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This report presents a case of Schloffer tumour at the small intestinal mesentery, mimicking a malignant tumour, treated laparoscopically. Six years prior, a 57-year-old woman underwent laparoscopic salpingo-oophorectomy for a benign, cystic, ovarian tumour, but she had no history of malignancy. She was treated at an outpatient clinic for gastrointestinal complaints and was relieved of these symptoms. Abdominal computed tomography showed an incidental mesenteric tumour of the small intestine, tending toward growth. Due to the tumour’s malignant potential, laparoscopic examination was performed. A spherical tumour with a base in the jejunum mesentery was observed. It was removed without damage. The post-operative course was uneventful, and the patient was discharged 3 days after the operation without complications. Histological diagnosis showed this to be a Schloffer tumour, but no malignancy was observed. Unidentified intraperitoneal tumours in patients with surgical histories may be Schloffer tumours, and this should be kept in mind. [ABSTRACT FROM AUTHOR]

Abstract Purpose  The type of anastomosis and its outcome can affect postoperative morbidity, mortality, and quality of life after esophagectomy. We compared the outcomes of cervical hand-sewn anastomosis (CHS) and intrathoracic stapled anastomosis (ITS) performed after esophagectomy and gastric reconstruction. Methods  Thirty-two patients with middle or lower thoracic esophageal cancer were prospectively randomized to undergo CHS (n = 18) or ITS (n = 14) after esophagectomy. We compared clinical data, postoperative symptoms, and long-term survival in the two groups. Results  The rates of anastomotic leak and stricture in the CHS and ITS groups were 16.7% versus 7.1% and 0% versus 14.2%, respectively, which do not represent significant differences. The respective rates of recurrent laryngeal nerve palsy were 38.8% versus 7.1% (P P Conclusions  The two methods of anastomosis yielded similar anastomotic outcomes. Although the incidence of recurrent laryngeal nerve injury was higher after CHS, and proximal esophageal resection was longer, this had little impact on postoperative symptoms and long-term survival. [ABSTRACT FROM AUTHOR]

OBJECTIVETo investigate the mechanism by which methylprednisolone protects the liver from hypoxia-induced injury.DESIGNProspective control study using the isolated rat liver.SETTINGAnimal research facility.SUBJECTSMale, fasted, pathogen-free Sprague-Dawley rats.INTERVENTIONSLow-flow hypoxia was produced by reducing afferent perfusate pressure from 10 to 2.5 cm H2O; isolated livers were portally perfused for 2 hrs.MEASUREMENTS AND MAIN RESULTSWe measured mitochondrial membrane potential and hydrogen peroxide production by imaging rhodamine 123 and 2''-7''-dichlorofluorescein fluorescence, respectively. Leakage of mitochondrial enzymes was also monitored by assaying mitochondrial aspartate aminotransferase activity in the outflow perfusate, and the radical-scavenging effect of methylprednisolone was assessed by measuring luminol-dependent hydrogen peroxide chemiluminescence. Apoptosis in liver cells was determined by using terminal deoxynucleotidyl transferase-mediated dUTP-digoxigenin nick-end labeling. Rhodamine 123 fluorescence was significantly diminished in the hypoxic liver, especially in the region of the terminal hepatic venules, which is indicative of membrane depolarization in the mitochondria in those areas. Hypoxia-induced mitochondrial dysfunction was indicated by leakage of aspartate aminotransferase into the outflow perfusate, and increased 2''-7''-dichlorofluorescein fluorescence indicated increased hydrogen peroxide levels, particularly in the midzone. Pretreatment with 30, 10, or 3 mg/kg of methylprednisolone inhibited the hypoxia-induced mitochondrial membrane depolarization and enzyme leakage, although hydrogen peroxide levels and apoptosis in sinusoidal endothelial cells were unaffected.CONCLUSIONSMethylprednisolone does not protect the liver from hypoxia-induced injury by suppressing hydrogen peroxide production. Instead, the beneficial effect of methylprednisolone seems to be related to its ability to protect against mitochondrial membrane depolarization under hypoxic conditions. [ABSTRACT FROM AUTHOR]