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Elodie Fallet Michel Rayar Amandine Landrieux Christophe Camus Pauline Houssel-Debry Caroline Jezequel Ludivine Legros Thomas Uguen Martine Ropert-Bouchet Karim Boudjema Dominique Guyader Edouard Bardou-Jacquet 《World journal of gastroenterology : WJG》2020,26(16):1938-1949
BACKGROUND Liver transplantation(LT) is the best treatment for patients with liver cancer or end stage cirrhosis, but it is still associated with a significant mortality. Therefore identifying factors associated with mortality could help improve patient management. The impact of iron metabolism, which could be a relevant therapeutic target, yield discrepant results in this setting. Previous studies suggest that increased serum ferritin is associated with higher mortality.Surprisingly iron deficiency which is a well described risk factor in critically ill patients has not been considered.AIM To assess the impact of pre-transplant iron metabolism parameters on posttransplant survival.METHODS From 2001 to 2011, 553 patients who underwent LT with iron metabolism parameters available at LT evaluation were included. Data were prospectively recorded at the time of evaluation and at the time of LT regarding donor and recipient. Serum ferritin(SF) and transferrin saturation(TS) were studied as continuous and categorical variable. Cox regression analysis was used to determine mortality risks factors. Follow-up data were obtained from the local and national database regarding causes of death.RESULTS At the end of a 95-mo median follow-up, 196 patients were dead, 38 of them because of infections. In multivariate analysis, overall mortality was significantly associated with TS 75% [HR: 1.73(1.14; 2.63)], SF 100 μg/L [HR: 1.62(1.12;2.35)], hepatocellular carcinoma [HR: 1.58(1.15; 2.26)], estimated glomerular filtration rate(CKD EPI Cystatin C) [HR: 0.99(0.98; 0.99)], and packed red blood cell transfusion [HR: 1.05(1.03; 1.08)]. Kaplan Meier curves show that patients with low SF( 100 μg/L) or high SF( 400 μg/L) have lower survival rates at 36 mo than patients with normal SF(P = 0.008 and P = 0.016 respectively). Patients with TS higher than 75% had higher mortality at 12 mo(91.4% ± 1.4% vs 84.6% ±3.1%, P = 0.039). TS 75% was significantly associated with infection related death [HR: 3.06(1.13; 8.23)].CONCLUSION Our results show that iron metabolism imbalance(either deficiency or overload)is associated with post-transplant overall and infectious mortality. Impact of iron supplementation or depletion should be assessed in prospective study. 相似文献
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The platelet release reaction plays a critical role in thrombosis and contributes to the events that follow hemostasis. Previous studies have shown that platelet secretion is mediated by Soluble NSF Attachment Protein Receptor (SNARE) proteins from granule and plasma membranes. The SNAREs form transmembrane complexes that mediate membrane fusion and granule cargo release. Although VAMP-8 (v-SNARE) and SNAP-23 (a t-SNARE class) are important for platelet secretion, the identity of the functional syntaxin (another t-SNARE class) has been controversial. Previous studies using anti-syntaxin Abs in permeabilized platelets have suggested roles for both syntaxin-2 and syntaxin-4. In the present study, we tested these conclusions using platelets from syntaxin-knockout mouse strains and from a Familial Hemophagocytic Lymphohistiocytosis type 4 (FHL4) patient. Platelets from syntaxin-2 and syntaxin-4 single- or double-knockout mice had no secretion defect. Platelets from a FHL4 patient deficient in syntaxin-11 had a robust defect in agonist-induced secretion although their morphology, activation, and cargo levels appeared normal. Semiquantitative Western blotting showed that syntaxin-11 is the more abundant syntaxin in both human and murine platelets. Coimmunoprecipitation experiments showed that syntaxin-11 can form SNARE complexes with both VAMP-8 and SNAP-23. The results of the present study indicate that syntaxin-11, but not syntaxin-2 or syntaxin-4, is required for platelet exocytosis. 相似文献
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Chamie K Daskivich TJ Kwan L Labo J Dash A Greenfield S Litwin MS 《Journal of general internal medicine》2012,27(5):492-499