I guess we'll just have to extrapolate what the numbers would be now, three more years into use and millions more users. What say Chinnis? Table 1. Cases of Statin-Associated Rhabdomyolysis by Drug (October 1997 through December 2000 Drug| Number of Cases| Percent of Total Cases| Cases without Fibrates| Percent of cases without Fibrates Atorvastatin| 86| 11.1%| 73| 84.9% Cerivastatin| 387| 50.1%| 187| 48.3% Fluvastatin| 10| 1.3%| 8| 80.0% Lovastatin| 32| 4.1%| 30| 93.8% Pravastatin| 70| 9.1%| 62| 88.6% Simvastatin| 187| 24.2%| 164| 87.7% TOTAL| 772 524| 67.9%| ============================= Table 2. Deaths reported in Statin-Associated Rhabdomyolysis (October 1997 through December 2000) Drug| Number of Cases(Deaths)| Percent of Total Deaths| Cases without Fibrates| Percent of cases of each drug without Fibrates Atorvastatin| 13| 18.1%| 11| 84.6% Cerivastatin| 20| 27.8%| 10| 50.0% Fluvastatin| 1| 1.4%| 1| 100% Lovastatin| 5| 6.9%| 5| 100% Pravastatin| 9| 12.5%| 8| 88.9% Simvastatin| 24| 33.3%| 19| 79.2% TOTAL| 72*| 54**| 75.0% *- 2 deaths were reported where there was use of 2 statins concurrently (1 with cerivastatin and simvastatin, 1 with pravastatin and simvastatin) ** - 1 death with use of 2 statins (pravastatin and simvastatin) ========================
On 6 Mar 2004 21:11:59 -0800, [email protected] (Zee) wrote: >I guess we'll just have to extrapolate what the numbers >would be now, three more years into use and millions more >users. What say Chinnis? > > >Table 1. Cases of Statin-Associated Rhabdomyolysis by Drug >(October 1997 through December 2000 > >Drug| Number of Cases| Percent of Total Cases| Cases >without Fibrates| Percent of cases without Fibrates >Atorvastatin| 86| 11.1%| 73| 84.9% > >Cerivastatin| 387| 50.1%| 187| 48.3% > >Fluvastatin| 10| 1.3%| 8| 80.0% > >Lovastatin| 32| 4.1%| 30| 93.8% > >Pravastatin| 70| 9.1%| 62| 88.6% > >Simvastatin| 187| 24.2%| 164| 87.7% > >TOTAL| 772 524| 67.9%| >============================= >Table 2. Deaths reported in Statin-Associated >Rhabdomyolysis (October 1997 through December 2000) > >Drug| Number of Cases(Deaths)| Percent of Total Deaths| >Cases without Fibrates| Percent of cases of each drug >without Fibrates > >Atorvastatin| 13| 18.1%| 11| 84.6% > >Cerivastatin| 20| 27.8%| 10| 50.0% > >Fluvastatin| 1| 1.4%| 1| 100% > >Lovastatin| 5| 6.9%| 5| 100% > >Pravastatin| 9| 12.5%| 8| 88.9% > >Simvastatin| 24| 33.3%| 19| 79.2% > >TOTAL| 72*| 54**| 75.0% > > >*- 2 deaths were reported where there was use of 2 statins >concurrently (1 with cerivastatin and simvastatin, 1 with >pravastatin and simvastatin) > >** - 1 death with use of 2 statins (pravastatin and >simvastatin) >======================== 72 deaths out of hundreds of millions of statin users, even then. A tragedy to be sure, but statistically speaking.....? Also, it's not made clear if there were underlying issues that precipitated a negative interaction. Jim, you've been paged. L.
"Zee" <[email protected]> wrote in message news:[email protected]... > I guess we'll just have to extrapolate what the numbers > would be now, three more years into use and millions more > users. What say Chinnis? > > > Table 1. Cases of Statin-Associated Rhabdomyolysis by Drug > (October 1997 through December 2000 > > Drug| Number of Cases| Percent of Total Cases| Cases > without Fibrates| Percent of cases without Fibrates > Atorvastatin| 86| 11.1%| 73| 84.9% > > Cerivastatin| 387| 50.1%| 187| 48.3% > > Fluvastatin| 10| 1.3%| 8| 80.0% > > Lovastatin| 32| 4.1%| 30| 93.8% > > Pravastatin| 70| 9.1%| 62| 88.6% > > Simvastatin| 187| 24.2%| 164| 87.7% > > TOTAL| 772 524| 67.9%| > ============================= > Table 2. Deaths reported in Statin-Associated > Rhabdomyolysis (October 1997 through December 2000) > > Drug| Number of Cases(Deaths)| Percent of Total Deaths| > Cases without Fibrates| Percent of cases of each drug > without Fibrates > > Atorvastatin| 13| 18.1%| 11| 84.6% > > Cerivastatin| 20| 27.8%| 10| 50.0% > > Fluvastatin| 1| 1.4%| 1| 100% > > Lovastatin| 5| 6.9%| 5| 100% > > Pravastatin| 9| 12.5%| 8| 88.9% > > Simvastatin| 24| 33.3%| 19| 79.2% > > TOTAL| 72*| 54**| 75.0% > > > *- 2 deaths were reported where there was use of 2 statins > concurrently (1 with cerivastatin and simvastatin, 1 with > pravastatin and simvastatin) > > ** - 1 death with use of 2 statins (pravastatin and > simvastatin) > ======================== Source? Also it is not clear what these numbers mean. But I think it means that, e.g., 11.1% of the total cases reported were taking Atorvastatin - not that 11.1% of the people taking Atorvastatin were afflicted. Right? What was the underlying population and how many of them were there? What does the total 772 524 mean? Thanks. Bill
Your numbers are absolutely insignificant out of a population totaling tens of millions (perhaps hundreds of millions) of users. Following the logic represented by your posting this information, we should stop driving our cars because of the many people killed in auto accidents. I don't think so...... "Zee" <[email protected]> wrote in message news:[email protected]... > I guess we'll just have to extrapolate what the numbers > would be now, three more years into use and millions more > users. What say Chinnis? > > > Table 1. Cases of Statin-Associated Rhabdomyolysis by Drug > (October 1997 through December 2000 > > Drug| Number of Cases| Percent of Total Cases| Cases > without Fibrates| Percent of cases without Fibrates > Atorvastatin| 86| 11.1%| 73| 84.9% > > Cerivastatin| 387| 50.1%| 187| 48.3% > > Fluvastatin| 10| 1.3%| 8| 80.0% > > Lovastatin| 32| 4.1%| 30| 93.8% > > Pravastatin| 70| 9.1%| 62| 88.6% > > Simvastatin| 187| 24.2%| 164| 87.7% > > TOTAL| 772 524| 67.9%| > ============================= > Table 2. Deaths reported in Statin-Associated > Rhabdomyolysis (October 1997 through December 2000) > > Drug| Number of Cases(Deaths)| Percent of Total Deaths| > Cases without Fibrates| Percent of cases of each drug > without Fibrates > > Atorvastatin| 13| 18.1%| 11| 84.6% > > Cerivastatin| 20| 27.8%| 10| 50.0% > > Fluvastatin| 1| 1.4%| 1| 100% > > Lovastatin| 5| 6.9%| 5| 100% > > Pravastatin| 9| 12.5%| 8| 88.9% > > Simvastatin| 24| 33.3%| 19| 79.2% > > TOTAL| 72*| 54**| 75.0% > > > *- 2 deaths were reported where there was use of 2 statins > concurrently (1 with cerivastatin and simvastatin, 1 with > pravastatin and simvastatin) > > ** - 1 death with use of 2 statins (pravastatin and > simvastatin) > ========================
> "Zee" <[email protected]> wrote in message > news:[email protected]... > > I guess we'll just have to extrapolate what the numbers > > would be now, three more years into use and millions > > more users. What say Chinnis? > > > > > > Table 1. Cases of Statin-Associated Rhabdomyolysis by > > Drug (October 1997 through December 2000 > > > > Drug| Number of Cases| Percent of Total Cases| Cases > > without Fibrates| Percent of cases without Fibrates > > Atorvastatin| 86| 11.1%| 73| 84.9% > > > > Cerivastatin| 387| 50.1%| 187| 48.3% > > > > Fluvastatin| 10| 1.3%| 8| 80.0% > > > > Lovastatin| 32| 4.1%| 30| 93.8% > > > > Pravastatin| 70| 9.1%| 62| 88.6% > > > > Simvastatin| 187| 24.2%| 164| 87.7% > > > > TOTAL| 772 524| 67.9%| > > ============================= > > Table 2. Deaths reported in Statin-Associated > > Rhabdomyolysis (October 1997 through December 2000) > > > > Drug| Number of Cases(Deaths)| Percent of Total Deaths| > > Cases without Fibrates| Percent of cases of each drug > > without Fibrates > > > > Atorvastatin| 13| 18.1%| 11| 84.6% > > > > Cerivastatin| 20| 27.8%| 10| 50.0% > > > > Fluvastatin| 1| 1.4%| 1| 100% > > > > Lovastatin| 5| 6.9%| 5| 100% > > > > Pravastatin| 9| 12.5%| 8| 88.9% > > > > Simvastatin| 24| 33.3%| 19| 79.2% > > > > TOTAL| 72*| 54**| 75.0% > > > > > > *- 2 deaths were reported where there was use of 2 > > statins concurrently (1 with cerivastatin and > > simvastatin, 1 with pravastatin and simvastatin) > > > > ** - 1 death with use of 2 statins (pravastatin and > > simvastatin) > > ======================== > > Source? Also it is not clear what these numbers mean. But > I think it means that, e.g., 11.1% of the total cases > reported were taking Atorvastatin - not that 11.1% of the > people taking Atorvastatin were afflicted. Right? What was > the underlying population and how many of them were there? > What does the total 772 524 mean? > > Thanks. > > Bill I think it originates with this, but that's not where I got it. http://www4nl.dr-rath- foundation.org/DE_STICHTING/Nieuws/2001/2001-08-20.htm Here's another. With both, it is *reported* rhabdomyolysis, *reported* adverse events. Reported adverse events are estimated to be ONE to Ten percent of all adverse events, and Terence Young, father of the young woman killed by cisapride estimates the number at 25 per cent. Also to consider, this is only to the FDA. Does that include Canada, Europe, Britain and Australia, for example? I can tell you categorically that my illness, disability and several types of side effects including spiked CK were NOT every reported. Not by my G.P, not by my endocrinologists, either of them, both of whom are principals in studies funded by pharma. :www.theannals.com/cgi/reprint/36/2/288.pdf+Cases+of+Statin- Associated+Rhabdomyolysis+by+Drug&hl=en&ie=UTF-8 I would also suggest everyone who goes on statins thinks they have to take them. We are all under the impression *we* have serious need to take this drug. Others may be able to get away without it, but not us. We are faced with our mortality, impressed by it in fact. I can tell you virtually every person I have talked to who has been put on statins says some variation of, but really not too varied "oh but I have to take them. I have very serious (fill in the blank). And there is still no concensus that high cholesterol is the problem or that lowerering cholesterol will protect you from anything. Case in point: a friend who recently had a heart attack and had a stent implanted had one blockage, was reassured his other arteries are "clean as a whistle". His total cholesterol is 6.1. He is on a statin to lower his cholesterol. Why? B'adant
[email protected] (Zee) wrote in message news:<[email protected]>... > I guess we'll just have to extrapolate what the numbers > would be now, three more years into use and millions more > users. What say Chinnis? > > > Table 1. Cases of Statin-Associated Rhabdomyolysis by Drug > (October 1997 through December 2000 It originates here: http://www.publiccitizen.org/publicatio- ns/release.cfm?ID=7051 And here for an overview of ADRs but not to date:2/288.pdf+fda+adverse+event+reports+on+statins&hl=en&ie=UTF- 8 And here for ADRs in under one year for Crestor in Canada alone. Type in Crestor, and limit 2003-2003. http://www.cbc.ca/news/adr/database/ Click on the numbers to the left to see what the actual side effects experienced were. Try your statin here, and keep in mind it is estimated no more than 10 percent of serious ADRs are ever reported. B'adant
On 7 Mar 2004 13:05:43 -0800, [email protected] (Zee) wrote: > >And here for an overview of ADRs but not to date:/288.pdf+fda+adverse+event+reports+on+statins&hl=en&ie=UTF- >8 Again, "....871 reports of statin-associated rhabdomyolysis in the 29-month time frame examined, representing 601 cases" out of *millions* of statin users is statistically extremely small. Isn't it? And MOST IMPORTANTLY as the study says: "....safety is not an absolute concept, since no drug is completely without adverse effects..." AND (get a load of this!): "In addition, assessing causality was not possible, since there was no certainty that a statin or its possible interaction with other drugs may have caused the rhabdomyolysis because the event may have occurred due to some other cause." >B'adant L.
"Zee" <[email protected]> wrote in message news:[email protected]... > [email protected] (Zee) wrote in message news:<[email protected]>... > Try your statin here, and keep in mind it is estimated no > more than 10 percent of serious ADRs are ever reported. > > > B'adant I would think that most serious cases would be recognized via the CPK test, but maybe not reported - I don't know most Drs. habits. But in case of death I would think it would be, but again I'm not sure. Also keep in mind that there are causes other than statins to Rhabdomyolysis and indeed it was known prior to the development of statins. Bill
On 7 Mar 2004 09:56:01 -0800, [email protected] (Zee) wrote: >And there is still no concensus that high cholesterol is >the problem or that lowerering cholesterol will protect you >from anything. > >Case in point: a friend who recently had a heart attack and >had a stent implanted had one blockage, was reassured his >other arteries are "clean as a whistle". His total >cholesterol is 6.1. He is on a statin to lower his >cholesterol. Why? > > > >B'adant Cholesterol levels are just a piece of the puzzle. Studies are beginning to show other factors involved in cardiovascular disease. (This actually has been known for some time). At the same time, studies are also showing *other* benefits from statins besides its effective cholesterol lowering abilities. I've been posting links to some of them in the past few weeks, in case you missed it.... I understand that CAUSers would never want to acknowledge that. L. Here is some useful information for you: Simvastatin reduces human atrial myofibroblast proliferation independently of cholesterol lowering via inhibition of RhoA. Porter KE, Turner NA, O'Regan DJ, Balmforth AJ, Ball SG. Institute for Cardiovascular Research, Worsley Building, University of Leeds, Leeds LS2 9JT, UK. Objective: Adverse atrial and ventricular myocardial remodeling is characterized by fibrosis, myocyte death or hypertrophy and fibroblast proliferation. HMG-CoA reductase inhibitors (statins) are widely prescribed cholesterol- lowering drugs that also appear to have beneficial effects on myocardial remodeling. Although statins are known to reduce myocyte hypertrophy, their effect on cardiac fibroblast proliferation is unknown. The purpose of this study was to investigate the effects of simvastatin on human atrial myofibroblast proliferation. Methods: Cardiac myofibroblasts were cultured from biopsies of human right atrial appendage. Proliferation was quantified by cell counting and cell cycle progression determined by immunoblotting for Cyclin A. The expression, activation and intracellular localization of RhoA were investigated using immunoblotting and immunocytochemistry. Results: Simvastatin (0.1-1.0 micromol/l) inhibited serum-induced myofibroblast proliferation in a concentration-dependent manner at a point upstream of Cyclin A expression. These effects were reversed by mevalonate or geranylgeranyl pyrophosphate (GGPP), but not squalene or farnesyl pyrophosphate (FPP), indicating a mechanism involving inhibition of Rho-family GTPases and independent of cholesterol synthesis. The effects of simvastatin were mimicked by inhibiting Rho geranylgeranylation or Rho-kinase activation. Furthermore, we demonstrated that simvastatin inhibited RhoA function by preventing its association with the plasma membrane and hence, its interaction with downstream effectors required for cell proliferation. Conclusions: Simvastatin reduced proliferation of cultured human atrial myofibroblasts independently of cholesterol synthesis via a mechanism involving inhibition of RhoA geranylgeranylation. Statins may therefore have an important role in preventing adverse myocardial remodeling associated with cardiac myofibroblast proliferation. PMID: 14985071 Cholesteryl ester transfer protein concentration is associated with progression of atherosclerosis and response to pravastatin in men with coronary artery disease (REGRESS). Klerkx AH, de Grooth GJ, Zwinderman AH, Jukema JW, Kuivenhoven JA, Kastelein JJ. Department of Vascular Medicine, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands. [email protected] BACKGROUND: The TaqIB polymorphism in the cholesteryl ester transfer protein (CETP) gene is associated with HDL-C, progression of coronary artery disease (CAD) and response to pravastatin treatment in men with angiographically proven CAD (REGRESS). We hypothesized that differences in CETP concentration could explain these associations and now investigated whether CETP concentration is an independent determinant of these parameters. MATERIALS AND METHODS: Plasma CETP concentrations at baseline and after 2 years' treatment with pravastatin or placebo were measured (n=674), and correlations with lipid and angiographic parameters (mean segment- and obstruction-diameter; MSD and MOD), and TaqIB genotype were studied. RESULTS: After segregation into three groups (baseline CETP<1.58, 1.58-2.21, >2.21 mg L(-1)), subjects with the highest CETP had significantly higher baseline total cholesterol, LDL-C and triglycerides (P<0.01), while HDL-C, MSD and MOD were not different among these groups. After 2 years of placebo, the MSD decreased threefold (P<0.001) and the MOD decreased 2.4-fold (P=0.042) more in the highest compared with the lowest CETP quartile. Pravastatin treatment reduced total cholesterol LDL-C and triglycerides significantly more in the highest CETP quartile. Moreover, only in the highest CETP quartile, pravastatin significantly reduced the MSD- (P=0.003) and MOD-decrease (P=0.014) compared with placebo, and, notably, this was independent of baseline lipids and differential lipid changes in these quartiles. Strikingly, baseline associations and treatment responses according to baseline CETP were independent of TaqIB genotype. CONCLUSIONS: High CETP concentration is associated with faster progression of coronary atherosclerosis in men with proven CAD. Second, pravastatin yielded the highest improvement of lipid and angiographic parameters in patients with high baseline CETP independent of baseline lipids, lipid changes and TaqIB genotype, indicating that the plasma CETP level itself is an important determinant of the response to statins. PMID: 14984434 Does atorvastatin influence serum C-reactive protein levels in patients on long-term hemodialysis? Vernaglione L, Cristofano C, Muscogiuri P, Chimienti S. Nephrology and Dialysis Unit, M. Giannuzzi Hospital, Manduria, Italy. [email protected] BACKGROUND: The increase in serum C-reactive protein (CRP) levels is an independent determinant of cardiovascular events in long-term hemodialysis (HD) patients. Recently, statins have shown anti-inflammatory properties in addition to their lipid-lowering effect. METHODS: We designed a 6- month, prospective, randomized, controlled study to assess the safety and efficacy of atorvastatin in reducing serum CRP levels in long-term HD patients. Patients on HD therapy for at least 6 months, with autologous vascular access, were included. Patients presenting with illnesses and/or use of drugs that may affect CRP levels were excluded. After randomization, group A included 16 patients treated with atorvastatin (10 mg/d orally), and group B included 17 patients treated with placebo. Body mass index, Kt/V, normalized protein catabolic rate, mean blood pressure, and levels of hemoglobin, serum CRP, albumin, creatinine, lipids, and enzymes were recorded at baseline and after 6 months. RESULTS: Qualitative/quantitative parameters were homogeneous between the groups at baseline. In group A, median serum CRP levels decreased from 9 mg/L (range, 5 to 22 mg/L) at baseline to 5 mg/L (range, 3 to 16 mg/L) after 6 months (P = 0.004). In group B, values were 8 mg/L (range, 4 to 14 mg/L) at baseline and 7 mg/L (range, 3 to 17 mg/L) after 6 months (P = 0.98). Serum CRP levels were lower in group A than group B at month- 4 (5 mg/L; range, 3 to 11 mg/L versus 7 mg/L; range, 3 to 10 mg/L, respectively; P = 0.054) and month-6 evaluations (5 mh/L; range, 3 to 16 mg/L versus 7 mg/L; range, 3 to 17 mg/L, respectively; P = 0.060). After 6 months, only in group A was there a significant decrease in serum cholesterol levels (P = 0.041) and a significant increase in serum albumin levels (P = 0.004). Enzyme levels were stable during the study in both groups. CONCLUSION: Administration of atorvastatin is safe in patients on long- term HD therapy and, in addition to its beneficial effects on lipid levels, induces a significant decrease in serum CRP levels, with a consequential increase in serum albumin levels. PMID: 14981605 Statin therapy is associated with improved survival in ischemic and non-ischemic heart failure. Horwich TB, MacLellan WR, Fonarow GC. Ahmanson-UCLA Cardiomyopathy Center, Los Angeles, California 90095-1679, USA. OBJECTIVES: This study aimed to investigate the impact of hydroxymethylglutaryl coenzyme A reductase inhibitor (statin) therapy in patients with advanced heart failure (HF). BACKGROUND: Although statins are known to reduce mortality in coronary artery disease (CAD), the impact of statin therapy in patients with HF has not been well studied. Both the potential risks and benefits of statins in HF have been described. METHODS: We studied a cohort of 551 patients with systolic HF (left ventricular ejection fraction [EF] <or=40%) referred to a single university center for clinical management and/or transplant evaluation. Survival without the necessity of urgent heart transplantation was determined. RESULTS: The patients' mean age was 52 +/- 13 years; mean EF was 25 +/- 7%. Forty-five percent of the cohort had CAD, and 45% were receiving statin therapy, including 73% and 22% of CAD and non-CAD patients with HF, respectively. Patients receiving statins were significantly older and more likely to be male, with higher rates of hypertension, diabetes, and smoking. The EF and cholesterol levels were similar between treated and non- treated patients. Statin use was associated with improved survival without the necessity of urgent transplantation in both non-ischemic and ischemic HF patients (91% vs. 72%, p < 0.001 and 81% vs. 63%, p < 0.001 at one-year follow-up, respectively). After risk adjustment for age, gender, CAD, cholesterol, diabetes, medications, hemoglobin, creatinine, and New York Heart Association functional class, statin therapy remained an independent predictor of improved survival (hazard ratio 0.41 95% confidence interval 0.18 to 0.94). CONCLUSIONS: Statin therapy is associated with improved survival in patients with ischemic and non-ischemic HF. Randomized trials are needed for confirmation of a therapeutic benefit. PMID: 14975476 Statins prevent bisphosphonate-induced gamma,delta-T-cell proliferation and activation in vitro. Thompson K, Rogers MJ. Bone Research Group, Department of Medicine and Therapeutics, Institute of Medical Sciences, University of Aberdeen, Foresterhill, Aberdeen, United Kingdom. [email protected] The acute phase response is the major adverse effect of intravenously administered N-BPs. In this study we show that N-BPs cause gamma,delta-T-cell activation and proliferation in vitro by an indirect mechanism through inhibition of FPP synthase, an effect that can be overcome by inhibiting HMG- CoA reductase with a statin. These studies clarify the probable initial cause of the acute phase response to N-BP drugs and suggest a possible way of preventing this phenomenon. INTRODUCTION: The acute phase response is the major adverse effect of intravenously administered nitrogen- containing bisphosphonate drugs (N-BPs), used in the treatment of metabolic bone diseases. This effect has recently been attributed to their action as non-peptide antigens and direct stimulation of gamma,delta-T-cells. However, because N-BPs are potent inhibitors of farnesyl diphosphate (FPP) synthase, they could cause indirect activation of gamma,delta-T-cells owing to the accumulation of intermediates upstream of FPP synthase in the mevalonate pathway, such as isopentenyl diphosphate/dimethylallyl diphosphate, which are known gamma,delta-T-cell agonists. MATERIALS AND METHODS: Peripheral blood mononuclear cells (PBMCs) were isolated from healthy volunteers and treated with N-BP, statin, or intermediates/inhibitors of the mevalonate pathway for 7 days in the presence of interleukin (IL)-2. Flow cytometric analysis of the T-cell-gated population was used to quantify the proportion of gamma,delta-T- cells in the CD3+ population. RESULTS AND CONCLUSIONS: The ability of N-BPs to stimulate proliferation of CD3+ gamma,delta-T- cells in human PBMC cultures matched the ability to inhibit FPP synthase. Gamma,delta-T-cell proliferation and activation (interferon gamma [IFNgamma] and TNFalpha release) was prevented by mevastatin or lovastatin, which inhibit HMG-CoA reductase upstream of FPP synthase and prevent the synthesis of isopentenyl diphosphate/dimethylallyl diphosphate. Desoxolovastatin, an analog of lovastatin incapable of inhibiting HMG-CoA reductase, did not overcome the stimulatory effect of N-BP. Furthermore, statins did not prevent the activation of gamma,delta-T- cells by a synthetic gamma,delta-T-cell agonist or by anti- CD3 antibody. Together, these observations show that N-BPs indirectly stimulate the proliferation and activation of gamma,delta-T- cells caused by inhibition of FPP synthase and intracellular accumulation of isopentenyl diphosphate/ dimethylallyl diphosphate in PBMCs. Because activation of gamma,delta-T- cells could be the initiating event in the acute phase response to bisphosphonate therapy, co-administration of a statin could be an effective approach to prevent this adverse effect. PMID: 14969398 Beneficial effects of statins in patients with non-ischemic heart failure. Laufs U, Wassmann S, Schackmann S, Heeschen C, Bohm M, Nickenig G. Klinik und Poliklinik Innere Medizin III, Universitat des Saarlandes, 66424, Homburg, Germany, [email protected] OBJECTIVE: HMG CoA reductase inhibitors (statins) may exert a wide array of cholesterolindependent effects including antihypertrophic effects on the heart. Their role in the treatment of heart failure has not been studied. METHODS AND RESULTS: 15 patients with heart failure NYHA II-III based on non-ischemic dilated cardiomyopathy were randomized in a double- blind study to 0.4 mg cerivastatin or placebo for an average treatment period of 20 weeks. Quality of life and exercise capacity increased significantly in the statin treatment but not in the placebo group (Minnesota Living with Heart Failure Questionnaire, 6 min walking test). Concomitantly, there was a trend towards increased left ventricular ejection fraction (radionuclear ventriculography) and improved endothelial function (forearm blood flow). Statins decreased plasma concentrations of troponine T, high sensitive C-reactive protein (hsCRP), plasminogen activator inhibitor-1 (PAI-1) and tumor necrosis factor alpha (TNFalpha). CONCLUSIONS: Statins induce benefical effects in patients with non-ischemic cardiomyopathy leading to improvement of quality of life and exercise capacity disclosing a promising novel treatment strategy for patients with heart failure. PMID: 14963675 Statins induce the regression of left ventricular mass in patients with angina. Nishikawa H, Miura S, Zhang B, Shimomura H, Arai H, Tsuchiya Y, Matsuo K, Saku K. Department of Cardiology, Fukuoka University School of Medicine, Japan. Background There is evidence that statins induce the regression of cardiac hypertrophy in a transgenic rabbit model of hypertrophic cardiomyopathy. Methods and Results The association between treatment with statins and the regression of cardiac mass (left ventricular mass index, LVMI) was investigated in a case - control study using transthoracic echocardiography in 304 patients with angina who underwent coronary angiography. Those who received pravastatin or index-matched controls (n=127) were selected. The cases showed a significant decrease in LVMI compared with the controls. Although the cases included a significantly higher percentage of patients with hypertension and calcium antagonist (CaA) treatment than the controls, there were no relationships between LVMI and either hypertension or CaA treatment. Because the cases had a significantly higher number of stenosed vessels than the controls, LVMI for each number of stenosed vessels was analyzed, and a significant interaction effect between the association of LVMI with statin and the number of stenosed vessels was found. Conclusions Treatment with statins was associated with a lower cardiac mass in patients with angina, suggesting that this is one of the drugs' pleiotropic effects. PMID: 14745145 Additive benefits of pravastatin and aspirin to decrease risks of cardiovascular disease: randomized and observational comparisons of secondary prevention trials and their meta-analyses. Hennekens CH, Sacks FM, Tonkin A, Jukema JW, Byington RP, Pitt B, Berry DA, Berry SM, Ford NF, Walker AJ, Natarajan K, Sheng-Lin C, Fiedorek FT, Belder R. Mount Sinai Medical Center-Miami Heart Institute, Department of Medicine & Epidemiology and Public Health, University of Miami School of Medicine, Boca Raton, FL 33432, USA. [email protected] BACKGROUND: In randomized trials of secondary prevention, pravastatin sodium and aspirin reduce risks of cardiovascular disease. Pravastatin has a predominantly delayed antiatherogenic effect, and aspirin has an immediate antiplatelet effect, raising the possibility of additive clinical benefits. METHODS: In 5 randomized trials of secondary prevention with pravastatin (40 mg/d), comprising 73 900 patient-years of observation, aspirin use was also prescribed in varying frequencies, and data were available on a large number of confounding variables. We tested whether pravastatin and aspirin have additive benefits in the 2 large trials (Long-term Intervention With Pravastatin in Ischaemic Disease trial and the Cholesterol and Recurrent Events trial) that were designed to test clinical benefits. We also performed meta-analyses of these 2 trials and 3 smaller angiographic trials that collected clinical end points. In all analyses, multivariate models were used to adjust for a large number of cardiovascular disease risk factors. RESULTS: Individual trials and all meta-analyses demonstrated similar additive benefits of pravastatin and aspirin on cardiovascular disease. In meta-analysis, the relative risk reductions for fatal or nonfatal myocardial infarction were 31% for pravastatin plus aspirin vs aspirin alone and 26% for pravastatin plus aspirin vs pravastatin alone. For ischemic stroke, the corresponding relative risk reductions were 29% and 31%. For the composite end point of coronary heart disease death, nonfatal myocardial infarction, coronary artery bypass graft, percutaneous transluminal coronary angioplasty, or ischemic stroke, the relative risk reductions were 24% and 13%. All relative risk reductions were statistically significant. CONCLUSION: More widespread and appropriate combined use of statins and aspirin in secondary prevention of cardiovascular disease will avoid large numbers of premature deaths. PMID: 14718320 Atorvastatin completely inhibits VEGF induced ACE upregulation in human endothelial cells. Saijonmaa O, Nyman T, Stewen P, Fyhrquist F. Minerva Institute for Medical Research, Helsinki, Finland; Department of Internal Medicine, Helsinki University Central Hospital, Helsinki, Finland. Objective: Angiotensin-converting enzyme (ACE) plays an important role in the pathophysiology of cardiovascular disease. We investigated whether atorvastatin, a powerful agent for the prevention and treatment of cardiovascular disease influences ACE production in endothelial cells. Methods and Results: Human umbilical cord vein endothelial cells were treated with VEGF (476pM) which induced ACE upregulation. Co-treatment with atorvastatin (0,1-10 micro M) dose dependently inhibited VEGF induced ACE upregulation. In the presence of mevalonate (100 micro M), atorvastatin failed to downregulate VEGF induced ACE production. Co- treatment of the cells with either farnesylpyrophosphate (FPP, 5 micro M) or geranylgeranylpyrophosphate (GGPP, 5 micro M) partially inhibited the suppressive effect of atorvastatin. Pretreatment of the cells with Rho associated protein kinase inhibitor, Y27632 (10 micro M), partially inhibited VEGF induced ACE upregulation. VEGF (476pM) caused PKC phosphorylation which was inhibited by co-treatment of the cells with atorvastatin. Conclusions: Atorvastatin inhibited VEGF induced ACE upregulation probably by inhibiting PKC phosphorylation. This effect was mediated via inhibition of the mevalonate pathway. ACE downregulation may be an additional beneficial effect of statins in the treatment of cardiovascular disease. PMID: 14704227 Usefulness of statin drugs in protecting against atrial fibrillation in patients with coronary artery disease. Young-Xu Y, Jabbour S, Goldberg R, Blatt CM, Graboys T, Bilchik B, Ravid S. Lown Cardiovascular Research Foundation, Brookline, Massachusetts, USA Atrial fibrillation (AF) is prevalent in the elderly, in patients with hypertension, and in patients with coronary artery disease (CAD). We hypothesized that statin therapy might be effective in preventing AF in patients with CAD and examined this hypothesis in a sample of patients with chronic stable CAD without AF, followed prospectively at a large outpatient cardiology practice. The association between statin use and the risk of developing AF was examined univariately and then with adjustment for potential confounding factors. Four hundred forty-nine men and women between the ages of 40 and 87 years were followed for an average of 5 years. Fifty-two patients (12%) developed AF during follow-up. Statin therapy was used by 59% of the patients during the study period and was associated with a significantly reduced risk of developing AF (crude odds ratio, 0.48, 95% confidence interval 0.28 to 0.83). This association remained significant after adjustment for potential confounders, including age, hypertension, left ventricular systolic function, occurrence of heart failure or acute ischemic events, and baseline cholesterol and changes in cholesterol levels (adjusted odds ratio 0.37, 95% confidence interval .18 to 0.76). Use of statins in patients with chronic stable CAD appears to be protective against AF. The underlying mechanism for this effect is unknown but appears to be independent of the reduction in serum cholesterol levels. PMID: 14675569 The cardioprotective effects of statins. Davignon J. Hyperlipidemia and Atherosclerosis Research Group, Clinical Research Institute of Montreal (IRCM), 110 Pine Avenue West, Montreal, QC H2W 1R7, Canada. [email protected] In addition to their lipid-modulating properties, statins have a large number of beneficial cardiovascular effects that have emerged over time and that were not anticipated during drug development. The lipid and nonlipid effects act in a concerted way to reduce the ischemic burden of the myocardium and to protect it against injury. By acting on the vessel wall, statins may prevent lesion initiation and repair injuries, enhance myocardial perfusion, slow lesion progression, and prevent coronary occlusion. They may also directly reduce myocardial damage, favor myocardial repair, and protect against immune injury. This review focuses on properties of statins that contribute to their cardioprotective effect. The first section includes information on modulation of vascular tone, endothelial permeability and function, inhibition of complement injury, curbing of foam cell formation, antioxidant and anti- inflammatory properties, and profibrinolytic and anticoagulant activities. The second section relates to reduction of myocardial necrosis, myocardial hypertrophy, blood pressure, and heart failure, as well as mobilization of endothelial progenitor cells for repair, angiogenic effects, and immunomodulation. In many instances, results of in vitro and animal studies have raised expectations and prompted studies in humans. Several clinical trials have confirmed these expectations and have strengthened the value of statins as valuable antiatherosclerotic and cardioprotective agents. PMID: 14662105 Atorvastatin reduces neurological deficit and increases synaptogenesis, angiogenesis, and neuronal survival in rats subjected to traumatic brain injury. Lu D, Goussev A, Chen J, Pannu P, Li Y, Mahmood A, Chopp M. Department of Neurosurgery, Henry Ford Health Sciences Center, Detroit. Statins administered postischemia promote functional improvement in rats, independent of their capability to lower cholesterol. We therefore tested the effect of statin treatment on traumatic brain injury (TBI) in rats. Atorvastatin was orally administered (1 mi/kg/day) to Wistar rats starting 1 day after TBI for 7 consecutive days. Control animals received saline. Modified Neurological Severity Scores and Corner tests were utilized to evaluate functional response to treatment. Bromodeoxyuridine (BrdU, 100 mg/kg) was also intraperitoneally injected daily for 14 consecutive days to label the newly generated endothelial cells. Rats were sacrificed at day 14 after TBI, and the brain samples were processed for immunohistochemical staining. Atorvastatin administration after brain injury significantly reduced the neurological functional deficits, increased neuronal survival and synaptogenesis in the boundary zone of the lesion and in the CA3 regions of the hippocampus, and induced angiogenesis in these regions. The results suggest that atorvastatin may provide beneficial effects in experimental TBI. PMID: 14987462 Prevention of atrial fibrillation recurrence by statin therapy in patients with lone atrial fibrillation after successful cardioversion. Siu CW, Lau CP, Tse HF. Cardiology Division, Department of Medicine, Queen Mary Hospital, The University of Hong Kong, Hong Kong, China. The aim of this study was to investigate the effect of statin therapy on arrhythmia recurrence in patients with lone atrial fibrillation (AF). From July 1998 to December 1999, 62 patients with lone persistent AF lasting >/=3 months underwent successful external cardioversion. After a mean follow-up of 44 months, 85% had recurrence of AF. The use of statins was associated with a significant decrease in the risk of arrhythmia recurrence after successful cardioversion of AF. The result of this retrospective study demonstrates that the use of statins in patients with lone AF was associated with a significant decrease in the risk of arrhythmia recurrence after successful cardioversion. PMID: 14636918 American Journal of Therapeutics: Volume 10(6) November/December 2003 Statins for Everybody? New Evidence on the Efficacy and Safety of the Inhibitors of HMG Co-A Reductase Alcocer, Luis* México City General Hospital and National Autonomous University of México, México City, Mexico. *Address for correspondence: Tuxpan 16, México D.F., 0676, México. E- mail: [email protected] Abstract Classically, the statins are the first choice drugs when treating dyslipidemias, especially in patients with hypercholesterolemia alone or accompanied by hypertriglyceridemia. The recent evidence of the effectiveness, safety and impact comes from hard endpoints, as demonstrated in 6 trials which included more than 40,000 subjects. The statins are being recommended for the treatment of a large number of patients with overt coronary heart disease, regardless of serum cholesterol levels, in patients with acute phases of coronary syndromes, and in patients without apparent coronary heart disease with moderate risk and average serum cholesterol and LDL cholesterol levels. These drugs are also being prescribed to patients with high-risk medical conditions that are equivalent to coronary heart disease, like diabetes, lower limb atherosclerosis, or vascular cerebral disease, independent of the basal serum cholesterol levels or LDL cholesterol ranging from normal to high. Despite all the evidence collected as to the efficacy and safety of these drugs, the statins are not sufficiently used in daily practice, probably due to the ignorance of new concepts and the doubts related to the safety that may be cleared by careful analysis of 6 major studies with these drugs. Benefits of statin treatment in cardiac syndrome-X1. Kayikcioglu M, Payzin S, Yavuzgil O, Kultursay H, Can LH, Soydan I. Ege University, Medical School, Department of Cardiology, Izmir, Turkey. [email protected] AIMS: The pathophysiological mechanism in cardiac syndrome- X (anginal chest pain, positive exercise test, and angiographically normal coronary arteries) has been suggested as an impairment in normal endothelial function of the coronary microvasculature, resulting in inadequate flow reserve. The aim of this study was to determine whether statins with proven beneficial effects on endothelium, have any effect on endothelial functions and exercise induced ischaemia in cardiac syndrome-X. METHODS AND RESULTS: Study population consisted of prospectively enrolled 40 patients with cardiac syndrome-X. Patients with left ventricular hypertrophy, hypertension, diabetes mellitus, and LDL levels >/=160 mg/dl were excluded. Half of the patients received pravastatin (40 mg/day) for 3 months irrespective of their lipid values, according to a single-blind, randomized, placebo-controlled design. Endothelial functions were assessed with high-resolution vascular ultrasound, which measured the brachial artery flow mediated dilatation (FMD). Lipid measurements, symptom limited exercise tests and vascular ultrasound images were obtained before and at the end of 3 months. After the treatment, FMD improved significantly in pravastatin group. Exercise duration, and time to 1mm-ST depression were significantly prolonged after statin therapy. Ischaemic symptoms and ECG findings during exercise test disappeared completely in 5 (26%) patients in the statin group. However, there were no significant changes in FMD and exercise parameters in placebo group. CONCLUSIONS: Statin therapy resulted in beneficial effects on both exercise induced ischaemia and FMD in cardiac syndrome-X. The mechanism of this beneficial effect is probably the result of improvement in endothelial functions. PMID: 14613735 Statin use is associated with enhanced collateralization of severely diseased coronary arteries. Pourati I, Kimmelstiel C, Rand W, Karas RH. Preventive Cardiology Center, Division of Cardiology, and Department of Medicine, New England Medical Center Hospitals, Boston, Mass, USA. BACKGROUND: The presence of coronary collateral vessels has been associated with improved clinical outcome in patients with coronary artery disease. Animal experiments have shown that hydroxymethyl glutaryl coenzyme A reductase inhibitors (statins) can promote angiogenesis in ischemic tissues in a cholesterol-independent manner. We hypothesized that statin therapy is associated with increased coronary collateral formation in patients with severe coronary artery disease. METHODS AND RESULTS: Patients undergoing clinically indicated coronary angiography at the Tufts-New England Medical Center from September 2000 to April 2001 who had at least 1 major coronary artery occlusion, or a stenosis of > or =95% with Thrombolysis In Myocardial Infarction (TIMI) trial grade < or =1 anterograde flow on their angiograms, were included. Fifty-one patients were taking statins before admission, and 43 patients were not. Their angiograms were reviewed and coronary collaterals were graded from 0 to 3 according to the Cohen-Rentrop method. The statin-treated group had a significantly higher mean collateral score compared with the patients not taking statins (2.05 vs 1.52, P =.005). Multivariate analysis supported the significance of the effect of statin therapy on the collateral score. There was no relation between collateral score and low- density lipoprotein levels (r = -0.06, P =.64). The statin- treated group also had a significantly higher left ventricular ejection fraction compared to the patients not taking statins (51% vs 44%, P <.05). CONCLUSIONS: Statin therapy is associated with enhanced coronary collateral formation in patients with severely diseased coronary arteries. PMID: 14597938 LIFE-SAVER: World's largest cholesterol-lowering trial reveals massive benefits for high-risk patients 13-NOV-2001 Los Angeles: Around a third of all heart attacks and strokes can be avoided in people at risk of vascular disease by using statin drugs to lower blood cholesterol levels - irrespective of the person's age or conclusion of UK researchers who have just completed the world's largest randomised trial on cholesterol-lowering therapy. Unveiling the key findings today (Tuesday 13 November) at the American Heart Association's Scientific Sessions 2001, lead researcher Professor Rory Collins said: "This is a stunning result, with massive public health implications. We've found that cholesterol-lowering treatment can protect a far wider range of people than was previously thought, and that it can prevent strokes as well as heart attacks." The MRC/BHF Heart Protection Study (HPS) involved 20,000 volunteers aged 40-80 years who were at high risk of coronary heart disease, but for whom there was substantial uncertainty about the balance of benefits and safety of cholesterol-lowering therapy. It specifically targeted groups of patients in which there was little direct evidence of benefit - including women, the over 70s, people with diabetes, those with non-coronary vascular disease, and those with average or below-average cholesterol levels. Volunteers were allocated either 40mg daily simvastatin as cholesterol-lowering therapy, or matching dummy tablets. Study treatment and follow-up continued for an average of five and a half years in 69 UK hospitals. The funding of £21 million (US $32 million) was provided by the UK's Medical Research Council (MRC), the British Heart Foundation (BHF), and the pharmaceutical companies Merck & Co. Inc. and Roche Vitamins Ltd. The study was, however, designed, conducted and analysed entirely independently of all funding sources by the Clinical Trial Service Unit of Oxford University. It started in 1994 and ended only last month. Summary of major findings o Cholesterol-lowering with statin treatment reduces the risk of heart attacks and of strokes by at least one-third, as well as reducing the need for arterial surgery, angioplasty and amputations. o Reductions of at least one-third in these 'major vascular' events were found in a very wide range of high-risk patients for whom there had previously been uncertainty about using cholesterol-lowering therapy: o women as well as men; o people aged over 70 as well as younger people; o people with blood levels of total cholesterol below 200mg/dl (approx. 5mmol/l) or of 'bad' LDL cholesterol below 120mg/dl (approx. 3mmol/l), as well as those considered to have 'high' levels. o About 5 years of statin treatment typically prevents heart attacks, strokes or other major vascular events in: o 100 of every 1000 people who've previously had a heart attack o 80 of every 1000 people with angina or some other evidence of coronary heart disease o 70 of every 1000 patients who've previously had a stroke o 70 of every 1000 people with occlusive disease in leg or other arteries o 70 of every 1000 people with diabetes o In addition, cholesterol-lowering reduces the risk of being hospitalised because of worsening angina - typically, about 30 fewer admissions per 1000 treated for 5 years. o The benefits increase throughout the study treatment period (so more prolonged therapy might be expected to produce even bigger benefits), and are additional to those of other treatments used to prevent heart attacks and strokes. o This trial provides uniquely reliable evidence about the safety of this simvastatin regimen, with no support for previous concerns about possible adverse effects of lowering cholesterol on particular non-vascular causes of death, on cancers or on strokes due to bleeding. Professor Collins, HPS lead investigator, said: "We knew from other studies that statins lowered 'bad' LDL cholesterol, and reduced heart disease risk in some circumstances. But, HPS now provides the first direct evidence that cholesterol-lowering therapy cuts the risk of heart attacks and strokes by at least one third not just in people who already have coronary disease but also in those who have diabetes, narrowing of arteries in their legs or a previous history of stroke. It shows that, for high-risk patients, cholesterol-lowering therapy produces substantial benefits even among those considered to have 'low' cholesterol levels. It also provides the first clear evidence of benefit in women and the over 70s. The study's size, and the wide range of high-risk patients included, means that doctors now have evidence that is uniquely clear and reliable. "In this trial, 10 thousand people were on a statin. If now, an extra 10 million high-risk people worldwide go onto statin treatment, this would save about 50,000 lives each year - that's a thousand a week. These results are at least as important as previous findings for aspirin's effects on heart attack and strokes. Those findings changed medical practice, and we expect these to have the same effect. In fact, statins are the new aspirin."
> "Zee" <[email protected]hoo.com> wrote in message > news:[email protected]... > > [email protected] (Zee) wrote in message > news:<[email protected]>... > > Try your statin here, and keep in mind it is estimated > > no more than 10 percent of serious ADRs are ever > > reported. > > > > > > B'adant > > I would think that most serious cases would be recognized > via the CPK test, but maybe not reported - I don't know > most Drs. habits. But in case of death I would think it > would be, but again I'm not sure. Also keep in mind that > there are causes other than statins to Rhabdomyolysis and > indeed it was known prior to the development of statins. > > Bill Apparently not Bill. It is only a voluntary reporting system. And there are many reasons a doctor would voluntarily choose not to report. I'll paraphrase a document I received recently. *Most get their drug information from pharma reps. Many take gifts from those same reps including jewellery, computers, prommissory notes and trips to luxury resorts. That this affects their prescribing habits is incontrovertible: just ask the drug company execs who happily put their signature to funding of this profitible expense. $$$$ *Most don't read the warnings from drugs companies or medical journals regularly. Some have little training on how drugs work, only what they are prescribed for, and do not know how common ADRs are or how to recognize them. *Many prescribe off-label based on incidental evidence and conversations with drugs reps (illegal) and other doctors. *Most doctors are paid for service rather than for patient so their income goes up if they write more prescriptions taking 2 minutes instead of taking more time discussing diet, exercise and other options. *No doctor ever wants to talk about the primary reason doctors don't want to write ADRs--fear of being sued or damage to their reputation. They cloud the issue talking about the time it takes... I'll continue this in a following post. B'adant
Top posting for this one. B'adant The Washington Times www.washingtontimes.com ------------------------------------------------------------ -------------------- FDA unaware of most drug complaints By Joyce Howard Price THE WASHINGTON TIMES Published March 7, 2004 ------------------------------------------------------------ -------------------- The Food and Drug Administration receives more than 300,000 reports annually about adverse effects caused by drugs on the market, but officials say those reports don't include most patients' concerns because local health care professionals are not required to report complaints to the federal level. "We've always estimated we get about 10 percent of all reports," said Dr. Paul Seligman, director of the FDA's Office of Pharmacoepidemiolgy and Statistical Science. A Harvard study two years ago, published in the Journal of the American Medical Association, cited previous research that estimated only 10 percent of serious adverse effects are given to the FDA through its MedWatch program. MedWatch is the voluntary system the FDA established in 1993 for health professionals to report serious adverse reactions and problems related to drugs, biologics, medical devices, dietary supplements, cosmetics and infant formulas. MedWatch followed another FDA voluntary-reporting program started in 1961. Pharmaceutical firms are required to report adverse effects to the FDA. "Ninety percent of the reports we receive about the most adverse effects come from manufacturers," said Dr. Seligman, noting that many doctors and pharmacists first report such complaints to manufacturers. Dr. Gregory A. Thompson, director of the Los Angeles County- University of Southern California Drug Information Center, which advises health care professionals about proper dosages and side effects of medications, said the proportion of serious drug complications voluntarily reported to the FDA is "far lower" than 10 percent. "[Health professionals] might report 10 percent of people who die of serious side effects of drugs," Dr. Thompson said. He stressed that there should be more reporting, noting that the hospital where he works ?? the USC Medical Center ?? "reports hundreds of serious complaints yearly" to the FDA. The 2002 Harvard study in JAMA found that one in five new drugs produced major side effects that were not discovered until after FDA approval. The FDA says no one should be surprised that it's not until a drug has been taken by hundreds of thousands -- or millions -- of people that some complications are discovered. One person trying to get Congress to require physicians to report adverse events after drug approval is Marvin Moskowitz, 76, of Lancaster, Calif. He said he took a drug for heartburn and developed an unwanted condition. "Tissue developed under my breasts, and I wanted someone to help me with the $9,000 medical bills I incurred," he said. Asked about Mr. Moskowitz's push for federal legislation that would require physicians to report to the FDA "all serious side effects and complications," Dr. Seligman said, "the practice of medicine is regulated on a state-by- state basis. The FDA has no legal authority over health care providers, only manufacturers." A spokeswoman for the American Medical Association said such a change "would put an incredible burden on the health care system." > "Zee" <[email protected]> wrote in message > news:[email protected]... > > [email protected] (Zee) wrote in message > news:<[email protected]>... > > Try your statin here, and keep in mind it is estimated > > no more than 10 percent of serious ADRs are ever > > reported. > > > > > > B'adant > > I would think that most serious cases would be recognized > via the CPK test, but maybe not reported - I don't know > most Drs. habits. But in case of death I would think it > would be, but again I'm not sure. Also keep in mind that > there are causes other than statins to Rhabdomyolysis and > indeed it was known prior to the development of statins. > > Bill
Thanks. In this case the reporting of deaths MAY be somewhat higher than typical because there is a good test for the condition (CPK) and a known correlation. Of course, one can not know for sure. Bill
All I know is my own Family doctor takes Crestor himself. He's late 40's very fit and hates taking meds. It's heresay, for sure but he seems to think its safe enough to take it himself.
