Distal pancreatectomy: what is the standard for laparoscopic surgery?

AbstractBackground/aimsDistal pancreatectomy (DP) is performed for a range of benign and malignant lesions. Accurate pre-operative diagnosis can be unreliable and morbidity remains high. This study evaluates a 12-year, single-centre experience with open DP to review indications, diagnoses and associated morbidity.MethodsRetrospective review of patients who underwent DP at a UK-based tertiary referral centre between 1994 and 2006.ResultsSixty-five patients (mean age 49.9 years) had final diagnoses of chronic pancreatitis ± pseudocyst (n= 22), benign cystadenoma (n= 15), neuroendocrine tumour (n= 8), primary pancreatic carcinoma (n= 6) and 14 other conditions. DP performed for presumed cystic neoplasm (n= 24) revealed a correct pre-operative diagnosis in 71% of patients. Histological examination confirmed that 59% of resected cystic tumours were either malignant or had malignant potential. When DP was undertaken for presumed pseudocyst (n= 12), 83% of cases were correctly diagnosed pre-operatively. Overall mortality and morbidity rates were 3% and 39%, respectively, with five patients (8%) developing a clinically significant pancreatic fistula. Ten (17%) patients developed diabetes mellitus and nine (14%) required long-term pancreatic exocrine supplementation.ConclusionsOpen DP can be performed with acceptable morbidity, low mortality and preservation of pancreatic function in the majority of cases, setting the standard for laparoscopic techniques

CSF1 Restores Innate Immunity Following Liver Injury in Mice and Serum Levels Indicate Outcomes of Patients With Acute Liver Failure

Background & Aims: Liver regeneration requires functional liver macrophages, which provide an immune barrier that is compromised after liver injury. The numbers of liver macrophages are controlled by macrophage colony-stimulating factor (CSF1). We examined the prognostic significance of the serum level of CSF1 in patients with acute liver injury and studied its effects in mice. Methods: We measured levels of CSF1 in serum samples collected from 55 patients who underwent partial hepatectomy at the Royal Infirmary Edinburgh between December 2012 and October 2013, as well as from 78 patients with acetaminophen-induced acute liver failure admitted to the Royal Infirmary Edinburgh or the University of Kansas Medical Centre. We studied the effects of increased levels of CSF1 in uninjured mice that express wild-type CSF1 receptor or a constitutive or inducible CSF1-receptor reporter, as well as in chemokine receptor 2 (Ccr2)-/- mice; we performed fate-tracing experiments using bone marrow chimeras. We administered CSF1-Fc (fragment, crystallizable) to mice after partial hepatectomy and acetaminophen intoxication, and measured regenerative parameters and innate immunity by clearance of fluorescent microbeads and bacterial particles. Results: Serum levels of CSF1 increased in patients undergoing liver surgery in proportion to the extent of liver resected. In patients with acetaminophen-induced acute liver failure, a low serum level of CSF1 was associated with increased mortality. In mice, administration of CSF1-Fc promoted hepatic macrophage accumulation via proliferation of resident macrophages and recruitment of monocytes. CSF1-Fc also promoted transdifferentiation of infiltrating monocytes into cells with a hepatic macrophage phenotype. CSF1-Fc increased innate immunity in mice after partial hepatectomy or acetaminophen-induced injury, with resident hepatic macrophage as the main effector cells. Conclusions: Serum CSF1 appears to be a prognostic marker for patients with acute liver injury. CSF1 might be developed as a therapeutic agent to restore innate immune function after liver injury