Successful treatment of gastric cancer with gastroduodenal intussusception by laparoscopic distal gastrectomy.

We report a case of a 93-year-old woman with gastric cancer who presented with gastroduodenal intussusception and was treated with laparoscopic distal gastrectomy. Esophagogastroduodenoscopy showed a giant protruding lesion in the gastric antrum extending into the duodenal bulb, and biopsy confirmed a well-differentiated adenocarcinoma. Abdominal contrast-enhanced computed tomography (CT) revealed a well-defined mass with homogeneous enhancement and a stalk arising from the distal stomach extending into the duodenal bulb. With a clinical diagnosis of gastric cancer with gastroduodenal intussusception, the patient underwent laparoscopic distal gastrectomy with regional lymph node dissection and reconstruction using the Billroth I method. Reduction of the intussusception was performed through a 4 cm incision under the xiphoid process in the epigastric region because it could not be laparoscopically reduced. Gross examination of the resected specimen showed a well-circumscribed, elevated lesion measuring 11.2 × 4.7 × 3.6 cm in the antrum. Microscopic examination of the elevated tumor confirmed the diagnosis of well-differentiated adenocarcinoma invading the gastric submucosal layer without lymph node metastasis. There was no lymphatic or venous invasion or lymph node metastasis. The postoperative course was uneventful, and her hemoglobin level improved to 11.9 g/dL. The patient has been postoperatively well without evidence of recurrence for 3 months. Part of the superficial spreading-type tumor may be drawn into the duodenum under strong peristaltic movement because it does not infiltrate the muscle layer.

[Non-alcoholic steatohepatitis : pathology and pathogenesis].

Nonalcoholic steatohepatitis (NASH) has become to be widely recognized as a significant cause of chronic liver injuries. Evidences suggest that development of NASH requires a double "hit". The "first hit" involves the accumulation of fat in the liver, and the "second hit" includes oxidative stress, cytokines, stellate cell activation, and fibrogenesis. Microscopically, some alcoholic hepatitis-like findings, hepatocellular steatosis, ballooning degeneration, Mallory body, acute and chronic lobular inflammation, and zone 3 perisinusoidal fibrosis are noted. Because ballooning degeneration and Mallory body denote progressive NASH, we should identify clearly these findings. The diagnosis of nonalcoholic steatohepatitis requires histopathologic evaluation, because the lesions of parenchymal injury and fibrosis cannot be detected by imaging studies or laboratory tests.

Polymorphisms of microsomal triglyceride transfer protein gene and manganese superoxide dismutase gene in non-alcoholic steatohepatitis.

BACKGROUND/AIMS: The pathogenesis of non-alcoholic steatohepatitis (NASH) is poorly understood. The aim of this study was to examine genetic influences on NASH pathogenesis. METHODS: Blood samples from 63 patients with biopsy-proven NASH and 150 healthy controls were analyzed by the polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP). Two functional polymorphisms were studied: the -493 G/T polymorphism in the promoter of microsomal triglyceride transfer protein (MTP) and the 1183 T/C polymorphism in the mitochondrial targeting sequence of manganese superoxide dismutase (MnSOD). RESULTS: NASH patients had a much higher incidence of the MTP gene G allele (P=0.001) and of the G/G genotype (P=0.002) compared to the controls. Fat occupied more area in liver lobules and the stage of NASH was advanced in patients with the G/G-genotype than in patients with G/T-genotype (P=0.04). NASH patients also had a higher incidence of the MnSOD T/T genotype (P=0.016). CONCLUSIONS: The G allele in the MTP promoter leads to decreased MTP transcription, less export of triglyceride from hepatocytes, and greater intracellular triglyceride accumulation. The T allele in MnSOD mitochondrial targeting sequence leads to less transport of MnSOD to the mitochondria. Therefore, functional polymorphisms in MTP and MnSOD may be involved in determining susceptibility of NASH.