Dysfunction in Patients with Chronic Pancreatitis and Newly Diagnosed Pancreatic Cancer.
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DOI：
10.1007/s10620-015-3972-6
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发表时间：
2016-04
影响因子：
3.1
通讯作者：
Małecka-Panas E
中科院分区：
文献类型：
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作者：
Gasiorowska A;Talar-Wojnarowska R;Kaczka A;Borkowska A;Czupryniak L;Małecka-Panas E
最近的研究表明，多种细胞因子可能在慢性胰腺炎(CP)和胰腺癌(PC)的发生发展中起重要作用。我们研究了新诊断的胰腺癌和慢性胰腺炎患者的内皮功能障碍和亚临床炎症。本研究共纳入45例患者，其中慢性前列腺炎27例，前列腺癌18例。此外，这项研究还包括13名年龄和体重匹配的健康受试者作为对照。检测血浆脂联素、肿瘤坏死因子-α、白介素6(IL-6)、白介素1β(IL-1β)、E-选择素、血栓调节蛋白、黏附分子细胞间黏附分子和血管细胞黏附分子、内皮素-1。与对照组比较，PC组和CP组的血浆脂联素(13,292和12,227 ng/ml比5,408 ng/ml；p<0.0003)、肿瘤坏死因子-α(22.1pg/ml比13 pg/ml；p<0.0002)和IL-6(6.6pg/ml和7.3pg/ml比3.3pg/ml；p<0.0001)显著升高。此外，PC和CP患者外周血中细胞间黏附分子(931和492vs290 ng/ml；P<0.005)和血管细胞黏附分子(1511和1080vs840 ng/ml；P<0.01)明显高于对照组。当单独考虑合并和不合并糖尿病的PC和CP患者时，脂联素、细胞因子和内皮功能障碍的参数没有差异。综上所述，我们的数据表明，与健康人相比，CP和PC患者表达多种细胞因子，尤其是脂联素、肿瘤坏死因子-α和IL-6。晚期CP患者血清肿瘤坏死因子-α和细胞间黏附分子水平呈协同升高趋势。此外，尤其是在PC受试者中，内皮功能障碍的标记物升高。这项研究提供了进一步的证据，表明PC和CP中炎性细胞因子和黏附分子的变化可能与内分泌紊乱无关。
Recent studies have suggested that various cytokines may be important players in the development and progression of chronic pancreatitis (CP) and pancreatic adenocarcinoma (PC). We studied endothelial dysfunction and subclinical inflammation in patients with newly diagnosed pancreatic adenocarcinoma and CP. A total of 45 patients were included in the present investigation, 27 with CP and 18 with PC. In addition, the study included 13 age- and body weight-matched healthy subjects served as controls. In all subjects, plasma adiponectin, TNF-alfa, interleukin 6 (IL-6), interleukin 1beta (IL-1β), E-selectin, thrombomodulin, adhesion molecules ICAM and VCAM, and endothelin-1 were assessed. PC and CP patients as compared with controls had significantly greater plasma adiponectin (13,292 and 12,227 vs 5408 ng/ml; p < 0.0003), TNF-alfa (22.1 and 23.1 vs 13 pg/ml; p < 0.0002), and IL-6 (6.6 and 7.3 vs 3.3 pg/ml; p < 0.0001). Moreover, there was significantly higher concentration of ICAM (931 and 492 vs 290 ng/ml; p < 0.005) and VCAM (1511 and 1080 vs 840 ng/ml; p < 0.01) in PC and CP patients. When PC and CP patients with and without diabetes were considered separately, there was no difference in adiponectin, cytokines, and parameters of endothelial dysfunction. In summary, our data indicate that patients with CP and PC express high levels of several cytokines compared with healthy individuals, especially adiponectin, TNF-α and IL-6. Serum TNF-α and ICAM concentrations coordinately increase in advanced CP. Furthermore, especially in PC subjects, elevated markers of endothelial dysfunction are present. This study provides additional evidence that changes in inflammatory cytokine and adhesion molecules in PC and CP are not likely related to endocrine disorders.