http://www.termedia.pl/Molecular-mechanisms-of-statin-intolerance,19,27579,0,1.html
Anna Gluba-Brzozka, Beata Franczyk, Peter P. Toth, Jacek Rysz, Maciej Banach
Arch Med Sci 2016; 12, 3: 645–658
DOI (digital object identifier): 10.5114/aoms.2016.59938
Statins reduce cardiovascular morbidity and mortality in primary and
secondary prevention. Despite their efficacy, many persons are unable to
tolerate statins due to adverse events such as hepatotoxicity and
myalgia/myopathy. In the case of most patients, it seems that
mild-to-moderate abnormalities in liver and muscle enzymes are not
serious adverse effects and do not outweigh the benefits of coronary
heart disease risk reduction. The risk for mortality or permanent organ
damage ascribed to statin use is very small and limited to cases of
myopathy and rhabdomyolysis. Statin-induced muscle-related adverse
events comprise a highly heterogeneous clinical disorder with numerous,
complex etiologies and a variety of genetic backgrounds. Every patient
who presents with statin-related side effects cannot undergo the type of
exhaustive molecular characterization that would include all of these
mechanisms. Frequently the only solution is to either discontinue statin
therapy/reduce the dose or attempt intermittent dosing strategies at a
low dose.
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