Severe biliary complications after hepatic artery embolization.
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AIM: To study the mechanism and treatment of severe biliary complications arising from hepatic artery embolization(HAE). METHODS: Of seven cases of intra- and extrahepatic biliary damage resulting from hepatic artery embolization reported since 1987, 6 patients suffered from hepatic haemangioma, the other case was due to injection of TH compound into the hepatic artery during operation. The hepatic artery was injected with ethanol so as to evaluate the liver damage in experimental rats. RESULTS: All the cases were found to have destructive damage of intra- and extrahepatic bile duct at the hilum with biliary hepatocirrhosis. Experimental results revealed necrosis of the liver parenchyma, especially around the portal tract and obliteration of intrahepatic bile duct. CONCLUSIONS: To prevent the severe biliary complications of HAE, the use of HAE for hepatic haemangioma which was widely practiced in China, should be re-evaluated. Hepatic arterial embolization of hepatic haemangioma may resulte in severe destructive biliary damages and its indiscriminate use should be prohibited. (+info)
Enhancement of hepatic hemangiomas with levovist on coded harmonic angiographic ultrasonography.
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OBJECTIVE: To evaluate the pattern of contrast enhancement with Levovist on coded harmonic angiographic ultrasonography of hepatic hemangiomas. METHODS: Twenty hemangiomas were evaluated with coded harmonic angiographic ultrasonography and a microbubble contrast agent. Verification of the diagnosis of a hemangioma was made by means of dynamic computed tomography (n = 8), dynamic magnetic resonance imaging (n = 1), radionuclide scanning (n = 6), or follow-up ultrasonography (n = 5). Ultrasonographic images were obtained before contrast agent administration and with a bolus injection of 2.5 g of a microbubble contrast agent (300 mg/mL Levovist; Schering AG, Berlin, Germany) every 10 to 15 seconds for 5 minutes. The contrast enhancement patterns of the 20 hemangiomas were assessed. RESULTS: The tumor diameters as measured on ultrasonography were 7 to 97 mm (mean, 26.7 mm). Of the 20 hemangiomas, peripheral globular enhancement with progressive centripetal fill-in was shown in 15 (75%), rimlike enhancement with progressive centripetal fill-in was shown in 2 (10%), and homogeneous enhancement was shown in 1 (5%). In the remaining 2 lesions (10%), the enhancement patterns could not be seen, because they were not found on coded harmonic angiographic ultrasonography. CONCLUSIONS: Coded harmonic angiographic ultrasonography with a microbubble contrast agent can depict the typical enhancement pattern in most hepatic hemangiomas. (+info)
A mouse model of TSC1 reveals sex-dependent lethality from liver hemangiomas, and up-regulation of p70S6 kinase activity in Tsc1 null cells.
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Tuberous sclerosis (TSC) is a autosomal dominant genetic disorder caused by mutations in either TSC1 or TSC2, and characterized by benign hamartoma growth. We developed a murine model of Tsc1 disease by gene targeting. Tsc1 null embryos die at mid-gestation from a failure of liver development. Tsc1 heterozygotes develop kidney cystadenomas and liver hemangiomas at high frequency, but the incidence of kidney tumors is somewhat lower than in Tsc2 heterozygote mice. Liver hemangiomas were more common, more severe and caused higher mortality in female than in male Tsc1 heterozygotes. Tsc1 null embryo fibroblast lines have persistent phosphorylation of the p70S6K (S6K) and its substrate S6, that is sensitive to treatment with rapamycin, indicating constitutive activation of the mTOR-S6K pathway due to loss of the Tsc1 protein, hamartin. Hyperphosphorylation of S6 is also seen in kidney tumors in the heterozygote mice, suggesting that inhibition of this pathway may have benefit in control of TSC hamartomas. (+info)
Primary hemangioma of the occipital bone in the region of the torcula--two case reports.
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Two rare cases of subtorcular occipital bone hemangioma occurred in 26-year-old and 30-year-old female patients. Partial resection was performed in both cases because of the proximity to the torcula. No recurrence was seen at follow-up examination at 9 and 12 months. (+info)
Premature infant with severe periventricular leukomalacia associated with a large placental chorioangioma: a case report.
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We present the first reported case of severe periventricular leukomalacia associated with a large placental chorioangioma. We believe that the large chorioangioma near the point of umbilical cord insertion was not only disrupting fetoplacental circulation but may also have led to the periventricular leukomalacia lesions. (+info)
Fetal axillary hemangiolymphangioma with secondary intralesional bleeding: serial ultrasound findings.
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A case of fetal axillary hemangiolymphangioma coexisting with intralesional hemorrhage is presented. At 27 weeks' gestation, the fetus was found to have a 52 x 43-mm left axillary multilocular cystic mass which showed no signals on color Doppler. The mass was composed mostly of sonolucent spaces. At 29 weeks' gestation, an arterial flow signal (15 cm/s) was detected within the mass. In addition, two low-density echogenic cystic spaces with bidirectional flow waveforms were found, which raised the suspicion of intratumoral bleeding. Two weeks later, a fine-needle aspiration of the mass revealed both straw-colored and chocolate-colored fluid. The tumor size increased from 52 x 43 mm at 27 weeks to 100 x 79 mm at 37 weeks. Blood clots developed gradually in the hemorrhagic spaces. The pregnancy proceeded smoothly to term and at 38 weeks an elective Cesarean section was performed. After a surgical excision of the mass at the age of 4 days, a mixed cavernous hemangioma and cystic lymphangioma with secondary intralesional hemorrhage was confirmed histopathologically. (+info)
Prenatal diagnosis and management of fetuses with liver hemangiomata.
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OBJECTIVES: To study the relationship between prenatal appearance and perinatal outcome of fetuses with hepatic hemangiomata with special emphasis on criteria that may help to improve perinatal management. METHODS: In a tertiary referral center six fetuses with hepatic hemangiomata were evaluated by gray-scale, color, and pulsed wave Doppler ultrasound between 1994 and 2000. Fetal blood sampling was performed in four cases. All data (computerized files and video tapes) were analyzed retrospectively. RESULTS: Two fetuses showed very similar sonographic findings. They had an isolated large ('giant') round hepatic hemangioma (diameter 43 and 68 mm, respectively) supplied by one hepatic artery and drained by one hepatic vein, both of them showing high velocity and low pulsatility blood flow. Fetal blood count and coagulation parameters were normal in one case, whereas the other fetus showed a Kasabach-Merritt sequence with severe thrombocytopenia (10 platelets/nL) and mild disseminated intravascular coagulation. Intrauterine platelet transfusion was performed immediately prior to planned Cesarean delivery. Rapid platelet consumption continued postnatally, requiring several thrombocyte transfusions. Platelet counts stabilized only after tumor resection on the second day of life. One fetus with diffuse neonatal hemangiomatosis developed high-output cardiac failure with hydrops in addition to Kasabach-Merritt sequence (15 platelets/nL), and died following premature delivery. Three fetuses, however, showing an isolated small hyperechogenic hepatic hemangioma (5, 5, and 6 mm in diameter, respectively) did not develop any perinatal complications. CONCLUSION: Large fetal liver hemangiomata and diffuse hemangiomatosis may cause severe perinatal complications, particularly high-output cardiac failure and/or Kasabach-Merritt sequence with severe consumption of platelets and clotting factors and hemolytic anemia. Fetal blood sampling enables the prenatal detection of these potential complications, allowing critical modification of perinatal management such as intrauterine platelet transfusion, especially directly before delivery. In contrast, isolated small hyperreflexic hepatic hemangiomata do not appear to be associated with any of these fetal and postnatal sequelae. (+info)
Glucose regulates insulin mitogenic effect by modulating SHP-2 activation and localization in JAr cells.
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The glucose effect on cell growth has been investigated in the JAr human choriocarcinoma cells. When JAr cells were cultured in the presence of 6 mm glucose (LG), proliferation and thymidine incorporation were induced by serum, epidermal growth factor, and insulin-like growth factor 1 but not by insulin. In contrast, at 25 mm glucose (HG), proliferation and thymidine incorporation were stimulated by insulin, serum, epidermal growth factor, and insulin-like growth factor 1 to a comparable extent, whereas basal levels were 25% lower than those in LG. HG culturing also enhanced insulin-stimulated insulin receptor and insulin receptor substrate 1 (IRS1) tyrosine phosphorylations while decreasing basal phosphorylations. These actions of glucose were accompanied by an increase in cellular tyrosine phosphatase activity. The activity of SHP-2 in HG-treated JAr cells was 400% of that measured in LG-treated cells. SHP-2 co-precipitation with IRS1 was also increased in HG-treated cells. SHP-2 was mainly cytosolic in LG-treated cells. However, HG culturing largely redistributed SHP-2 to the internal membrane compartment, where tyrosine-phosphorylated IRS1 predominantly localizes. Further exposure to insulin rescued SHP-2 cytosolic localization, thereby preventing its interaction with IRS1. Antisense inhibition of SHP-2 reverted the effect of HG on basal and insulin-stimulated insulin receptor and IRS1 phosphorylation as well as that on thymidine incorporation. Thus, in JAr cells, glucose modulates insulin mitogenic action by modulating SHP-2 activity and intracellular localization. (+info)