修回日期: 2005-08-08
接受日期: 2005-08-26
在线出版日期: 2005-09-28
目的: 研究血小板参数在轻症急性胰腺炎(MAP)与重症急性胰腺炎(SAP)中的变化特点及善宁治疗后对其的影响.
方法: 用全自动血球计数仪测定MAP与SAP患者入院及用善宁治疗1 wk后血小板计数(PLT)、平均血小板体积(MPV)和血小板分布宽度(PDW).
结果: 入院时MAP患者血小板参数无变化, 治疗1 wk后PLT无显著性升高, MPV、PDW明显增高(10.88±2.40 vs10.11±1.66, P<0.05; 17.98±4.41 vs 16.62±1.38, P<0.05); SAP组入院时PLT明显降低(161.61±68.30 vs191.60±31.98, P<0.05), MPV、PDW明显增高(11.82±2.33 vs 9.81±0.79, P<0.01; 19.33±7.07 vs 16.36±0.51, P<0.05), 1 wk后PLT增高(251.61±84.07 vs 161.61±68.30, P<0.01), MPV、PDW变化不明显(P>0.05); SAP经治疗1 wk后善宁组较一般治疗组PLT增高更为显著(57.81±68.24 vs 112.53±89.31, P<0.05), MPV、PDW下降明显(1.29±2.79vs -0.17±2.04, P<0.01; 2.75±8.81 vs -0.89±3.44, P<0.01).
结论: MAP与SAP患者血小板参数变化明显不同, 可反映不同病情程度; 善宁治疗可使SAP患者PLT增多, MPV、PDW下降, 降低血小板活性, 从而改善微循环, 有重要的治疗作用.
引文著录: 黄坚, 陆士奇, 陈建荣. 善宁对急性胰腺炎患者血小板参数变化的影响. 世界华人消化杂志 2005; 13(18): 2281-2283
Revised: August 8, 2005
Accepted: August 26, 2005
Published online: September 28, 2005
AIM: To investigate the changes of platelet parameters in patients with mild and severe acute pancreatitis (MAP and SAP) after treated with octreotide.
METHODS: The full-automatic blood cell counter was used to obtain the platelet count (PLT), mean platelet volume (MPV), and platelet distribution width (PDW) in the patients with MAP and SAP before and 1 wk after treatment with octreotide.
RESULTS: The platelet parameters of the patients with MAP were not significantly different from that of the normal controls. One week after treatment, there was still no significant change in the PLT. However, the MPV and PDW were increased markedly (10.88±2.40 vs 10.11±1.66, P < 0.05; 17.98±4.41 vs 16.62±1.38,P < 0.05). In patients with SAP, the PLT was decreased markedly (161.61±68.30 vs 191.60±31.98, P < 0.05), and the MPV and PDW were increased markedly (11.82±2.33vs 9.81±0.79, P < 0.01; 19.33±7.07 vs 16.36±0.51,P < 0.05) as compared with those in the normal controls. One week after treatment, the PLT was notably elevated (251.61±84.07 vs 161.61±68.30, P < 0.01), while the MPV and PDW were not changed (P >0.05) as compared with those before treatment. For SAP, the PLT increased more (112.53±89.31 vs 57.81±68.24, P<0.05), and the MPV and PDW decreased more (1.29±2.79 vs -0.17±2.04, P < 0.01; 2.75±8.81 vs -0.89±3.44, P < 0.01) at 1 wk in the octreotide treatment patients as compared with those of general treatment ones.
CONCLUSION: The platelet parameters can reflect the severeness of acute pancreatitis. Octreotide can improve the microcirculation by decreasing MPV and PDW, increasing PLT.
- Citation: Huang J, Lu SQ, Chen JR. Effects of octreotide on platelet parameters in patients with acute pancreatitis. Shijie Huaren Xiaohua Zazhi 2005; 13(18): 2281-2283
- URL: https://www.wjgnet.com/1009-3079/full/v13/i18/2281.htm
- DOI: https://dx.doi.org/10.11569/wcjd.v13.i18.2281
急性胰腺炎(acute pancreatitis,AP)是常见急腹症之一, 其发病过程常伴有胰腺微循环障碍, 血管通透性增加, 血小板聚集活化, 凝血和纤溶系统改变, 血小板参数会发生一定改变, 从而影响疾病的进程和预后[1,2]. 本文主要探讨急性胰腺炎患者外周血中的血小板参数: 血小板计数(PLT)、平均血小板体积(MPV) 和血小板分布宽度(PDW)的变化在AP发生、发展中的作用, 以及经善宁治疗后对其的影响.
我院2002-01/2005-05住院急性胰腺炎患者132例, 所有患者均符合急性胰腺炎诊断标准(症状、体征、实验室检查、B超、CT等)[3],并按APACHEⅡ评分≥8分、Bathazar CT分级≥Ⅱ级为判断重症标准, 其中轻症急性胰腺炎(mild acute pancreatitis,MAP)81例, 男49例, 女32例, 年龄25-78岁; 重症急性胰腺炎(severe acute pancreatitis,SAP)51例, 男31例, 女20例, 年龄28-88岁. 对照组30例为同期健康体检者, 男18例, 女12例, 年龄23-69岁.
51例SAP分为: 一般治疗组(禁食、胃肠减压、输液、抑酸、抑酶、抗炎等治疗)21例, 男14例、女7例; 善宁治疗组(一般治疗基础上加用善宁0.1 mg/次, 每8小时一次皮下注射, 5-7 d, 善宁为诺华制药公司合成的天然生长抑素八肽衍生物)30例, 男17例、女13例. 测定方法: 取患者入院24 h内及治疗1 wk后外周静脉血, 以全自动血球计数仪(Coulter STKS 美国生产)进行测定.
统计学处理 均数以mean±SD表示, 行t检验, P<0.05为有统计学意义.
MAP组入院时与健康对照组PLT、MPV、PDW无显著性差异(P>0.05), 治疗一周后PLT变化无显著性(P>0.05), MPV、PDW较入院时增高明显(P<0.05); SAP组入院时较对照组PLT明显减少(P<0.05), MPV、PDW明显增高(P<0.01, P<0.05), 治疗1 wk后较入院时PLT增高(P<0.01), MPV、PDW变化不明显(P>0.05); 入院时,SAP组较MAP组PLT低(P<0.05), MPV、PDW高(P<0.01, P<0.01), 1 wk后SAP组PLT较MAP组高(P<0.05), MPV、PDW无显著性差异(P>0.05, P>0.05).
SAP经治疗1 wk后善宁组较一般治疗组PLT明显增高(P<0.05), MPV、PDW降低(P<0.01, P<0.01); 治疗前后数值变化, 一般治疗组与善宁组比较PLT、MPV有显著性差异(P<0.05, P<0.05), PDW无显著性差异(P>0.05).
AP发病机制至今未能完全明了, 不仅涉及免疫防御系统, 激肽、补体、溶血及纤溶系统也参与其中. 近年来, 对胰腺微循环障碍与急性胰腺炎关系有了更深入研究, 包括微血管内皮细胞损伤、微血管通透性增加、胰腺缺血-再灌注损伤、血液流变学改变、血小板聚集活化等, 这些都是改变急性胰腺炎病程的重要因素[4-6]. 血小板是外周血中对化学和物理因素最敏感的成分, AP患者体内大量血小板破坏, 释放高浓度的5-羟色胺, 血栓素A等血管活性物质, 这些物质一方面有强烈缩血管作用, 另一方面与内皮细胞作用进一步介导炎症介质的释放, 并作为炎症介质参与全身炎症反应过程, 促进全身炎症反应综合征(SIRS)发生[7], 这可能是MAP病情恶化、SAP患者并发多脏器功能不全(MODS)及死亡的重要因素. Mitchell et al[8]研究证实持续SIRS时间与血小板计数呈负相关.
本文MAP初期PLT、MPV、PDW较健康组变化无显著性, 1 wk后, PLT无显著性变化, 而MPV、PDW渐增高, 血小板体积增大, 推测可能与胰腺微循环障碍时血小板破坏, 通过反馈机制使巨核细胞激活产生大体积血小板有关, 此种血小板的致密小体多, 酶活力高, 功能活跃, 其出现是一种应激代偿作用, 以适应机体的需要[9]. 研究表明大体积血小板代谢活跃, 聚集黏附力强和止血性强, 故平均血小板体积(MPV)与血小板体外功能明显相关[10], 可根据MPV和PDW来估计血小板的活性.
SAP初期较对照组、MAP组PLT降低明显, MPV、PDW增高, 表明患者体内有大量血小板黏附、聚集而高度活化, 造成循环血中血小板明显减少, 骨髓中巨核细胞反应性生成大体积血小板, 使循环血中血小板均一性降低, 导致MPV、PDW值增大, 因此监测AP患者循环血中血小板参数变化有助于病情判断[11,12].1 wk后, PLT显著性增高, 而MPV、PDW变化不明显, 可能与经治疗后微循环改善, 阻止血小板进一步聚集破坏有关. 善宁(生长抑素八肽衍生物)治疗SAP患者1 wk后与一般治疗组比较: PLT增高, MAP和PDW降低明显, 说明善宁治疗可降低血小板活性, 增加血小板数量, 其机制可能是善宁阻断细胞因子(包括血小板活化因子等)及炎症介质的释放[13,14],从而减轻了全身炎症反应进程, 改善微循环及血液流变学, 防止血小板过度聚集活化, 改善SAP的病程和预后, 降低死亡率[15,16]. 因此善宁在SAP治疗中具有极其重要作用, 应广泛推广.
电编:张勇 编辑:潘伯荣 审读:张海宁
1. | Sugimoto M, Takada T, Yasuda H. A new experimental pancreatitis by incomplete closed duodenal loop: the influence of pancreatic microcirculation on the development and progression of induced severe pancreatitis in rats. Pancreas. 2004;28:e112-e119. [PubMed] [DOI] |
2. | Chen HM, Sunamura M, Shibuya K, Yamauchi JI, Sakai Y, Fukuyama S, Mikami Y, Takeda K, Matsuno S. Early microcirculatory derangement in mild and severe pancreatitis models in mice. Surg Today. 2001;31:634-642. [PubMed] [DOI] |
4. | de la Mano AM, Sevillano S, Manso MA, Pérez M, de Dios I. Cholecystokinin blockade alters the systemic immune response in rats with acute pancreatitis. Int J Exp Pathol. 2004;85:75-84. [PubMed] [DOI] |
6. | Wittel UA, Rau B, Gansauge F, Gansauge S, Nussler AK, Beger HG, Poch B. Influence of PMN leukocyte-mediated pancreatic damage on the systemic immune response in severe acute pancreatitis in rats. Dig Dis Sci. 2004;49:1348-1357. [PubMed] [DOI] |
10. | Mimidis K, Papadopoulos V, Kotsianidis J, Filippou D, Spanoudakis E, Bourikas G, Dervenis C, Kartalis G. Alterations of platelet function, number and indexes during acute pancreatitis. Pancreatology. 2004;4:22-27. [PubMed] [DOI] |
11. | Dabrowski A, Gabryelewicz A, Chyczewski L. The effect of platelet activating factor antagonist (BN 52021) on acute experimental pancreatitis with reference to multiorgan oxidative stress. Int J Pancreatol. 1995;17:173-180. [PubMed] |
12. | Hackert T, Pfeil D, Hartwig W, Gebhard MM, Büchler MW, Werner J. Platelet function in acute experimental pancreatitis induced by ischaemia-reperfusion. Br J Surg. 2005;92:724-728. [PubMed] [DOI] |
13. | Andoh A, Hata K, Shimada M, Fujino S, Tasaki K, Bamba S, Araki Y, Fujiyama Y, Bamba T. Inhibitory effects of somatostatin on tumor necrosis factor-alpha-induced interleukin-6 secretion in human pancreatic periacinar myofibroblasts. Int J Mol Med. 2002;10:89-93. [PubMed] |
14. | Nikou GC, Giamarellos-Bourboulis EJ, Grecka P, Toumpanakis Ch, Giannikopoulos G, Katsilambros N. Effect of octreotide administration on serum interleukin-6 (IL-6) levels of patients with acute edematous pancreatitis. Hepatogastroenterology. 2004;51:599-602. [PubMed] |
15. | Piri M, Alhan E, Küçüktülü U, Erçin C, Deger O, Yücel K, Cicek R. The effects of somatostatin on the microperfusion of the pancreas during acute necrotizing pancreatitis in rats. Hepatogastroenterology. 2002;49:833-837. [PubMed] |
16. | 王 艳蕾, 贾 玉杰, 王 立娜, 姜 妙娜, 赵 景霞. 善宁对重症急性胰腺炎胰腺细胞的保护作用. 四川大学学报(医学版). 2005;36:134-135. |