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Article: Spontaneous rupture of hepatocellular carcinoma and vascular injury

TitleSpontaneous rupture of hepatocellular carcinoma and vascular injury
Authors
Issue Date2001
PublisherAmerican Medical Association. The Journal's web site is located at http://www.archsurg.com
Citation
Archives Of Surgery, 2001, v. 136 n. 6, p. 682-687 How to Cite?
AbstractHypothesis: Because spontaneous rupture of hepatocellular carcinoma (HCC) is one kind of bleeding complication related to the blood vessels, the possible mechanism of this rupture should occur on the blood vessel itself. Our hypothesis, which has not yet been investigated, is that the vascular integrity of HCC might be damaged during vascular injury. Design: We examined semiquantitatively the expression of von Willebrand factor, elastin, neutrophil elastase, type IV collagen, and collagenase in 23 specimens of HCC with spontaneous rupture by immunohistochemistry, and compared them with 30 specimens of HCC without rupture. Results: There was a significant decrease of von Willebrand factor, proliferation of degenerated elastin, abnormal distribution of neutrophil elastase, degradation of type IV collagen, and increase in collagenase production around the blood vessels in ruptured HCC. Since the decreased expression of von Willebrand factor is an indicator of vascular injury and elastase and collagenase are present in inflammatory processes, we postulate that the vascular injury probably exists before spontaneous rupture of HCC occurs. The blood vessel dysfunction resulting from the degeneration of elastin and the degradation of type IV collagen can render the blood vessels stiff and weak, causing them to split easily when the vascular load increases from hypertension or minor mechanical trauma. Conclusion: Spontaneous rupture of HCC may be related to the vascular dysfunction.
Persistent Identifierhttp://hdl.handle.net/10722/84276
ISSN
2014 Impact Factor: 4.926
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorZhu, LXen_HK
dc.contributor.authorGeng, XPen_HK
dc.contributor.authorFan, STen_HK
dc.date.accessioned2010-09-06T08:51:02Z-
dc.date.available2010-09-06T08:51:02Z-
dc.date.issued2001en_HK
dc.identifier.citationArchives Of Surgery, 2001, v. 136 n. 6, p. 682-687en_HK
dc.identifier.issn0004-0010en_HK
dc.identifier.urihttp://hdl.handle.net/10722/84276-
dc.description.abstractHypothesis: Because spontaneous rupture of hepatocellular carcinoma (HCC) is one kind of bleeding complication related to the blood vessels, the possible mechanism of this rupture should occur on the blood vessel itself. Our hypothesis, which has not yet been investigated, is that the vascular integrity of HCC might be damaged during vascular injury. Design: We examined semiquantitatively the expression of von Willebrand factor, elastin, neutrophil elastase, type IV collagen, and collagenase in 23 specimens of HCC with spontaneous rupture by immunohistochemistry, and compared them with 30 specimens of HCC without rupture. Results: There was a significant decrease of von Willebrand factor, proliferation of degenerated elastin, abnormal distribution of neutrophil elastase, degradation of type IV collagen, and increase in collagenase production around the blood vessels in ruptured HCC. Since the decreased expression of von Willebrand factor is an indicator of vascular injury and elastase and collagenase are present in inflammatory processes, we postulate that the vascular injury probably exists before spontaneous rupture of HCC occurs. The blood vessel dysfunction resulting from the degeneration of elastin and the degradation of type IV collagen can render the blood vessels stiff and weak, causing them to split easily when the vascular load increases from hypertension or minor mechanical trauma. Conclusion: Spontaneous rupture of HCC may be related to the vascular dysfunction.en_HK
dc.languageengen_HK
dc.publisherAmerican Medical Association. The Journal's web site is located at http://www.archsurg.comen_HK
dc.relation.ispartofArchives of Surgeryen_HK
dc.titleSpontaneous rupture of hepatocellular carcinoma and vascular injuryen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0004-0010&volume=136&spage=682&epage=687&date=2001&atitle=Spontaneous+rupture+of+hepatocellular+carcinoma+and+vascular+injuryen_HK
dc.identifier.emailFan, ST: stfan@hku.hken_HK
dc.identifier.authorityFan, ST=rp00355en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.pmid11387009-
dc.identifier.scopuseid_2-s2.0-0034995701en_HK
dc.identifier.hkuros59320en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0034995701&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume136en_HK
dc.identifier.issue6en_HK
dc.identifier.spage682en_HK
dc.identifier.epage687en_HK
dc.identifier.isiWOS:000169033800022-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridZhu, LX=36248128300en_HK
dc.identifier.scopusauthoridGeng, XP=7102141591en_HK
dc.identifier.scopusauthoridFan, ST=7402678224en_HK

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