Bargnoux A.-S.,Montpellier University |
Arnaud J.,Grenoble University Hospital Center |
Cavalier E.,University of Liège |
Pieroni L.,Center Hospitalier dAvignon |
And 28 more authors.
Annales de Biologie Clinique | Year: 2015
A better knowledge of physiopathologic mechanisms responsible for vascular calcification leads to emerging biological markers of calcifications. The use of these biomarkers in daily practice requires both clinical and analytical validation. This latter point is of particular importance to implement "researchgrade"diagnostic kits into daily practice. Data in the literature underline the lack of method standardization and the non-transferability of results. Depending on the method used, important biological associations might be hidden. © 2015, John Libbey Eurotext. All rights reserved.
Pelletier S.,University of Lyon |
Jean G.,Nephrocare Tassin Charcot |
Fouque D.,University of Lyon |
Fouque D.,Lyon University Hospital Center |
And 22 more authors.
Annales de Biologie Clinique | Year: 2015
Sclerostin is an osteocyte-specific glycoprotein secreted by the osteocyte and involved in the regulation of bone mass. High sclerostin levels are associated with osteoporosis, whereas low sclerostin levels are correlated with higher bone mineral density. It seems interesting to investigate a potential association between sclerostin levels and vascular calcifications since sclerostin is considered as a potent inhibitor of bone formation. In chronic kidney disease, serum sclerostin levels rise as renal function declines. Preliminary studies show a positive association between serum sclerostin and vascular calcification, but the link between sclerostin and survival of patients remains unclear in the absence of large-scale studies. © 2015, John Libbey Eurotext. All rights reserved.
Farhat S.,Endoscopy Unit |
Chaussade S.,Endoscopy Unit |
Chaussade S.,University of Paris Descartes |
Ponchon T.,Hopital Edouard Herriot |
And 21 more authors.
Endoscopy | Year: 2011
Background and study aims: Endoscopic submucosal dissection (ESD) is a technique for en bloc resection of superficial tumors of the gastrointestinal tract. In France, experience with this technique is still limited. We wanted to assess the development of ESD in France, with special attention to short term outcomes. Patients and methods: Members of the Société Française d'Endoscopie Digestive (SFED) who declared performing ESD reported their cases prospectively on a voluntary basis. Demographic, clinical, and technical data, and the results of immediate complications were collected. Case reports were completed prospectively by each investigator before pooled analysis. Results: A total of 188 consecutive case reports were collected from 16 centers. The median case mix per center was 6 patients (range 143). The lesion sites treated by ESD were the stomach (n=75), esophagus (n=27), duodenum (n=1), cecum (n=2), right colon (n=3), transverse colon (n=5), sigmoid (n=3), and rectum (n=72). The median size of the lesions was 26mm (range 2150mm). En bloc resection was achieved in 77.1% of cases, with complete R0 resection in 72.9%. Histopathology results showed high grade dysplasia or superficial cancer in 71.2%. The median duration of ESD was 105 minutes (range 20450 minutes). The short term morbidity was 29.2% including 34 cases of perforation (18.1%), and 21 hemorrhages (11.2%) during the 24 hours following ESD, 89% of which were managed conservatively or endoscopically. Conclusion: In this early experience, the feasibility of ESD appeared to be good but R0 resection and complication rates did not match those reported by Japanese authors and must be improved by an extended practice. © Georg Thieme Verlag KG Stuttgart New York.
Evrard S.,University of Liège |
Delanaye P.,University of Liège |
Kamel S.,Laboratoire Of Biochimie |
Kamel S.,University of Picardie Jules Verne |
And 24 more authors.
Clinica Chimica Acta | Year: 2014
The link between vascular calcification (VC) and increased mortality is now well established. Over time, as clinical importance of this phenomenon has begun to be fully considered, scientists have highlighted more and more physiopathological mechanisms and signaling pathways that underlie VC. Several conditions such as diabetes, dyslipidemia and renal diseases are undoubtedly identified as predisposing factors. But even if the process is better understood, many questions still remain unanswered. This review briefly develops the various theories that attempt to explain mineralization genesis. Nonetheless, the main purpose of the article is to provide a profile of the various existing biomarkers of VC. Indeed, in the past years, a lot of inhibitors and promoters, which form a dense and interconnected network, were identified. Given importance to assess and control mineralization process, a focusing on accumulated knowledge of each marker seemed to be necessary. Therefore, we tried to define their respective role in the physiopathology and how they can contribute to calcification risk assessment. Among these, Klotho/fibroblast growth factor-23, fetuin-A, Matrix Gla protein, Bone morphogenetic protein-2, osteoprotegerin, osteopontin, osteonectin, osteocalcin, pyrophosphate and sclerostin are specifically discussed. © 2014 Elsevier B.V.