Re: Prilosec (continued)

[Guest guest]

> How does this correlate to UC

The only explanation that I can offer for the positive effects of Prilosec [or Nexium] (proton-pump inhibitors) on ulcerative colitis:

http://www.ncbi.nlm.nih.gov/pubmed/8071518

is that by suppressing acid production in the gut, these agents may lead to a more alkaline environment in the gut/intestine. An alkaline environment would allow for higher activity of intestinal alkaline phosphatase. The main function of this enzyme seems to be to detoxify the bacterial toxin lipopolysaccharide (endotoxin) produced by gut bacteria:

http://www.am-pharma.com/download/0710%20alkaline%20phosphatase%20in%20uc%20oct07.pdf

Some recent research in zebrafish suggest that intestinal alkaline phosphatase is critical for preventing gut inflammation caused by resident bacteria:

http://www.ncbi.nlm.nih.gov/pubmed/18078689

As the name implies "alkaline" phosphatase means that it functions best in alkaline environments, and does not work well in "acid" environments. So Prilosec or Nexium might create the alkaline (i.e. less acidic) environment required to detoxify lipopolysaccharide. Could this be relevant to PSC? Possibly? One theory is that endotoxin/lipopolysaccharide reaching the liver via the portal vein from a leaky gut might contribute to the liver inflammation and bile-duct injury in PSC. PSC is associated with abnormal endotoxin accumulation in biliary epithelial cells.

http://www.ncbi.nlm.nih.gov/pubmed/9764987

But this is not scientific fact, only my conjecture!

Best regards,

Dave

(father of (23); PSC 07/03; UC 08/03)