Peliosis hepatis pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:
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Overview
The pathogenesis of peliosis hepatis is unknown. There are several hypotheses, such as, it arise from sinusoidal epithelial damage[1], increased sinusoidal pressure due to obstruction in blood outflow from the liver, or hepatocellular necrosis[2].
Pathophysiology
The pathogenesis of peliosis hepatis is unknown. There are several hypotheses, such as, it arise from sinusoidal epithelial damage[3], increased sinusoidal pressure due to obstruction in blood outflow from the liver, or hepatocellular necrosis[2].
Two morphologic patterns of hepatic peliosis were described by Yanoff and Rawson [4]. In the phlebectatic type, the blood-filled spaces are lined with endothelium and are associated with aneurismal dilatation of the central vein; in the parenchymal type, the spaces have no endothelial lining and they usually are associated with haemorrhagic parenchymal necrosis. Some considers both pattern to be one process, initiated by focal necrosis of liver parenchyma observed in parenchymal type progressing into formation of fibrous wall and endothelial lining around haemorrhage of phebectatic type. Fibrosis, cirrhosis, regenerative nodules, and tumours may also be seen.
References
- ↑ Gushiken FC (2000). "Peliosis hepatis after treatment with 2-chloro-3'-deoxyadenosine". South. Med. J. 93 (6): 625–6. PMID 10881786.
- ↑ 2.0 2.1
- ↑ Gushiken FC (2000). "Peliosis hepatis after treatment with 2-chloro-3'-deoxyadenosine". South. Med. J. 93 (6): 625–6. PMID 10881786.
- ↑ YANOFF M, RAWSON AJ (1964). "PELIOSIS HEPATIS. AN ANATOMIC STUDY WITH DEMONSTRATION OF TWO VARIETIES". Archives of pathology. 77: 159–65. PMID 14088761.