Tasmar and Liver (cont.) 1 December 1998 As (I think) I mentioned just before the Thanksgiving holiday, I reluctantly decided to quit Tasmar, until more is known about a very rare but extremely dangerous side effect, fulminant hepatitis. I'm now back to 800mg/day, vice the former 400mg/day of Sinemet, and unhappy about it. BTW: Tasmar, like many other drugs, should not be stopped abruptly- see your neuro first. The crux of the matter is ignorance about fulminant hepatitis (FH). Unlike most other liver diseases, FH external symptoms develop within a few hours, followed shortly, if not treated, by coma and death. Encephalopathy (e.g., coma) is a hallmark. The last I knew, 3 deaths from FH were reported among the 100,000 or so Tasmar recipients in the past couple of years, prompting suspension of approval in Europe and warning letters to doctors in the U.S. and Canada. It's unclear how FH incidence among Tasmar users compares with that in the general population. One recent review mentions studies of 364 cases in the general population worldwide, and one warning letter suggests "10- to 100-fold" higher incidence in Tasmar users. A feature of FH seems to be virtual destruction of the liver, either by atrophy or necrosis. The most successful treatment has been immediate surgical replacement (graft) of all or part of the liver. Authorities now require informed consent by those wishing to continue taking Tasmar, and frequency of blood tests (to detect liver disease in general) increased from monthly to biweekly, for at least a year. The problem with periodic blood tests, for raised levels of the enzymes alanine aminotransferase (ALT) or aspartate aminotransferase (AST), is that they may not give timely warning of FH, because of its very rapid onset. FH may be caused by a virus. Viruses specific to hepatitis are so numerous they are named by letters of the alphabet. Suspects mentioned include hepatitis A, B, C, D, and G, as well as the Epstein-Barr virus that is associated with other disease. Since the viruses are all contagious, transmissible via food, blood, etc., it's quite possible for FH to result from liver transplant surgery done for some other reason. FH is also associated with some (medical) drugs other than tolcapone, such as halothane, amiodarone, or topiramate, to name a few. But my time, facility, and access aren't up to the task of checking out all the possibilities. What's needed is an up-to-date review of FH and tolcapone, preferably by a liver specialist who keeps abreast of literature on that subject. Now, risk by itself isn't all bad. It depends on what may be gained. A PD patient who likes the benefits of Tasmar urgently needs answers to these two questions, presently unknown, to decide whether the benefits to him/her outweigh the risk: (a) Given that FH may happen to anyone, what is the nature and extent of the additional risk from taking Tasmar? (b) Does the frequent blood test now required, or any other test, reduce that risk by providing warning in time to avoid the disaster of FH? Until then, stay tuned. Cheers, Joe -- J. R. Bruman (818) 789-3694 3527 Cody Road Sherman Oaks, CA 91403-5013