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Tasmar And Liver Failure; More 18 Nov 1998 I'm getting a picture now, that may now resolve the conundrums regarding the current Tasmar scare. First, a very respectful take on the news releases is in the Awakenings website at http://www.parkinsonsdisease.com/ which is supported as a public service by the makers of Tasmar. Now my (layman's) hypothesis: In illness, just as in failure of an auto engine or any other appliance, one may draw two broad categories- gradually progressive, and catastrophic. There are many examples, but consider PD versus, say, cerebral "stroke". PD usually develops so slowly that initial symptoms are not even noticed, but careful screening tests can permit earlier diagnosis. The exact time of a "stroke" on the other hand, is inherently unpredictable, and only a gradually more ominous predisposition can be uncovered by screening tests. So, the liver monitoring advocated for Tasmar recipients may find a gradually worsening condition, but seems unlikely to predict a sudden viral onslaught such as fulminant hepatitis, at least in time to do anything about it. So much for alanine aminotransferase (ALT) monitoring. The alternative is to depend on accumulated statistical experience, and play the odds. Now, why is fulminant hepatitis such a very rare condition? Either the virus itself is rare, or it is ubiquitous but the lack of resistance to it is rare. On the other hand, if Tasmar can directly cause fulminant hepatitis, why don't all the recipients get it, instead of only 2 or 3 per 100,000? I suggest that it takes a combination of _two_ events: a rare infection, (say by HAV or NANB), _and_ a common predisposition (all Tasmar users). Is it possible that Tasmar alone doesn't cause fulminant hepatitis directly, but somehow lowers resistance to whatever does cause it? The answer is crucial, because if my guess is correct, the risk is now reduced to that of the rare event, namely infection (probably the 2 or 3 per 100,000 of current experience). That doesn't seem so bad, compared to some other PD drugs, or to various invasive PD surgeries such as pallidotomy, with mortality of about 1 per 100. The "combined event" hypothesis has a striking example in current PD science: If a very common environmental hazard such as pesticide exposure can cause PD, why doesn’t virtually everyone have PD? Answer: In at least one important variant of PD, it takes both the common exposure hazard _and_ a rare inherited mutation of an enzyme (glutathione S-transferase) that protects most people against it. (see Menegon A et al; Lancet, 24 Oct 1998, 1344- 1346, and related postings here). I hope I'm right, because I like what Tasmar does for me, but I'm too young to die. Cheers, Joe -- J. R. Bruman (818) 789-3694 3527 Cody Road Sherman Oaks, CA 91403-5013