Operative treatment of hepatic hydatid cysts: A single center experience

Summary: Background: Hydatid cyst is a zoonotic disease caused by Echinococcus genera. Surgery is needed in most cases. We aimed to describe our center's experience in the surgical management of hepatic hydated cysts (HHC). Methods: Data was retrospectively collected for patients who underwent operative management for HHC between the years 1994–2014. Results: Sixty-nine underwent surgical treatment for HHC. Group A included 34 treated with an unroofing procedure, group B included 24 patients who underwent hepatectomy and group C included 11 patients who underwent peri-cystectomy. The median ± (range) age for groups A, B and C were 39.5 (6.5–69), 40 (17–74) and 32 (20–62), respectively (P > 0.1). Post-operative complications occurred in 16, 11 and 5 patients in group A, B and C, respectively, as assessed by clavien-dindo classification (CDC). The average CDC was significantly higher in the hepatectomy group as compared to the unroofing group (2.3 vs.1.5, P = 0.04). Recurrence was significantly higher after the unroofing procedure as compared to the hepatectomy group (P = 0.05). Conclusion: Surgery remains the mainstay of treatment for HHC, once surgery is pursued, the results are satisfactory. Keywords: Echinococcus, Hydated cyst, Liver surgery, Morbidity, Mortalit

Role of the ductal transcription factors HNF6 and Sox9 in pancreatic acinar-to-ductal metaplasia

OBJECTIVE: Growing evidence suggests that a phenotypic switch converting pancreatic acinar cells to duct-like cells can lead to pancreatic intraepithelial neoplasia and eventually to invasive pancreatic ductal adenocarcinoma. Histologically, the onset of this switch is characterised by the co-expression of acinar and ductal markers in acini, a lesion called acinar-to-ductal metaplasia (ADM). The transcriptional regulators required to initiate ADM are unknown, but need to be identified to characterise the regulatory networks that drive ADM. In this study, the role of the ductal transcription factors hepatocyte nuclear factor 6 (HNF6, also known as Onecut1) and SRY-related HMG box factor 9 (Sox9) in ADM was investigated. DESIGN: Expression of HNF6 and Sox9 was measured by immunostaining in normal and diseased human pancreas. The function of the factors was tested in cultured cells and in mouse models of ADM by a combination of gain and loss of function experiments. RESULTS: Expression of HNF6 and Sox9 was ectopically induced in acinar cells in human ADM as well as in mouse models of ADM. HNF6 and, to a lesser extent, Sox9 were required for repression of acinar genes, for modulation of ADM-associated changes in cell polarity and for activation of ductal genes in metaplastic acinar cells. CONCLUSIONS: HNF6 and Sox9 are new biomarkers of ADM and constitute candidate targets for preventive treatment in cases when ADM may lead to cancer. This work also shows that ectopic activation of transcription factors may underlie metaplastic processes occurring in other organs