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For these reasons, it has been postulated that statins may reduce mortality in critically ill patients.
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It has been postulated that the anti-neoplastic effects of statins could be attributed to their ability to increase HMG-CoAR activity in tumour cells, thus leading to the production of non-sterol bi-products of the mevalonate pathway [ 2].
High-dose statin therapy may be hepatotoxic and may cause peripheral neuropathy, and it has also been postulated that it can promote tumor growth, particularly in women [4] [7].
It has been postulated that 2-hydroxylated estradiol is anticarcinogenic.
It is postulated that previously restricted epitopes are exposed by statins and this may trigger an autoimmune myopathy.
Since all statins require hepatic transporters for their transmembrane flux, it was postulated that polymorphisms in this gene would affect serum levels of all statins and thus the risk for myopathy.
It is postulated that PACAP is involved in nociception.
It is postulated that the underlying mechanism concerns diminished cardiotoxicity.
Many mechanisms have been postulated to explain why statins may influence sepsis [ 5], and it is possible some of these may be of particular benefit in pneumonia [ 6- 8].
Statins have been postulated to have an effect on sepsis outcomes that is mediated by their anti-inflammatory effects [10,11].
Statins have been postulated to have an effect on sepsis outcomes that is mediated by their anti-inflammatory effects [ 10, 11].
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