JAMA & ARCHIVES
JAMA & Archives
SEARCH
GO TO ADVANCED SEARCH
HOME  EMBARGOED CONTENT  PAST ISSUES  EVENTS  HELP  SEARCH RELEASES

July 11, 2005

JAMA news releases are made available to the public after 3 pm US Central time on the first 4 Tuesdays of each month. the Archives of Journals news releases are made available to the public after 3 pm Central time on Mondays. We also provide a list of previous news releases.

THIS WEEK'S CONTENTS

ARCHIVES OF NEUROLOGY NEWS RELEASES

(Embargoed Until: 3 P.M. (CT), Monday, July 11, 2005)

>   SPECIAL ONLINE PUBLICATION — PARKINSON'S DISEASE DRUGS MAY CAUSE PATHOLOGICAL GAMBLING

>   LORENZO'S OIL SHOWS PROMISE IN REDUCING RISK OF DEBILITATING DISEASE IN GENETIC DISORDER

>   STATINS NOT ASSOCIATED WITH REDUCED DEMENTIA RISK

ARCHIVES OF INTERNAL MEDICINE NEWS RELEASES

(Embargoed Until: 3 P.M. (CT), Monday, July 11, 2005)

>   HOSPITAL COSTS OF CORONARY ARTERY BYPASS GRAFT SURGERY IN U.S. MORE THAN 80 PERCENT HIGHER IN U.S. THAN IN CANADA

ARCHIVES OF OPHTHALMOLOGY NEWS RELEASES

(Embargoed Until: 3 P.M. (CT), Monday, July 11, 2005)

>   NEARLY TWO MILLION EYE INJURIES IN THE U.S. EACH YEAR

INFORMATION CONTAINED IN THESE NEWS RELEASES IS PROTECTED BY COPYRIGHT. JOURNAL ATTRIBUTION IS REQUIRED.

JOURNALISTS CAN NOW ACCESS EMBARGOED JAMA/ARCHIVES STUDIES ON-LINE. Go to www.jamamedia.org for more information and to apply for access.

Please Note: The FOR THE MEDIA website now has a search feature to enable media to find previous JAMA/Archives news releases on specific medical topics. This search feature link is located on the home page at www.jamamedia.org

EMBARGOED FOR RELEASE UNTIL 3 P.M. (CT), MONDAY, July 11, 2005
Media Advisory: To contact M. Leann Dodd, M.D., call Lisa Lucier at 507-284-5005.

PARKINSON'S DISEASE DRUGS MAY CAUSE PATHOLOGICAL GAMBLING

CHICAGO—Eleven patients with Parkinson's disease (PD) developed pathological gambling behavior following dopamine agonist therapy, a drug therapy to control movement problems caused by Parkinson's disease, according to a study posted online today which will appear in the September print issue of the Archives of Neurology, one of the JAMA/Archives journals.

Parkinson's disease, a degenerative disorder marked by the death of the neurons of an area of the brain called the substantia nigra, is primarily treated by drugs that restore or improve brain chemical signaling system dependent on dopamine, according to background information in the article. Brain dopamine, a chemical that helps regulate movement, balance and walking, also plays a central role in the behavioral reward system, reinforcing a myriad of behaviors. It has been implicated in the reward of gambling behavior.

M. Leann Dodd, M.D., of the Mayo Clinic, Rochester, Minn., and colleagues, present reports of eleven patients seen and evaluated between 2002 and 2004 in the Mayo movement disorders clinic with Parkinson's disease who had recently developed pathological gambling and review similar cases from the medical literature. Pathological gambling is defined as a failure to resist gambling impulses despite severe personal, family or vocational consequences

The researchers describe the clinical features of 11 patients. Pathological gambling developed in seven of these 11 patients within one to three months of either reaching the maintenance dose, or increasing their dose of a dopamine agonist, the researchers report. While the other four patients did not report compulsive gambling until 12 to 30 months after initiating the therapy, in all four the gambling resolved within months of discontinuing agonist treatment. "The relationship of pathological gambling to dopamine agonist therapy in these cases is striking," the researchers write.

Six of the patients developed additional behavioral problems simultaneously with the pathological gambling, which resolved as the gambling subsided. These included compulsive eating, increased alcohol consumption, increased spending and hypersexuality.

"In summary, dopamine agonist drugs appear to be uniquely implicated as a cause of pathological gambling," the authors conclude. "Both our series and prior reports have especially linked this to administration of the selective dopamine D3 agonist pramipexole. Disproportionate stimulation of dopamine D3 receptors might be responsible for pathological gambling in these PD cases."
(Arch Neurol. 2005;62:1-5. Available to the media pre-embargo at www.jamamedia.org)

For more information, contact JAMA/Archives media relations at 312/464-JAMA (5262) or e-mail mediarelations{at}jama-archives.org.

Go back to the top.


EMBARGOED FOR RELEASE UNTIL 3 P.M. (CT), MONDAY, July 11, 2005
Media Advisory: To contact Hugo W. Moser, M.D., call Colleen O'Malley or Corrie Allen at 202-955-6222. To contact editorial author Raymond Ferri, M.D., Ph.D., call Pam Sowers at 206-543-3620.

LORENZO'S OIL SHOWS PROMISE IN REDUCING RISK OF DEBILITATING DISEASE IN GENETIC DISORDER

CHICAGO—Treatment of boys with X-linked adrenoleukodystrophy (ALD) with Lorenzo's oil (LO) reduced their risk of developing the severe debilitating form of the disease, according to a study in the July issue of the Archives of Neurology, one of the JAMA/Archives journals.

Individuals with ALD accumulate high levels of saturated very long-chain fatty acids (VLCFA) in their brains. The course of the disease results in a number of different manifestations [phenotypes], according to background information in the article. The rapidly progressive cerebral ALD (CERALD) type typically begins between ages four and eight and progresses rapidly to total disability within a few years. An adult form is non-inflammatory, progresses slowly and is far less disabling. Children who do not develop abnormalities as measured by magnetic resonance imaging (MRIs) by age seven or clinical symptoms by age 10, have greatly diminished risk of developing cerebral ALD.

In 1989, one of the authors of this study, Augusto Odone, pioneered a treatment (Lorenzo's oil), which was shown to normalize the levels of saturated very long-chain fatty acids within four weeks in most patients with ALD. "The striking effect of LO on plasma C26:0 [a saturated very long-chain fatty acid] levels engendered the hope that it would be of clinical benefit for patients with ALD," the authors write. However, previous clinical trials led to the conclusion that Lorenzo's oil did not alter the rate of progression of the disease in patients who already had neurological symptoms.

Hugo W. Moser, M.D., of the Kennedy Kreiger Institute, Baltimore, and colleagues treated 89 boys with ALD who had no neurological symptoms and normal brain MRIs with moderate dietary fat restriction and Lorenzo's oil between 1989 and 2002. Sixty-four of the patients were younger than seven years old when they began treatment and all were followed up for an average of approximately seven years. Because of the devastating nature of cerebral ALD, and the hope that the striking reduction of very long chain fatty acid levels would lead to clinical benefit, none of the boys were given placebo. Fatty acids blood levels were assessed every month for the first six months after enrollment in the study and every three to six months thereafter. Neurological examinations and MRIs were scheduled every six to 12 months.

Sixty-six patients (74 percent) were well at last follow-up. Twenty-one patients (24 percent) developed MRI abnormalities and 10 patients (11 percent) developed neurological abnormalities. The researchers found a significant association between the development of MRI abnormalities and an increase in the levels of the saturated very long chain fatty acid C26:0. "Patients who had a neurological abnormality had significantly higher weighted average C26:0 levels than those who did not have an abnormality, suggesting that an LO-induced decrease in the C26:0 level could protect against the inflammatory cerebral disease," the authors report.

"We recommend that LO therapy be offered to male patients with ALD who are neurologically asymptomatic, have normal brain MRI results, and are at risk of developing CERALD," the authors conclude. "This recommendation is based on strongly suggestive, albeit not fully definitive, evidence of a preventive effect combined with our awareness of the severe prognosis of the untreated patients with CERALD. ...The patients who are younger than seven years represent prime candidates for this therapy. We hypothesize that intensive LO therapy during the ages at which the risk for CERALD is greatest may protect against this phenotype until they reach the ages at which the risk for CERALD diminishes."
(Arch Neurol. 2005;62:1073-1080. Available to the media pre-embargo at www.jamamedia.org)

Editor's Note: This study was supported by grants from the Johns Hopkins University School of Medicine General Clinical Research Center, from the National Center for Research Resources/National Institutes of Health, Bethesda, Md., the National Institutes of Health, Bethesda, Md., the Office of Orphan Drug Products of the Food and Drug Administration, Rockville, Md., and the Myelin Project, Dunn Loring, Va.

EDITORIAL: LORENZO'S OIL: ADVANCES IN THE TREATMENT OF NEUROMETABOLIC DISORDERS

In an editorial accompanying the article, Raymond Ferri, M.D., Ph.D. and Phillip F. Chance, M.D., of the University of Washington, Seattle, write "In recent years, extraordinary progress has also been made in developing effective treatments, and ALD serves as an excellent model for the treatment of neurometabolic diseases. ...Current treatment includes hematopoietic stem cell transplantation (HSCT) to stabilize neurologic progression, steroid therapy for adrenal insufficiency, and symptomatic treatments. The article by Moser et al in this issue may establish new standards for the treatment of this degenerative disorder."

"Therefore, Moser and colleagues propose LO therapy for all asymptomatic patients with biochemical evidence of ALD to slow the progression of disease and to prevent symptoms until the child is past the age for the development of the childhood cerebral form of the disorder," the authors write. "Successful implementation of this practice requires early identification of at-risk patients. However, because almost 20 percent of the patients are either asymptomatic or have Addison disease only, at-risk children may not be identified. As also mentioned in the article, neonatal screening would identify more at-risk patients at a very early age. This would allow for further studies to examine very early treatment with LO for affected children, and dietary therapy can be studied in other ALD phenotypes [manifestations]. Also, this study can be extended to follow patients for an even greater duration to establish the full treatment effects of LO."

"X-linked ALD is a rare, progressive neurometabolic disorder, but coordinated, worldwide research efforts have made it a treatable disease," the authors conclude. "Dietary therapy started early in life and HSCT have markedly improved the longevity and quality of life for affected people, and new standards for treatment have been established."

For more information, contact JAMA/Archives media relations at 312/464-JAMA (5262) or e-mail mediarelations{at}jama-archives.org.

Go back to the top.


EMBARGOED FOR RELEASE UNTIL 3 P.M. (CT), MONDAY, July 11, 2005
Media Advisory: To contact Thomas D. Rea, M.D., M.P.H., call Pam Sowers at 206-685-4232.

STATINS NOT ASSOCIATED WITH REDUCED DEMENTIA RISK

CHICAGO—The use of statins and other lipid-lowering agents by older adults was not associated with a reduced risk of Alzheimer's disease or other types of dementia, according to a study in the July issue of the Archives of Neurology, one of the JAMA/Archives journals.

Statins may reduce cardiovascular risk by inhibiting cholesterol synthesis or through anti-inflammatory effects, biological mechanisms which may play a role in the development of dementia, particularly Alzheimer's disease, according to background information in the article. Previous studies have suggested that statins may have a protective effect on the process of dementia, preventing or delaying onset.

Thomas D. Rea, M.D., M.P.H., of the University of Washington, Seattle, and colleagues assessed data on 2,798 participants 65 years or older in the Cardiovascular Health Study who underwent baseline magnetic resonance imaging (MRI) and took a standardized mental test to determine that they were free of dementia when enrolled in the study (between 1991 and 1994). At baseline, information on their health status, cognitive function and medication use, as well as laboratory assessments and diagnostic testing was collected. Participants were followed up annually to assess their health status, medication use and whether they had developed dementia. During a total of 15,030 person years (number of individuals followed over time until development of disease or end of the study) of follow-up, there were 480 cases of dementia, including 245 attributable to Alzheimer's disease alone.

After controlling for other known or suspected risk factors, the researchers found that patients who had ever used statins had no reduction in their risk of developing dementia from any cause (Alzheimer's disease, mixed Alzheimer's disease and vascular dementia or vascular dementia alone) compared with those who had never used statins.

"Several factors may explain why statin use was not associated with a lower risk of dementia," the authors write. "Participants were on average 75 years of age, and statin use was assessed for a median of five years. Statin exposure may need to occur earlier in adulthood or for longer periods to prevent dementia, although analyses that stratified the duration of statin use did not suggest a duration-dependent association."

"In this investigation, statin therapy was not associated with a lower risk of dementia," the authors concluded. "Although statin use is an important treatment for cardiovascular disease, additional investigation is needed to determine whether and for whom statin use may affect dementia risk."
(Arch Neurol. 2005;62:1047-1051. Available to the media pre-embargo at www.jamamedia.org)

Editor's Note: This study was supported by grants from the National Heart, Lung, and Blood Institute, Bethesda, Md. and the National Institute on Aging, Bethesda, Md.

For more information, contact JAMA/Archives media relations at 312/464-JAMA (5262) or e-mail mediarelations{at}jama-archives.org.

Go back to the top.


EMBARGOED FOR RELEASE UNTIL 3 P.M. (CT), MONDAY, July 11, 2005
Media Advisory: To contact Mark J. Eisenberg, M.D., M.P.H., call Suzanne Gold at 514-340-8222, ext. 4120.

HOSPITAL COSTS OF CORONARY ARTERY BYPASS GRAFT SURGERY IN U.S. MORE THAN 80 PERCENT HIGHER IN U.S. THAN IN CANADA

CHICAGO—Although there are no differences in clinical outcome, the in-hospital cost of coronary artery bypass graft surgery (CABG) in the U.S. is 82.5 percent higher in the U.S. than in Canada, according to a study in the July 11 issue of the Archives of Internal Medicine, one of the JAMA/Archives journals.

Cardiovascular disease is a leading cause of illness and death in the U.S. and Canada, with an estimated direct cost in the U.S. of $209.3 billion in 2003, including $94.1 billion in in-hospital costs alone, according to background information in the article. In 2000, more than 500,000 CABGs were performed in the U.S.

Mark J. Eisenberg, M.D., M.P.H., of Jewish General Hospital, Montreal, and colleagues compared the outcomes and costs of treatment of 12,017 consecutive patients (4,698 U.S. and 7,319 Canadian patients) undergoing CABG at five U.S. and four Canadian hospitals.

"In-hospital costs of treatment were substantially higher in the United States than in Canada [an average cost of $20,673 vs. $10,373]," the authors report. "After controlling for demographic and clinical differences, length of stay in Canada was 16.8 percent longer than in the United States; there was no difference in in-hospital mortality [death]; and the cost in the United States was 82.5 percent higher than in Canada."

"Coronary artery bypass graft surgery requires substantial resources in Canada and the United States," the authors conclude. "However, patients undergoing CABG at U.S. hospitals incur approximately twice as much cost compared with those at Canadian hospitals, with little difference in clinical outcome and despite shorter average LOS [length of stay]. The difference in total in-hospital costs is almost equally attributable to differences in direct and overhead costs between the Canadian and U.S. hospitals. This cost differential primarily reflects higher resource prices for products and labor and higher overhead costs in the United States resulting from a nonsocialized medical system. However, U.S. hospitals also appear to streamline services better to reduce LOS, a strategy Canadian hospitals might emulate to further reduce treatment costs."
(Arch Intern Med. 2005;165:1506-1513. Available to the media pre-embargo at www.jamamedia.org)

Editor's Note: This study was supported by an unrestricted research grant from Pfizer, Inc., Groton/New London, Conn. Dr. Eisenberg is a Senior Physician-Scientist of the Quebec Foundation for Health Research, Montreal. Co-author Kristian B. Filion, B. Sc., was supported by a Canadian Cardiovascular Outcomes Research Team Summer Studentship. Co-author Louise Pilote, M.D., M.P.H., Ph.D., is a Physician-Scientist of the Canadian Institutes of Health Research, Ottawa, Ontario.

For more information, contact JAMA/Archives media relations at 312/464-JAMA (5262) or e-mail mediarelations{at}jama-archives.org.

Go back to the top.


EMBARGOED FOR RELEASE UNTIL 3 P.M. (CT), MONDAY, July 11, 2005
Media Advisory: To contact Gerald McGwin, Jr., M.S., Ph.D., call Bob Shepard at 205-934-8934.

NEARLY TWO MILLION EYE INJURIES IN THE U. S. EACH YEAR

CHICAGO—Nearly two million Americans are treated for eye injuries per year, with males experiencing twice the rate of injury than that of females, according to a study in the July issue of the Archives of Ophthalmology, one of the JAMA/Archives journals.

Because eye injuries are rarely serious enough to require hospitalization, to understand the extent of eye injuries in the U.S., inpatient and outpatient facilities, in addition to other settings, must be considered, according to background information in the article.

Gerald McGwin, Jr., M.S., Ph.D., from the University of Alabama at Birmingham, and colleagues combined data from the National Ambulatory Medical Care Survey, the National Hospital Ambulatory Medical Care Survey, and the National Hospital Discharge Survey for 2001, to estimate eye injuries in the U.S. Eye injuries treated in emergency departments, inpatient and outpatient facilities, and private physicians' offices, as well as their causes and characteristics, were included in the study.

The researchers found that in 2001 an estimated 1,990,872 individuals (6.98 per 1,000) experienced an eye injury in the U.S. Most of the eye injuries were treated in emergency departments (50.7 percent); 38.7 percent were treated in private physicians' offices, 8.1 percent in outpatient facilities, and 2.5 percent in inpatient facilities. Overall, males had more than twice the eye injury rate than that of females (9.5 injuries per 1,000 compared with 4.5 injuries per 1,000). White males in their 20s had the highest rate of eye injury (more than 20 injuries per 1,000). Injury rates were highest for superficial injuries, foreign bodies, contusions, and open wounds.

The authors state: "While the epidemiologic pattern of eye injury presented in this article is consistent with previous research from other settings, some important differences emerged. Private physicians represent an important source of care for eye injury in the United States, particularly for middle-aged adults. Future research should focus on a more detailed documentation of the causes of eye injuries as well as long-term functional outcomes as, despite the relatively frequent nature of eye injury documented in this study, injuries with potential visual significance more accurately reflect the public health impact of eye injury in the United States."
(Arch Ophthalmol. 2005;123:970-976. Available to the media pre-embargo at www.jamamedia.org)

Editor's Note: This research was supported by a grant from the National Institutes of Health, Bethesda, Md.; Research to Prevent Blindness Inc., New York; and the EyeSight Foundation of Alabama, Birmingham. Dr. Owsley, co-author, is a Research to Prevent Blindness Senior Scientific Investigator.


For more information, contact JAMA/Archives media relations at 312/464-JAMA (5262) or e-mail mediarelations{at}jama-archives.org.

Go back to the top.


HOME | EMBARGOED CONTENT | PAST ISSUES | EVENTS | HELP | SEARCH RELEASES
CONDITIONS OF USE | PRIVACY POLICY | CONTACT US | SITE MAP
 
© 2009 American Medical Association. All Rights Reserved.