LOGIC March 2018 Vol 17 Vol 1 - Page 22

Comorbidities including diabetes mellitus, hypothyroidism, impaired liver or kidney function, acute infection, severe trauma, HIV and Vitamin D deficiency increase risk for SAMS. Major surgery is also a risk factor and statins may be stopped prior to this (Best Tests Team 2014; Pirillo 2015; Stroes 2015). Pathophysiology of SAMS The mechanism by which statins cause myopathy is not fully understood (Best Tests 2014; Pirillo 2015; Stroes 2015) however it is thought that more than one mechanism may be involved (Best Tests Team 2014; Stroes 2015). The most likely explanation based on current studies is that statins adversely affect the function of mitochondria, reduce cellular energy production and change the way muscle protein is broken down, all of which on their own may cause myopathy (Stroes 2015). Statins do this by reducing levels of cholesterol which is involved in maintaining cell membrane function. Lower cholesterol levels affect cell membrane ion channels and therefore excitability of muscle cells which can lead to myopathy However, myopathy is not observed when March 2018 L.O.G.I.C another enzyme involved in the synthesis of cholesterol is inhibited (Best Tests Team 2014). taking statins and therefore it is not currently recommended (Best Tests Team 2014; Pirillo 2015; Skarlovnik 2014). The inhibition of HMGCoA reductase by statins also reduces the biosynthesis of cholesterol precursors and downstream metabolites such as ubiquinone (coenzyme Q10), all of which may have a role to play in maintaining muscle cells. Reduced levels of them therefore may be a factor in the development of myopathy (Best Tests Team 2014). Statins may also affect calcium movement in muscle cells based on animal studies which have shown this reduces muscle strength. Statins may cause apoptosis (programmed cell death) in skeletal muscle which could lead to SAMS. More studies and evidence is required to fully elucidate the mechanism, however (Best Tests Team 2014). Coenzyme Q10 is a downstream metabolite from a cholesterol precursor called mevalonate. It is involved with electron transport in the mitochondria of cells and helps to prevent oxidative stress during cellular aerobic metabolism. Lower serum and muscle tissue levels of coenzyme Q10 have been seen in people taking statins (Skarlovnik 2014). It has been suggested that this may affect cellular respiration and aerobic metabolism in muscles which could cause myopathy (Best Tests Team 2014; Pirillo 2015; Skarlovnik 2014). Evidence is not clear about the usefulness of supplementation with Coenzyme Q10 to prevent muscle symptoms in people Management of SAMS a. Check for Causes Non-Statin If a patient has myalgia, then any risk factors for SAMS should be determined and non-statin causes of the pain should be ruled out e.g. hypothyroidism, Vitamin D deficiency, hypercalcaemia, fibromyalgia, vigorous exercise, infection or polymyalgia rheumatica. If a person has had muscle symptoms prior to starting their statin, then the cause may not be the statin. Patient adherence and history should be checked to see if they have increased their dose of statin or if they are on any drugs that may interact with the statin to increase statin exposure and 20