Cases reported "Liver Cirrhosis"

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11/1533. Posttraumatic intra-gallbladder hemorrhage in a patient with liver cirrhosis.

    We report a case of intra-gallbladder hemorrhage secondary to blunt abdominal trauma in a patient with liver cirrhosis. A 58-year-old man was admitted to a local hospital with persistent right upper quadrant abdominal pain. anemia was detected, and computed tomography (CT) revealed a high-density mass in the gallbladder lumen. He was transferred to our hospital because a gallbladder tumor was suspected. He had a history of habitual alcohol abuse and had sustained blunt abdominal trauma in the right upper quadrant 29 days before admission to our hospital (4 days before to the admission local hospital). The intra-gallbladder high-density mass depicted on the CT scan, observed as non-shadowing low-level echoes, was deemed to represent a blood clot on ultrasonography (US) performed 31 days after the trauma. US-guided percutaneous transhepatic gallbladder aspiration and cholecystography confirmed the presence of an old blood clot in the lumen. Because of the patient's persistent pain, a cholecystectomy was performed. The distended gallbladder was filled with old clotted blood. ( info)

12/1533. Case report: rupture of a gastric varix in liver cirrhosis associated with glycogen storage disease type iii.

    glycogen storage disease type iii, or Cori's disease, is caused by a deficiency of amylo-1,6-glucosidase (debranching enzyme), which leads to the storage of an abnormal glycogen in the liver and in skeletal and heart muscle. glycogen storage disease type iii is usually characterized by hepatic symptoms, growth failure and myopathy. Even though liver cirrhosis is reported, portal hypertension is a rare complication of this disease. We describe the case of a glycogen storage disease type III patient who was diagnosed at 3 years of age and developed complications (liver cirrhosis and rupture of a gastric varix) at 31 years of age. We discuss the histological progression to cirrhosis of the liver and describe the liver enzyme profile at 3 and 31 years of age. ( info)

13/1533. Septic shock due to helicobacter fennelliae in a non-human immunodeficiency virus-infected heterosexual patient.

    helicobacter fennelliae (formerly campylobacter fennelliae) has been reported to cause bacteremia in homosexual men with or without human immunodeficiency virus (hiv) infection. We report here a 48-year-old, non-hiv-infected, heterosexual man with diabetes mellitus and cirrhosis of the liver who developed bacteremia and septic shock due to H. fennelliae. The patient was treated successfully initially with intravenous ampicillin-sulbactam and ceftazidime, followed by ampicillin-sulbactam only. These agents were active in vitro against the isolate by E-test results. To our knowledge, this is the first documented case of septic shock due to H. fennelliae in a non-hiv-infected, heterosexual, immunocompromised patient. ( info)

14/1533. Cirrhosis in a child with hypothalamic syndrome and central precocious puberty treated with cyproterone acetate.

    Before the advent of gonadotropin-releasing-hormone analogues, cyproterone acetate (CPA) had been widely prescribed for the treatment of precocious puberty. Although it is usually well tolerated, liver toxicity has been recognized as a complication of its long-term use. We report the occurrence of cirrhosis in a 10-year-old boy with hypothalamic syndrome and precocious puberty who was treated with CPA for over 50 months. Despite discontinuation of the medication, the liver disease progressed. The patient died of sepsis and multiorgan failure at the age of 14 years. This is the first paediatric report of substantial liver damage and liver toxicity progressing to cirrhosis associated with CPA treatment. CONCLUSION: Prolonged cyproterone acetate treatment may induce cirrhosis. Monitoring of liver function both during treatment and for several months after discontinuation of therapy is recommended. ( info)

15/1533. Late manifestation of Indian childhood cirrhosis in a 3-year-old German girl.

    We report on a 3.8-year-old German girl who presented with signs of subacute liver failure based on a 4-month history. Investigations done before admission excluded infectious, metabolic and immunological diseases. Laboratory findings were increased values of aminotransferases, hyperbilirubinaemia, hyperammonaemia and deteriorated plasmatic coagulation. Caeruloplasmin and serum copper concentrations were normal; however, urinary copper excretion was elevated (80 microg/l). Liver biopsy showed a micronodular liver cirrhosis and an extremely high liver copper concentration (1400 microg/g dry weight). Epidemiological investigations revealed an elevated copper concentration (8645 microg/l, normal: <2000) and a low pH value (6.3) of the drinking water supplied by copper pipes. The girl had been exposed to copper-contaminated drinking water since the age of 2 years. CONCLUSION: Laboratory, histopathological findings and a proven chronic copper intoxication lead to the diagnosis of Indian childhood cirrhosis in a German girl. Whereas this disease is mostly described in patients with increased copper intake in infancy, our patient developed toxic liver cirrhosis with relatively late copper exposure. Indian childhood cirrhosis should be considered in the differential diagnosis of early childhood liver cirrhosis. ( info)

16/1533. Case report: two cases of biliary papillomatosis with unusual associations.

    Papillomatosis arising from the biliary tree is a well recognized but rare entity. We encountered two patients with this condition. However, one of them had associated hepatocellular carcinoma and cirrhosis and the other had concomitant recurrent pyogenic cholangitis. To our knowledge, these associations have not been reported before. We, therefore, present these clinical problems and highlight the added difficulty in the management of these patients. ( info)

17/1533. Complete remission of multiple hepatocellular carcinomas associated with hepatitis c virus-related, decompensated liver cirrhosis by oral administration of enteric-coated tegafur/uracil.

    We report a case of complete remission of multiple hepatocellular carcinomas after oral administration of enteric-coated tegafur/uracil. A 77-yr-old woman was diagnosed as having recurrent hepatocellular carcinoma associated with decompensated liver cirrhosis. We administered enteric-coated tegafur/uracil to this patient. After 1 month of oral administration, there was a decrease in tumor markers. An image analysis showed disappearance of hepatocellular carcinoma. No recurrence of the hepatocellular carcinoma was recognized for 18 months up to the time of the patient's death, which was due to massive bleeding from a hemorrhagic rectal ulcer. At autopsy, the tumor lesion had necrotized. Oral administration of enteric-coated granules containing tegafur/uracil may provide an effective treatment for hepatocellular carcinoma. ( info)

18/1533. Recurring fibro-obliterative venopathy in liver allografts.

    Recurrent diseases in liver allografts are not uncommon. These occur most frequently in those transplanted for viral hepatitis b and C. We report an unusual case of recurrent process in two consecutive liver allografts received by a 37-year-old woman, who previously had an unremarkable past medical history but developed a rapidly progressive cholestatic liver failure. Histopathologic examination of the native liver showed fibroocclusive lesions of both terminal hepatic venules and portal vein branches. The exuberant fibroobliterative process created dense fibrosis with whorled appearance, and broad fibrous septa connecting adjacent central areas, and sometimes bridging portal to central areas. Dense portal fibrosis resulted in compression atrophy and loss of bile ducts. The first allograft, which failed within 3 months, showed histopathologic findings similar to that of the native liver. A liver biopsy that was performed 20 months after the second liver transplant again showed similar histopathology. The histopathologic features and clinical presentation of this patient suggest an unusual form of recurring progressive fibroobliterative venopathy causing liver failure. ( info)

19/1533. Control of solitary gastric fundal varices and portosystemic encephalopathy accompanying liver cirrhosis by balloon-occluded retrograde transvenous obliteration (B-RTO): a case report.

    In a patient with liver cirrhosis complicated by solitary gastric fundal varices and portosystemic encephalopathy, Balloon-occluded retrograde transvenous obliteration (B-RTO) of the varices was performed. The gastric varices were decreased in size 2 weeks after treatment and had not recurred after 1 year. B-RTO successfully occluded the portosystemic shunt (gastrorenal shunt). Accordingly, the patient's blood ammonia levels, total bile acid level, and 15 min retention rate of indocyanine green decreased, and his hepatic encephalopathy improved. However, since consecutive increase in blood flow through the portal collateral vessels except for gastrorenal shunt vessel at 6 months and 1 year after B-RTO was noted, further careful follow-up may be required. ( info)

20/1533. Endoscopic management of bleeding ectopic varices with histoacryl.

    Bleeding from antral and duodenal varices is an uncommon feature in patients with portal hypertension. We report a patient with cirrhosis and portal vein thrombosis, who had a massive bleed from antral and duodenal varices. Bleeding was controlled with endoscopic injection of varices using histoacryl. Endoscopic treatment and the relatively uncommon occurrence of antral and duodenal varices are highlighted. ( info)
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