Statins; an expensive way to damage your health!

There is to much evidence Statins serve only one: the producer

 

Here's a list of many studies, showing the dangerous effects and side effects of statins. The first one shows how statins can be used after organ transplantation to reduce the efficacy of the immunesystem to inhibit organ rejection. Oeps, does that mean statins reduce the immune system, raising the risk for cancer? YES!!!

Potential immunologic effects of statins in cancer following transplantation.

Fildes JE, Shaw SM, Williams SG, Yonan N. Cancer Immunol Immunother. 2008 Jun 4.
The Transplant Centre, University Hospital of South Manchester NHS Foundation Trust, Wythenshawe Hospital, Manchester, M23 9LT, UK, james.fildes@manchester.ac.uk.

3-hydroxy-3-methyglutaryl CoA reductase inhibitors (statins) are frequently used following organ transplantation and have well reported pleiotropic effects, including immunomodulation, which may be of benefit in preventing graft rejection.

However, the immunomodulatory effects of statins on cell transformation and malignancy, combined with the immunologic processes and administration of immunosuppression are almost completely unknown. The administration of immunosuppression is well recognised as the main cause of cancer following transplantation, so the addition of an immunomodulatory agent should be associated with an increased incidence of cancer, as immune surveillance and response may be suppressed, allowing cellular transformation and proliferation combined with lack of recognition to occur. This hypothetical review attempts to delineate the mode of action of statins in terms of pro/anti-carcinogenic mechanisms, while considering graft rejection and the presence of immunosuppression.

Rapid onset of muscle weakness (rhabdomyolysis) associated with the combined use of simvastatin and colchicine.

Justiniano M, Dold S, Espinoza LR .J Clin Rheumatol. 2007 Oct;13(5):266-8.
Rheumatology Section, Department of Internal Medicine, LSU Health Sciences Center, 2020 Gravier Street, New Orleans, LA 70112, USA.

We report a case of a patient with mild chronic renal insufficiency who had been taking simvastatin for over a year and developed acute weakness within 3 weeks after the start of treatment with colchicine for acute gouty bursitis. Profound muscle weakness of lower extremities with inability to stand up and/or walk was present. Elevated muscle enzymes and findings on electromyography were consistent with myopathy. Rapid improvement in muscle strength accompanied by prompt resolution of abnormal elevation of muscle enzymes followed cessation of both medications. Both colchicine and statin therapy may be associated with myopathy, which usually occurs after several months of therapy. The concomitant use, however, of colchicine and statin has been associated with the rapid onset of muscle weakness. Four patients with similar clinical and laboratory characteristics to our patient's after the combined use of colchicine and statins have been described in the literature. Patients receiving combination therapy with colchicine and simvastatin, particularly in the presence of renal insufficiency, should be monitored for the development of myopathy, including rhabdomyolysis.

Drug-induced myopathies.

Klopstock T. Curr Opin Neurol. 2008 Oct;21(5):590-5.
Friedrich-Baur-Institute, Department of Neurology, Ludwig-Maximilians-University, Munich, Germany. Thomas.Klopstock@med.uni-muenchen.de

PURPOSE OF REVIEW: Drug-induced muscle disorders are important causes of morbidity, but the risk-benefit profile of the incriminated drugs must be put into perspective. This review highlights some recent advances on statin-induced and antiretroviral drug-induced myopathies and calls attention to some less familiar myotoxic disorders.

RECENT FINDINGS: In statin myopathy, reduction of coenzyme Q has been discussed as a key mechanism. However, data on coenzyme Q concentration and mitochondrial dysfunction in muscle of these patients are not conclusive. The first two controlled trials on coenzyme Q supplementation in statin myopathy have yielded contradictory results and do not support a routine supplementation.

In human immunodeficiency virus infection, the advent of highly active antiretroviral therapy has led to a shift from virus-related to drug-induced morbidity. The knowledge of these distinct syndromes allows rational management. In addition, an omnium-gatherum is presented with recent findings on drug-induced dermatomyositis, tendinopathy, rhabdomyolysis, and local myotoxicity. These latter topics are intended to direct attention to less familiar but still clinically relevant myotoxic events.

SUMMARY: Statin myotoxicity may be prevented in many cases by anticipation of drug-drug interactions. On the contrary, undue withdrawal of statins owing to minor myalgias should be avoided. A large and appropriately powered trial is required to finally determine whether supplementation of coenzyme Q can mitigate statin myopathy. The identification of individual genetic risk factors for myotoxicity is a key challenge for future pharmacogenomic research.

Statin myopathy as a metabolic muscle disease.

Phillips PS, Haas RH. Expert Rev Cardiovasc Ther. 2008 Aug;6(7):971-8.
Catheterization Laboratories, Scripps Mercy Hospital, 4077 4th Avenue, San Diego, CA 92103, USA. phillips.paul@scrippshealth.org


The etiology of statin myopathy remains unclear and concern about this toxicity is a leading reason that statins are underutilized. A number of observations suggest that this toxicity may be due to the metabolic effects of lipid-lowering in patients with minor muscle disorders. These patients have a high frequency of mutations for metabolic muscle diseases and often have depleted mitochondrial enzymes. Their exercise physiology and biopsy findings indicate reduced oxidation of fats and mitochondrial dysfunction. These subjects are often intolerant of other lipid-lowering therapies in addition to statins, which suggests that the myopathy is due to lipid-lowering itself more than a simple pharmacokinetic reaction to high statin levels. Altogether, these findings support the concept that statin myopathy is a metabolic muscle disease.

Combination drug products: an indication for medication reconciliation and pharmacist counseling.

Stroup J, Stephens J. J Am Pharm Assoc (2003). 2008 Jul-Aug;48(4):541-3.
Department of Internal Medicine, Center for Health Sciences, Oklahoma State University, Tulsa 74127, USA. jeffrey.stroup@okstate.edu

OBJECTIVE: To describe a case of drug-induced rhabdomyolysis that occurred because of an inadvertent duplication in statin therapy.

SETTING: Tertiary care academic teaching hospital in Oklahoma, December 2005.

PATIENT PRESENTATION: A 45-year-old white man received the combination therapy simvastatin 80 mg/ezetimibe 10 mg (Vytorin-Merck/Schering-Plough) daily after a coronary artery bypass graft (CABG) procedure. This patient was also receiving simvastatin 80 mg daily and cyclosporine 150 mg twice daily, which had been prescribed before CABG. The use of two simvastatin products prescribed at high doses subsequently led to rhabdomyolysis and renal failure.

RESULTS: Statin therapy was discontinued at admission, and the patient was aggressively hydrated with 0.45% sodium chloride injection containing 50 mEq of sodium bicarbonate per liter at a rate of 250 mL/hour to alkalinize his urine. Hydration therapy alone decreased the patient's serum creatine kinase level to 910 units/L by day 7, but his serum creatinine remained elevated at 2.7 mg/dL. To manage rhabdomyolysis during hospitalization, the patient received a total of 6.7 liters of 0.45% sodium chloride injection with 50 mEq of sodium bicarbonate per liter. The patient was discharged 7 days after admission to a rehabilitation facility for continued strengthening of muscle tissue.

CONCLUSION: The increased use of combination drug products poses an increased risk of therapeutic duplication in patients. The medication reconciliation process and proper counseling by pharmacists is necessary to avoid these potentially harmful errors.

Expensive drug compared to placebo give hardly any benefit, but higher rates in cancer. What if the "placebo" would have been replaced with omega 3 fatty acids and K2/D3?

Intensive lipid lowering with simvastatin and ezetimibe in aortic stenosis.

N Engl J Med. 2008 Sep 25;359(13):1343-56. Epub 2008 Sep 2.
Comment in:
N Engl J Med. 2008 Sep 25;359(13):1357-66.
N Engl J Med. 2008 Sep 25;359(13):1395-8.
N Engl J Med. 2008 Sep 25;359(13):1398-9.
N Engl J Med. 2008 Sep 25;359(13):1400-2.

Rossebø AB, Pedersen TR, Boman K, Brudi P, Chambers JB, Egstrup K, Gerdts E, Gohlke-Bärwolf C, Holme I, Kesäniemi YA, Malbecq W, Nienaber CA, Ray S, Skjaerpe T, Wachtell K, Willenheimer R; SEAS Investigators.
Collaborators (445)
Division of Cardiology, Aker University Hospital, Trondheimsveien 235, N-0514 Oslo, Norway. anne@rossebo.net

BACKGROUND: Hyperlipidemia has been suggested as a risk factor for stenosis of the aortic valve, but lipid-lowering studies have had conflicting results.

METHODS: We conducted a randomized, double-blind trial involving 1873 patients with mild-to-moderate, asymptomatic aortic stenosis. The patients received either 40 mg of simvastatin plus 10 mg of ezetimibe or placebo daily. The primary outcome was a composite of major cardiovascular events, including death from cardiovascular causes, aortic-valve replacement, nonfatal myocardial infarction, hospitalization for unstable angina pectoris, heart failure, coronary-artery bypass grafting, percutaneous coronary intervention, and nonhemorrhagic stroke. Secondary outcomes were events related to aortic-valve stenosis and ischemic cardiovascular events.

RESULTS: During a median follow-up of 52.2 months, the primary outcome occurred in 333 patients (35.3%) in the simvastatin-ezetimibe group and in 355 patients (38.2%) in the placebo group (hazard ratio in the simvastatin-ezetimibe group, 0.96; 95% confidence interval [CI], 0.83 to 1.12; P=0.59).

Aortic-valve replacement was performed in 267 patients (28.3%) in the simvastatin-ezetimibe group and in 278 patients (29.9%) in the placebo group (hazard ratio, 1.00; 95% CI, 0.84 to 1.18; P=0.97).

Fewer patients had ischemic cardiovascular events in the simvastatin-ezetimibe group (148 patients) than in the placebo group (187 patients) (hazard ratio, 0.78; 95% CI, 0.63 to 0.97; P=0.02), mainly because of the smaller number of patients who underwent coronary-artery bypass grafting.

Cancer occurred more frequently in the simvastatin-ezetimibe group (105 vs. 70, P=0.01).

CONCLUSIONS: Simvastatin and ezetimibe did not reduce the composite outcome of combined aortic-valve events and ischemic events in patients with aortic stenosis. Such therapy reduced the incidence of ischemic cardiovascular events but not events related to aortic-valve stenosis. (ClinicalTrials.gov number, NCT00092677.) 2008 Massachusetts Medical Society