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Statine

Vreau s v vorbesc despre o problem de sntate foarte serio n America. Pentru


milioane de oameni, medicii prescriu o clas de medicamente numite statine (Lipantil,
Crestor, etc.). Se presupune c acestea reduc colesterolul i, in consecin, previn
atacurile de cord. !ar eu v spun ceva ce avei dreptul s tii despre acest tip de
medicamente. "nt#i de toate$ Scad ele colesterolul% &spunsul este da, l scad. !ar iat o
ntrebare mai important$ previn ele infarctul miocardic% &spunsul este nu, nu'l previn.
Sunt ele si(ure% )u, nu sunt. !eci dac iei statine, iei un medicament pentru a'ti preveni
un eventul infarct i care, de fapt, mu'l previne. *ai mult, iei un medicament care nu este
si(ur, adic i poate face ru. Are asta vreo lo(ic% !e fapt medicamentul tu pe ba+ de
statine te pune ntr'un pericol foarte mare, pre(tind terenul pentru pentru boli de inim i
alte afeciuni (rave, inclu+#nd o boal de rinic,i letal.
Avnd n vedere c statinele sunt complet nefolositoare i periculoase, de ce sunt
prescrise% -i bine, cei mai muli medici cred c un nivel ridicat de colesterol este
principala cau+ a bolilor cardiace i vd statinele sunt complet nefolositoare i
periculoase, dece sunt prescrise% -i bine, cei mai muli medici cred c un nivel ridicat de
colesterol este principala cau+ a bolilor cardiace i vd statinele ca pe nite medicamente
salvatoare de viei. Aceast lo(ic este fundamental (reit. !ac colesterolul contea+
aa de mult n apariia bolilor cardiace, cum v e.plicai c cei mai muli oameni care fac
infarct au un nivel al colesterolului perfect normal% !e fapt este e.act invers$ riscul de
infarct crete la cei care iau statine. Prin urmare, statinele cau+ea+ boli de inim.
/n doctor care pre+int n mod cura0os despre pericolul statinelor este cardiolo(ul
!r.Peter Lan(s0oen (1,2), care ntr'o petiie adresat 3!A (a(enia S/A responsabil cu
introducerea pe pia a medicamentelor) a scris, cite+, 4statinele pre0udicia+ (rav
sntatea oamenilor i pe muli i omoar5. 6oi pacianii care iau statine devin deficieni
n coen+ima 718 ntr'un interval de 9'12 luni (:). Persoanele tinere i sntoase pot tolera
statinele c#iva ani nainte de a ncepe neca+urile, ca oboseala, slbiciunile, dureri
musculare i, n final, afecuni cardiace.
Statinele sunt prescrise cu o uurin de nedescris, n concentraii din ce n ce mai mari,
nu numai oamenilor n v#rst, ci i oamenilor ce au colesterolul normal, numai n ideea
de a preveni o boal cardiac, dei nu au aceat calitate. Adevarul este c bolile de inim
i infarcturile sunt din ce n ce mai numeroase ca re+ultat al administrrii de statine. A
aprut c,iar o boal nou denumit, cardiomiopatie statinic. Suntem n pre+ent
martoriiuneia dintre cele mai mari tra(edii ale timpului nostru. )iciodat n istorie,
tiima medical nu a mai creat, cu bun tiin, un medicament care s amenine viaa a
milioane de oameni, de altfel sntoi, aa cum se nt#mpl acum cu statinele. Statinele
afectea+ esutul muscular, provoc#nd dureri permanente i slbiciune. /n studiu din
2818 publicat n reista Current Atherosclerosis Reports afirm c 1;< dintre consumatori
de statine acu+ probleme musculare. *ai mult, esutul muscular afectat produce o
protein numit mio(lobin, care se descompune ntr'o substan c,imic ce perturb
activitatea rinic,ilor i cau+ea+ o boal fatal numit, rabdomioli+. Alte complicaii
includ, tulburri de coa(ulare i stop cardiac.
Statinele distru( ficatul, d#nd dureri abdominale, urini nc,ise la culoare, n(lbenirea
pielii i a scleroticii, ca semne ale afectrii serioase ale acestui or(an.
Statinele perturb sistemul nervos. )europatia periferic cau+at de statine este tradus
prin simptome precum, furnicturi i tresriri necontrolate ale m#inilor i picioarelor, care
pot escalada p#n la sen+aii dureroase de aresur i parali+ia membrelor. C,iar i atunci
cnd sunt luate n do+e relativ mici, statinele cau+ea+ o reducere a funciilor motorii cu
=8< fa de cei ce nu iau statine.
Statinele acionea+ nefast asupra creierului cau+#nd pierderi de memorie, confu+ie
(simtome similare bolii Al+,eimer), sc,imbri brute de dispo+iie, depresie, ostilitate
a(resivitate.
!iabetul este o alt complicaie. /n studiu al cercettorilor de la >arvard publicat in
ianuarie 2812 a conclu+ionat c, folosirea pe termen lun( a statinelor, crete
probabilitatea de+voltrii unui diabet +a,arat de tip ?? cu cca ;8<. /n studiu din 2811 din
Journal of American Medical Association a stabilit c riscul de a face diabet crete cu
12< la captul a ; ani de administrare de statine.
*ulte alte boli pot fi asociate cu statinele$ cancer, scelro+ lateral amiotrofic, boala Lou
@e,ri( (afectarea mduvei spinrii i a bulbului ra,idian cu parali+ie muscular
pro(resiv. !e fapt 3!A a anunat recent c sunt necesare averti+ri priviind efectele
secundare ale meicaiei cu statine (pierderi de memorie, creterea (licemiei).
Av#nd n vedere c statinele nu au nicio eficien n prvenirea atacurlor de cord, nu aduc
niciun beneficiu or(anismului i, mai mult, date fiind aceste stricciuni pe care le
provoac se impune o intrebare$ ce rost mai fie prescrise de medici %
1. Advice on statin risA .3!A 0anuarB 281=
2. Littarru @P, Lan(s0oen P. Coen+Bme 718 and statins$ bioc,emical and clinical
implications. *itoc,ondrion. 288C DunEC Suppl$S19F'C=. -pub 288C *ar 2C
:. *ortensen SA, Let, A, A(ner -, &o,de *. !ose'related decrease of serum coen+Bme
718 durin( treatment Git, >*@'CoA reductase in,ibitors. *ol Aspects *ed 1HHC, 1F
Suppl$S 1:C'1==.
=. Collins &, Armita(e D, Paris, S, Slei(, P, Peto & . *&CIJ>3 >eart Protection StudB of
c,olesterol'loGerin( Git, simvastatin in ;H9: people Git, diabetes$ a randomised
placebo'controlled trial. Lancet. 288: Dun 1=E:91(H:C=)$288;'19.
-pub 288; Dul ;.
;. 6onelli *, ?sles C, Craven 6,et al. -ffect of pravastatin on rate of AidneB function loss
in people Git, or at risA for coronarB disease Circulation. 12E112(2)$1C1'F, 288;.
9. &avi V, S,a, *!, Allison J, @oldfine *!. Statins and risA of neG'onset diabetes
mellitus.Circulation, 129$e2F2'2F=, 2812
C. Palmer SC, Craig JC, Navaneethan SD, Tonelli M, Pellegrini F, Strippoli GF. Jenefits and
,arms of statin t,erapB for persons Git, c,ronic AidneB disease$ a sBstematic revieG and
meta'analBsis. Ann ?ntern *ed1;C(=)$29:'C;. doi$ 18.C:29I888:'=F1H'1;C'='28128F218'
8888C, 2812.
8. *iBaAe K, S,ou+u A, )is,iAaGa *B Konemoto 6, S,imi+u >, Lmoto S, >aBaAaGa 6, ?nada *. -ffect
of treatment Git, : ',Bdro.B': 'met,Bl(lutarBl coen+Bme A reductase in,ibitors on serum coen+Bme 7lo in
diabetic patients. Ar+neimittelforsc,un( 1HHH AprE=H(=)$:2='H.
Statins are dru(s of AnoGn and undisputed efficacB in t,e treatment of
,Bperc,olesterolemia, usuallB Gell tolerated bB most patients. ?n some cases treatment
Git, statins produces sAeletal muscle complaints, andIor mild serum CM elevationE t,e
incidence of r,abdomBolBsis is verB loG. As a result of t,e common biosBnt,etic pat,GaB
Coen+Bme 7 (ubiNuinone) and dolic,ol levels are also affected, to a certain de(ree, bB
t,e treatment Git, t,ese >*@'CoA reductase in,ibitors. Plasma levels of Co718 are
loGered in t,e course of statin treatment. 6,is could be related to t,e fact t,at statins
loGer plasma L!L levels, and Co718 is mainlB transported bB L!L, but a decrease is
also found in platelets and in lBmp,ocBtes of statin treated patients, t,erefore it could
trulB depend on in,ibition of Co718 sBnt,esis. 6,ere are also some indications t,at statin
treatment affects muscle ubiNuinone levels, alt,ou(, it is not Bet clear to G,ic, e.tent
t,is depends on some effect on mitoc,ondrial bio(enesis. Some papers indicate t,at
Co718 depletion durin( statin t,erapB mi(,t be associated Git, subclinical
cardiomBopat,B and t,is situation is reversed upon Co718 treatment. Oe can reasonablB
,Bpot,esi+e t,at in some conditions G,ere ot,er Co718 depletin( situations e.ist
treatment Git, statins maB seriouslB impair plasma and possible tissue levels of
coen+Bme 718. O,ile Gaitin( for a lar(e scale clinical trial G,ere patients treated Git,
statins are also monitored for t,eir Co718 status, Git, a (roup also bein( (iven Co718,
p,Bsicians s,ould be aGare of t,is dru('nutrient interaction and be vi(ilant to t,e
possibilitB t,at statin dru(s maB, in some cases, impair sAeletal muscle and mBocardial
bioener(etics.
?ndividuals Git, diabetes are at increased risA of cardiovascular morbiditB and mortalitB,
alt,ou(, tBpicallB t,eir plasma concentrations of L!L c,olesterol are similar to t,ose in
t,e (eneral population. Previous evidence about t,e effects of loGerin( c,olesterol in
people Git, diabetes ,as been limited, and most diabetic patients do not currentlB receive
c,olesterol'loGerin( t,erapB despite t,eir increased risA.
METHODS:
;H9: /M adults (a(ed =8'F8 Bears) AnoGn to ,ave diabetes, and an additional 1=;C: Git,
occlusive arterial disease (but no dia(nosed diabetes), Gere randomlB allocated to receive
=8 m( simvastatin dailB or matc,in( placebo. Prespecified analBses in t,ese prior disease
subcate(ories, and ot,er relevant subcate(ories, Gere of first ma0or coronarB event (ie,
non'fatal mBocardial infarction or coronarB deat,) and of first ma0or vascular event (ie,
ma0or coronarB event, stroAe or revascularisation). AnalBses Gere also conducted of
subseNuent vascular events durin( t,e sc,eduled treatment period. Comparisons are of all
simvastatin'allocated versus all placebo'allocated participants (ie, intention to treat),
G,ic, Bielded an avera(e difference in L!L c,olesterol of 1.8 mmolIL (:H m(IdL)
durin( t,e ;'Bear treatment period.
FINDINGS:
Jot, amon( t,e participants G,o presented Git, diabetes and amon( t,ose G,o did not,
t,ere Gere ,i(,lB si(nificant reductions of about a Nuarter in t,e first event rate for ma0or
coronarB events, for stroAes, and for revascularisations. 3or t,e first occurrence of anB of
t,ese ma0or vascular events amon( participants Git, diabetes, t,ere Gas a definite 22<
(H;< C? 1:':8) reduction in t,e event rate (981 P28.2<Q simvastatin'allocated vs C=F
P2;.1<Q placebo'allocated, pR8.8881), G,ic, Gas similar to t,at amon( t,e ot,er ,i(,'
risA individuals studied. 6,ere Gere also ,i(,lB si(nificant reductions of ::< (H;< C?
1C'=9, pS8.888:) amon( t,e 2H12 diabetic participants G,o did not ,ave anB dia(nosed
occlusive arterial disease at entrB, and of 2C< (H;< C? 1:'=8, pS8.888C) amon( t,e 2=29
diabetic participants G,ose pretreatment L!L c,olesterol concentration Gas beloG :.8
mmolIL (119 m(IdL). 6,e proportional reduction in risA Gas also about a Nuarter amon(
various ot,er subcate(ories of diabetic patient studied, includin($ t,ose Git, different
duration, tBpe, or control of diabetesE t,ose a(ed over 9; Bears at entrB or Git,
,BpertensionE and t,ose Git, total c,olesterol beloG ;.8 mmolIL (1H: m(IdL). ?n
addition, amon( participants G,o ,ad a first ma0or vascular event folloGin(
randomisation, allocation to simvastatin reduced t,e rate of subseNuent events durin( t,e
sc,eduled treatment period.
INTERPRETATION:
6,e present studB provides direct evidence t,at c,olesterol'loGerin( t,erapB is beneficial
for people Git, diabetes even if t,eB do not alreadB ,ave manifest coronarB disease or
,i(, c,olesterol concentrations. Allocation to =8 m( simvastatin dailB reduced t,e rate of
first ma0or vascular events bB about a Nuarter in a Gide ran(e of diabetic patients studied.
After maAin( alloGance for non'compliance, actual use of t,is statin re(imen Gould
probablB reduce t,ese rates bB about a t,ird. 3or e.ample, amon( t,e tBpe of diabetic
patient studied Git,out occlusive arterial disease, ; Bears of treatment Gould be e.pected
to prevent about =; people per 1888 from ,avin( at least one ma0or vascular event (and,
amon( t,ese =; people, to prevent about C8 first or subseNuent events durin( t,is
treatment period). Statin t,erapB s,ould noG be considered routinelB for all diabetic
patients at sufficientlB ,i(, risA of ma0or vascular events, irrespective of t,eir initial
c,olesterol concentrations.
SSSSSSSSSSSSSSSSSSSSSSSSSSSSSSSSSSSSSSSSSSSSSSSSSSSSSSSSSSSSSSS
Limited data su((est t,at >*@'CoA reductase in,ibitors (statins) reduce rates of AidneB
function loss. Oe performed t,is analBsis to determine G,et,er pravastatin reduced t,e
rate of AidneB function loss over appro.imatelB ; Bears in people Git, or at ,i(, risA for
coronarB disease.
METHODS AND RESULTS:
6,is Gas a post ,oc sub(roup analBsis of data from : randomi+ed double'blind controlled
trials comparin( pravastatin =8 m(Id and placebo in sub0ects Git, a previous acute
coronarB sBndrome or G,o Gere at ,i(, cardiovascular risA. 6,e primarB outcome Gas
t,e rate of c,an(e in estimated (lomerular filtration rate (@3&E in mLImin per 1.C:
m2IB). 6,e *odified !iet and &enal !isease StudB (*!&!) and CocAcroft'@ault
eNuations Gere used to estimate @3&. Oe studied 1F,;9H participants, :=82 (1F.:<) of
G,om ,ad moderate c,ronic AidneB disease as defined bB an estimated @3& of :8 to ;H.H
mLImin per 1.C: m2 bodB surface area. ?n sub0ects Git, moderate c,ronic AidneB disease
at baseline, pravastatin reduced t,e ad0usted rate of AidneB function loss bB
appro.imatelB :=<, alt,ou(, t,e absolute reduction in t,e rate of loss Gas small (8.22
mLImin per 1.C: m2IB bB *!&!'@3&E H;< C?, 8.8C to 8.:C). Pravastatin did not reduce
t,e freNuencB of T or S2;< decreases in AidneB function in t,is (roup G,en *!&!'
@3& Gas used to estimate @3& (relative risA P&&Q, 8.F=E H;< C?, 8.99 to 1.89). O,en all
1F,;9H sub0ects Gere considered, pravastatin reduced t,e ad0usted rate of AidneB function
loss bB F< (8.8F mLImin per 1.C: m2IB bB *!&!'@3&E H;< C?, 8.81 to 8.1;) and t,e
risA of acute renal failure (&&, 8.98E H;< C?, 8.=1 to 8.F9) but did not si(nificantlB
reduce t,e freNuencB of a T or S2;< decline in AidneB function bB *!&!'@3& (&&,
8.H=E H;< C?, 8.FF to 1.81).
CONCLUSIONS:
Pravastatin modestlB reduced t,e rate of AidneB function loss in people Git, or at risA for
cardiovascular disease. >oGever, t,e primarB indication for t,e use of statins in people
Git, or at risA for coronarB events remains t,e reduction in mortalitB t,at results from
t,eir use.
.
Statins ,ave uncertain benefits in persons Git, c,ronic AidneB disease (CM!) because
individual trials maB ,ave insufficient poGer to determine G,et,er treatment effects
differ Git, severitB of CM!.
PURPOSE:
6o summari+e t,e benefits and ,arms of statin t,erapB for adults Git, CM! and e.amine
G,et,er effects of statins varB bB sta(e of AidneB disease.
DATA SOURCES:
Coc,rane and -*JAS- databases (inception to 3ebruarB 2812).
STUDY SELECTION:
&andomi+ed trials comparin( t,e effects of statins Git, placebo, no treatment, or anot,er
statin on mortalitB and cardiovascular outcomes.
DATA EXTRACTION:
6Go independent revieGers e.tracted data and assessed risA of bias.
DATA SYNTHESIS:
-i(,tB trials comprisin( ;18HH participants compared statin Git, placebo or no treatment.
6reatment effects varied Git, sta(e of CM!. *oderate' to ,i(,'NualitB evidence
indicated t,at statins reduced all'cause mortalitB (relative risA P&&Q, 8.F1 PH;< C?, 8.C=
to 8.FFQ), cardiovascular mortalitB (&&, 8.CF PC?, 8.9F to 8.FHQ), and cardiovascular
events (&&, 8.C9 PC?, 8.C: to 8.F8Q) in persons not receivin( dialBsis. *oderate' to ,i(,'
NualitB evidence indicated t,at statins ,ad little or no effect on all'cause mortalitB (&&,
8.H9 PC?, 8.FF to 1.8=Q), cardiovascular mortalitB (&&, 8.H= PC?, 8.F2 to 1.8CQ), or
cardiovascular events (&&, 8.H; PC?, 8.FC to 1.8:Q) in persons receivin( dialBsis. -ffects
of statins in AidneB transplant recipients Gere uncertain. Statins ,ad little or no effect on
cancer, mBal(ia, liver function, or Git,draGal from treatment, alt,ou(, adverse events
Gere evaluated sBstematicallB in feGer t,an ,alf of t,e trials.
LIMITATION:
6,ere Gas a reliance on post ,oc sub(roup data for earlier sta(es of CM!.
CONCLUSION:
Statins decrease mortalitB and cardiovascular events in persons Git, earlB sta(es of CM!,
,ave little or no effect in persons receivin( dialBsis, and ,ave uncertain effects in AidneB
transplant recipients.