Health Report:

Hormone Replacement Therapy (HRT) & Breast Cancer

 

Stool DNA Testing & Cancer of the Colon & Rectum

 

“A critical weekly review of important new research findings for health-conscious readers…”

 

By, Robert A. Wascher, MD, FACS

Last Updated:  02/08/2009

The information in this column is intended for informational purposes only, and does not constitute medical advice or recommendations by the author.  Please consult with your physician before making any lifestyle or medication changes, or if you have any other concerns regarding your health.

 

HORMONE REPLACEMENT THERAPY (HRT) & BREAST CANCER

 

 

Hormone replacement therapy (HRT) came of age during the sexual revolution in the United States in the 1960s.  During this revolution, premenopausal women not only finally gained control over their reproductive systems with the advent of oral contraceptives, but postmenopausal women could also effectively alleviate the symptoms of menopause by taking HRT pills.  However, despite a recent avalanche of clinical research data linking the most commonly prescribed form of HRT with an increased risk of breast cancer, diehard supporters of HRT continue to cling to alternative explanations for the lock-step rise and fall of breast cancer cases relative to the number of HRT prescriptions filled in the United States (and around the world).  While the cloak of obfuscation and overstated benefits that has obscured the risks of HRT finally began to be peeled away with the 2002 publication of the preliminary results of the enormous Women’s Health Initiative Study, entrenched proponents of HRT are not going down without a fight.  Recently, persistent HRT advocates have attempted to link a modest and recent decrease in the incidence of screening mammograms with the recent and historical decline in the number of breast cancer cases diagnosed in the United States, despite highly compelling research evidence that breast cancer rates are falling as a direct consequence of declining HRT use by women.  Now, a new study, just published in the New England Journal of Medicine, substantially adds to the findings of other recent studies in debunking this alternate hypothesis.

 

 

In this new study, the Women’s Health Initiative (WHI) study researchers have gone back and reviewed their data on the nearly 17,000 women who volunteered for this pivotal women’s health study (the average duration of follow-up in this prospective, randomized, placebo-controlled study has already exceeded 12 years, rendering it an exceedingly powerful clinical research study).  In particular, the significant increase in breast cancer incidence that was observed among the WHI study women who had received HRT pills for an average of almost 6 years was then compared to the subsequent decline in breast cancer rates in this same group of women after the premature termination of the combination HRT portion of the WHI study in 2002. 

 

 

Among the group of women randomized to receive HRT pills, the incidence of new breast cancer cases after 5.6 years of HRT was almost twice as high as was observed in the “control group” of women that received only placebo pills.  However, within two years of discontinuing HRT, following the premature termination of the WHI study in 2002, the breast cancer rate rapidly declined in the original HRT group of women.  During this phase of the WHI study, there was no significant difference in the incidence of screening mammograms between the two groups of women.  Thus, the incidence of breast cancer rose dramatically over a 5 to 6 year period among women randomized to receive standard combination HRT, and then fell just as dramatically among this same group of women as fewer and fewer women in this group continued to use HRT.  As this “experimental group” of women were confirmed to have utilized mammograms to the same degree as the “control group” of women did during this prolonged phase of the WHI study, the potential impact, if any, of declining mammogram rates on the incidence of breast cancer among these nearly 17,000 postmenopausal women is automatically eliminated with respect to the seminal findings of the WHI study.

 

 

The history of the dramatic rise of HRT after World War II, and its gradual and still ongoing decline, is a fascinating (and disturbing) story of hubris, bias, and ignorance; as well as the crass commercial exploitation of momentous cultural shifts in the United States (and around much of the world) for financial gain.  Look for a new book on this unsettling medical drama from me in the coming year or two.

 

 

 

STOOL DNA TESTING & CANCER OF THE COLON & RECTUM

 

 

Depending upon your age and your risk profile for colorectal cancer, you may be advised to undergo colonoscopy every 5 to 10 years.  Although there are several available options for colorectal cancer screening, colonoscopy remains the “gold standard” screening test, as it allows for evaluation of the entire colon and rectum.  Unlike other methods of screening, colonoscopy also allows physicians to biopsy or remove suspicious lesions identified during the screening examination.  Let’s face it, though, undergoing colonoscopy is no picnic.  For most people (myself included), the “prep” is the worst part of the experience. 

 

 

On the day before colonoscopy, powerful purgatives are used to flush out the colon.  Although there are several different types of “bowel prep” solutions available, all of them result in some degree of abdominal cramps and nausea, and they all produce the same “end result.”  Hours spent sitting on the toilet, with profuse diarrhea throughout the day, make for a miserable day, indeed.  At the end of the prep day, most people feel rather spent and hungry from a day of purging and consuming only liquids.  In most cases, colonoscopy is performed with intravenous sedation and, fortunately, most patients have little or no recall of the actual procedure. 

 

 

While thousands of colonoscopies are safely performed every day, colonoscopy is an invasive procedure, and there is a very small (but not completely insignificant) risk of complications, including bleeding and bowel perforation. 

 

 

Because of the negative aspects of colonoscopy, alternative colorectal cancer screening methods are always being evaluated.  “Virtual colonoscopy,” using computed tomography (CT) scans, is still undergoing evaluation, but many experts have already noted that patients still have to purge their colons before CT-colonography, and any polyps or other abnormalities that are detected during CT-colonography will still require that a separate colonoscopy be performed.   There is also the issue of being exposed to not inconsequential doses of radiation each time a patient undergoes CT-colonography. 

 

 

Given the unpleasantness associated with conventional colonoscopy, studying the stool for signs of premalignant or malignant polyps or tumors is an attractive option.  In fact, various tests that detect tiny amounts of shed blood in the stool have been used for decades as colorectal cancer screening tests.  Unfortunately, fecal occult blood testing is not sensitive or specific enough to rely upon as a single screening method for cancers, or precancerous lesions, of the colon and rectum.  (There are multiple non-cancer causes of occult blood loss into the stool, and not all precancerous polyps, or even small colon or rectal cancers, will consistently shed enough blood into the stool to be detected by fecal occult blood testing.) 

 

 

Recently, a new approach to screening the stool for signs of precancerous and cancerous lesions has been developed.  Unlike fecal occult blood testing, which detects a substance in the stool (e.g., traces of blood) that is not specific to cancer, the most recent generation of stool studies detect genetic material specific to malignant or premalignant cells that are also shed into the stool.  Of particular interest, currently, are stool DNA studies.  In this method of colorectal cancer screening, DNA is extracted from stool samples and, using a powerful DNA amplification test (polymerase chain reaction, or PCR), DNA mutations specific to cancer cells can often be detected.  However, these stool DNA tests currently miss about half of all colorectal cancers, and they are largely incapable of detecting the precancerous polyps that can easily be detected and removed during colonoscopy.  However, a new study, just published in the journal Gastroenterology, reveals a potentially important advance in stool DNA testing for colorectal cancer screening.

 

 

In this new study, PCR was combined with another test known as digital melt curve analysis.  Adding digital melt curve analysis further increases the already exquisite sensitivity of PCR in detecting tiny traces of mutated DNA that are shed into the stool by colorectal cancers, and by many premalignant polyps as well.  Using this approach in patients already diagnosed with colorectal cancer, and in whom specific cancer-related DNA mutations were known to be present, evidence of tumor DNA was identified in 90 percent of the stool samples that were tested with the new DNA test.  In another group of patients known to have precancerous polyps (advanced adenomas) containing a specific cancer-associated DNA mutation called KRAS, this new method of stool DNA testing was able to detect the KRAS mutation in an impressive 75 percent of patients. 

 

 

The results of this small pilot study are extremely impressive, and will likely lead to a new generation of stool DNA testing that will overcome many of the limitations associated with currently available stool DNA tests.  As this study evaluated only a very small number of patients, however, it will be necessary to repeat this study with larger numbers of patients before stool DNA testing can be considered equivalent to screening colonoscopy.  Until then, colonoscopy, in my opinion, remains the current gold standard for colorectal cancer screening.  Perhaps one day, in the near future, however, colonoscopy will only be reserved for the approximately 20 to 25 percent of patients who have colorectal polyps or other neoplastic lesions (including cancer) at the time of their periodic colorectal cancer screening exams.  Fortunately, I have another four years left before I have to repeat my next colonoscopy prep.  Perhaps stool DNA testing will be a reasonable colorectal cancer screening alternative for me, and for millions of other patients, by then!

 

Disclaimer:  As always, my advice to readers is to seek the advice of your physician before making any significant changes in medications, diet, or level of physical activity

Dr. Wascher is an oncologic surgeon, a professor of surgery, a widely published author, and a Surgical Oncologist at the Kaiser Permanente healthcare system in Orange County, California

Send your feedback to Dr. Wascher at:

 rwascher@doctorwascher.net

Dr. Wascher’s Biography

 

Links to Other Health & Wellness Sites

http://doctorwascher.com

 

Copyright 2009  

Robert A. Wascher, MD, FACS  

All rights reserved

 

 

Dr. Wascher’s Archives:

 

2-1-2009:   Obesity and the Complications of Diverticulosis (Diverticulitis & Bleeding); Obesity, Weight Loss & Urinary Incontinence

1-25-2009:  Prostate Cancer, Fatigue & Exercise; Does your Surgeon “Warm-up” Before Surgery?

1-18-2009:  Cancer and Vitamins; Teenagers, MySpace and Risky Behaviors

1-11-2009:  Exercise Reverses Some Effects of Fatty Meals; Vitamin C and Blood Pressure

1-4-2009:  Secondhand Smoke & Heart Attack Risk; Poor Physical Fitness During Childhood & Heart Disease Risk During Adulthood

12-28-2008:  Stress & Your Risk of Heart Attack; Vitamin D & the Prevention of Colon & Rectal Polyps

12-21-2008:  Breast Cancer Incidence & Hormone Replacement Therapy; Circumcision & the Risk of HPV & HIV Infection

12-14-2008:  Vitamin E, Vitamin C and Selenium Do Not Prevent Cancer;  Postscript: A Possible Cure for Down’s Syndrome

12-7-2008:  Generic vs. Brand-Name Drugs, Stress & Breast Cancer Survival

11-30-2008:    A Possible Cure for Down’s Syndrome?; Smoking & Cognitive Decline; Calcium & Vitamin D & Breast Cancer Risk

11-23-2008:  Breast Cancer & Fish Oil; Lymphedema after Breast Cancer Treatment; Vasectomy & Prostate Cancer Risk

11-16-2008:  Vitamin E & Vitamin C: No Impact on Cardiovascular Disease Risk; Does Lack of Sleep Increase Stroke & Heart Attack Risk in Hypertensive Patients?

11-9-2008:  Statins Cut Heart Attack Risk Even with Normal Cholesterol Levels; Statins & PSA Level

11-2-2008:  Radiation Treatment of Prostate Cancer & Second Cancers; Sexual Content on TV & Teen Pregnancy Risk

10-26-2008:  Smoking & Quality of Life

10-19-2008:  Agent Orange & Prostate Cancer

10-12-2008:  Pomegranate Juice & Prostate Cancer

10-5-2008:  Central Obesity & Dementia; Diet, Vitamin D, Calcium, & Colon Cancer

9-28-2008:  Publication & Citation Bias in Favor of Industry-Funded Research?

9-21-2008:  Does Tylenol® (Acetaminophen) Cause Asthma?

9-14-208:   Arthroscopic Knee Surgery- No Better than Placebo?; A Healthy Lifestyle Prevents Stroke

8-23-2008:  Alcohol Abuse Before & After Military Deployment; Running & Age; Running & Your Testicles

8-12-2008:  Green Tea & Diabetes; Breastfeeding & Adult Cholesterol Levels; Fish Oil & Senile Macular Degeneration

8-3-2008:   Exercise & Weight Loss; Green Tea, Folic Acid & Breast Cancer Risk; Foreign Language Interpreters & ICU Patients

7-26-2008:  Viagra & Sexual Function in Women; Patient-Reported Adverse Hospital Events; Curcumin & Pancreatic Cancer

7-13-2008:  Erectile Dysfunction & Frequency of Sex; Muscle Strength & Mortality in Men; Cryoablation for Prostate Cancer

7-6-2008:  Sleep, Melatonin & Breast Cancer Risk; Mediterranean Diet & Cancer Risk; New Treatment for Varicose Veins

6-29-2008:  Bone Marrow Stem Cells & Liver Failure; Vitamin D & Colorectal Cancer Survival; Green Tea & Colorectal Cancer

6-22-2008:  Obesity, Lifestyle & Heart Disease; Effects of Lifestyle & Nutrition on Prostate Cancer; Ginkgo Biloba, Ulcerative Colitis & Colorectal Cancer

6-15-2008:  Preventable Deaths after Coronary Artery Bypass Graft (CABG) Surgery; Green Tea & Colorectal Cancer; Attention-Deficit/Hyperactivity Disorder (ADHD) & St. John’s Wort

6-8-2008:  Vitamin D & Prostate Cancer Risk; Radiofrequency Ablation (RFA) of Kidney (Renal) Cancer; Antisense Telomerase & Cancer

6-2-2008:  Acute Coronary Syndrome- Do You Know the Symptoms?; Green Tea & Lung Cancer; Episiotomy & Subsequent Deliveries- An Unkind Cut

5-25-2008:  Early Childhood Screening Predicts Later Behavioral Problems; Psychiatric Disorders Among Parents of Autistic Children; Social & Psychiatric Profiles of Young Adults Born Prematurely

5-18-2008:  Can Statins Reverse Coronary Artery Disease?; Does Breast Ultrasound Improve Breast Cancer Detection?; Preventive Care Services at Veterans Administration (VA) Medical Centers

5-11-2008:  Smoking Cessation & Risk of Death; Childhood Traumas & Adult Suicide Risk; “White Coat Hypertension” & Risk of Cardiovascular Disease

5-4-2008:  Super-Size Me: Fast Food’s Effects on Your Liver; Exercise, Weight & Coronary Artery Disease; Contamination of Surgical Instruments in the Operating Room

4-27-2008:  Stents vs. Bypass Surgery for Coronary Artery Disease; The “DASH” Hypertension Diet & Cardiovascular Disease Prevention; Testosterone Therapy for Women with Decreased Sexual Desire & Function

4-20-2008:  BRCA Breast Cancer Mutations & MRI Scans; Bladder Cancer Prevention with Broccoli?; Diabetes: Risk of Death Due to Heart Attack & Stroke

4-13-2008:  Breast Cancer Recurrence & Hormone Replacement Therapy (HRT); Carotid Artery Disease: Surgery vs. Stents?; Statin Drugs & Cancer Prevention

4-6-2008:  Human Papilloma Virus (HPV), Pap Smear Results & Cervical Cancer; Human Papilloma Virus (HPV) Infection & Oral Cancer; Hormone Replacement Therapy (HRT) & the Risk of Gastroesophageal Reflux Disorder (GERD)

3-30-2008:  Abdominal Obesity & the Risk of Death in Women; Folic Acid Pretreatment & Heart Attacks; Pancreatic Cancer Regression after Injections of Bacteria

3-23-2008:  Age of Transfused Blood & Risk of Complications after Surgery; Obesity, Blood Pressure & Heart Size in Children

3-16-2008:  Benefits of a Full Drug Coverage Plan for Medicare Patients?; Parent-Teen Conversations about Sex; Soy (Genistein) & Prostate Cancer

3-9-2008:  Flat Colorectal Adenomas & Cancer; Health Risks after Stopping Hormone Replacement Therapy (HRT); Television, Children & Obesity 

3-2-2008:  Medication & Risk of Death After Heart Attack; Hormone Replacement Therapy (HRT) & Mammogram Results; Selenium: Cancer, Heart Disease & Death

2-23-2008:  Universal Healthcare Insurance Study; Glucosamine & Arthritis

2-17-2008:  Exceptional Longevity in Men; Testosterone & Risk of Prostate Cancer; Smoking & Pre-malignant Colorectal Polyps

2-10-2008:  Thrombus Aspiration from Coronary Arteries; Intensive Management of Diabetes & Death; Possible Cure for  Down’s Syndrome?

2-3-2008:  Vitamin D & Cardiovascular Health; Vitamin D & Breast Cancer; Green Tea & Colorectal Cancer

1-27-2008:  Colorectal Cancer, Esophageal Cancer & Pancreatic Cancer: Update from the 2008 American Society of Clinical Oncology’s Gastrointestinal Cancers Symposium

1-20-2008:  Testosterone Levels & Risk of Fractures in Elderly Men; Air Pollution & DNA Damage in Sperm; Statins & Trauma Survival in the Elderly

1-12-2008:  Statins, Diabetes & Stroke and Obesity; GERD & Esophageal Cancer

1-7-2008:  Testosterone Supplements in Elderly Men; Colorectal Cancer– Reasons for Poor Compliance with Screening Recommendations

12-31-2007:  Minority Women, Hormone Replacement Therapy & Breast Cancer; Does Health Insurance Improve Health?

12-23-2007:  Is Coffee Safe After a Heart Attack?; Impact of Divorce on the Environment; Hypertension & the Risk of Dementia; Emotional Vitality & the Risk of Heart Disease

12-16-2007:   Honey vs. Dextromethorphan vs. No Treatment for Kids with Night-Time Cough, Acupuncture & Hot Flashes in Women with Breast Cancer, Physical Activity & the Risk of Death, Mediterranean Diet & Mortality 

12-11-2007:  Bias in Medical Research; Carbon Nanotubes & Radiofrequency: A New Weapon Against Cancer?; Childhood Obesity & Risk of Adult Heart Disease

12-2-2007:  Obesity & Risk of Cancer; Testosterone Level & Risk of Death; Drug Company Funding of Research & Results; Smoking & the Risk of Colon & Rectal Cancer 

 

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LOW TESTOSTERONE LEVELS & FRACTURE RISK IN ELDERLY MEN

Following a recent column in which I discussed the risks versus benefits of testosterone supplementation in older men, a reader wrote to ask me if there were still any medically appropriate reasons for men to receive testosterone replacement therapy.  Aside from its use to treat flagging libido in men with documented low levels of this primary male sex hormone in the blood, the indications for testosterone supplementation in older men have been rather controversial.  The only other mainstream clinical indication for testosterone replacement therapy, to date, has been to treat—or prevent—osteoporosis (a weakening of the bones due to loss of mineral content), in an effort to prevent the skeletal fractures that become more common as we age.  Unfortunately, there is far more clinical data to support the use of hormonal and non-hormonal therapies in elderly, postmenopausal women (who suffer from osteoporosis and osteoporosis-related fractures more commonly than older men do) than is the case for men. 

Both testosterone in men and estrogen in women play an important role in maintaining strong, healthy bones (as does a calcium-rich diet and adequate Vitamin D levels throughout one’s adult life).  Both of these sex hormones naturally decline as we age, however (it should be noted that women’s bodies naturally produce small amounts of testosterone, and men’s bodies also produce small amounts of estrogen).  In women, the ovaries stop producing estrogen altogether after menopause, and only very low levels of estrogen are produced, mainly by the body’s fat cells, thereafter.  This places older women at a considerably greater risk of osteoporosis, and fractures, than elderly men, as testosterone levels gradually decline with age in men, but the testes of most men continue to produce significant amounts of testosterone throughout life.  Another significant factor is that the larger and more heavily mineralized skeletal system of men offers added protection against osteoporosis and fractures in later life, when compared to the thinner, smaller, and less heavily mineralized bones of women.

A new study, just published in the Archives of Internal Medicine, suggests that decreased levels of testosterone in the blood (and to a slightly lesser degree, decreased levels of estrogen in the blood as well) may indeed be linked to an increased risk of fractures in older men.  In this study, more than 600 men, aged 60 years or greater, were monitored between 1989 and 2005, for an average observation period of about 6 years.  Levels of testosterone and estradiol (the active form of estrogen) in the blood were measured in all study volunteers upon entry into the study.  Additionally, clinical risk factors for osteoporosis and osteoporosis-related fractures were assessed, including bone mineral density, calcium intake history, age, weight, and smoking history.

During the period of observation, 113 of the study volunteers experienced an osteoporosis-related fracture.  When the data collected in this study were analyzed, the men with the lowest testosterone levels in their blood were noted to have a 48% relative increase in the risk of osteoporosis-related fractures, and hip fractures in particular, for which the relative risk was almost double of that experienced by the men with the highest testosterone levels.  At the same time, a 21% relative increase in the risk of fractures was also noted for men with the lowest levels of estradiol in their blood.  While testosterone supplementation is not without risk, the results of this study certainly suggest that older men with very low testosterone levels in the blood should at least be considered for testosterone replacement (although only under the supervision of physicians who are knowledgeable and experienced in Endocrinology, a specialty that focuses of the body’s hormones and hormone-producing glands).  Older men with a family history of osteoporosis and very low testosterone levels should particularly consider a consultation with an experienced Endocrinologist. 

EXPOSURE TO AIR POLLUTION & GENETIC DAMAGE IN SPERM CELLS

In our increasingly urban, industrialized world, chronic exposure to environmental pollutants has become a major public health concern.  Long-term exposure to particulate air pollution, and especially to diesel engine exhaust, has previously been linked to an increased risk of both chronic lung disease and cancer by previous studies.  As a research and clinical fellow in Surgical Oncology, a few years back, I lived in an area of west Los Angeles that abutted I-405, an extremely busy interstate highway that was always jam-packed with big commercial trucks and their rattling, wheezing big diesel engines.  No matter how often, or how thoroughly, we cleaned our home, the very next morning, every window sill that faced I-405 would again be covered with a thin layer of black soot, hurled into the air by thousands of passing diesel-powered vehicles.  These particulate pollutants, which are capable of reaching the deepest recesses of our lungs, are considered to be carcinogenic, based upon previous animal and human research data.

A new research study, published in the journal Proceedings of the National Academy of Sciences, provides further scientific evidence that particulate air pollutants can directly cause mutations and other damage to our DNA which, in turn, may increase the risk for cancer development.  What is especially unique about this study, and worrisome as well, was the finding that exposure to particulate air pollutants also appears to damage the DNA of sperm cells in male mice (more about the potential significance of this finding in a moment…).

Male mice were divided into two groups for this study.  All mice were housed in a facility situated near a major highway and steel mill, where the ambient air was known to contain high levels of particulate air pollutants.  One group of mice was housed in cages that were fully exposed to the polluted ambient air around them, while the second group of mice was housed in special cages outfitted with high-efficiency HEPA air filtration systems.  At the end of the study, the animals were euthanized, and their testicles were then subjected to multiple standard tests for DNA mutations and damage known to be associated with an increased risk of cancer.  Strikingly, the sperms cells in the mice that were exposed to high levels of particulate air pollutants revealed significant DNA mutations and other signs of “DNA injury” when compared to the animals that were housed in cages with HEPA filters. 

The most striking aspect of this study is that it revealed that exposure to particulate air pollutants not only increases mutations in the DNA of our bodies’ cells, but also in our reproductive cells as well.  This raises at least the possibility that high levels of air pollution may not only have an adverse potential impact on the health of individual human beings, but that these adverse health effects might also be passed along to our offspring as a result of DNA damage occurring in sperm cells as well (this study did not evaluate the effects of exposure to particulate air pollutants on the ova of female mice, so the effects, if any, of such exposure on the ovaries of mice is unknown at this time). 

A couple of major caveats must be raised before applying the worrisome findings of this study to humans, however.  First of all, this was an animal study that involved the use of mice, and not men (undoubtedly, very few men would have volunteered for such a study…).  As we have learned from many other previous studies, mice and men are similar in many ways, but not in every way.  Unfortunately, what is observed to happen in mice in the laboratory does not always prove to also happen in humans.  Secondly, because the ambient air in urban areas contains a very complex stew of chemical and particulate contaminants, and because this study did not specifically identify the individual pollutants that caused the observed damage to sperm cells, we cannot be certain which substances in the polluted air actually caused the DNA damage.  These caveats aside, however, this is a very important public health study, and it should compel further study in humans in an effort to learn whether or not chronic exposure to polluted air might be exposing our unborn children and grandchildren to diseases (both benign and malignant) transmitted through sperm and, possibly, ova, damaged by such exposure. 

STATINS & TRAUMA SURVIVAL IN THE ELDERLY

Despite recent reports calling into question the degree of cardiovascular protections offered by statins in patients who are not already at very high risk of coronary artery disease or stroke, the preponderance of clinical data regarding these extremely popular drugs continues to show a marked reduction in the risk of heart attack and stroke in most patients who take statins for the appropriate indications.  Although still the subject  of debate by experts, there is also a growing body of evidence that certain statins might be associated with at least a mild reduction in the incidence of some types of cancer as well (I have summarized several of these studies in previous columns, which are archived and still available for online review).  Although the mechanism behind the anti-cancer effect of statins, if any, is not clearly understood, many experts believe that the anti-inflammatory effects of statins drugs may play an important role in both the prevention of heart disease and in cancer risk reduction.  Now, a new study takes a rather novel look at the protective effects of statins on an unusual group of patients, and once again, the anti-inflammatory heart-protective effects of statin drugs may have an important role to play.

A new research paper in the Journal of Trauma, Injury, Infection & Critical Care looked at the impact of chronic statin use on the survival of elderly patients admitted to 69 different hospitals following moderate-to-severe traumatic injuries.  More than 1,200 patients, 65 years of age and older, were included in this study.  Multiple clinical factors were analyzed, and then correlated with mortality in this large group of elderly trauma patients.  Among the factors evaluated were ongoing statin use prior to injury, gender, age, and associated health conditions (e.g., a history of cardiovascular disease, heart attack, stroke, diabetes, high blood pressure, emphysema, kidney disease, and smoking).  The severity of these patients’ traumatic injuries was then graded using the previously validated Abbreviated Injury Scale.  All of the resulting data was statistically analyzed and correlated to the risk of death following admission to the hospital.

Overall, the pre-injury use of statin drugs among these seriously injured elderly patients was associated with a whopping 67% reduction in the risk of death while in the hospital!  When the researchers further analyzed the data, they found that this apparent life-saving effect of statin drugs only applied to those patients with a previous history of cardiovascular disease.  In this group of patients, pre-injury use of statins was associated with a 70% reduction in the risk of death while hospitalized.  Among the elderly patients taking statins, but without any significant history of cardiovascular disease, the death rate was actually somewhat greater, by 40%, when compared to patients with a similar health history and who were note taking statin drugs at the time of injury.  This intriguing study dovetails nicely with existing data showing that the initiation of statin drugs immediately after a heart attack appears to reduce mortality, as well as the risk of subsequent heart attacks.  Based upon this trauma research study, it would appear that long-term statin use may also protect the cardiovascular system of patients with heart and vascular disease when these body systems are under the tremendous physiological stress that results from serious injury. 

http://www.sbhcs.com/hospitals/newark_beth_israel/mservices/oncology/surgical.html

Send your feedback to Dr. Wascher at rwascher@doctorwascher.net

Copyright 2008.  Robert A. Wascher, MD, FACS.  All rights reserved. 

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