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Recent News and Articles on the Keywords: tylenol + liver + linked  Related to the article below (Last Update: 8/5/2008)

Alex "Iron Doc" McDonald: Water and Salt: Separate but Equal
Xtri.com -
If you want to take a pain reliever on race day, use Tylenol/acetaminophen as this medication is metabolized by the Liver and does not have a major effect ...
HIV-positive migrants accuse US of neglect
Macon Telegraph, GA -
"It was so advanced that it involved her brain, her liver, her lungs, her heart, and a couple of other organs. She died in terrible pain. ...
Source: Google News

… quantitation of 3-(cystein-S-yl) acetaminophen adducts in serum and liver proteins of acetaminophen … -
NR Pumford, JA Hinson, DW Potter, KL Rowland, RW … - J Pharmacol Exp Ther, 1989 - ncbi.nlm.nih.gov
... enzyme-linked immunosorbent assay specific for 3-(cystein-S-yl)acetaminophen adducts
we have quantitated the formation of these specific adducts in liver and ...

… necrosis factor genomic polymorphism and outcome of acetaminophen (paracetamol)-induced acute liver -
W Bernal, P Donaldson, J Underhill, J Wendon, R … - J Hepatol, 1998 - ncbi.nlm.nih.gov
... plays a role in the development of acetaminophen (paracetamol)-induced liver injury
and ... of tumor necrosis factor-alpha have been linked to genomic ...

… Expression and Prevents Acetaminophen-Induced Programmed and Unprogrammed Cell Death in Mouse Liver -
SD Ray, MA Kumar, D Bagchi - Archives of Biochemistry and Biophysics, 1999 - Elsevier
... in AAP-induced apoptotic death of liver cells (Ray ... 4 Abbreviations used: AAP,
acetaminophen; ALT, alanine amino ... and apoptosis are intimately linked pro- cesses. ...

… mitochondrial glutathione depletion by ethanol enhances acetaminophen toxicity in rat liver -
P Zhao? - Hepatology, 2002 - doi.wiley.com
... Abbreviations: APAP, acetaminophen; NAPQI, N-acetyl-p-benzoquinone imi ... de- hydrogenase;
ELISA, enzyme-linked immunosorbent assay. ... for the Study of Liver Diseases ...

A sensitive immunochemical assay for acetaminophen-protein adducts. -
DW Roberts, NR Pumford, DW Potter, RW Benson, JA … - J Pharmacol Exp Ther, 1987 - ncbi.nlm.nih.gov
... We have developed an avidin biotin-amplified competitive enzyme-linked
immunosorbent assay to detect protein-bound acetaminophen. ...

In vitro effects of acetaminophen metabolites and analogs on the respiration of mouse liver -
RR Ramsay, MS Rashed, SD Nelson - Arch Biochem Biophys, 1989 - ncbi.nlm.nih.gov
... is toxic in overdose to liver and kidney. ... on mitochondrial respiration of acetaminophen,
its less ... parent compounds inhibited NADH-linked respiration reversibly ...

Alpha-fetoprotein is a predictor of outcome in acetaminophen-induced liver injury -
LE Schmidt, K Dalhoff - Hepatology, 2005 - doi.wiley.com
... patients with severe acetaminophen-induced liver injury ... in 239 patients with
acetaminophen intoxication and ... was measured using an enzyme- linked immunoassay ( ...

Lipopolysaccharide-binding protein modulates acetaminophen-induced liver injury in mice -
GL Su, KQ Gong, MH Fan, WM Kelley, J Hsieh, JM Sun … - Hepatology, 2005 - doi.wiley.com
... in the amount or pattern of acetaminophen adduct formation ... Animals With LBP In- creased
Liver Injury ... levels were measured via enzyme-linked immunosorbent assay ...

Mechanism of acetaminophen-induced liver disease -
SD NELSON, SA BRUSCHI - Drug-induced liver disease - books.google.com
13 Mechanisms of Acetaminophen- Induced Liver Disease SIDNEY D. NELSON and SAM A.
BRUSCHI University of Washington School of Pharmacy, Seattle, Washington, USA ...

Alterations in the Rat Serum Proteome during Liver Injury from Acetaminophen Exposure -
BA Merrick, ME Bruno, JH Madenspacher, BA Wetmore, … - Journal of Pharmacology and Experimental Therapeutics, 2006 - ASPET
... and histopathology revealed the greatest liver damage at ... h after high-dose acetaminophen
corresponding to ... Antibody array and enzyme-linked immunosorbent assay ...

Source: Google Scholar

High Tylenol Doses Linked to Liver Woes

Healthy adults taking maximum doses of Tylenol for two weeks had abnormal liver test results in a small study, researchers found, raising concerns that even recommended amounts of the popular painkiller might lead to liver damage.

In the study, 106 participants took four grams of Tylenol - equivalent to eight extra-strength Tylenol tablets - each day for two weeks. Some took Tylenol alone and some took it with an opioid painkiller. Dummy pills were given to 39 others.

There were no alarming liver test results among the people who took the placebos. But nearly 40 percent of people in all the other groups had abnormal test results that would signal liver damage, according to the study that appears in Wednesday's Journal of the American Medical Association.

"I would urge the public not to exceed four grams a day. This is a drug that has a rather narrow safety window," said a study co-author, Dr. Neil Kaplowitz of the University of Southern California.

Heavy drinkers should take no more than two grams daily, Kaplowitz said.

Another co-author, Dr. Paul Watkins of the University of North Carolina, said he's less worried than Kaplowitz, noting that acetaminophen, the active ingredient in Tylenol, has been used for 50 years and has a good safety record.

The maker of Tylenol, McNeil Consumer & Specialty Pharmaceuticals, said its own research found much lower rates of abnormal liver results. The company's studies tracked high-dose users over longer periods than did the new study.

"It doesn't lead to liver disease and it usually resolves as patients continue to take acetaminophen," said Dr. Edwin Kuffner, senior director of medical affairs at McNeil.

The researchers had been hired by the drug company Purdue Pharma LP, maker of the prescription painkiller OxyContin, to find out why abnormal liver tests were showing up in people testing a combination drug containing the acetaminophen and the opiate hydrocodone.

Purdue Pharma stopped its hydrocodone study early because of the abnormal liver tests. Researchers Watkins and Kaplowitz thought they would find the culprit in hydrocodone's interaction with acetaminophen.

"Our jaws dropped when we got the data," Watkins said. "It doesn't have anything to do with the opiate. It's good ol', garden-variety acetaminophen."

Acetaminophen is more popular than aspirin or ibuprofen. Each week, one in five U.S. adults uses it for pain or fever, a 2002 survey found.

Acetaminophen is included in numerous over-the-counter and prescription medications, making overdose possible as people unwittingly combine drugs. Overdoses of acetaminophen are the leading cause of acute liver failure.

"A week doesn't go by when I don't have to talk to someone about how much they're taking," said Kathleen Besinque of the USC School of Pharmacy.

Watkins said people considering switching painkillers should know that others have their own side effects, such as internal bleeding and stomach irritation.

New research under way at the University of North Carolina may determine if acetaminophen's effect on the liver continues for long-term, high-dose users, or if the body adapts, Watkins said.

Early Drinking Linked to Higher Lifetime Alcoholism Risk

Data from a survey of 43,000 U.S. adults heighten concerns that early alcohol use, independent of other risk factors, may contribute to the risk of developing future alcohol problems. Those who began drinking in their early teens were not only at greater risk of developing alcohol dependence at some point in their lives, they were also at greater risk of developing dependence more quickly and at younger ages, and of developing chronic, relapsing dependence. Among all respondents who developed alcoholism at some point, almost half (47 percent) met the diagnostic criteria for alcohol dependence (alcoholism) by age 21.

The associations between early drinking and later problems held even after investigators controlled for other risk factors for dependence, adding to concerns that drinking at a young age might raise the risk of future alcohol problems rather than being an identifying feature of young people predisposed to risky behavior. The study appears in the July issue of Archives of Pediatrics & Adolescent Medicine (volume 160, pages 739-746).

Elias A. Zerhouni, M.D., director of the NIH, said, “This is a very good example of how insights gained from health research can inform public policy. Converging research suggests that youthful drinking is associated with an increased risk of long-term, not just acute, health consequences.”

Scientists at the Boston University School of Public Health and Youth Alcohol Prevention Center, led by Dr. Ralph Hingson*, carried out the analysis using data from the 2001-2002 National Epidemiologic Survey on Alcohol and Related Conditions (NESARC), a representative survey of the U.S. civilian noninstitutionalized population aged 18 years and older.

NESARC involved face to face interviews with adults ages 18 and older. The survey used questions based on diagnostic criteria for alcohol abuse and alcohol dependence from the American Psychiatric Association’s Diagnostic and Statistical Manual of Mental Disorders-Fourth Edition (DSM-IV). In the study, “starting to drink” meant the age when respondents first drank alcohol, not counting tastes or sips.

NIAAA Director Dr. Ting-Kai Li said “this work underscores the need for research to clarify how early drinking relates to the risk of lifetime alcohol problems. In particular, it is important to learn whether early alcohol use may affect the developing brain in ways that increase vulnerability to dependence.”

In results that echo earlier studies, of those individuals who began drinking before age 14, 47 percent experienced dependence at some point, vs. 9 percent of those who began drinking at age 21 or older. In general, each additional year earlier than 21 that a respondent began to drink, the greater the odds that he or she would develop alcohol dependence at some point in life. While one quarter of all drinkers in the survey started drinking by age 16, nearly half (46 percent) of drinkers who developed alcohol dependence began drinking at age 16 or younger.

New findings showed that among all drinkers, early drinking was associated not only with a higher risk of developing alcoholism at some point, but also within 10 years of first starting to drink, before age 25, and within any year of adult life. Early drinking was also associated with increased risk of having multiple episodes of alcoholism. Further, among respondents who had had alcohol dependence at some point, those who began drinking young had episodes of longer duration and with a wider range of symptoms than those who started later.

Previous research has established the link between early onset of drinking and lifetime diagnosis of alcoholism. Key to understanding the relationship between early drinking and alcoholism risk is whether the act of drinking while young raises lifetime risk, or whether early drinking reflects an underlying predisposition for risky behavior in particular young people. In the latter case, early drinking would be considered a marker identifying individuals already at risk for developing alcoholism. In this study, investigators attempted to account for factors — such as family history of alcoholism, childhood antisocial behavior and depression, and smoking and drug use — known to be associated with higher risk. Even controlling for a number of risk factors and the effects of age differences among respondents, early drinking was associated with an increased risk of lifetime alcohol diagnosis.

In calculating the impact of early drinking on the risk of experiencing alcoholism, the study used statistical methods that account for the fact that older respondents have had a longer window of opportunity to develop alcoholism than younger respondents. The risk of those who began drinking before age 14 was multiplied by a factor (or “hazard ratio”) of 1.78 relative to those who started drinking at age 21 or older.

The recently released 2005 Youth Risk Behavior Survey — conducted by the Centers for Disease Control and Prevention — found that among high school students nationwide, 26 percent had drunk alcohol (other than a few sips) for the first time before age 13.

The authors conclude that the results of both studies support the need to take measures to delay alcohol consumption by underage youth. Dr. Hingson said, “This analysis suggests that interventions that delay drinking onset may not only reduce the acute consequences of drinking among youth, but may help reduce alcohol dependence among adolescents and adults. It’s an important public health issue for longitudinal research to resolve.”

The National Institute on Alcohol Abuse and Alcoholism, part of the National Institutes of Health, is the primary U.S. agency for conducting and supporting research on the causes, consequences, prevention, and treatment of alcohol abuse, alcoholism, and alcohol problems and disseminates research findings to general, professional, and academic audiences. Additional alcohol research information and publications are available at www.niaaa.nih.gov.

The National Institutes of Health (NIH) — The Nation's Medical Research Agency — includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. It is the primary federal agency for conducting and supporting basic, clinical and translational medical research, and it investigates the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit www.nih.gov.

 
 
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