Reye's Syndrome and Coenzyme A Sequestration

Here's an article that discusses CoA sequestration, in response to aspirin, as a mechanism leading to Reye's syndrome. I'm not sure if it's saliciloyl-CoA, the acetyl- group donation by acetylsalicylic acid, or some other, more direct inhibitory effect on beta-oxidation that's the most important mechanism. But aspirin definitely can produce significant inhibition of beta-oxidation:

http://jpet.aspetjournals.org/cgi/content/abstract/259/2/894 (pubmed: http://www.ncbi.nlm.nih.gov/pubmed/1941634?dopt=Abstract) (Deschamps et al., 1991)

The "microvesicular steatosis" the authors mention is fatty liver disease, the accumulation of lipids due to, and in association with, mitochondrial damage or at least the more short-term impairment in mitochondrial function due to acyl-CoA accumulation. I know they used to use carnitines and CoA precursors to treat Reye's syndrome, but there's been more research, in recent years, on the use of nucleotides and the maintenance of one-carbon metabolism with L-methylfolate/methylcobalamin, as approaches to treating fatty liver disease, than on the use of CoA precursors and acetyl-L-carnitine, etc.