Note to Houston-area patients: |
Sorry, not currently accepting new patients due to research/work schedule. Please check back periodically. Email/phone consultations are available only for established patients. |
| Front page |
| Main page |
| Credentials and Overview |
Office Location |
| Appointments and Consultations |
| Clinical Art and Sciences |
| Textbooks and Seminars for Doctors |
| Contents of This Site |
|
|
|
“Bastyr is the leading academic force in natural medicine. I have great respect for the school...” Andrew Weil, MD |
|
|
|
Dr Vasquez has relocated to Fort Worth and is still available by 
Adverse effects of cholesterol-lowering drugs:
These drugs are sold as Atorvastatin, cerivastatin, fluvastatin, lovastatin, pravastatin, and simvastatin under the names Lescol, Lipitor, Mevacor, Pravachol, Zocor, Baycol (Baycol was removed from the U.S. market in August 2001.)
BAYER VOLUNTARILY WITHDRAWS BAYCOL
FDA today announced that Bayer Pharmaceutical Division is voluntarily withdrawing Baycol (cerivastatin) from the U.S. market because of reports of sometimes fatal rhabdomyolysis, a severe muscle adverse reaction from this cholesterol-lowering (lipid-lowering) product. The FDA agrees with and supports this decision.
Baycol (cerivastatin), which was initially approved in the U.S. in 1997, is a member of a class of cholesterol lowering drugs that are commonly referred to as "statins." Statins lower cholesterol levels by blocking a specific enzyme in the body that is involved in the synthesis of cholesterol. While all statins have been associated with very rare reports of rhabdomyolysis, cases of fatal rhabdomyolysis in association with the use of Baycol have been reported significantly more frequently than for other approved statins.
Fatal rhabdomyolysis reports with Baycol have been reported most frequently when used at higher doses, when used in elderly patients, and particularly, when used in combination with gemfibrozil (LOPID and generics), another lipid lowering drug. FDA has received reports of 31 U.S. deaths due to severe rhabdomyolysis associated with use of Baycol, 12 of which involved concomitant gemfibrozil use.
- Carcinogenicity of lipid-lowering drugs.
Newman TB, Hulley SB. - Department of Laboratory Medicine, School of Medicine, University of California, San Francisco, USA.
- JAMA 1996 Jan 3;275(1):55-60
OBJECTIVE--To review the findings and implications of studies of rodent carcinogenicity of lipid-lowering drugs. DATA SOURCES--Summaries of carcinogenicity studies published in the 1992 and 1994 Physicians' Desk Reference (PDR), additional information obtained from the US Food and Drug Administration, and published articles identified by computer searching, bibliographies, and consultation with experts. STUDY SAMPLE--We tabulated rodent carcinogenicity data from the 1994 PDR for all drugs listed as "hypolipidemics." For comparison, we selected a stratified random sample of antihypertensive drugs. We also reviewed methods and interpretation of carcinogenicity studies in rodents and results of clinical trials in humans. DATA SYNTHESIS--All members of the two most popular classes of lipid-lowering drugs (the fibrates and the statins) cause cancer in rodents, in some cases at levels of animal exposure close to those prescribed to humans. In contrast, few of the antihypertensive drugs have been found to be carcinogenic in rodents. Evidence of carcinogenicity of lipid-lowering drugs from clinical trials in humans is inconclusive because of inconsistent results and insufficient duration of follow-up. CONCLUSIONS--Extrapolation of this evidence of carcinogenesis from rodents to humans is an uncertain process. Longer-term clinical trials and careful postmarketing surveillance during the next several decades are needed to determine whether cholesterol-lowering drugs cause cancer in humans. In the meantime, the results of experiments in animals and humans suggest that lipid-lowering drug treatment, especially with the fibrates and statins, should be avoided except in patients at high short-term risk of coronary heart disease.
- FDA adverse event reports on statin-associated rhabdomyolysis.
Omar MA, Wilson JP.
Division of Pharmacy Practice and Administration, College of Pharmacy, University of Texas at Austin, Austin, TX, USA.Ann Pharmacother 2002 Feb;36(2):288-95
OBJECTIVE: To determine the number of cases of statin-associated rhabdomyolysis reported to the Food and Drug Administration for 6 statins and to profile the cases. METHODS: A retrospective analysis of all domestic and foreign reports of statin-associated rhabdomyolysis between November 1997 and March 2000 was conducted. Outcome measures included the total number of reports (initial plus follow-up), the number of unique cases, age, gender, percentages of report codes and role codes, and frequencies of concomitant interacting drugs that may have precipitated rhabdomyolysis, outcomes codes, and report source codes. RESULTS: There were 871 reports of statin-associated rhabdomyolysis in the 29-month time frame examined, representing 601 cases. The following number of cases were associated with each of the individual statins: simvastatin, 215 (35.8%); cerivastatin, 192 (31.9%); atorvastatin, 73 (12.2%); pravastatin, 71 (11.8%); lovastatin, 40 (6.7%); and fluvastatin, 10 (1.7%). Drugs that may have interacted with the statins were present in the following number of cases: mibefradil (n = 99), fibrates (n = 80), cyclosporine (n = 51), macrolide antibiotics (n = 42), warfarin (n = 33), digoxin (n = 26), and azole antifungals (n = 12). The reports of 62.1% of cases were classified as expedited. Statins were designated as the primary suspect in 72.0% of the cases. Death was listed as the outcome in 38 cases. The majority of reports (n = 556) were from health professionals. CONCLUSIONS: Compared with the other statins, simvastatin and cerivastatin were implicated in a relatively higher number of reports. Because of the various limitations of a spontaneous reporting-system database, caution is urged when interpreting the relative number of cases reported.
- Fatal rhabdomyolysis caused by lipid-lowering therapy.
Federman DG, Hussain F, Walters AB.
Department of Medicine and the Pharmacy Service, VA Connecticut Health Care System, West Haven, CT 06516, USA. - South Med J 2001 Oct;94(10):1023-6
Treatment of hypercholesterolemia has been shown to reduce mortality in patients with coronary artery disease. Patients with severe lipid abnormalities may require high-dose statin therapy, at times used in combination with additional agents. We report a case of fatal rhabdomyolysis caused by the combination of simvastatin and gemfibrozil. Clinicians should be aware of risk factors for rhabdomyolysis, which include underlying renal insufficiency, high-dose statin therapy, and combination therapy with a fibrate.
- Simvastatin-associated memory loss.
-
Orsi A, Sherman O, Woldeselassie Z.
Pharmacy Program, Bronx VA Medical Center, New York 10468, USA. - Pharmacotherapy 2001 Jun;21(6):767-9
-
The statins are widely used to treat dyslipidemias. They are generally associated with mild adverse effects, but rarely, more serious reactions may occur. A 51-year-old man experienced delayed-onset, progressive memory loss while receiving simvastatin for hypercholesterolemia. His therapy was switched to pravastatin, and memory loss resolved gradually over the next month, with no recurrence of the adverse effect.
Statins and risk of polyneuropathy: a case-control study.
Gaist D, Jeppesen U, Andersen M, Garcia Rodriguez LA, Hallas J, Sindrup SH.
Department of Neurology, Odense University Hospital, Denmark.- Neurology 2002 May 14;58(9):1333-7
BACKGROUND: Several case reports and a single epidemiologic study indicate that use of statins occasionally may have a deleterious effect on the peripheral nervous system. The authors therefore performed a population-based study to estimate the relative risk of idiopathic polyneuropathy in users of statins. METHOD: The authors used a population-based patient registry to identify first-time-ever cases of idiopathic polyneuropathy registered in the 5-year period 1994 to 1998. For each case, validated according to predefined criteria, 25 control subjects were randomly selected among subjects from the background population matched for age, sex, and calendar time. The authors used a prescription register to assess exposure to drugs and estimated the odds ratio of use of statins (ever and current use) in cases of idiopathic polyneuropathy compared with control subjects. RESULTS: The authors verified a diagnosis of idiopathic polyneuropathy in 166 cases. The cases were classified as definite (35), probable (54), or possible (77). The odds ratio linking idiopathic polyneuropathy with statin use was 3.7 (95% CI 1.8 to 7.6) for all cases and 14.2 (5.3 to 38.0) for definite cases. The corresponding odds ratios in current users were 4.6 (2.1 to 10.0) for all cases and 16.1 (5.7 to 45.4) for definite cases. For patients treated with statins for 2 or more years the odds ratio of definite idiopathic polyneuropathy was 26.4 (7.8 to 45.4). CONCLUSIONS: Long-term exposure to statins may substantially increase the risk of polyneuropathy. - Statin-induced fibrotic nonspecific interstitial pneumonia.
Lantuejoul S, Brambilla E, Brambilla C, Devouassoux G.
Dept of Cellular Pathology, Centre Hospitalier Universitaire de Grenoble, Universite J. Fourier, France. - Eur Respir J 2002 Mar;19(3):577-80
Statins inhibit the 3-hydroxy-3-methylglutaryl coenzyme A reductase, reduce the serum level of low-density lipoprotein cholesterol, and are extensively prescribed to prevent cardiovascular mortality and morbidity. Few systemic adverse effects, such as pseudopolymyositis, lupus-like syndromes, and anecdotal hypersensitivity pneumonitis, have been reported. A simvastatin-induced diffuse interstitial pneumonia associated with a nonspecific interstitial pneumonia pattern at histological analysis is repoted here. Ultrastructural analysis showed a diffuse cytoplasmic accumulation of intralysosomial lamellar inclusions in type II pneumonocytes, histiocytes and endothelial cells, suggesting a shared pathogenesis with amphiphilic drug-induced toxic lung injury. Because statins are increasingly prescribed, statin-induced interstitial lung disorders may be more frequently observed and early recognition will be required. - Statins as immunosuppressive agents.
Kobashigawa JA.
Division of Cardiology University of California at Los Angeles Medical Center 100 UCLA Medical Plaza, #630 Los Angeles, CA 90095. - Liver Transpl 2001 Jun;7(6):559-61
BACKGROUND: Coronary artery disease in the transplanted heart, also known as cardiac allograft vasculopathy, is one of the major causes of mortality late after heart transplantation. This accelerated form of atherosclerosis also affects the donor organs of other transplant recipients including that of liver, kidney and lung. There are multiple immune and non-immune risk factors associated with this disease process, one of which is hyperlipidemia. Use of lipid lowering agents, specifically HMG-CoA reductase inhibitors (statins) was initially reported to have outcomes benefit and possibly immunosuppressive effects in a single center study of heart transplant recipients. Other subsequent studies have supported this beneficial effect. Method and Results: In a recent paper by Kwak and colleagues, the specific mechanism for this immunosuppressive effect has been elucidated through the use of experiments monitoring cell surface expression assayed by fluorescence-activated cell sorting and by immunofluorescence as well as mRNA levels of major histocompatibility complex class II (MHC-II). They report that statins repress induction of MHC-II by interferon-gamma and that this in turn represses activation of T-lymphocytes and other cell types including primary human smooth muscle cells and fibroblasts, as well as in established cell lines such as ThP1, melanomas, and HeLa cells. CONCLUSION: In addition to previous clinical and laboratory publications this work by Kwak and colleagues has provided a firm scientific rationale to support the use of statins as adjunct immunosuppressive agents in organ transplantation. - Acute hepatitis induced by HMG-CoA reductase inhibitor, lovastatin.
Grimbert S, Pessayre D, Degott C, Benhamou JP.
Service d'Hepatologie, Unite de Recherches de Physiopathologie Hepatique (INSERM U 24), Hopital Beaujon, Clichy, France. - Dig Dis Sci 1994 Sep;39(9):2032-3
The HMG-CoA reductase inhibitor, lovastatin, is known to induce asymptomatic liver dysfunction in a few patients. We report the case of an adult who suffered from clinical hepatitis three months after the onset of lovastatin administration. Manifestations included asthenia, jaundice, and increased aminotransferase and alkaline phosphatase activities. Histologic examination showed centrilobular necrosis, centrilobular cholestasis, and infiltrates with mononuclear and polymorphonuclear cells, including eosinophils. Withdrawal of lovastatin was followed by complete normalization of liver tests within two months. - Simvastatin reduces levels of CoQ-10, an important nutrient for cellular function. Low levels of CoQ-10 correlate with increased risk for cancer, allergies, and low survival in patients with HIV. Not surprisingly, some people develop allergic skin problems with use of these drugs.
- Dermatology 1993;186(4):248-52
- All lipid-lowering drugs in the "statin" class cause cancer in animals. Some studies have shown that these drugs cause cancer in humans, too, and that these drugs should therefore be used only for the short-term.
- JAMA 1996 Jan 3;275(1):55-60 - See abstract below.
- There is one case report of a patient developing cancerous changes in her thyroid gland after starting simvastatin.
- Tenn Med 2000 Jun;93(6):210-2
- Yet, another larger study showed that simvastatin did not increase the risk for cancer.
- Am J Cardiol 2000 Aug 1;86(3):257-62
- High Lp(a) levels are a strong risk factor for cardiovascular disease. Treatment with simvastatin is associated with a significant increase in Lp(a) levels.
- Cardiovasc Drugs Ther 1995 Dec;9(6):785-9
- Minerva Med 1995 Jul-Aug;86(7-8):299-303
- HMG-CoA reductase inhibitors can cause liver damage, muscle injury, and kidney problems - these problems can be fatal.
- Tenn Med 2000 Jun;93(6):210-2
- Tenn Med 2000 Jun;93(6):210-2
Why choose a treatment approach that 1) does not address the cause of the problem, 2) potentially causes liver damage, and 3) may increase the risk for cancer, when a safe and natural alternative is available? For many people, there are effective ways to lower cholesterol without the risks associated with using simvastatin or other HMG-CoA reductase inhibitors. Opting instead for safe and natural treatments, many patients choose to avoid the risks associated with synthetic drugs.
Simvastatin lowers cholesterol levels by inhibiting the enzyme that makes cholesterol in the body: HMG CoA reductase. Although attaining lower cholesterol helps to lower the risk of cardiovascular disease, inhibiting HMG CoA reductase with chemical drugs is associated with some problems, such as the following:
Natural medicines provide the most safe and effective approach to treating and preventing many chronic diseases.
