Statins Cause Muscle Damage Without Pain

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Statins Cause Muscle Damage Without Pain

http://www.spacedoc.net/statins_muscle_damage_no_pain.html

 

In previous articles I have cited possible mechanisms of statin associated

muscle damage from cell wall breakdown to fundamental changes in essential

transcriptases.

 

Now we have we have a mechanism of statin action just reported that points

directly at cholesterol lowering per se within the muscle fiber as the offending

action and the vital changes of muscle structure occur with or without muscle

symptoms and occur in most statin users!

 

In the Journal of Pathology 210: 94-102, 2006, Draeger A and others of the

University of Bern, Switzerland report: Statin therapy induces ultrastructural

damage in skeletal muscle in patients without myalgia.

 

Muscle pain and weakness are frequent complaints in patients treated with

statins drugs, also known as HMG CoA reductase inhibitors. Many patients with

myalgia have Creatine Kinase (CK) levels that are either normal or only

marginally elevated and no obvious structural defects have been reported with

myalgia

only.

 

 

Draeger’s group did skeletal muscle biopsies from statin treated and

non-statin treated patients and examined them using electron microscopy and

biochemical approaches. They reported clear evidence of skeletal muscle damage

in statin

treated patients despite their being asymptomatic. Although the degree of

overall damage was minimal, it was the characteristic pattern of damage,

including rupture of critical structures that caught the attention of the

investigators.

 

These findings support the hypothesis that statin induced cholesterol

lowering per se contributes to myocyte damage and suggests further that it is

the

specific lipid/protein organs of the skeletal muscle itself that renders it

particularly vulnerable.

 

 

Was it only a decade ago that that the drug companies were reporting the

possibility of up to 2% incidence of muscle damage when statins were used? Then

along came our rhabdomyolysis deaths and reported real life myopathy levels much

closer to 40% than to two, depending upon which team does the reporting. And

now it seems that muscle effects might be universal! Of course this depends

upon the sensitivity of the tests being used. Does this remind you of the 100%

incidence of cognitive damage in statin users, reported by Muldoon (if

sufficiently sensitive testing is done) versus the negligible to no cognitive

damage

reported by other studies, even those using 80mg doses, based upon more casual

observation? None are so blind as those who will not see.

 

Of course the problem here is one of awareness. With respect to cognitive

function, we are not precise creatures. Rarely can we remember what we had for

breakfast two days ago, your boss’s wife’s name or when you last registered

your domain name. Because of this natural tendency for forgetfulness we accept

imprecision and a 5-10 % cognitive loss might be barely noticeable in some.

Similarly only our athletes might notice a slight deterioration of skeletal

muscle

function, whereas most of us explain it away as old age or simple

deconditioning.

 

The problem we face is in bringing this new information to the attention of

the prescribing physicians. As this study demonstrates some of statin damage is

occurring in the absence of symptoms. Does this mean they are not important.

I think not!

 

Duane Graveline MD MPH