WARNING: ANECDOTAL "EVIDENCE" FOLLOWS; FAINT OF HEART SHOULD AVERT THEIR
EYES:
After a doc froze the AK off my forehead, he told me to virtually avoid
the sun for the rest of my life. That was a hundred thousand miles of
desert and tropical windsurfing ago, and we do *not* take mid-day
breaks, and my AK hasn't flared up again.

The short answer: There is growing evidence, especially outside the
U.S., that statins cause far more muscle and joint pain and amnesia than
previously thought. Severe and debilitating pain [as I had] was
virtually ubiquitous with statin-treated pro athletes in one study.
After all, statin pts are strongly warned to report muscle pain
*immediately*; my doctor had me in her office, tested me for muscle
damage, and obtained the test results within hours of my initial phone
call. I encounter people fighting statin-induced muscle pain everywhere
I bring it up, especially in medical circles.

Caveat: I haven't yet researched this as extensively as I did ADT SEs,
because that urgent test showed my pain is not life-threatening, as some
statin-induced pain is. It was, however, more *urgent* than ADT, because
of the level (6-8?) and frequency (every time I moved) of pain, so I
quit my statin immediately.

For starters and effect, slam the book "Statin Drugs - Side Effects" by
astronaut physician Duane Graveline (see http://www.spacedoc.net/ ) down
on her desk. I know we can find books touting or pooh-poohing any
hypothesis under the sun, and I don't know where on the scale of gospel
to BS this one stands, but the man has qualifications out the wazoo,
footnotes many pages of specific references, presents convincing
arguments for laymen and physicians, was personally devastated by
statins, and the most brilliant man I've ever known personally was an
astronaut physician who met the same tough standards.

WARNING: LOOOOOOOONG references, with no pony underneath unless you have
 unexplained or statin-blamed muscle or joint pain or transient global
amnesia episodes:

Beyond that, Google. Examples:

Dear Dr. Mirkin: How common is muscle pain from cholesterol-
lowering drugs?
   
    Some patients with high cholesterol levels are afraid to
take statins because off fear of developing side effects such as
muscle pain.  A study from Scripps Mercy Hospital in San Diego
reviews the latest data on side effects of statins  (The American
Journal of Medicine, May 2006).  This review found that statin-
induced muscle damage is more common in Asians, people who
exercise, have had recent surgery, have kidney, liver or
thyroid disease, or have high triglycerides.  The incidence of
muscle pain and damage from statins is extremely low in non-
exercisers, three to ten percent in those who exercise, and very
high in competitive athletes.  Most athletes refuse to take statin
drugs because they train by taking a hard workout that damages
their muscles.  Then they must take easy workouts until the
soreness disappears and muscles heal. When statins prevent
this muscle healing, the athlete must train at reduced intensity for
a much longer period of time.  Brand names of statins include:
Altoprev, Crestor, Lipitor, Mevacor, Pravachol and Zocor.

Statins and muscle pains

From
http://www.blackwell-synergy.com/doi/full/10.1111/j.1365-2125.2003.02044.x
.
Professional athletes suffering from familial hypercholesterolaemia
rarely tolerate statin treatment because of muscular problems
H. Sinzinger & J. O'Grady*
 Aims
Muscular problems are the major group of side-effects during statin
treatment. They are known to occur much more frequently during and after
exercise.
 Methods and results
For the last 8 years we have monitored 22 professional athletes in whom,
because of familial hypercholesterolaemia, treatment with different
statins was attempted. Only six out of the 22 finally tolerated at least
one member of this family of drugs. In three of these six the first
statin prescribed allowed training performance without any limitation.
Changing the drug demonstrated that only two tolerated all the four or
five statins examined (atorvastatin, fluvastatin, lovastatin,
pravastatin, simvastatin). Cerivastatin was not among the statins
prescribed.
 Conclusions
These findings indicate that in top sports performers only about 20%
tolerate statin treatment without side-effects. Clinical decision making
as to lipid lowering therapy thus becomes a critical issue in this small
subgroup of patients.
 Introduction    Go to:    ChooseTop of pageIntroduction
<<MethodsResultsDiscussionReferencesThis article is cited by the
following articles in Blackwell Synergy and CrossRef               
Statins are one of the most widely used drugs worldwide because of their
clinical effectiveness [1]. Although rare, top sports performers
suffering from familial hypercholesterolaemia (FH) may require drug
treatment even at a young age. Muscular symptoms are the major group of
adverse side-effects among statin users, totaling about 5% in
multicentre-controlled studies [2]. The HPS-Study reported muscular
symptoms at a rate of 32.9% in the active treatment group and 33.2% in
the placebo group [3]. The number of more severe side-effects is quite
low, ranging below 0.1%[4, 5]. However, some years ago we found that
muscular side-effects during exercise clearly are related to statin
treatment even in the absence of elevated creatine kinase (CK) [6]. In
another study examining the role of exercise in patients with statin
treatment we realized that in those people performing regular strenuous
exercise side-effects, characterized as ache- and cramp-like symptoms as
well as muscular weakness, may increase, raising the possibility that as
many as 25% may suffer. In recent reviews [7, 8] exercise-induced pain
and the problem of statin use in top athletes is not even mentioned.
Throughout the years we have monitored a number of professional athletes
in whom FH had been diagnosed and at different stages statin treatment
was initiated. In this paper we describe the individual cases and
response to attempts to treat with various members of this family of
compounds.
 Methods    Go to:    ChooseTop of pageIntroductionMethods
<<ResultsDiscussionReferencesThis article is cited by the following
articles in Blackwell Synergy and CrossRef               
Patients were considered as professional athletes when they had attended
an Austrian championship at any age class during the last 2 years or
were playing in the top two leagues of their respective discipline (for
characteristics of athletes see Table 1). They all were suffering from
FH as diagnosed at the receptor level. No other drugs including vitamins
were taken for at least 4 weeks. Testing for anabolic steroids was done
in all athletes to exclude any possible influence. According to a
recommendation of the Austrian Cholesterol Consensus [9] the starting
dose of the respective statin was always the lowest available dose.
Logic for switching patients who tolerated a statin was that they did
not achieve target values. The shortest duration of treatment before
switching was 8 weeks.
Blood samples for CK and liver enzymes (GOT, GPT, γGT) were regularly
drawn at each monitoring interval.
 Results    Go to:    ChooseTop of pageIntroductionMethodsResults
<<DiscussionReferencesThis article is cited by the following articles in
Blackwell Synergy and CrossRef               
Except for cerivastatin all the other statins available were tried. Some
of the athletes refused to try a further compound (Table 2). When
initiating a statin therapy only three (numbers 5, 11, 15) out of 22
athletes (11%) tolerated the chosen drug (Table 2). Another three
patients (numbers 1, 2, 20) tolerated at least one statin, while only
two athletes (numbers 11 and 15) tolerated all the compounds used.
Switching to other compounds we realized that toleration was rare and 16
(78%) athletes did not tolerate any of the compounds tested (Table 2).
Symptoms experienced on the different statins in one and the same
athlete were very similar. The delay in reporting onset of symptoms was
longer during the first drug attempt, possibly because the athletes were
more alert to the possible emergence of muscle problems. After drug
withdrawal, symptoms in most of the patients disappeared within a few
days (< 1 week) and in all of them within 3 weeks. Patients 1 and 2 were
already reported in part in our earlier work describing statin
associated exercise-induced muscle pain without CK-alteration for the
first time [6]. An increase in CK above the value usually found in
professional athletes was not seen. In the present study an increase in
any of the liver enzymes was not observed in any of the athletes.
Testing for anabolic steroids was negative in all of them. Fenofibrate
given finally mainly to those athletes with extremely elevated Lp(a) did
not produce any adverse reaction in the six athletes treated so far.
 Discussion    Go to:    ChooseTop of
pageIntroductionMethodsResultsDiscussion <<ReferencesThis article is
cited by the following articles in Blackwell Synergy and CrossRef               
Thompson et al. first described exercise-induced skeletal muscle injury
with CK-elevation but in the absence of symptoms after lovastatin [10].
Prevalence of muscle pain without exercise may increase in hobby
athletes and even further in professional athletes. Regardless of the
biochemical background statin therapy and top athletics seem to be
almost incompatible. Whether top athletes are more likely to report
side-effects affecting the results remains open. Switching to nonstatin
lipid reduction therapy or (in less severe FH) to postpone treatment
seemed to be the only options available. As biopsy studies [2] and blood
examination [11] revealed an oxidation injury which may be further
aggravated by heavy exercise (the underlying pathogenesis being
unknown), withdrawal of statins until after finishing an athletic career
considering the usually high HDL these patients have may be advisable.
The decision, however, remains a very individual one based only on
experience and risk calculation rather than facts or recommendations
available.
The case report that incidental vitamin E administration improved
statin-induced muscle pains [12] led to the discovery that many of these
patients show increased lipid peroxidation while normally statin therapy
causes a decrease [13]. It has been described that in patients with
muscle problems on all the statins a withdrawal of the drug results in
cessation in muscular symptoms [14] as also seen in the athletes.
In the original description on exercise-induced muscle pain on statins
[6] problems in all the eight patients (six of them performing hobby
sports activities) disappeared after fluvastatin; in our group of top
athletes, however, the prevalence of side-effects on all the compounds
examined seemed to be comparable. The limitation of this observation is
the lack of a control. However, at least six of them tolerated some
statin. Our data are raising a concern on the use of statins in elite
professional athletics. In order to definitely test the hypothesis,
however, there is a strong need for a placebo-controlled trial of
statins in subjects undergoing intensive exercise.
In conclusion, our findings demonstrate that the great majority of
professional athletes with severe FH do not tolerate any of the statins
available.

From http://www.medicinenet.com/script/main/art.asp?articlekey=16431 ,
Myositis (Muscle Inflammation)...Check The Meds!
Medical Author: William C. Shiel Jr., MD, FACP, FACR
I am a rheumatologist - an internal medicine specialist who is trained
to evaluate, diagnose, and treat diseases that involve the muscles and
joints. Because rheumatologists have a keen interest in undiagnosed
conditions, I see a number of patients every week who are seeking a
first diagnosis.
It is commonplace for doctors to refer patients to a rheumatologist for
the evaluation of painful muscles. There are many diseases that are
associated with inflammation of muscles. Furthermore, many conditions
may appear to involve muscles, but may actually be a result of disease
of the tendons, joints, or bones.
By way of illustration, I want to call viewers' attention to a patient
that I just saw in the office this week. I feel that this patient is
very representative of a muscle condition that is under appreciated
nowadays. I also know that patients and doctors should have a heightened
awareness of this condition since it is easily managed when discovered
early. When discovered late, it can lead to serious injury - not only to
the muscles, but also potentially to the kidneys and heart.
Mr. Jones is a 75 year old man who was referred by a cardiologist
because of pains and stiffness in the muscles of his arms, shoulders,
thighs, and buttocks. He has been taking Lipitor (atorvastatin) for six
months to control elevated cholesterol levels in his blood. Mr. Jones
reported muscle aching for the past eight weeks. He was also weak in the
locations of pain. Blood testing for the muscle enzyme, CPK, was mildly
elevated.
Now, here's the point:
Lipitor is a member of a class of cholesterol-lowering drugs called
statins. The statins include lovastatin (brand name: Mevacor),
simvastatin (Zocor), pravastatin (Pravachol), fluvastatin (Lescol),
atorvastatin (Lipitor), and cerivastatin (Baycol) (Baycol was withdrawn
from the market in August, 2001). Statin drugs are known to cause muscle
pains and inflammation around the muscle cells (myositis). It should
also be noted that the risk of muscle injury is greater when a statin is
combined with other drugs that also cause muscle damage by themselves.
For example, when lovastatin (Mevacor) is used alone to lower
cholesterol, muscle damage occurs on the average in one person out of
about every 500. However, if lovastatin (Mevacor) is used in combination
with other drugs such as niacin, gemfibrozil (Lopid) or fenofibrate
(Tricor) to further reduce cholesterol levels, the risk of muscle injury
skyrockets to one person out of every 20 to 100 who receive the
combination. The risk of muscle damage is thus multiplied 5 to 25-fold
by using a combination of a statin and another cholesterol-lowering drug
rather than by just using statin alone.
In fact, the manufacturers of statins recommend that any patient taking
a statin "should be advised to report promptly any unexplained muscle
pain, tenderness or weakness.... When a muscle disease is suggested, the
doctor stops the statin drug."
You see, statin drugs cause three types of muscle conditions. First,
they can cause muscle aching. This condition generally reverses itself
within weeks of discontinuing the drugs. Second, they can cause muscle
pains and mild muscle inflammation that may also be accompanied by minor
weakness. Blood testing for the muscle enzyme, CPK, is mildly elevated.
This condition also generally reverses, but it may take several months
to resolve. Third, statins can cause severe muscle inflammation and
damage so that not only are the muscles painful all over the body, they
also become severely weakened. Heart muscle can even (rarely) become
affected. Blood testing for the muscle enzyme, CPK, is markedly
elevated. When the muscles are severely damaged, the muscle cells
release proteins into the blood that collect in and can damage the
kidneys. This can lead to kidney failure and require dialysis.
In each of the above three forms of muscle conditions that result from
statin drugs, the outcome is always much better when the condition is
detected early.
My patient is expected to do well. I have discontinued his Lipitor and
his muscle pain and stiffness will resolve in the upcoming weeks. He
will follow-up with me in a month for a progress report.
There are many other medications (aside from statins) and diseases that
can cause muscle aching. Of all causes, however, statin drugs are what I
see as the most common culprits. If you or someone you know has muscle
pains, check the medications being taken first!
Finally, please understand that the statin drugs have been shown to be
the most effective (and widely prescribed) medications to optimally
lower cholesterol and prevent heart attacks and stroke. This perspective
article is intended to highlight the fact that even the best drugs
require monitoring and can have side effects.

For additional Doctor's Views written by Dr. Shiel, visit the Doctor's
Views Library.

From http://www.gpnotebook.co.uk/cache/x20020702113831768120.htm ,
myalgia and myositis associated with statin treatment

The topic of side effects of statin therapy has become more prominent
since the precautionary withdrawal of cerivastatin following reports of
death and rhabdomyolysis with cerivastatin, particularly when given in
simultaneous combination therapy with gemfibrozil. Also many patients
complain of myalgia when on treatment with statins with this side effect
having an incidence of up to 5%.
Myositits
mild myositis is associated with painful muscles and CK elevation. Some
suggest withdrawal of statin therapy is indicated in patients whose CK
rises 10-fold to levels about 2,000 IU/L (1) whilst others suggest that
'patients experiencing muscle pain, weakness or cramps whilst should
have their CK level measured. If this is significantly elevated (>5x
upper limit of normal) or if myopathy is suspected, treatment should be
stopped (2)'
rhabdomyolysis (characterised by plasma CK > 20,000 IU/L, myoglobinuria
and extreme muscular pain) occurs in about 1 in 250,000 patients and is
commoner in females, the elderly, hypothyroidism and with concomitant
therapy with cytochrome P450 3A4 metabolised drugs e.g. cyclosporin,
erythromycin, and fibrates (particularly gemfibrozil)
Myalgia
far commoner than myositis and is not accompanied by any rise in CK levels
the mechanism is obscure but it has been noted that by inhibiting
hydroxy-methyl-glutaryl (HMG)-CoA reductase, statins also reduce
isoprenoid intermediates of cholesterol synthesis, including those that
are utilised in the manufacture of ubiquinone which is essential for
electron transport in mitochondria
The Committee on Safety of medicines recommends various measures to
reduce the risk of myopathy with HMG CoA reductase inhibitors (1):
dosage instructions should be adhered to strictly (see product
information). The maximum recommended dosage should not be exceeded and
any adjustment of dosage should be made at intervals of 4 weeks or more
careful consideration should be given to statin use in patients who are
at an increased risk of developing myopathy (see below):
patients with underlying muscle disorders, renal impairment,
hypothyroidism or alcohol abuse
concomitant use of other lipid lowering agents i.e. gemfibrozil, other
fibrates or nicotinic acid
concomitant use of cytochrome P450 3A4 inhibitors including macrolide
antibiotics, cyclosporin, azole antifungals (e.g. ketoconazole and
itraconazole) and protease inhibitors
in these patients baseline measurement and monitoring of CK should be
considered. If CK is >5 times the upper limit of normal (ULN) at
baseline then treatment with a statin should not be commenced
patients are made aware of the risk of myopathy, including
rhabdomyolysis, and asked to report promptly any muscle pain, weakness
or tenderness, particularly if accompanied by fever, malaise or dark urine
if a patient experiences muscle pain weakness or cramps whilst on
treatment then this is an incidation for CK measurement. If CK is
significantly elevated (>5x ULN) or if myopathy is suspected then
treatment should be stopped, while the patient is monitored for muscular
symptoms and cardiovascular risk
if the symptoms resolve and CK levels return to normal, re-introduction
of the statin or introduction of an alternative statin may be
considered. This should initially be at the lowest dose and with close
monitoring
Reference:
The British Journal of Cardiology (2002), 9 (4), 193-4.
Current Problems in Pharmacovigilance (2002), 28, 8-9.

From http://medrants.com/index.php/archives/564#comment-436 :
Coenzyme Q and Statins - Plausible Mechanism for Statin-Induced Myopathy
and Neuropathy.
Theory was clear for over a decade How Statins Cause
Myopathy & Neuropathy
Statins inhibit the enzyme HMG-CoA Reductase, many
steps before the final formation of Cholesterol in the mevalonate pathway.
This same pathway is used to synthesize the essential biochemical
Coenzyme Q10 (aka Coenzyme Q 10, CoQ10, Ubiquinone).
Thus a major side effect predicted for statins is to reduce Coenzyme
Q10, with consequent danger to Heart and Skeletal Muscle. This was
trivially obvious for theoretical reasons before statins came to be used
medically, to medical research scientists or pre-medical students. The
effect would be most pronounced in cells that have high metabolic rates,
for instance muscle cells and nerve cells.
Reduction in Coenzyme Q10 may cause Myopathy, Neuropathy,
Rhabdomyolysis, Exercise Intolerance, and recurrent Myoglobinuria, based
on decades of research:
Scarlato G, Comi GP.
Metabolic and drug-induced muscle disorders.
Curr
Opin Neurol. 2002 Oct;15(5):533-8
Farley TM, Scholler J, Folkers K.
Response of genetically dystrophic
mice to therapy with hexahydrocoenzyme Q4.
Biochem Biophys Res Commun.
1966 Aug 12;24(3):299-303.
These aspects of Statin action were also noted in patents that issued in
1990, Patent numbers 4,933,165 (May 29, 1990) and 4,929,437 (June 12,
1990) both to Merck.

From a footnote in http://www.ptjournal.org/cgi/content/full/85/5/459  :
“We conclude that HMG-CoA reductase inhibitors exacerbate
exercise-induced skeletal muscle injury.”

Dr. Mercola has a BIG statin file at
http://www.mercola.com/2004/jul/21/statin_drugs.htm.

From http://www.thecureforheartdisease.com/owen/coq10.htm  :
Very brief entry from large body of literature research: “Ubiquinone
(CoQ10) is a popular heart medication.  Until 2001, it was only
available by prescription in Japan. The public is hardly aware that an
increasingly popular class of cardiovascular drugs called statins
(HMG-CoA reductase inhibitors) interfere with the body’s synthesis of
CoQ10. [*] Top selling statin drugs, such as LipitorÒ and ZocorÒ, earn
their makers in excess $20 billion per year. These drugs lower the
endogenous production of cholesterol and are often touted as “life
saving” by cardiologists and the Media.
Are the statin drugs really good for us, or are cardiologists mistaken?
 How can drugs that lower the body’s production of CoQ10 benefit heart
patients?  Are the health benefits attributed to CoQ10 supplementation
hype or is it that there is something fundamentally wrong with the
thinking and science being used by those who market statin drugs?

Adverse Side Effects of Statin Cholesterol Lowering Drugs:
The following headlines from BOLENREPORT.COM reveal the many
little-known side effects of the 'artificial' Statin drugs, some of
which are required to be reported in Canadian statin drug ads, but not
the U. S. versions.
Statin Cholesterol Lowering Drugs:

1.   Deplete the ubiquinone (vitamin-like) Coenzyme Q10 causing
cardiomyopthy and heart failure
2.      Change, weaken, damage or destroy muscle (depending on dose and
concomitant use of other drugs)
3.      Do not slow atherosclerosis
4.      Induce sudden total memory loss
5.      Increase eye cataract risk
6.      Suppress immune function
7.      Are linked to cancer
8.      Have been linked for 10-years with Rhabdomyolysis and Myoglobinuria
9.      Have been linked with elevated transaminase (indicator of liver
and kidney damage)
10.  Are linked to nerve damage
11.  Induce muscle pain
12.  Do not extend life
13.  Increase serum Lp(a) concentrations** (Increasing odds of heart
attack or stroke up to 70% SOURCE: CIRCULATION)
14.  Reduce left ventricular function,
15.  Elevate the lactate to pyruvate ratio
16.  Enhance LDL cholesterol oxidation
17.  Would be expected to interfere with any function (e.g. sex hormone
production, hair growth, sleep, or proper brain and nerve function) that
depends on cholesterol or CoQ10
18.  Are prescribed to 13 million (in the U.S., 25 million worldwide)
creating a $20b market
19.  Are MORTAL (else will cause 65,000 predicted myopathies Source:
Merck Patent)
NOTE: Biopsy only reliable test for statin induced myopathy
Conclusion
Apparently a 20 billion dollar market has blinded some scientists.
Merck and the other pharmaceutical companies have known about the CoQ10
biosynthesis “issue” for more than a decade.  (Few medical doctors in
the U.S. are aware of this problem.) There exists no theory that
justifies the use of statin drugs. This author has seen no data or
evidence that demonstrates any real health benefit for statin drug use
in most people that overcomes the proven detriment of hampering the
production of CoQ10.  ”

From
http://www.cbc.ca/story/science/national/2005/03/02/Crestor050302.html  :
Roles of Exercise and Pharmacokinetics in Cerivastatin-Induced Skeletal
Muscle Toxicity
Jennifer L. Seachrist*,1, Cho-Ming Loi, Mark G. Evans*, Kay A. Criswell*
and Charles E. Rothwell*
* Safety Sciences Department, and  Pharmacokinetics, Dynamics and
Metabolism Department, Pfizer Global Research & Development, 2800
Plymouth Road, Ann Arbor, Michigan 48105
Received July 21, 2005; accepted August 24, 2005
Three-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors
are associated with adverse skeletal muscle effects, but the underlying
mechanisms remain unclear. To determine whether toxicity involves the
level of drug exposure in muscle tissue and to test the effect of
exercise on cerivastatin (CVA)-induced skeletal muscle damage, female
rats were administered vehicle or CVA at 0.1, 0.5, and 1.0 mg/kg/day by
gavage for two weeks and exercised or not on treadmills for 20 min/day.
Clinical chemistry and plasma and tissue pharmacokinetics were
evaluated; light and transmission electron microscopy (TEM) of Type I
and Type II fiber-predominant skeletal muscles were performed. Serum
levels of AST, ALT, CK, and plasma lactic acid were significantly
elevated dose-dependently. CVA treatment decreased psoas and quadriceps
weights. At 1 mg/kg all muscles except soleus demonstrated degeneration.
Exercise-exacerbated severity of CVA-induced degeneration was evident in
all muscles sampled except soleus and quadriceps. Early mitochondrial
involvement in toxicity is suggested by the numerous membranous whorls
and degenerate mitochondria observed in muscles at 0.5 mg/kg. No
significant differences in CVA concentrations between either EDL and
soleus or plasma and muscle were found. We found that CVA had no effect
on cleaved caspase 3. In summary, we found that treadmill exercise
exacerbated the incidence and severity of CVA-induced damage in Type II
fiber-predominant muscles. Tissue exposure is likely not the key factor
mediating CVA-induced skeletal muscle toxicity.

From
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=Abstra
ctPlus&list_uids=14728975&query_hl=2&itool=pubmed_docsum

Evaluation of ubiquinone concentration and mitochondrial function
relative to cerivastatin-induced skeletal myopathy in rats.
Schaefer WH, Lawrence JW, Loughlin AF, Stoffregen DA, Mixson LA, Dean
DC, Raab CE, Yu NX, Lankas GR, Frederick CB.
SNIP The results of this study suggest that neither mitochondrial
injury, nor a decrease in muscle ubiquinone levels, is the primary cause
of skeletal myopathy in cerivastatin-dosed rats.

But the next one seems to contradict that:
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=Abstra
ctPlus&list_uids=15902968&query_hl=2&itool=pubmed_docsum

Statin-induced muscle necrosis in the rat: distribution, development,
and fibre selectivity.
Westwood FR, Bigley A, Randall K, Marsden AM, Scott RC.
Safety Assessment, AstraZeneca, Macclesfield, Cheshire SK10 4TG, United
Kingdom. russell.westwood@astrazeneca.com
Simvastatin and cerivastatin have been used to investigate the
development of statin-induced muscle necrosis in the rat. This was
similar for both statins and was treatment-duration dependent SNIP
These findings suggest an important early involvement of mitochondria in
selective glycolytic muscle fibre necrosis following inhibition of the
enzyme HMG-CoA reductase.

I.P.