1.
The predictive value of the prealbumin-to-fibrinogen ratio in patients with acute pancreatitis.
Yue, W, Liu, Y, Ding, W, Jiang, W, Huang, J, Zhang, J, Liu, J
International journal of clinical practice. 2015;(10):1121-8
Abstract
OBJECTIVE Early identification of severe acute pancreatitis (SAP) progression is important in acute pancreatitis (AP) treatment. The Ranson, APACHE II and CTSI systems are difficult to use and exhibit limited predictive value. Prealbumin and fibrinogen are acute phase reactants generally used to assess the nutritional statuses and coagulation functions of AP patients, respectively. Here, we explored the value of the combination of these two markers for evaluating AP severity and prognosis. METHODS One hundred and sixty-nine AP patients, including mild AP (MAP) (n = 101) and severe AP (SAP) patients (n = 68), were enrolled. Their Ranson, APACHE II and CTSI scores, routine laboratory test results, and prealbumin and fibrinogen levels were determined after admission. Multivariate regression analysis was performed to determine the independent predictors of AP severity. ROC curves were generated to determine the suitabilities of prealbumin and fibrinogen levels and the above-mentioned scores for SAP prediction. RESULTS The SAP patients exhibited higher scores, white blood cell counts, CRP and fibrinogen levels but lower calcium, prealbumin levels and prealbumin/fibrinogen ratio than the MAP patients (p < 0.05). The multivariate regression analysis demonstrated that the prealbumin/fibrinogen ratio was a good predictor of severity and outperformed CRP. The prealbumin/fibrinogen ratio was correlated with CRP, hospitalisation length and complication occurrence in SAP. The ROC curve analyses showed that the prealbumin/fibrinogen ratio exhibited superior sensitivity, specificity, PPV and NPV for SAP prediction over the scoring systems. With a cut-off of 31.70 mg/g, the sensitivity, specificity, PPV and NPV were 76.5%, 94.1%, 89.6% and 85.6%, respectively. CONCLUSIONS The prealbumin/fibrinogen ratio is a promising predictor of AP severity and prognosis.
2.
No evidence for genome-wide interactions on plasma fibrinogen by smoking, alcohol consumption and body mass index: results from meta-analyses of 80,607 subjects.
Baumert, J, Huang, J, McKnight, B, Sabater-Lleal, M, Steri, M, Chu, AY, Trompet, S, Lopez, LM, Fornage, M, Teumer, A, et al
PloS one. 2014;(12):e111156
Abstract
Plasma fibrinogen is an acute phase protein playing an important role in the blood coagulation cascade having strong associations with smoking, alcohol consumption and body mass index (BMI). Genome-wide association studies (GWAS) have identified a variety of gene regions associated with elevated plasma fibrinogen concentrations. However, little is yet known about how associations between environmental factors and fibrinogen might be modified by genetic variation. Therefore, we conducted large-scale meta-analyses of genome-wide interaction studies to identify possible interactions of genetic variants and smoking status, alcohol consumption or BMI on fibrinogen concentration. The present study included 80,607 subjects of European ancestry from 22 studies. Genome-wide interaction analyses were performed separately in each study for about 2.6 million single nucleotide polymorphisms (SNPs) across the 22 autosomal chromosomes. For each SNP and risk factor, we performed a linear regression under an additive genetic model including an interaction term between SNP and risk factor. Interaction estimates were meta-analysed using a fixed-effects model. No genome-wide significant interaction with smoking status, alcohol consumption or BMI was observed in the meta-analyses. The most suggestive interaction was found for smoking and rs10519203, located in the LOC123688 region on chromosome 15, with a p value of 6.2 × 10(-8). This large genome-wide interaction study including 80,607 participants found no strong evidence of interaction between genetic variants and smoking status, alcohol consumption or BMI on fibrinogen concentrations. Further studies are needed to yield deeper insight in the interplay between environmental factors and gene variants on the regulation of fibrinogen concentrations.