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Original Article
June 2001

Spontaneous Rupture of Hepatocellular Carcinoma and Vascular Injury

Author Affiliations

From the Institute of Surgery, Affiliated Hospital of Anhui Medical University, Anhui, Hefei, China (Drs Zhu and Geng); and the Department of Surgery, the University of Hong Kong, Hong Kong, China (Dr Fan).

Arch Surg. 2001;136(6):682-687. doi:10.1001/archsurg.136.6.682
Abstract

Hypothesis  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.

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