Gamma-glutamyl transpeptidase to platelet ratio predicts short-term outcomes in hepatocellular carcinoma patients undergoing minor liver resection

2018 ◽  
Vol 231 ◽  
pp. 403-410 ◽  
Author(s):  
Meng-yun Ke ◽  
Mei Zhang ◽  
Qing Su ◽  
Shasha Wei ◽  
Jia Zhang ◽  
...  
2020 ◽  
Author(s):  
Hongxing Zhang ◽  
Yu Zhou ◽  
Yicheng Li ◽  
Wanying Qin ◽  
Yunhua Zi ◽  
...  

Abstract Background: Microvascular invasion (MVI) is an independent risk factor for poor prognosis in hepatocellular carcinoma (HCC). However, there is still a lack of preoperative markers to predict MVI in HCC. This study intends to explore the potential application value of the gamma-glutamyl transpeptidase (GGT) to lymphocyte count ratio (GLR) in predicting MVI in HCC and provide guidance for clinical diagnosis and treatment. Methods: From March 2010 to December 2015, 230 HCC patients who underwent surgical treatment in the Affiliated Hospital of Guilin Medical University were selected. Clinicopathological parameters between the MVI group (n = 115) and the non-MVI group (n = 115) were comparatively analyzed. The GLR was used as the potential risk factor for HCC with MVI, and its optimal cut-off value was estimated by using the receiver operating characteristic (ROC) curve. The Kaplan-Meier method was used to analyze the survival of HCC patients, and univariate and multivariate Cox regression analyses were used to establish independent predictors affecting postoperative HCC patients. Results: The GLR levels in the MVI group and non-MVI group were 84.83 ± 61.84 and 38.42 ± 33.52 (p < 0.001), respectively. According to ROC curve analysis, the optimal cut-off value of GLR was 56.0, and the area under the ROC curve (AUC) was 0.781 (95% CI, 0.719-0.833) for the risk prediction of MVI in HCC patients. Multivariate analysis showed that tumor size > 5 cm, HCC combined with MVI and GLR > 56.0 were independent risk factors for poor prognosis in HCC patients. In addition, compared with the non-MVI group, patients in the MVI group had shorter progression-free survival (PFS) and overall survival (OS). Conclusion: GLR could be a predictive biomarker of HCC after operation and a potential predictor of HCC combined with MVI. Keywords: Hepatocellular carcinoma, Microvascular invasion, GLR, Predictive


1982 ◽  
Vol 1 (1) ◽  
pp. 119-144 ◽  
Author(s):  
Stanley Goldfarb ◽  
Thomas D. Pugh

Results of many studies, summarized in this review, support the hypothesis that carcinogen-induced hepatocellular carcinomas develop from phenotypically-altered hyperplastic hepatocellular nodules; these in turn apparently arise from smaller focal collections of hyperplastic cells referred to as hepatocellular islands. The very recent recognition that phenobarbital, when administered after carcinogens, fosters the outgrowth of hepatocellular islands and carcinomas, now provides the means for studying stages of initiation and promotion in hep-atocarcinogenesis. In addition, the recognition that enzymatic alterations, particularly the acquisition of canalicular gamma glutamyl transpeptidase activity, loss of ATP'ase activity, and loss of glucose-6-phosphatase activity that characterize many islands, have been particularly useful for measuring and evaluating the growth kinetics and heterogeneity of the islands. Evidence is presented that periportal gamma glutamyl transpeptidase positive hepatocytes are considerably more abundant after four weeks of feeding .02% 2-acetyl-aminofluorene to young rats than in control animals, and that the outgrowth of these cells is fostered by a distinctive type of periportal reparative hyperplasia. The cells appear to arise from a pool of cells that are normally abundant in periportal location in young growing rats. The studies suggest that it may now be possible to develop short term in vivo bioassays for initiators, promoters, and complete carcinogens in the rodent liver.


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