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By
sulthan on Tuesday, May 17, 2011
Two U.S. Food and Drug Administration advisory committees plan to meet Tuesday and Wednesday to decide whether to recommend that the dosing instructions on the labels of medicines containing acetaminophen
need to be fine-tuned to protect children under the age of 2 against possible liver failure and even death. Currently, the labels of such
fever-reducing medications, which include Children's Tylenol, have dosing instructions for children aged 2 and up. For kids under 2, the labels simply tell parents to "ask a doctor." The American Academy of Pediatrics (AAP) and drug manufacturers are both strongly in favor of giving parents the additional dosing information.
"
If we give parents better information, they will be able to give enough of the medicine to work well, at the same time minimizing the side effects," said Dr. Daniel Frattarelli, a pediatrician in Dearborn, Mich. who chairs the academy's drug committee and who plans to testify before a joint, two-day meeting of the Nonprescription
Drugs Advisory Committee and the Pediatric Advisory Committee. "Parents want to do the right thing for their children," he said. "
We as a medical community have to give them that information so they are able to do this." Although the evidence shows that acetaminophen is safe for young children, parents have to be careful with it, pediatricians noted. Giving too much can be toxic to the liver, causing poisoning and even liver failure.
In 2010, there were 270,000 reported overdoses of acetaminophen, according to the American Association of Poison Control Centers. Dosing errors involving children's acetaminophen products accounted for almost 7,500 cases nearly 3 percent. In an ideal world, the parents of infants and toddlers would still consult with their pediatrician or pharmacist to get the proper medication dosing, said Dr. William Basco, director of general pediatrics at the Medical University of South Carolina. But the reality is that many parents aren't doing that and are instead guessing about proper dosing. "There is no benefit to having parents guess at the right dose," Basco said.
By
sulthan on Wednesday, April 20, 2011
A 39-year-old woman is referred to Washington University's Siteman
Cancer Center in St. Louis with suspected acute myeloid leukemia (AML), a cancer that can be treated relatively simply with medication, or not so
simply with a high-risk stem cell transplant, depending on the tumor subtype. But finding out which type of cancer she has proves trickier than expected. While the pathologist sees a type of leukemia known as M3AML, which generally has a
good outcome and can be treated with the drug ATRA, the cytogeneticist sees something entirely different.
In his analysis, the
woman has a type of leukemia with poor long-term survival that is usually treated with stem cell transplantation a risky therapy that sometimes leads to
death. Fortunately, in this case study, documented in the April 20 issue of the Journal of the American Medical Association, the woman's oncologist is aware of a clinical trial and, deferring treatment for six weeks, refers her there so the researchers can do a full scan of her genome and come up with an answer.
Full-genome sequencing involves scanning all the thousand of
genes on the human genome to try to find a mistake. It's different from the more common gene testing these days, which looks only for
specific DNA that might or might not be responsible for a particular problem. In the St. Louis case, the more in-depth sequencing, done in only seven weeks, uncovered a new genetic "mistake" that showed the woman could be treated with ATRA and not the more-complicated, risky stem cell transplantation.
By
sulthan on Tuesday, April 19, 2011
New research suggests that
HIV-infected patients are most likely to stay clear of AIDS longer if they start drug therapy when their immune systems are still relatively strong. However, starting treatment earlier, compared to waiting, didn't affect dying from AIDS. "
There wasn't a clear benefit in terms of preventing death" by prescribing the drugs before some guidelines suggest, said Dr. Keith Henry, director of
HIV clinical research at Hennepin County Medical Center in Minneapolis and co-author of a commentary accompanying the study, published in the April 19 edition of Annals of Internal Medicine.
The issue of when to begin drug treatment is a hot topic in the field of AIDS/HIV medicine. If physicians wait to begin treatment, patients can delay the expense not to mention the side effects of pricey anti-HIV
drugs. But such delays may also give the virus a chance to become more powerful and better able to fend off medications.
If they're not treated with drugs, HIV-infected people almost always go on to develop AIDS. So when should doctors turn to the drugs? In the U.S., guidelines suggest that HIV-infected patients take them when the level of CD4 cells an important part of the immune system dips below 0.500 X 109 cells per liter (cells/L).
In Europe, the guideline number is frequently lower meaning a weaker immune system at under 0.350 X 109 cells/L.In the new study, researchers examined how patients did when they began drug therapy with their CD4
cells at a variety of levels. The study authors examined the medical records of
almost 21,000 HIV-infected patients who sought treatment in HIV clinics in Europe and through the Veterans
Health Administration system in the United States. The researchers found that the
death rate was about the same regardless of whether patients began treatment when their CD4 levels dipped under 0.500 X 109 cells/L or if they waited until their immune systems deteriorated more and reached below the level of 0.350 X 109 cells/L.
By
sulthan on Monday, April 18, 2011
New research suggests that the development of insulin resistance and type 2
diabetes may be linked to an immune system reaction gone awry. "
The main point of this study is trying to shift the emphasis in thinking of type 2 diabetes as a purely metabolic disease, and instead emphasize the role of the immune system in type 2," said study co-author Dr. Daniel Winer, an endocrine pathologist at Toronto General Hospital in Canada. When the research began, Winer was a postdoctoral fellow at Stanford University in California. The researchers have
identified immune system antibodies in people who are obese and insulin-resistant that aren't present in people who are obese without insulin resistance. They also tested a
drug that modifies the immune system in mice fed a fatty diet, and found that the medication could help maintain normal blood sugar levels.
The findings were published online April 17 in the journal Nature Medicine. Funding for the study was provided by the U.S. National Institutes of
Health. Nearly
26 million Americans have diabetes, according to the U.S. Centers for Disease Control and Prevention. Between 90 percent and 95 percent of these cases are type 2 diabetes, where the body doesn't use insulin efficiently, so the pancreas must make increasing amounts of insulin. Eventually, the
pancreas stops making enough insulin to meet the increased demand. The less common form of the disease, type 1 diabetes, occurs when the immune system mistakenly destroys the
insulin-producing beta cells in the pancreas. This type of diabetes is considered an autoimmune disease, and isn't linked to how much a person weighs.
Although the
causes of type 2 haven't been clear, it's known that the disease runs in families, suggesting a genetic component. Also, while type 2 is strongly linked to increased weight, not everyone who is overweight gets type 2 diabetes. And, that's what got the researchers searching for another factor.
Winer explained that excess weight has been linked to inflammation, which can cause the immune system to react. As visceral
fat (abdominal fat) expands, it eventually runs out of room, explained Winer. At that point, the fat cells may become stressed and inflamed, and eventually the cells die. When that happens, immune system cells known as macrophages come to sweep up the mess.
By
sulthan on Thursday, February 10, 2011
Few eligible stroke patients get an injectable clot-busting
drug within the recommended 60-minute window after their hospital arrival, new research finds. "
It has been widely recommended that the 'door-to-needle' time should be 60 minutes," said study author Dr. Gregg C. Fonarow, a professor of cardiovascular medicine at the University of California Los Angeles David Geffen School of Medicine. The phrase refers to the
timeframe between when the patient arrives at the hospital and when that patient is given the clot-buster, known as tissue plasminogen activator (tPA).
In his analysis of
stroke patients from 1,083 hospitals, he found the
60-minute window was not the typical reality. "That occurs only in 26.6 percent of patients," he said. Fonarow was slated to present the findings Thursday at the American Stroke Association's International Stroke Conference in Los Angeles; the research is being published simultaneously in the journal Circulation.
Perhaps even more surprising, the hospitals in the study were all participating in the American Heart Association/American Stroke Association's Get with The Guidelines-Stroke quality improvement program, which recommends early tPA administration.
"
It involved some of the largest, best-known hospitals for stroke care," Fonarow said. The study looked at more than 25,500 patients who had suffered ischemic stroke in which a
blood clot obstructs
blood flow and had been treated with tPA within three hours of the start of symptoms. Just 6,790 got the intravenous drug within 60 minutes. During the course of the study, there was only modest improvement in the hospitals' track records.
By
sulthan on Monday, February 7, 2011
Middle-aged
breast cancer survivors face an
increased risk for hip fractures, a condition normally uncommon in women younger than 70, a new study has found. Researchers at Northwestern University in Chicago say that this may be because early menopause caused by
breast cancer treatment and the effects of breast cancer
drugs could
weaken the bones by the time women reach middle age. The finding came from a study of six women who had survived breast cancer and, in their early 50s, were being treated for hip fractures.
Most of the women did not have osteoporosis, but they did have lower-than-normal
bone mineral density (osteopenia). This suggests that
rapid changes in bone architecture caused by chemotherapy, early menopause and
adjuvant breast cancer therapy may not be detected on a bone mineral density test, said Dr. Beatrice Edwards, an associate professor of medicine and orthopedic surgery and director of the bone
health and osteoporosis program Northwestern University's Feinberg School of Medicine, who led the research.
The women had been diagnosed with early-stage
breast cancer, and their treatments had included lumpectomy, radiation therapy and chemotherapy with cytoxan and a
driamycin for one to four years before they broke a hip. All of the women were perimenopausal at the time of the fracture. In four of the women, their
breast cancer had grown in response to estrogen, and their
cancer therapy had included aromatase inhibitors to prevent their bodies from making estrogen. Recent research has linked aromatase inhibitors with possible bone loss in women.
By
sulthan on Wednesday, December 22, 2010
Scientists are
reporting early but promising results from a new drug that blocks
HIV as it attempts to invade human cells. The approach differs from most current antiretroviral therapy, which tries to
limit the virus only after it has gained entry to cells. The medication, called VIR-576 for now, is still in the early phases of development. But researchers say that if it is successful, it might also
circumvent the drug resistance that can undermine standard therapy, according to a report published Dec. 22 in Science Translational Medicine.
The new approach is an attractive one for a number of reasons, said Dr. Michael Horberg, director of HIV/AIDS for Kaiser Permanente in Santa Clara, Calif. "
Theoretically it should have fewer side effects and there's probably less of a chance of mutation in developing resistance to medication," said Horberg, who was not involved in the study. Viruses replicate inside
cells and scientists have long known that this is when they tend to mutate potentially developing new ways to resist drugs. "
It's generally accepted that it's harder for a virus to mutate outside cell walls," Horberg explained.
The new
drug focuses on HIV at this pre-invasion stage. "
VIR-576 targets a part of the virus that is different from that targeted by all other HIV-1 inhibitors," explained study co-author Frank Kirchhoff, a professor at the Institute of Molecular Virology, University Hospital of Ulm in Ulm, Germany, who, along with several other researchers, holds a patent on the new medication.
The target is the gp41 fusion peptide of HIV, the "sticky" end of the virus's outer membrane, which "
shoots like a 'harpoon'" into the body's cells, the authors said. The launch of this peptide is a first step in the virus's bid to inhabit host cells.
