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Medical Forum / General / Cardiology / April 2007Vytorin: let's compare possible side effects.
I'm wondering if anyone else is experiencing any side effects while using Vytorin? I have been taken Vytorin 10/20 for one year now, and about a month ago, I started to experience muscle pain (myalgia). Examples of locations; in the right shoulder I'm experiencing pain and up that side of the neck, also on the left side but not up the neck. Also, in the bicep muscles of both legs, in both hips and water retention in both calves and feet. I am not sure if this is Vytorin side effects. How about you? russ > I'm wondering if anyone else is experiencing any side effects while > using Vytorin? [quoted text clipped - 5 lines] > both calves and feet. > I am not sure if this is Vytorin side effects. It is possible. > How about you? Not taking Vytorin but have seen this side effect is some of my patients. It should be a simple matter for your doctor(s) to switch you to alternative lipid-lowering medications once you inform him/her/them about your symptoms. May GOD bless you. Prayerfully in Jesus' ever-lasting love, Andrew <>< -- Andrew B. Chung, MD/PhD http://EmoryCardiology.com May HIS immortal brethren pray for our dying mortal friends and neighbors: http://HeartMDPhD.com/Convicts Especially dear Bob(this one) Pastorio: http://bobs-amanuensis.livejournal.com/4211.html http://pics.livejournal.com/bobs_amanuensis/pic/0000z24f/g1 As for knowing who are the very elect, these you will know by the unconditional love they have for everyone including their enemies (Matthew 5:44-45, 1 Corinthians 13:3, James 2:14-17). http://HeartMDPhD.com/Love > I'm wondering if anyone else is experiencing any side effects while > using Vytorin? [quoted text clipped - 7 lines] > > russ Started taking this drug over one year ago. The only side effects have been very small elevations of ALT and AST over the limits that define the upper end of the normal range. These levels are being periodically monitored. The drug has been very effective: total cholesterol 114 mg at last test. My HDL and LDL levels are influenced more by exercise than by the drug. For me HDLs become more elevated if I maintain higher levels of aerobic exercise and maintain regular sessions of weight training. You definitely need to give your physician feedback regarding the issues you are having. You should be given periodic blood tests (so-called lipid-liver panel) and if the pain persists and/or the numbers come out wrong, your physician should discontinue the Vytorin and see if that reduces or eliminates the symptoms. I am not a doctor. Best wishes, Steve  SignatureThe above posting is neither a legal opinion nor legal advice, because we do not have an attorney-client relationship, and should not be construed as either. This posting does not represent the opinion of my employer, but is merely my personal view. To reply, delete _spamout_ and replace with the numeral 3 Steve >I'm wondering if anyone else is experiencing any side effects while >using Vytorin? [quoted text clipped - 7 lines] > >russ I had myalgia (between the shoulder blades and in my thighs) after taking Zetia, which is a Vytorin component. Also severe nerve pain. It all went away a couple of days after discontinuing Zetia. Previous to using Zetia My MD tried Zocor which is the other ingredient in Vytorin. This also induced myalgia and muscle twitching but not nerve pain. Took a couple of weeks to go away after discontinuing Zocor > >I'm wondering if anyone else is experiencing any side effects while > >using Vytorin? [quoted text clipped - 16 lines] > but not nerve pain. Took a couple of weeks to go away after > discontinuing Zocor No one knows if Zetia reduces cardiovascular disease risk because no studies have been done looking at clinical endpoints. In other words, no one knows if Zetia is a safe medicine to take. Marilyn >> >I'm wondering if anyone else is experiencing any side effects while >> >using Vytorin? [quoted text clipped - 22 lines] > >Marilyn They have done the FDA safety testing, but without clinical endpoints no one knows how effective Zetia is in reducing mortality or morbidity. > They have done the FDA safety testing, but without clinical endpoints > no one knows how effective Zetia is in reducing mortality or > morbidity. What does it mean to say that it is safe without clinical endpoints? What if ezetimibe raises the risk of cardiac events or increases all-cause mortality? (This isn't an idle possibility: torcetrapib raises HDL, lowers LDL, and increased mortality so much that trials were recently stopped early.) SignatureDavid Rind drind@caregroup.harvard.edu > > They have done the FDA safety testing, but without clinical endpoints > > no one knows how effective Zetia is in reducing mortality or [quoted text clipped - 9 lines] > David Rind > d...@caregroup.harvard.edu I agree with David. Australian Adverse Drug Reactions Bulletin, October 2006, reports 265 reports of suspected adverse reactions with ezetimibe (Zetia) since June 2003, twelve of which describe depression or depressed mood in patients 60 to 82 years. In all cases, ezetimibe was the sole suspected drug. "An unusual feature was the rapid onset of symptoms . . . . In 5 patients, symptoms abated on withdrawal of ezetimibe but recurred on rechallenge." http://www.tga.gov.au/adr/aadrb/aadr0610.htm. Marilyn >> They have done the FDA safety testing, but without clinical endpoints >> no one knows how effective Zetia is in reducing mortality or [quoted text clipped - 5 lines] > HDL, lowers LDL, and increased mortality so much that trials were >recently stopped early.) OK - should have said it is not an immediate poison but in the long term it can have real benefits or not. This is an interesting dilemma for high risk patients. Do you go with a drug that superficially seems to accomplish significant risk reduction or do you wait 5+ years until there are solid results for cardiovascular risk. I was one one the high risk initial statin patients who switched from Questran and niacin to lovastatin based on the fact that it lowered cholesterol and that was good. At that time there was no mortality information. It could have been a bad decision but wasn't. Ezetimibe has not been shown to improve endothelial dysfunction. This is the response I got from one doctor when I said my daughter was on it: Its interesting that she is on zetia. It is generally thought that > the drug does not act systemically. However, the drug is taken up to > some degree from the intestine. [quoted text clipped - 6 lines] > to work (ie to lower the risk for CVD) and has not been demonstrated > to be safe. There is a clinical trial called IMPROVE-IT that is comparing ezetimibe/simvastatin combination 10/40 with simvastatin 40 in patients with high-risk acute coronary syndrome. www.clinicaltrials.gov/ct/show/NCT00202878. "Clinical benefit will be defined as the reduction in the risk of the occurrence of the composite endpoint of CV death, major coronary events, and stroke." I'm not clear what they mean by "composite endpoint." Marilyn > Ezetimibe has not been shown to improve endothelial dysfunction. > [quoted text clipped - 24 lines] > > Marilyn They mean that they intend to analyze the combination of all three of those endpoints as the main outcome of the study. This is common in cardiovascular trials, though sometimes is problematic. Notice that they do not seem to have included all-cause mortality in the primary endpoint. I would view that as concerning, but the study will certainly report the effect on all-cause mortality allowing some judgment to be made about benefits and harms. SignatureDavid Rind drind@caregroup.harvard.edu Thanks. The AHA just put out a scientific statement, McCrindle et al., Drug Therapy of High-Risk Lipid Abnormalities In Children and Adolescents, Circulation pub online 3/21/07. They mention ezetimibe and characterize it as "safe and well tolerated." They also say that there are some trials going on using ezetimibe as an adjunct to a statin in kids with familial hypercholesterolemia. Such trials would not provide very useful information because they would not be looking at clinical events and mortality. Marilyn > Thanks. > [quoted text clipped - 8 lines] > > Marilyn I think use of ezetimibe would be justified in the case of homozygous FH, or in certain other limited situations, but I wouldn't support using it routinely at the present time. In any case, they should discuss with the parents the lack of evidence that it works and is safe. In my case, my daughter's doctor did not do that. That's one reason I'm changing doctors. Marilyn There is a trial going on comparing ezetimibe plus simvastatin vs simvastatin on atherosclerosis progression in familial hypercholesterolemia. It's called the Ezetimibe and Simvastatin in Hypercholesterolemia Enhances Atherosclerosis Regression (ENHANCE) trial. The primary end point is mean change from baseline to 2 years in carotid artery intima-media thickness (CA IMT). Secondary endpoints include (1) the proportion of participants who exhibit reductions in CA IMT, (2) the change in maximum far wall IMT, (3) the proportion of participants who develop new carotid artery plaques, and (4) the changes in carotid plus common femoral artery IMT. I guess this will provide a little more info than just how much it lowers LDL. Marilyn Would the results of a study focusing on ACS have general applicability? Marilyn > Would the results of a study focusing on ACS have general > applicability? > > Marilyn Hard to know without seeing the actual results. ACS is the one area where we have a suggestion that the choice of statin matters. In PROVE-IT, high dose atorvastatin was immediately better than regular dose pravastatin in ACS (survival benefit started to become apparent within a few days). In contrast, in Phase Z of the A to Z trial, moderate dose simvastatin had no immediate benefits compared with placebo. So if simvastatin plus ezetimibe outperformed simvastatin alone in ACS during the first few weeks of the study, that would be pretty interesting, though still wouldn't tell you whether to use that combo or high dose atorvastatin for ACS. If the study follows out long enough (months to years), it should be possible to tell whether ezetimibe has an additive benefit once an ACS becomes stable CHD, particularly if they look at mortality as an endpoint. SignatureDavid Rind drind@caregroup.harvard.edu > OK - should have said it is not an immediate poison but in the long > term it can have real benefits or not. [quoted text clipped - 7 lines] > there was no mortality information. It could have been a bad decision > but wasn't. The problem from my point of view is that nearly every study of a drug to lower cholesterol that is not a statin has shown a trend toward increased mortality. So a better question would have been why to be on Questran or niacin at all prior to studies showing clinical benefits, rather than why to switch to lovastatin. I do not buy that a drug that lowers LDL "seems to accomplish significant risk reduction" in the absence of studies of clinical endpoints, given the mostly negative outcomes of studies with drugs other than statins. That said, if someone were extremely high risk, had a very high LDL, and could not tolerate a statin, I think it would be reasonable to treat with ezetimibe while awaiting better data. SignatureDavid Rind drind@caregroup.harvard.edu > David Rind wrote: > The problem from my point of view is that nearly every study of a drug > to lower cholesterol that is not a statin has shown a trend toward > increased mortality. Do you think this trend toward increased mortality is due to adverse effects of lowering LDL or other adverse effects of the drugs? Or maybe we just don't know. Marilyn >>David Rind wrote: > [quoted text clipped - 7 lines] > > Marilyn I don't think we know. I've never really thought that lowering LDL itself was bad, since in population studies having a lower LDL is good (except when you are old and it's a marker of illness and malnutrition to have a low LDL). I don't feel like I know enough to really have an opinion about underlying mechanisms. I just am completely unconvinced that effect on cholesterol (total, LDL, or HDL) is a good marker for whether a drug will have clinical benefits, given the many negative results over the past three decades. SignatureDavid Rind drind@caregroup.harvard.edu Thanks. Marilyn > I don't think we know. I've never really thought that lowering LDL > itself was bad, since in population studies having a lower LDL is good > (except when you are old and it's a marker of illness and malnutrition > to have a low LDL). This is interesting: Jacobs & Iribarren, Invited Commentary: Low Cholesterol and Nonatherosclerotic Disease Risk: A Persistently Perplexing Question, Am J Epidem 2000, Vol 151, No. 8, 748-751. Marilyn > > I don't think we know. I've never really thought that lowering LDL > > itself was bad, since in population studies having a lower LDL is good [quoted text clipped - 8 lines] > > Marilyn Am J Epidemiol. 2000 Apr 15;151(8):748-51. Links Comment on: Am J Epidemiol. 2000 Apr 15;151(8):739-47. Invited commentary: low cholesterol and nonartherosclerotic disease risk: a persistently perplexing question. € Jacobs DR Jr, Iribarren C. Division of Epidemiology, University of Minnesota, Minneapolis, USA. In contrast to clinical trials using statin drugs, which suggest that cholesterol lowering from high to moderate levels is safe, many, but not all, prospective studies report higher nonatherosclerotic disease rates in people with low serum total cholesterol, even after deleting deaths in the 5 years after cholesterol determination. A perplexing and unanswered question is whether low cholesterol is causally related to nonatherosclerotic disease risk. Cholesterol is reduced during the acute phase reaction; a state of immune activation that persists for more than 5 years may explain the prospective observations. Higher cholesterol may be a marker for other protective substances such as fat-soluble antioxidants. Low cholesterol might mark poor nutrition, for example, during depression. Alternatively, higher cholesterol levels may result in enhanced delivery of lipids to cells during the immune response or tissue repair or may enhance defense against endotoxins and viruses. Although we believe that populationwide efforts to lower cholesterol should continue, we think that important biology may be reflected in the repeatedly observed associations of low cholesterol with nonatherosclerotic disease. The authors urge that research continue to elucidate any biologic bases of these relations. PMID: 10965971 [PubMed - indexed for MEDLINE] SignatureS Jersey USA Zone 5 Shade http://www.ocutech.com/ High tech Vison aid This article is posted under fair use rules in accordance with Title 17 U.S.C. Section 107, and is strictly for the educational and informative purposes. This material is distributed without profit. > > I don't think we know. I've never really thought that lowering LDL > > itself was bad, since in population studies having a lower LDL is good [quoted text clipped - 8 lines] > > Marilyn Here is another TC as a marker for Aids. Bill "These findings suggest that low serum TC levels should be considered a marker of increased risk of HIV infection in men already at heightened risk of HIV infection." : J Acquir Immune Defic Syndr Hum Retrovirol. 1998 Jan 1;17(1):51-7. Links Association between serum total cholesterol and HIV infection in a high-risk cohort of young men. € Claxton AJ, Jacobs DR Jr, Iribarren C, Welles SL, Sidney S, Feingold KR. Division of Epidemiology, School of Public Health, University of Minnesota, Minneapolis 55454-1015, USA. Low serum total cholesterol (TC) is associated with a variety of nonatherosclerotic diseases, but the association of TC with infectious disease has been little studied. In this study, we examined the relationship between serum TC and HIV infection in members of a large health maintenance organization in Northern California. The cohort consisted of 2446 unmarried young men 15 to 49 years of age at high risk of HIV infection, defined as self-reported history of sexually transmitted disease or liver disease. Baseline measurements were taken between 1979 and 1985, and subjects were passively followed for HIV infection until the end of 1993 (average length of follow-up, 7.7 years). From a multivariate-adjusted Cox regression, the rate ratio (RR) of HIV infection was 1.66 (95% CI = 1.07, 2.56) for men with serum TC levels <160 mg/dl compared with those with TC levels between 160 and 199 mg/dl. Similar excess risk of AIDS and AIDS-related death was observed. These findings suggest that low serum TC levels should be considered a marker of increased risk of HIV infection in men already at heightened risk of HIV infection. PMID: 9436759 [PubMed - indexed for MEDLINE] SignatureS Jersey USA Zone 5 Shade http://www.ocutech.com/ High tech Vison aid This article is posted under fair use rules in accordance with Title 17 U.S.C. Section 107, and is strictly for the educational and informative purposes. This material is distributed without profit. On Apr 23, 8:24 am, William Wagner <not-to-here-william...@gmail.com> wrote: > In article <1177329234.170038.320...@p77g2000hsh.googlegroups.com>, > [quoted text clipped - 53 lines] > Title 17 U.S.C. Section 107, and is strictly for the educational > and informative purposes. This material is distributed without profit. Its shocking to even consider it, however, HIV is NOT the cause of AIDS. And is simply the largest medical blunder in the history of western civilization brought to you in 1984 by Robert Gallo, NIH virologist who was previously involved in scientific FRAUD. See the Book Science Fiction by Crewdson http://www.allbookstores.com/book/9780316090049/John_Crewdson/Science_Fictions.html http://findarticles.com/p/articles/mi_m1430/is_n9_v14/ai_12508167 http://www.ourcivilisation.com/aids/chap6.htm http://www.hiv-aids-factorfraud.com/producer.htm Important video relating to HIV and AIDS. http://www.aidsfraudvideo.com http://aidsmyth.addr.com/enteraidsmyth.htm My understanding is that apolipoprotein B (apoB) is a risk marker for CVD. I read the following study, but I'm afraid it's a little over my head. So I'm hoping someone will help me understand what it means (David R., are you out there?). Tremblay et al., Effect of Ezetimibe on the In Vivo Kinetics of ApoB-48 and ApoB-100 in Men With Primary Hypercholesterolemia, Arterioscler Thromb Vasc Biol May 2006. Objective- To examine the impact of ezetimibe, a selective inhibitor of intestinal cholesterol absorption, on the in vivo kinetics of apolipoproteins (apo) B-48 and B-100 in humans. Methods and Results- Kinetics of triglyceride-rich lipoprotein (TRL) apoB-48 and very-low-density lipoprotein (VLDL), intermediate-density lipoprotein (IDL), and low-density lipoprotein (LDL) apoB-100 labeled with a stable isotope were assessed at baseline and at the end of 8 weeks of treatment with 10 mg/d of ezetimibe in 8 men with moderate primary hypercholesterolemia. Data were fit to a multicompartmental model using SAAMII to calculate fractional catabolic rate (FCR) and production rate (PR). Ezetimibe significantly decreased total and LDL cholesterol concentrations by -14.5% and -22.0% (P=0.004), respectively, with no significant change in plasma triglyceride and high-density lipoprotein (HDL) cholesterol levels. Ezetimibe had no significant effect on TRL apoB-48 kinetics and pool size (PS). However, VLDL and IDL apoB-100 FCRs were significantly increased (+31.2%, P=0.02 and +20.8%, P=0.04, respectively) with a concomitant elevation of VLDL apoB-100 PR (+20.9%, P=0.04). Furthermore, LDL apoB-100 PS was significantly reduced by -23.2% (P=0.004), caused by a significant increase in FCR of this lipoprotein fraction (+24.0%, P=0.04). Conclusions- These results indicate that reduction of plasma LDL cholesterol concentration after treatment with ezetimibe is associated with an increase in FCR of apoB-100-containing lipoproteins. Ezetimibe, a selective inhibitor of intestinal cholesterol absorption, has been shown to decrease plasma low-density lipoprotein cholesterol (LDL-C) levels. To determine mechanism, apolipoprotein B kinetic studies were conducted in 8 hypercholesterolemic men. Reduction of LDL- C concentrations after treatment with ezetimibe was mainly associated with an increase in fractional catabolic rate of apoB-100-containing lipoproteins The authors state: "In conclusion, the present study indicates that the LDL-C lowering effect of ezetimibe is mainly caused by an increase in the catabolism of apoB-100-containing lipoproteins. Our study also shows that ezetimibe has no significant effect on TRL apoB-48 kinetics although variability in apoB-48 measurements could have reduced the power to detect a true effect of ezetimibe. Finally, our results suggest that the ezetimibe-induced reduction in cholesterol delivery to the liver is associated with a compensatory increase in hepatic VLDL apoB-100 production, which may limit the lipid-lowering effect of ezetimibe." I take it that this increase in VLDL apoB-100 production is not a good thing. Marilyn > My understanding is that apolipoprotein B (apoB) is a risk marker for > CVD. I read the following study, but I'm afraid it's a little over my [quoted text clipped - 56 lines] > > Marilyn The biochemistry here is a little over my head as well. They are certainly saying that in response to ezetimibe, liver production of VLDL apoB-100 increases and that this means that the reduction in LDL levels may not be as great with ezetimibe as would otherwise be expected from the degree to which ezetimibe apparently causes breakdown of apoB-100 associated with LDL. Ultimately, though, I think this is just a study looking into cholesterol kinetics in patients taking ezetimibe. Ezetimibe lowers LDL (in this study by 22%), and it's not clear why it would matter to someone taking it that if there weren't liver compensation it might lower LDL by a larger number. I suppose it might matter to someone trying to design a new drug with improved characteristics. My concerns about ezetimibe aren't because I've looked deeply into how it works and think that it's not a good drug. My concerns are based on the lack of published data on clinical endpoints in patients treated with ezetimibe. It's not as if I would have had any clue 20 years ago that a drug that lowered LDL by blocking HMG Co-A reductase (the mechanism by which statins lower LDL) would be a particularly great drug for CHD. SignatureDavid Rind drind@caregroup.harvard.edu Thanks. Marilyn "My concerns are based on the lack of published data on clinical endpoints in patients treated with ezetimibe." Yes, I have that same concern, as did the doctor I quoted in my 4/17 post. I don't want to say who he is since it was a private communication, but his research relates to metabolism of lipoproteins. I guess that article drew my interest because people with FH are said to have high levels of apoB. Marilyn |
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