We report a case of inferior mesenteric arteriovenous fistula without portal hypertension or mesenteric ischemia. A 64-year-old man had developed frequent mucous diarrhea during the previous month. Colonoscopy showed highly edematous mucosa of the rectum. Barium enema demonstrated localized stricture of the same part but no evidence of malignancy. Finally we established a diagnosis by 3D-CT and selective abdominal angiography. Transcatheter arterial embolization was successfully performed. After that, his symptoms gradually improved as all abnormal findings on colonoscopy, barium enema and abdominal CT disappeared.
An 81-year-old man who had under gone two abdominal surgeries and temporary colostomy 30 years previously was admitted due to lower abdominal pain and vomiting. An abdominal X-ray film and abdominal CT scan showed intestinal distension and multiple calcareous deposits in the colon. Gastrografin enema examination revealed smooth stenosis at the sigmoid colon and many additional defects. Endoscopy could not be perfomed due to the stenosis. He did not agree to surgery. Seven months later, he was admitted again, due to colonic obstruction. Surgery was performed which revealed colonic obstruction as the source of post-operative stenosis of the sigmoid colon and multiple enteroliths. The stones consisted of a core and a hull and contained ammonium magnesium phosphate.
We report a case of hepatitis B type liver cirrhosis with portal venous thrombosis in which danaparoid sodium was very effective. The portal venous thrombosis in this case disappeared 2 weeks commencing after administration of danaparoid sodium. The patient had not adverse effects or complications such as hemorrhage, and the clinical course was good. We consider that danaparoid sodium is an anticoagulant unlikely to cause adverse effects such as hemorrhage, and that it might be effective for treatment of portal venous thrombosis. We intend to examine the indications of treatment with danaparoid sodium, clarify the best administration method, and establishment of maintenance therapy by investigating more cases.
It is well known that long-term infection with Clonorchis sinensis often causes bile duct cancer, usually. It occurs in the intrahepatic bile duct. We encountered a rare case of clonorchiasis complicated with duodenal papillary cancer. The patient was a woman from China. Although clonorchiasis is rarely found in Japan, the promotion of international exchange may increase the number of visitors from endemic areas. Thus we must pay sufficient attention to this disease. Also, we reported that the microplate ELISA technique was useful in the diagnosis of clonorchiasis with high accuracy in this case.
A 40-year-old man, who had suffered from general malaise and brown urine during his stay in China, was addmitted with remarkable jaundice and hepatocellular disorders soon after he returned to Japan. Because his coagulation test results worsened, he was transferred to our hospital. No evidence of hepatitis A-D virus infection, autoimmune hepatitis, or metabolic disorders was noticed. His prothrombin time was extended (18%), grade II encephalopathy appeared on the second hospital day, and fulminant hepatitis was diagnosed. Artificial liver support was introduced, and his hepatic coma and coagulation parameters gradually recovered. Genotype IV hepatitis E virus RNA was detected in his early phase sera and also both IgG and IgM type anti-hepatitis E virus antibodies were detected. Fulminant hepatitis E resulting from infection in China was diagnosed.
We report a case of superficial bile duct carcinoma showing extensive intraductal spread without dilatation of the bile duct in which diagnosis was established preoperatively by transpapillary forceps biopsy and intraductal ultrasonography. A 78-year-old man was given a diagnosis of acute cholecystitis, and percutaneous transhepatic gallbladder drainage (PTGBD) was performed. Cholangiography via the PTGBD tube revealed a tiny irregularity in the hilar bile duct. Transpapillary intraductal ultrasonography showed that this irregularity extended from the intrahepatic bile duct to the middle of the bile duct. Bile duct biopsy revealed malignancy, and thus bile duct resection and hepaticojejunostomy were performed. Hisological examination verified a well-differentiated adenocarcinoma confined to the epithelium and the fibromuscular layer.
We report a case of pancreatic ductal adenocarcinoma producing granulocyte-colony stimulating factor (G-CSF). A 56-year-old Japanese man was admitted to our hospital with back pain and high fever. An abdominal CT scan revealed masses in the pancreatic body to the tail, and both lobes of the liver. A biopsy specimen of the hepatic tumor demonstrated metastatic poorly differentiated adenocarcinoma. We administered oral S-1 in combination with gemcitabine. However, his general condition gradually worsened, and a high serum level of G-CSF persisted. He died 135 days after admission. The diagnosis of autopsy was pancreatic ductal adenocarcinoma. Immunohistochemical staining showed the presence of G-CSF in tumor cells. The final diagnosis was G-CSF-producing pancreatic carcinoma.
In 1998 a 74-year-old man, he had a medical checkup and mediastinal and hilar lymph node hyperplasia were discovered. Since the lymph nodes showed a tendency to increase in size, mediastinal lymph node biopsy was performed in the following year. Castlemans disease was diagnosed, and he was followed up. In 2005, autoimmune pancreatitis (AIP) developed. At this time, the mediastinal lymph node that had been biopsied was stained with anti-IgG4 antibody. Further examinations on pancreatic lesions associated with Castlemans disease and AIP are necessary in relation to IgG4-related systemic diseases.