Angiogenesis is a dynamic,hypoxia-stimulated and growth factor-dependent process,and is currently referred to as the formation of new vessels from preexisting blood vessels.Experimental and clinical studies have unequ...Angiogenesis is a dynamic,hypoxia-stimulated and growth factor-dependent process,and is currently referred to as the formation of new vessels from preexisting blood vessels.Experimental and clinical studies have unequivocally reported that hepatic angiogenesis,irrespective of aetiology,occurs in conditions of chronic liver diseases(CLDs) characterized by perpetuation of cell injury and death,inflammatory response and progressive fibrogenesis.Angiogenesis and related changes in liver vascular architecture,that in turn concur to increase vascular resistance and portal hypertension and to decrease parenchymal perfusion,have been proposed to favour fibrogenic progression of the disease towards the end-point of cirrhosis.Moreover,hepatic angiogenesis has also been proposed to modulate the genesis of portal-systemic shunts and increase splanchnic blood flow,thus potentially affecting complications of cirrhosis.Hepatic angiogenesis is also crucial for the growth and progression of hepatocellular carcinoma.Recent literature has identified a number of cellular and molecular mechanisms governing the cross-talk between angiogenesis and fibrogenesis,with a specifi c emphasis on the crucial role of hypoxic conditions and hepatic stellate cells,particularly when activated to the myofibroblast-like pro-fibrogenic.Experimental anti-angiogenic therapy has been proven to be effective in limiting the progression of CLDs in animal models.From a clinical point of view,anti-angiogenic therapy is currently emerging as a new pharmacologic intervention in patients with advanced fibrosis and cirrhosis.展开更多
Carcinoids are tumors derived from neuroendocrine cells and often produce functional peptide hormones.Approximately 54.5% arise in the gastrointestinal tract and frequently metastasize to the liver.Primary hepatic car...Carcinoids are tumors derived from neuroendocrine cells and often produce functional peptide hormones.Approximately 54.5% arise in the gastrointestinal tract and frequently metastasize to the liver.Primary hepatic carcinoid tumors(PHCT) are extremely rare;only 95 cases have been reported.A 65-year-old man came to our attention due to occasional ultrasound findings in absence of clinical manifestations.His previous medical history,since 2003,included an echotomography of the dishomogeneous parenchymal area but no focal lesions.A computed tomography scan performed in 2005 showed an enhanced pseudonodular-like lesion of about 2 cm.Cholangio-magnetic resonance imaging identified the lesion as a possible cholangiocarcinoma.No positive findings were obtained with positron emission tomography.Histology suggested a secondary localization in the liver caused by a low-grade malignant neuroendocrine tumor.Immunohistochemistry was positive for anti chromogranin antibodies,Ki67 antibodies and synaptophysin.Octreoscan scintigraphy indicated intense activity in the lesion.Endoscopic investigations were performed to exclude the presence of extrahepatic neoplasms.Diagnosis of PHCT was established.The patient underwent left hepatectomy,followed by hormone therapy with sandostatine LAR.Two months after surgery he had a lymph nodal relapse along the celiac trunk and caudate lobe,which was histologically confirmed.The postoperative clinical course was uneventful,with a negative follow-up for hematochemical,clinical and radiological investigations at 18 mo post-surgery.Diagnosis of PHCT is based principally on the histopathological confi rmation of a carcinoid tumor and the exclusion of a non-hepatic primary tumor.Surgical resection is the recommended primary treatment for PHCT.Recurrence rate and survival rate in patients treated with resection were 18% and 74%,respectively.展开更多
文摘Angiogenesis is a dynamic,hypoxia-stimulated and growth factor-dependent process,and is currently referred to as the formation of new vessels from preexisting blood vessels.Experimental and clinical studies have unequivocally reported that hepatic angiogenesis,irrespective of aetiology,occurs in conditions of chronic liver diseases(CLDs) characterized by perpetuation of cell injury and death,inflammatory response and progressive fibrogenesis.Angiogenesis and related changes in liver vascular architecture,that in turn concur to increase vascular resistance and portal hypertension and to decrease parenchymal perfusion,have been proposed to favour fibrogenic progression of the disease towards the end-point of cirrhosis.Moreover,hepatic angiogenesis has also been proposed to modulate the genesis of portal-systemic shunts and increase splanchnic blood flow,thus potentially affecting complications of cirrhosis.Hepatic angiogenesis is also crucial for the growth and progression of hepatocellular carcinoma.Recent literature has identified a number of cellular and molecular mechanisms governing the cross-talk between angiogenesis and fibrogenesis,with a specifi c emphasis on the crucial role of hypoxic conditions and hepatic stellate cells,particularly when activated to the myofibroblast-like pro-fibrogenic.Experimental anti-angiogenic therapy has been proven to be effective in limiting the progression of CLDs in animal models.From a clinical point of view,anti-angiogenic therapy is currently emerging as a new pharmacologic intervention in patients with advanced fibrosis and cirrhosis.
文摘Carcinoids are tumors derived from neuroendocrine cells and often produce functional peptide hormones.Approximately 54.5% arise in the gastrointestinal tract and frequently metastasize to the liver.Primary hepatic carcinoid tumors(PHCT) are extremely rare;only 95 cases have been reported.A 65-year-old man came to our attention due to occasional ultrasound findings in absence of clinical manifestations.His previous medical history,since 2003,included an echotomography of the dishomogeneous parenchymal area but no focal lesions.A computed tomography scan performed in 2005 showed an enhanced pseudonodular-like lesion of about 2 cm.Cholangio-magnetic resonance imaging identified the lesion as a possible cholangiocarcinoma.No positive findings were obtained with positron emission tomography.Histology suggested a secondary localization in the liver caused by a low-grade malignant neuroendocrine tumor.Immunohistochemistry was positive for anti chromogranin antibodies,Ki67 antibodies and synaptophysin.Octreoscan scintigraphy indicated intense activity in the lesion.Endoscopic investigations were performed to exclude the presence of extrahepatic neoplasms.Diagnosis of PHCT was established.The patient underwent left hepatectomy,followed by hormone therapy with sandostatine LAR.Two months after surgery he had a lymph nodal relapse along the celiac trunk and caudate lobe,which was histologically confirmed.The postoperative clinical course was uneventful,with a negative follow-up for hematochemical,clinical and radiological investigations at 18 mo post-surgery.Diagnosis of PHCT is based principally on the histopathological confi rmation of a carcinoid tumor and the exclusion of a non-hepatic primary tumor.Surgical resection is the recommended primary treatment for PHCT.Recurrence rate and survival rate in patients treated with resection were 18% and 74%,respectively.
