ABSTRACT
Portal venous gas (PVG) generally suggests critically ill conditions such as severe bowel ischemia. We herein report a rare case of gallbladder torsion with PVG. An 88-year-old woman complained of right hypogastric pain. Ultrasonography (US) showed diffuse wall thickening of her gallbladder and mobile echogenic foci moving inside the portal venous branches. Computed tomography showed a thickened wall of the gallbladder with poor enhancement and tiny pockets of air in the portal venous branches (segments 4 and 5). There was no evidence of other visceral ischemia. She was diagnosed with necrotic cholecystitis and immediately underwent an emergency operation. We found a gangrenous gallbladder with 180° clockwise rotation along the longitudinal axis and performed cholecystectomy. We confirmed the disappearance of PVG with US after the operation. Her postoperative course was uneventful. Gallbladder diseases can produce PVG, and US might be a useful diagnostic modality to evaluate changes in PVG.
ABSTRACT
Were port a caseof an 82-year-old man who presented with vomiting. Computed tomography(CT)revealed a jejunum tumor and small bowel obstruction. Enteroscopy revealed a protruded lesion and biopsy indicated adenocarcinoma. PET-CT revealed nothing without jejunal tumor. Therefore, with a preoperative diagnosis of primary small bowel cancer, we performed operation. Surgery indicated peritoneal disseminations and a jejunal tumor 40 cm distal from the ligament of Treitz, and we performed small bowel partial resection. Pathological examination revealed adenocarcinoma originating from a Heinrich type I ectopic pancreas in the jejunum. Ectopic pancreatic cancer in the jejunum is rare, and we review case reports in the literature.
Subject(s)
Adenocarcinoma , Intestinal Obstruction/etiology , Jejunal Neoplasms/pathology , Pancreatic Neoplasms/pathology , Adenocarcinoma/complications , Adenocarcinoma/drug therapy , Adenocarcinoma/surgery , Aged, 80 and over , Antineoplastic Combined Chemotherapy Protocols/therapeutic use , Chemotherapy, Adjuvant , Humans , Intestinal Obstruction/surgery , Jejunal Neoplasms/complications , Jejunal Neoplasms/drug therapy , Jejunal Neoplasms/surgery , Male , Pancreatic Neoplasms/complications , Pancreatic Neoplasms/drug therapy , Pancreatic Neoplasms/surgeryABSTRACT
Glucose-6-phosphatase (G6Pase) is a key regulator of gluconeogenesis. We previously found that administration of glycerol, a substrate for gluconeogenesis, transactivates G6Pase in the mouse liver. To clarify its cell-autonomous transcriptional activation in hepatocytes, we examined the mechanism of expression of the gene G6pc, which encodes G6Pase, in rat hepatoma cell line FAO cells. Endogenous G6pc expression in FAO cells was increased by glycerol administration as well as by the fatty acid oleate. Luciferase reporter assay revealed that the ~2.0 kb mouse G6pc promoter contains the element(s) responsible for glycerol-stimulated G6pc transactivation. Using several deletion- or chimeric-constructs of G6pc promoter, we found that the DNA response element for hepatocyte nuclear factor 4α (HNF4α) (-77/-65) in the G6pc promoter is essential for transactivation by glycerol. Similarly to glycerol, oleate also increased G6pc expression through its action on the HNF4α element (-77/-65). Furthermore, the reporter activities were higher in the cells co-treated with glycerol plus oleate than in those singly treated with glycerol or oleate. In addition, the temporal profiles of G6pc expression differed between glycerol and oleate administration. Our present results suggest that glycerol and oleate induce G6pc expression both via the HNF4αelement (-77/-65) and also through other regulatory mechanisms.
Subject(s)
Gene Expression , Glucose-6-Phosphatase/genetics , Glycerol/metabolism , Hepatocyte Nuclear Factor 4/metabolism , Liver/metabolism , Animals , Base Sequence , Cell Line, Tumor , Gene Expression Regulation, Enzymologic , Genes, Reporter , Glycerol/pharmacology , Liver/drug effects , Mice , Oleic Acid/metabolism , Oleic Acid/pharmacology , Promoter Regions, Genetic , Rats , Sequence Deletion , Transcriptional ActivationABSTRACT
We report the case of a 77-year-old woman with mediastinal lymph node metastasis of combined hepatocellular and cholangiocarcinoma who was successfully treated with S8 segmentectomy and lymphadenectomy. A hepatic nodule was detected in segment 8 during follow-up computed tomography (CT) after left iliac arterial aneurysm repair. The patient was diagnosed with a hepatocellular carcinoma (HCC), and transcatheter arterial chemoembolization (TACE) was selected for HCC because of the patient's condition. The levels of tumor markers did not change after TACE was performed twice. Therefore, TACE treatment was considered to be ineffective for HCC, and the patient was admitted to our hospital for surgical resection. In addition to the primary lesion, a lymph node with a diameter of 20 mm was detected in the anterior mediastinum using CT and magnetic resonance imaging(MRI). We did not find any other metastases, and therefore, S8 segmentectomy and lymphadenectomy in the anterior mediastinum were performed. Recovery was uneventful, and the patient was discharged from the hospital on postoperative day 12. Based on histopathologic findings, combined hepatocellular and cholangiocarcinoma with mediastinal lymph node metastasis was confirmed. Levels of tumor markers normalized, and the patient survived without recurrence for 6 months.
