Ascitic fluid acidosis in bacterial peritonitis: A poor prognostic sign?

✍ Scribed by Norman Gitlin

• Publisher: John Wiley and Sons
• Year: 1990
• Tongue: English
• Weight: 393 KB
• Volume: 11
• Category: Article
• ISSN: 0270-9139
• DOI: 10.1002/hep.1840110532

✦ Synopsis

proliferation and secretion by production of interleukins 3 and 4. In PCT, another mechanism may be active. Photoactivation causes complement activation in PCT both in vitro and in vivo (8). Complement activation products include such anaphylatoxins as C5a, which, in turn, can cause mast cell secretion. Does chronic PCT skin resemble scleroderma skin because mast cell activation is a "final common pathway" to fibrosis, even though the factors "behind the mast cell" in these conditions are quite different?

To come to the liver (at last), are there any lessons here? Mast cells are not common in the normal liver, nor are they prominent in alcoholic cirrhosis (9). However, fibrosis of the liver is common in systemic mastocytosis, and hepatic mast cells are conspicuous in that disorder (10). Fibrosis is also common in the liver in PCT, but mast cells are not usually mentioned, perhaps because the correct stains are not used. Would the increased iron found in the liver in PCT stimulate fibrosis? Possibly. However, any link with the mast cell in this situation has not yet been forged to my knowledge. Would the inquisitive pathologist, looking for both granulated and "phantom" mast cells, find the number of either or both to be increased in the liver of patients with PCT? Perhaps, it is time to find out.

Clinicopathological correlations can be tantalizing.