For HIV-Positive Patients, Delayed Treatment a Costly Decision

"We know that it's important clinically to get people into care early because they will stay healthier and do better over the long run," says Kelly Gebo, M.D., M.P.H., an associate professor of medicine in the Division of Infectious Diseases at the Johns Hopkins University School of Medicine and the study's senior author. "But now we know it's also more costly to the health care system for potentially decades and a serious drain on our limited health care dollars."

Gebo says her team's findings highlight the importance of motivating people who are at risk to seek HIV testing and of reducing the time between the first positive HIV test and the first visit to an HIV clinic for care.

Patients with HIV are living longer and healthier lives, thanks to advances in antiretroviral therapy, but those successes may erode when some wait too long into the course of their disease to get treatment -- whether because they don't know they are infected with HIV, aren't sure how to access the health care system or have competing needs like mental health or substance abuse issues.

Dr. Gebo and her team's research, published in the December issue of the journal Medical Care, reviewed medical records of 8,348 patients at nine HIV clinics across the United States between 2000 and 2007. They found that more than 43 percent of patients were considered late entrants into the health care system, presenting at a clinic with extremely weakened immune systems, characterized by having CD4 counts below 200. CD4 cells are keys to a healthy immune system -- healthy people have counts between 800 and 1,000. When CD4 cells are damaged, as they are by HIV, counts can fall dramatically, making patients more susceptible to infection and certain types of cancer.

Low CD4 counts "make it more likely that patients are going to have complications and more likely that their CD4 counts won't ever recover to normal levels even with antiretroviral treatment," Gebo says. Previous studies have shown that those who come to care late in the course of their disease have shorter survival and benefit less from antiretroviral therapy.

Gebo and her colleagues found that the average difference in cumulative treatment expenditures between early and late presenters ranged from $27,275 to $61,615 higher over the course of the first seven to eight years of treatment. Costs are higher for the late presenters because they tend to be sicker than early presenters, particularly the first year of treatment -- and the cost gap doesn't shrink over time, she says. Late presenters are hospitalized more often, need to be put on costly antiretroviral therapy and antibiotics, and often must be treated for other diseases that have been exacerbated by a weakened immune system.

The study was supported by the Agency for Healthcare Research and Quality and the National Institutes of Aging and Drug Abuse. Richard D. Moore, M.D., M.H.Sc., a professor of general internal medicine at Johns Hopkins, also contributed to the research.

For more info- http://www.sciencedaily.com/releases/2010/11/101122111514.htm

DEET of the sea

If you were to find yourself in the jungle without a mosquito net, slathering yourself in snot might be a good alternative. It works for fish: Scientists have discovered that some coral reef fish protect themselves from biting isopods, a marine equivalent of mosquitoes, by covering themselves in mucus before going to sleep at night.

Researchers had speculated that the reason certain parrot fish and wrasses envelop themselves each night with a big blob of mucus might be to protect against settling silt or to deter hungry predators such as moray eels. But definitive experiments were lacking. Now scientists from the University of Queensland in Australia have done the dirty work. The team placed parrot fish in plastic tubs and after midnight, when all the fish had made their mucus cocoons, the researchers gently scraped off the cocoons from half the fishes. Then the team introduced tiny parasitic isopods — blood-sucking crustaceans that are taxonomically closer to lice than to mosquitoes — into the tubs.

Tallying each fish’s blood-engorged parasites showed that the mucus acts as a slimy sea version of bug netting: 94 percent of fish without cocoons had bites, versus 10 percent of fish with intact cocoons. The cocoon-challenged fish also had far more bites on average than their counterparts, the researchers report in a paper to appear in Biology Letters.

Making the mucus cocoon, which begins at the fish’s mouth and envelops the entire body within an hour, is an efficient protection strategy, costing a mere 2.5 percent of the fishes’ daily energy budget, the researchers estimate. This is relatively cheap, compared with scraping yourself on rocks or sand, avoiding areas with parasites or seeking parasite-eating cleaner fish (which the fish do during waking hours).

Keeping bugs at bay is a new role for fish mucus — the thinner slime layer employed by some species appears to protect against UV rays and pollutants, or can aiding in maintaining the proper balance of electrolytes and fluids.

Collected from- http://www.sciencenews.org/view/generic/id/65567/title/DEET_of_the_sea

New drug bumps up good cholesterol

An experimental drug shows the ability to more than double a person’s good cholesterol score, potentially filling a huge gap in cardiovascular care, scientists report. If the findings hold up in a larger trial, the drug, called anacetrapib, stands poised to become the best medication yet for boosting levels of the heart-disease preventer HDL.

“This is a very exciting era we are entering,” said Christopher Cannon, a cardiologist at Harvard Medical School and Brigham and Women’s Hospital in Boston. He presented the findings at a meeting of the American Heart Association on November 17, the same day they appeared online in the New England Journal of Medicine.

“These preliminary data are very promising,” agreed Sidney Smith, a cardiologist at the University of North Carolina at Chapel Hill and a past president of the AHA. “They show dramatic differences in HDL.” High-density lipoprotein, or HDL, ushers low-density bad cholesterol, or LDL, out of the blood. High levels of HDL are closely associated with low risk of heart attack and stroke.

Cannon and his colleagues randomly assigned 1,623 people, average age 63, who had heart disease to receive either anacetrapib or a placebo for 18 months. All were already taking a statin drug to lower LDL. In the anacetrapib group, HDL levels shot up from an average of 41 milligrams per deciliter of blood to 101 mg/dl within the first few weeks of the study and stayed there. Anacetrapib also lowered LDL from an average of 81 mg/dl to around 45 mg/dl. People who received a placebo experienced very slight changes in their HDL and LDL scores.

Only eight people getting anacetrapib — compared with 28 in the placebo group, which was the same size — needed to undergo coronary revascularization during the trial, in which doctors surgically reopen or bypass a blocked artery to restore blood flow to the heart. “We’re very encouraged by this,” Cannon said.

“These were people who were doing fine” at the outset, despite having heart disease, Cannon says. The revascularization data indicate that in some of them, the heart disease was progressing despite being on medication.

But the data in this study are not enough to change medical guidelines, Smith cautioned, and Cannon agreed. Further work will be needed to establish that the higher HDL levels seen in patients taking anacetrapib are truly functional HDL, and that can be established only by a long-term reduction in heart attacks, stroke, angina and other tangible cardiac events. “If it does have a significant benefit on events, then we will have a very valuable potent new therapy to add,” Smith said.

Some people naturally have higher HDL than others. Apart from niacin, which has a side effect of flushed skin, no drug has previously been shown to safely increase HDL substantially. Stopping smoking, losing weight and exercising can add 5 to 10 points to a person’s HDL score, Smith said.

Anacetrapib works by inhibiting CETP, or cholesteryl ester transfer protein, a compound that influences how much LDL and HDL a person carries in the blood at any given moment. A promising drug called torcetrapib had shown the ability to neutralize CETP (SN: 5/1/04, p. 285). But research pitting the drug against a placebo was stopped in 2006 when it became clear that people taking torcetrapib were more likely to develop high blood pressure, experience heart problems or die than those getting a statin alone. The result was a blow to the drug’s maker, Pfizer, and left HDL-boosting drug hopes in limbo, although some work is ongoing (SN: 4/14/07, p. 237).

Anacetrapib has now shown “a very potent and impressive change in lipid profiles,” said Thomas Lüscher, a cardiologist at University Hospital Zurich. “And such change occurred without a change in blood pressure.” The number of deaths was roughly the same in the two groups.

But 142 people had their LDL drop so low on anacetrapib plus a statin that they were taken off the experimental drug as a precaution. Scientists will next test anacetrapib, manufactured by Merck, in a trial of 30,000 heart disease patients over four years, paying close attention to that risk and any other that arises, said cardiologist Rory Collins of the University of Oxford.

Collected from- http://www.sciencenews.org/view/generic/id/65684/title/New_drug_bumps_up_good_cholesterol