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Dr Vasquez has relocated to Fort Worth and is still available by 
Let's look at the advantages and disadvantages of "cure" versus "palliative treatment."
pal·li·a·tive (pal' ee ate' iv) adj. 1. Tending or serving to palliate. 2. Relieving or soothing the symptoms of a disease or disorder without effecting a cure. --pal·li·a·tive n. One that palliates, especially a palliative drug or medicine. From the American Heritage Dictionary, 3rd Edition.
In healthcare, palliative treatment is supposedly reserved for patients with health conditions that are not curable. Ideally, the disease should be treated and eliminated, and "cure" is what all physicians should seek to accomplish. When the disease cannot be cured, then suppression of symptoms and manifestations of the disease is the next best treatment approach because it improves the patient's quality of life and may help prevent other complications of the disease.
For example, high blood pressure (hypertension) can be considered a disease. Effectively curing the patient of this condition would mean helping the patient to arrive at a condition where he/she no longer has hypertension because the underlying cause of the hypertension was treated, and therefore no longer exists. Thus the patient could described as "cured" because they no longer have that health problem.
cured, cur·ing, cures. --tr. 1. To restore to health. 2. To effect a recovery from. 3. To remove or remedy (something harmful or disturbing). From the American Heritage Dictionary, 3rd Edition.
Today, however, many physicians do not take the time and effort to seek the cure of their patients' conditions. Unfortunately, "palliative medicine" is what most people receive. This means that the underlying cause of the hypertension is never even pursued, let alone treated, let alone treated to completion. This means that a patient with hypertension is given blood pressure-lowering medications for the rest of his or her life because they continue to have hypertension for the rest of their life because the underlying cause of the hypertension has never been treated to completion. It is true that the patient may have fewer symptoms of hypertension (such as headaches) and they may have reduced risk of complications from hypertension (such as kidney failure), but they may also suffer from "medication side-effects" such as sexual dysfunction or "impotence", fatigue, depression, dizziness, dry mouth, skin rash, kidney failure, stomach upset, constipation, diarrhea, nausea, vomiting.... Additionally, the cost of such medications can place an undue financial burden on many patients.
Summary and comparison | COMPREHENSIVE HEALTHCARE: treating the cause, attempting to reach "cure" | NON-COMPREHENSIVE TREATMENT: palliative treatment , suppression of disease and symptoms |
advantages |
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disadvantages |
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I believe that comprehensive healthcare which aims at identifying and treating the cause of the illness to thus effect "cure" is superior to non-comprehensive palliative treatment, which simply suppresses the disease and and its symptoms while the disease may still progress and which often forces the patient to assume life-long financial burden and risk of medication side-effects.
This does not mean to say that palliative treatment has no role in healthcare. Palliative treatment is excellent for patients with incurable diseases and for patients who are not willing to invest the time and energy that may be necessary to find and treat the cause of their problem. Palliative treatment is also excellent in emergency situations that need immediate resolution or suppression. However, in my judgment, the routine use of long-term palliative symptom-suppressing treatment for health problems is to the disadvantage of the patient, who in most cases prefers to be cured of their condition and helped to a state of greater health, rather than take medications for the rest of their life while the disease process continues to fester. Ultimately the patient must choose, but many patients are never given the full range of options; often they are not told by their doctors that cure is possible; they are simply told, "Here, take these pills." Curing disease is superior to covering disease.
Let's look at one more common example: high cholesterol.
- The "holistic" approach is to use vitamins and nutrients to help optimize health so that cholesterol levels naturally become lower as the body becomes more healthy. Side effects of this approach are improved overall health and increased longevity
- The chemical/suppressive approach is to use drugs that inhibit the formation of cholesterol. Adverse effects from this type of treatment are not uncommon:
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.
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.
Natural medicines provide the most safe and effective approach to treating and preventing many chronic diseases.
