Giovannini Ivo, Chiarla Carlo, Giuliante Felice, Vellone Maria, Nuzzo Gennaro
Department of Surgery (Hepatobiliary Unit, Surgical Intensive Care), IASI-CNR Center for Pathophysiology of Shock, Catholic University Medical School, Rome, Italy.
Clin Chem Lab Med. 2004 Mar;42(3):261-5. doi: 10.1515/CCLM.2004.048.
In acute-phase response, the use of amino acids is redirected to supporting the synthesis of proteins for host defence and tissue repair. Fibrinogen is one of these proteins, and its plasma levels commonly increase in acute-phase conditions. After hepatectomy, this pattern may be modified by the variable impact of postoperative liver dysfunction. Our study was performed to specifically assess and quantify this aspect. Data were collected prospectively on 82 hepatectomized patients; 62 recovered normally, 20 had major complications (most commonly sepsis). Plasma fibrinogen and a large series of complementary variables were determined preoperatively and at postoperative days 1, 3 and 7 in all patients and until recovery, or death in those with complications. Multiple regression analysis showed that postoperative changes in fibrinogen (deltaFIB, micromol/l) were simultaneously related to the number of resected liver segments (NSEG), total bilirubin (BIL, micromol/l), aspartate aminotransferase (AST, U/l, n.v. 5-45), albumin (ALB, g/l), prothrombin activity (PA, % of standard reference), age (AGE, years) and basal preoperative fibrinogen (PFIB, micromol/l): deltaFIB = -0.51(NSEG) - 0.71(Log(n)BIL) - 0.74(Log(n)AST) + 0.11(ALB) + 0.09(PA) - 0.06(AGE) - 0.55(PFIB) + 7.74 (n=362, r2=0.68, p<0.001). In addition, an early postoperative tendency for low fibrinogen was associated with the subsequent development of complications or death. Our study quantifies the impact of size of hepatectomy and dysfunction of residual liver in modulating postoperative fibrinogen level and suggests that failure of fibrinogen to increase may signal an unfavorable condition limiting up-regulation of acute-phase response and increasing liability to complications.
在急性期反应中，氨基酸的使用被重新导向，以支持用于宿主防御和组织修复的蛋白质合成。纤维蛋白原就是这些蛋白质之一，其血浆水平在急性期通常会升高。肝切除术后，这种模式可能会因术后肝功能障碍的不同影响而改变。我们进行这项研究是为了具体评估和量化这一方面。前瞻性收集了82例肝切除患者的数据；62例恢复正常，20例出现严重并发症（最常见的是败血症）。在所有患者术前以及术后第1、3和7天直至恢复，或有并发症者直至死亡，测定血浆纤维蛋白原和一系列补充变量。多元回归分析表明，纤维蛋白原术后变化（deltaFIB，微摩尔/升）与切除肝段数量（NSEG）、总胆红素（BIL，微摩尔/升）、天冬氨酸转氨酶（AST，U/升，正常范围5 - 45）、白蛋白（ALB，克/升）、凝血酶原活性（PA，标准参考值的百分比）、年龄（AGE，岁）和术前基础纤维蛋白原（PFIB，微摩尔/升）同时相关：deltaFIB = -0.51（NSEG） - 0.71（Log(n)BIL） - 0.74（Log(n)AST） + 0.11（ALB） + 0.09（PA） - 0.06（AGE） - 0.55（PFIB） + 7.74 （n = 362，r2 = 0.68，p < 0.001）。此外，术后早期纤维蛋白原水平偏低的趋势与随后并发症或死亡的发生相关。我们的研究量化了肝切除大小和残余肝功能障碍对术后纤维蛋白原水平调节的影响，并表明纤维蛋白原未能升高可能预示着一种不利状况，限制急性期反应的上调并增加并发症的易感性。
