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In Vivo
RESEARCH BRIEFS
Chickenpox Booster Needed Years Earlier
One out of every four children inoculated with a single dose of the chickenpox vaccine may not develop immunity, according to a new study by CUMC infectious disease researchers. The results indicate that a second booster shot is needed months later, not years, as is currently recommended.
   Since its approval by the FDA in 1995, the chickenpox vaccine has dramatically decreased the number of chickenpox cases, hospitalizations, and pediatric deaths.
   Still, outbreaks of chickenpox periodically flare up in schools and daycare centers even among vaccinated children. In response, the CDC in 2006 recommended all children receive a second dose of the vaccine between age 4 and 6.
   It’s important that a second dose be given routinely, says Anne Gershon, MD, professor of pediatrics – infectious disease, but the timing is too late. “The timing of the second shot assumes that more than 95 percent of children develop immunity after the first dose, but that immunity slowly wanes over years. We’ve found that for many children that immunity never existed.”
   In the study, 148 1-year-olds were vaccinated with a single dose of the chickenpox vaccine. Four months later assays revealed that 24 percent of the children had no detectable antibodies to the virus, leaving them vulnerable to the disease.
   The failure of the first dose is much higher than the <5 percent figure reported in the vaccine’s pre-licensure studies. Dr. Gershon attributes the discrepancy to the tests used to measure antibodies. The current study used the FAMA test, developed years ago in Dr. Gershon’s lab. This assay is considered the gold standard in measuring chickenpox antibodies, but it cannot be automated. Most other studies use a less laborious, and less accurate, ELISA test.
   About 4 million children are vaccinated against chickenpox each year. “If one-quarter are unprotected and we wait five years before giving a second dose, that leaves us with 5 million vaccinated, but vulnerable, children,” Dr. Gershon says. “Not only will this continue to produce outbreaks, but it may also cause an epidemic of serious disease in unprotected adults.”
Journal of Infectious Disease (2008) 197: 944-949 Research supported by the NIH.


Gastric Bypass Impacts Type 2 Diabetes
A new study shows that gastric bypass surgery itself – and not the weight loss it causes – alters activity of a hormone that may help explain why the operation cures diabetes.
   Almost immediately after gastric bypass surgery, about 80 percent of diabetic patients can discard their diabetes drugs and stop insulin injections.
   Many researchers suspect that the effect of gastric bypass surgery on diabetes works by increasing the secretion of the hormone incretin, which is released by the gut after a meal and helps stimulate the release of insulin. Incretin release in patients with type 2 diabetes is sluggish but bounces back to normal after gastric bypass surgery. Since weight loss may also improve hormone release, however, it is unclear if changes in incretin hormones are due to the sudden weight loss after surgery or surgery itself.
   To find out, Blandine Laferrère, MD, assistant professor of medicine at St. Luke’s-Roosevelt, and her colleagues at the Obesity Research Center compared 10 gastric bypass diabetic patients with 10 similar subjects who rapidly lost the same amount of weight through dieting.
   “Surgery increased the levels of the incretins that improve diabetes, and we did not see that after dieting,” Dr. Laferrère says. Surgery raised both the level of incretins and their ability to stimulate insulin release, while diet had no effect on either. Glucose levels did improve in both groups, but the improvement was far greater among the surgical patients. None of the surgical patients needed diabetes drugs after surgery, compared with 80 percent of the dieters.
   Should everyone get gastric bypass? “I don’t think so,” Dr. Laferrère says. “We don’t have good data on hormone levels 10 years down the road. We need more research to see what is going on, which may also lead to alternatives that increase incretins without surgery.”
J Clin Endocrin Metab, published online Apr 22 ahead of print
The work was funded by the American Diabetes Association, NIH, and the Merck Investigator Initiated Studies Program.


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