Acute pancreatitis is the most common and feared complication of endoscopic retrograde cholangiopancreatography (ERCP). The aim of the study was to review the current knowledge on the nomenclature, etiology, pathophysiology, clinical presentation, diagnostic workup, and risk stratification of post-ERCP pancreatitis (PEP). A structured search in PubMed and Scopus databases was performed using search terms related to the subject of diagnosis, pathophysiology, risk stratification of post-ERCP pancreatitis, including full text articles and abstracts in the English language. Several causes, operating both at a local and systemic level, might play an important role in the pathogenesis of PEP. Different patient-related risk factors can help predict post-ERCP pancreatitis; diagnosis depends on clinical presentation, imaging and laboratory investigations. As an outpatient procedure, post-ERCP pancreatitis may be safe in a selected group of low-risk patients. Further investigation of the etio-pathogenesis of post-ERCP pancreatitis is required in order to improve diagnosis and treatment. Early identification and severity stratification of post-ERCP pancreatitis greatly affects the patient's outcome. There is still controversy concerning the risk factors related to PEP. More studies are needed to clarify early and definite diagnosis, risk and severity stratification, as well as treatment of post-ERCP pancreatitis.
ObjectiveRecent guidelines recommend more aggressive lipid-lowering in secondary prevention protocols. We examined whether this resulted in improved endothelial function.MethodsWe studied saphenous vein specimens of patients undergoing surgical coronary revascularisation in 2007 and compared results with those of patients examined in 2003. Endothelium-dependent vasodilation was assessed by relaxation to calcium ionophore A23187, and vascular superoxide production by lucigenin enhanced chemiluminescence.ResultsStatin dose increased from 26 ± 16 mg/d in 2003 to 37 ± 17 mg/d in 2007 (P < 0.001), and total (4.0 ± 0.9 mmol/L vs 4.8 ± 1.0 mmol/L) and LDL-cholesterol levels (2.0 ± 0.7 mmol/L vs 3.0 ± 0.9 mmol/L) were lower in 2007 compared to 2003 (P < 0.001; n = 90 each). Endothelium-dependent vasodilation was greater in 2007 (44 ± 15%) compared to 2003 (28 ± 12%; n = 36 each; P < 0.001). Vascular superoxide derived from endothelial NO synthase (eNOS) was lower in 2007 than in 2003 (reduction by NG-nitro-l-arginine-methyl ester, 0.29 ± 0.21 nmol/(mg min) vs 0.09 ± 0.20 nmol/(mg min); P = 0.002). In linear regression analysis, LDL-cholesterol levels have been shown to be the major determinant of endothelial function in the combined 2003 and 2007 cohort.ConclusionIntensive lipid-lowering is associated with improved endothelial function and reduced superoxide production from eNOS. Further improvement in vascular function could be achieved by targeting other sources of superoxide including xanthine oxidase.
BNP is an independent predictor of long-term survival after major non-cardiac surgery. A simple preoperative blood test can provide predictive information on future risk of death, and potentially has a role in preoperative risk assessment.
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