Shifting perspectives in liver diseases after kidney transplantation.

Liver diseases after kidney transplantation range from mild biochemical abnormalities to severe hepatitis or cirrhosis. The causes are diverse and mainly associated with hepatotropic viruses, drug toxicity and metabolic disorders. Over the past decade, the aetiology of liver disease in kidney recipients has changed significantly. These relates to the use of direct-acting antiviral agents against hepatitis C virus, the increasing availability of vaccination against hepatitis B and a better understanding of drug-induced hepatotoxicity. In addition, the emergence of the severe acute respiratory syndrome coronavirus 2 pandemic has brought new challenges to kidney recipients. This review aims to provide healthcare professionals with a comprehensive understanding of recent advances in the management of liver complications in kidney recipients and to enable them to make informed decisions regarding the risks and impact of liver disease in this population.

Approach to persistent ascites after liver transplantation.

Persistent ascites (PA) after liver transplantation (LT), commonly defined as ascites lasting more than 4 wk after LT, can be expected in up to 7% of patients. Despite being relatively rare, it is associated with worse clinical outcomes, including higher 1-year mortality. The cause of PA can be divided into vascular, hepatic, or extrahepatic. Vascular causes of PA include hepatic outflow and inflow obstructions, which are usually successfully treated. Regarding modifiable hepatic causes, recurrent hepatitis C and acute cellular rejection are the leading ones. Considering predictors for PA, the presence of ascites, refractory ascites, hepato-renal syndrome type 1, spontaneous bacterial peritonitis, hepatic encephalopathy, and prolonged ischemic time significantly influence the development of PA after LT. The initial approach to patients with PA should be to diagnose the treatable cause of PA. The stepwise approach in evaluating PA includes diagnostic paracentesis, ultrasound with Doppler, and an echocardiogram when a cardiac cause is suspected. Finally, a percutaneous or transjugular liver biopsy should be performed in cases where the diagnosis is unclear. PA of unknown cause should be treated with diuretics and paracentesis, while transjugular intrahepatic portosystemic shunt and splenic artery embolization are treatment methods in patients with refractory ascites after LT.

Aberrant expression of SFRP1, SFRP3, DVL2 and DVL3 Wnt signaling pathway components in diffuse gastric carcinoma.

Diffuse gastric carcinoma (DGC) is characterized by poorly cohesive cells, highly invasive growth patterns, poor prognosis and resistance to the majority of available systemic therapeutic strategies. It has been previously reported that the Wnt/ß-catenin signaling pathway serves a prominent role in the tumorigenesis of gastric carcinoma. However, the mechanism underlying the dysregulation of this pathway in DGC has not been fully elucidated. Therefore, the present study aimed to investigate the expression profiles of Wnt antagonists, secreted frizzled-related protein 1 (SFRP1) and secreted frizzled-related protein 3 (SFRP3), and dishevelled protein family members, dishevelled segment polarity protein 2 (DVL2) and dishevelled segment polarity protein 3 (DVL3), in DGC tissues. The association between the expression levels of these factors and the clinicopathological parameters of the patients was determined. Protein and mRNA expression levels in 62 DGC tumor tissues and 62 normal gastric mucosal tissues obtained from patients with non-malignant disease were measured using immunohistochemical and reverse transcription-quantitative PCR (RT-qPCR) analysis. Significantly lower protein expression levels of SFRP1 (P<0.001) and SFRP3 (P<0.001), but significantly higher protein expression levels of DVL2 (P<0.001) and DVL3 (P<0.001) were observed in DGC tissues compared with in control tissues by immunohistochemistry. In addition, significantly lower expression levels of SFRP1 (P<0.05) and higher expression levels of DVL3 (P<0.05) were found in in DGC tissues compared with those in normal gastric mucosal tissues using RT-qPCR. According to correlation analysis between the SFRP1, SFRP3, DVL2 and DVL3 protein expression levels and the clinicopathological characteristics of patients with DGC, a statistically significant correlation was found between the SFRP3 volume density and T stage (r=0.304; P=0.017) and between the SFRP3 volume density and clinical stage (r=0.336; P=0.008). In conclusion, the findings of the present study suggested that the Wnt signaling pathway components SFRP1, SFRP3, DVL2 and DVL3 may be aberrantly expressed in DGC tissues, implicating their possible role in the development of this malignant disease. The present data also revealed a positive relationship between SFRP3 protein expression and the clinical and T stage of DGC.

Intramural Stomach Gas with Hepatic Portal Venous Gas Indicating Spontaneous Stomach Necrosis.

Intramural gas in the stomach associated with hepatic portal venous gas is a rare entity, which suggests ischemic or infectious pathology of the stomach. We report a case of a 73-year-old man who presented with epigastric pain and nausea of 6 hours duration followed by hematemesis. The patient had pale skin, anemia, and a diffusively tender and distended abdomen. Abdominal radiography and computed tomography (CT) revealed gas in thickened gastric wall and gas in intrahepatic portal vein branches. Surgery was indicated, which consisted of partial gastrectomy with Roux en esophago-jejunal anastomosis. Postoperative course was uneventful, and pathohistological analysis indicated stomach wall necrosis with emphysametous gastritis (EG). The patient was free of symptoms at 2 years follow-up. Intramural gas in the stomach should always be meticulously investigated to differentiate between emphysematous gastritis and gastric emphysema, as this would direct the therapeutic approach to be adopted.

Comparison of single incision laparoscopic totally extraperitoneal and laparoscopic totally extraperitoneal inguinal hernia repair: initial experience.

BACKGROUND AND PURPOSE: Laparoendoscopic single-site (LESS) surgery has been implemented recently in many laparoscopic (LAP) surgical procedures. We report our initial experience with LESS totally extraperitoneal (LESS-TEP) inguinal hernia repair in relation to conventional LAP-TEP. PATIENTS AND METHODS: Between November 2008 and May 2009, 25 LESS-TEP repairs of inguinal hernia and 29 LAP-TEP repairs of inguinal hernia were performed in 44 patients. Data regarding patient demographics, type of hernia, operative time, complications, postoperative hospital stay, and recurrence were prospectively collected and analyzed. RESULTS: All 44 patients were men, aged 17 to 84 years. Of 44 men, 3 had bilateral inguinal hernias in the LESS-TEP group and 7 in the LAP-TEP group. The operative time for bilateral LESS-TEP was 60 ± 15.3 min (range 40-70 min) and 40 ± 21.6 min (range 20-100 min) for unilateral LESS-TEP, while for bilateral hernia LAP-TEP it was 60 ± 24.8 min (range 40-100 min) and for unilateral LAP-TEP it was 50 ± 14.2 min (range 40-80 min). Comparison of operative times in the LESS-TEP and LAP-TEP groups between the first and second half cohort resulted in significant reduction of operative time in the second half of the LESS-TEP group (P<0.001). There were no intraoperative complications. Discharge was within 72 hours for most patients in both groups. There was one early recurrence (mesh displacement) during a median follow-up period of 11.5 ± 2.5 months in the LESS-TEP group and no recurrences during the 11 ± 1.6 months in the LAP-TEP group. CONCLUSION: In our experience, LESS-TEP is a safe and feasible procedure with a short learning curve. In all analyzed parameters, it is comparable to conventional LAP-TEP. Further studies that compare LESS-TEP and conventional multiport LAP-TEP repairs with long-term follow-up evaluation are needed to confirm the initial experience.