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T Suou

Publications and source records attributed to T Suou.

68 records · Page 4Linked to original sources
PubMed1982

Spontaneous rupture of the spleen secondary to metastatic hepatocellular carcinoma: a report of a case and review of the literature.

An extremely rare case of splenic rupture at the site of metastasis of hepatocellular carcinoma is reported. A 62-yr-old woman with hepatocellular carcinoma and its suspected metastasis to the spleen died of intraperitoneal hemorrhage. Autopsy disclosed a laceration of the spleen as the definitive cause of the hemorrhage. There were multiple nodules of metastatic hepatocellular carcinoma in the spleen, some of which were exposed at the lacerated portion of the splenic capsule. This may be the first report of a case of spontaneous rupture of the spleen secondary to metastatic hepatocellular carcinoma. Splenic rupture can be one of the causes of hemoperitoneum in patients with hepatocellular carcinoma.

Carcinoma, Hepatocellular↗
PubMed1980

Antibodies to denatured bovine collagens in sera of patients with liver disease.

Sera from 101 patients with liver disease were studied for the presence of antibodies to three types of denatured bovine collagens by passive haemagglutination assay. A high incidence and titres were found especially in chronic active hepatitis, liver cirrhosis and primary hepatoma. The incidence and titres of antibodies to Type I and Type III collagens were significantly higher than those of antibodies to Type II collagen. Analysis by gel filtration on Sephadex G-200 or absorption with anti-IgG and IgM antisera revealed that the antibodies belonged to both IgG and IgM classes. They correlated with serum gamma-globulin levels, but not with rheumatoid factor.

Adolescent↗
PubMedDate not supplied

Elevated serum aminotransferase induced by isoniazid in relation to isoniazid acetylator phenotype.

Of 143 patients with pulmonary tuberculosis receiving isoniazid therapy, 52 (36%) had a transient elevation in serum aminotransferases. Among 74 patients taking isoniazid, rifampicin and streptomycin, 35 (47%) had such an increase, while of 69 patients taking isoniazid, amino-salicylic acid and streptomycin, 17 (24%) did; this difference was significant. Isoniazid therapy could be continued in all patients with the abnormal test results. In 36 of the patients receiving isoniazid, rifampicin and streptomycin, isoniazid and its metabolites were studied in the serum and urine using high-performance liquid chromatography after the oral administration of 10 mg per kg of isoniazid. We had chosen for this test 18 patients with normal aminotransferase levels and 18 with abnormal levels. There were 14 rapid acetylators in the patients with abnormal aminotransferase levels and 7 rapid acetylators in the patients with normal levels; this difference was significant. These results indicate that liver dysfunction is more often caused by an isoniazid/rifampicin regimen, and patients who are rapid acetylators are more susceptible.

Acetylation↗
PubMedDate not supplied

Is choledocholithiasis a late complication of nonresectional therapies for hepatocellular carcinoma?

We present 3 patients who developed choledocholithiasis 10, 13, and 12 months after percutaneous ethanol injection and/or transcatheter arterial chemoembolization for hepatocellular carcinoma. Since none of these patients had stones in the gallbladder or in the bile ducts before treatment, bile duct stones might have resulted from local injury in the bile ducts by percutaneous ethanol injection and/or transcatheter arterial chemoembolization. Choledocholithiasis may be a late complication of nonresectional and local therapies for hepatocellular carcinoma tumors.

Aged↗
PubMedDate not supplied

Liver perforation: a serious complication of percutaneous acetic acid injection for hepatocellular carcinoma.

A 75-year-old cirrhotic man, after undergoing percutaneous acetic acid injection therapy for hepatocellular carcinoma, presented high fever and right hypochondralgia. Computed tomography disclosed an area of low attenuation in the liver and a crescent-shaped intraperitoneal lesion adjacent to it. We diagnosed liver perforation and localized peritonitis due to the leakage of acetic acid following acetic acid injection. It is important to consider this serious complication when evaluating the indications for percutaneous acetic acid injection for hepatocellular carcinoma.

Acetic Acid↗
PubMedDate not supplied

Asymptomatic extrahepatic portal obstruction without portal hypertensive findings detected in ultrasonic mass screening.

BACKGROUND/AIMS: We report three adult cases of extrahepatic portal obstruction (EHPO) detected by ultrasonic (US) mass screening. MATERIAL AND METHODS: All these cases were asymptomatic with no abnormalities on hematological or biochemical tests. Only indocynanine green clearance test revealed a slight abnormality. By imaging modalities, the portal trunk could not be visualized and cavernous transformation could be visualized. RESULTS: There were no findings of portal hypertension, such as splenomegaly, esophageal varices and hepatofugal collaterals, in any of these cases. CONCLUSIONS: As many EHPOs without symptoms can be detected on US mass survey, US is considered to be the best modality for screening for this disease.

Adult↗
PubMedDate not supplied

Extrahepatic portal obstruction without hepatopetal pathway associated with congenital arterioportal fistula: a case report.

Extrahepatic portal obstruction is one of the causes of portal hypertension, in which well-developed hepatopetal pathways are commonly recognized. Herein an extremely rare case of extrahepatic portal obstruction without hepatopetal pathway, probably caused by arterioportal fistula, is reported. The patient was a normally matured 16-year-old girl admitted for further evaluation of jaundice, presenting with the clinical manifestations of the portal hypertension associated with hypersplenism and portosystemic venous shunt. Celiac angiography clearly demonstrated an intrahepatic arterial aneurysm fed by the right hepatic artery shunting to the superior mesenteric vein, and portography disclosed complete obstruction of the portal trunk with conspicuous hepatofugal pathway but no hepatopetal collateral veins. The exact mechanism of this phenomenon is not known and whether the extrahepatic portal obstruction was primary or secondary is still obscure. However, this is the first case report in the world literature describing extrahepatic portal obstruction with absence of hepatopetal pathway.

Adolescent↗
PubMedDate not supplied

Hypoplasia of the left hepatic lobe associated with floating gallbladder: a case report.

Agenesis or hypoplasia of the hepatic lobe and floating gallbladder are both rare. We report an extremely rare case of hypoplasia of the left hepatic lobe accompanied by floating gallbladder. The patient was a 71-year-old woman, with no past history of related symptoms, who was admitted for further evaluation of postprandial epigastralgia, nausea, and diarrhea. Laboratory data on admission showed chronic liver disease with positive anti-hepatitis C virus antibody. Abdominal ultrasonography and computed tomography revealed the absence of the left hepatic lobe and displacement of the gallbladder to the left. On endoscopic retrograde cholangiography, the cystic duct originated from the right side of the bile duct, but the gallbladder was displaced to the left. Poor yolk-induced gallbladder contraction suggested the existence of hypotonic biliary dyskinesia. Angiography demonstrated no middle or left hepatic arteries, indicating congenital hypoplasia of the left hepatic lobe. Open cholecystectomy was carried out, and a diagnosis of hypoplasia of the left hepatic lobe accompanied by floating gallbladder and chronic hepatitis was confirmed. We believe that this is the first reported case of a hypoplasia of the left hepatic lobe coexisting with floating gallbladder.

Aged↗
PubMedDate not supplied

Refractory ascites due to portal vein thrombosis in liver cirrhosis--report of two cases.

Portal vein thrombosis as a complication of liver cirrhosis has been reported to be extremely rare in Japan, as compared with European countries. There are few reports discussing the correlation of portal vein thrombosis with refractory ascites. Between January 1994 and December 1995, 20 cases (91%) of 22 patients with liver cirrhosis with ascites admitted to our hospital responded well within 2 months to a combination therapy of diuretics and albumin infusion, and the other two cases (9%) with refractory ascites were associated with portal vein thrombosis. The ascites in the first patient continued for 1 year, despite diuretics and albumin infusion therapy, and portal vein thrombosis was confirmed by autopsy. The ascites in the other patient continued for more than 4 months, and portal vein thrombosis was detected by ultrasound. Portal vein thrombosis was not found in the other 20 cirrhotic patients with ascites. These two cases suggest that portal vein thrombosis may be a contributing factor to refractory ascites in patients with decompensated liver cirrhosis.

Ascites↗