Could dog food additive prevent disabling chemotherapy side effect?

Contact: Stephanie Desmon sdesmon1@jhmi.edu 410-955-8665 Johns Hopkins Medicine

Johns Hopkins researchers find, in mice, that common preservative may thwart pain and damage of peripheral neuropathy

Working with cells in test tubes and in mice, researchers at Johns Hopkins have discovered that a chemical commonly used as a dog food preservative may prevent the kind of painful nerve damage found in the hands and feet of four out of five cancer patients taking the chemotherapy drug Taxol.

The Food and Drug Administration-approved preservative, an antioxidant called ethoxyquin, was shown in experiments to bind to certain cell proteins in a way that limits their exposure to the damaging effects of Taxol, the researchers say.

The hope, they say, is to build on the protective effect of ethoxyquin’s chemistry and develop a drug that could be given to cancer patients before taking Taxol, in much the same way that anti-nausea medication is given to stave off the nausea that commonly accompanies chemotherapy. While half of Taxol users recover from the pain damage, known as peripheral neuropathy, the other half continue to have often debilitating pain, numbness and tingling for the rest of their lives.

“Millions of people with breast cancer, ovarian cancer and other solid tumors get Taxol to treat their cancer and 80 percent of them will get peripheral neuropathy as a result,” says Ahmet Höke, M.D., Ph.D., a professor of neurology and neuroscience at the Johns Hopkins University School of Medicine and director of the Neuromuscular Division. “They’re living longer thanks to the chemotherapy, but they are often miserable. Our goal is to prevent them from getting neuropathy in the first place.”

A report on Höke’s research is published online in the Annals of Neurology.

Höke and his team knew from previous experiments that adding Taxol to a nerve cell line growing in a petri dish would cause neurodegeneration. In a series of experiments, they set out to hunt for compounds that might interrupt the degenerative process by adding Taxol to nerve cells along with some 2,000 chemicals — one at a time — to see which, if any, could do that.

Ethoxyquin did so, Höke says, apparently by making the cells resistant to the toxic effects of the Taxol.

Once they identified ethoxyquin’s effects, they gave intravenous Taxol to mice, and saw nerves in their paws degenerate in a couple of weeks. But when they gave ethoxyquin to the mice at the same time as the Taxol, it prevented two-thirds of the nerve degeneration, which Höke says would have a big impact on quality of life if the same effects were to occur in humans.

Specifically, Höke and his team discovered that molecules of ethoxyquin were binding to Hsp90, one of the so-called heat shock proteins that cells defensively make more of whenever they are stressed. Hsp90 acts as a cell’s quality control officer, determining whether a protein is properly formed before sending it out where it is needed.  When ethoxyquin binds to Hsp90, two other proteins — ataxin-2 and Sf3b2 — can’t bind to Hsp90. When they can’t bind, the cell senses that these two proteins are flawed, so they are degraded and their levels in the cell diminished.

Höke says his team is not certain why too much of those two proteins appears to have a negative effect on nerves, but reducing their levels clearly appears in their studies to make cells more resistant to Taxol toxicity.

Höke and his colleagues are looking into whether this medication could also make nerves more resistant to damage in peripheral neuropathy caused by HIV and diabetes, two other major causes of the pain. A previous study, Höke says, showed that ataxin-2 may cause degeneration in motor neurons in a rare form of ALS, commonly known as Lou Gehrig’s disease, suggesting that ethoxyquin or some version of it might also benefit people with this disorder.

Twenty to 30 million Americans suffer from peripheral neuropathy. Höke says it’s a “huge public health issue” that doesn’t get much attention because it is not fatal.

Höke’s team is hoping to conduct safety studies with ethoxyquin in animals in advance of possible testing in people. He says that while too much ethoxyquin is thought to be potentially harmful to dogs, the needed dose for humans would likely be 20-to-30-fold lower than what is found in dog food. Ethoxyquin was developed in the 1950s as an antioxidant, a compound to prevent pears and other foods from becoming discolored and spoiling.

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Other Johns Hopkins researchers involved in the study include Jing Zhu, Ph.D.; Weiran Chen, M.D.; Ruifa Mi, M.D., Ph.D.; Chunhua Zhou, B.S.; and Nicole Reed, M.S.

The research was supported by the Foundation for Peripheral Neuropathy, Dr. Miriam and Sheldon G. Adelson Medical Research Foundation, the National Institutes of Health’s National Institute of Neurological Disorders and Stroke (R01 NS43991) and Johns Hopkins Brain Science Institute.

For more information about Höke, click here.

Johns Hopkins Medicine (JHM), headquartered in Baltimore, Maryland, is a $6.5 billion integrated global health enterprise and one of the leading health care systems in the United States. JHM unites physicians and scientists of the Johns Hopkins University School of Medicine with the organizations, health professionals and facilities of the Johns Hopkins Hospital and Health System. JHM’s mission is to improve the health of the community and the world by setting the standard of excellence in medical education, research and clinical care. Diverse and inclusive, JHM educates medical students, scientists, health care professionals and the public; conducts biomedical research; and provides patient-centered medicine to prevent, diagnose and treat human illness.  JHM operates six academic and community hospitals, four suburban health care and surgery centers, and more than 30 primary health care outpatient sites. The Johns Hopkins Hospital, opened in 1889, was ranked number one in the nation from 1990 to 2011 by U.S. News & World Report.

Johns Hopkins Medicine Media Relations and Public Affairs Media Contacts:

Stephanie Desmon 410-955-8665; sdesmon1@jhmi.edu

Helen Jones 410-502-9422; hjones49@jhmi.edu

There’s life after radiation for brain cells

Contact: Stephanie Desmon sdesmon1@jhmi.edu 410-955-8665 Johns Hopkins Medicine

Johns Hopkins researchers suggest neural stem cells may regenerate after anti-cancer treatment

Scientists have long believed that healthy brain cells, once damaged by radiation designed to kill brain tumors, cannot regenerate. But new Johns Hopkins research in mice suggests that neural stem cells, the body’s source of new brain cells, are resistant to radiation, and can be roused from a hibernation-like state to reproduce and generate new cells able to migrate, replace injured cells and potentially restore lost function.

“Despite being hit hard by radiation, it turns out that neural stem cells are like the special forces, on standby waiting to be activated,” says Alfredo Quiñones-Hinojosa, M.D., a professor of neurosurgery at the Johns Hopkins University School of Medicine and leader of a study described online today in the journal Stem Cells. “Now we might figure out how to unleash the potential of these stem cells to repair human brain damage.”

The findings, Quiñones-Hinojosa adds, may have implications not only for brain cancer patients, but also for people with progressive neurological diseases such as multiple sclerosis (MS) and Parkinson’s disease (PD), in which cognitive functions worsen as the brain suffers permanent damage over time.

In Quiñones-Hinojosa’s laboratory, the researchers examined the impact of radiation on mouse neural stem cells by testing the rodents’ responses to a subsequent brain injury. To do the experiment, the researchers used a device invented and used only at Johns Hopkins that accurately simulates localized radiation used in human cancer therapy. Other techniques, the researchers say, use too much radiation to precisely mimic the clinical experience of brain cancer patients.

In the weeks after radiation, the researchers injected the mice with lysolecithin, a substance that caused brain damage by inducing a demyelinating brain lesion, much like that present in MS. They found that neural stem cells within the irradiated subventricular zone of the brain generated new cells, which rushed to the damaged site to rescue newly injured cells. A month later, the new cells had incorporated into the demyelinated area where new myelin, the protein insulation that protects nerves, was being produced.

“These mice have brain damage, but that doesn’t mean it’s irreparable,” Quiñones-Hinojosa says. “This research is like detective work. We’re putting a lot of different clues together. This is another tiny piece of the puzzle. The brain has some innate capabilities to regenerate and we hope there is a way to take advantage of them. If we can let loose this potential in humans, we may be able to help them recover from radiation therapy, strokes, brain trauma, you name it.”

His findings may not be all good news, however. Neural stem cells have been linked to brain tumor development, Quiñones-Hinojosa cautions. The radiation resistance his experiments uncovered, he says, could explain why glioblastoma, the deadliest and most aggressive form of brain cancer, is so hard to treat with radiation.

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The research was supported by grants from the National Institutes of Health’s National Institute of Neurological Disorders and Stroke (RO1 NS070024), the Maryland Stem Cell Research Fund, the Robert Wood Johnson Foundation, the Howard Hughes Medical Institute, the PROMETEO grant, the Red de Terapia Celular (TerCel) from Instituto de Salud Carlos III, and the Consejo Nacional de Ciencia y Tecnología.

Other Johns Hopkins researchers involved in the study include Vivian Capilla-Gonzalez, Ph.D.; Hugo Guerrero-Cazares, M.D., Ph.D.; Janice Bonsu; Oscar Gonzalez-Perez, M.D.; Pragathi Achanta, Ph.D.; John Wong, Ph.D.; and Jose Manuel Garcia-Verdugo, Ph.D.

For more information: http://tinyurl.com/ofqkea3

JOHNS HOPKINS MEDICINE

Johns Hopkins Medicine (JHM), headquartered in Baltimore, Maryland, is a $6.7 billion integrated global health enterprise and one of the leading health care systems in the United States. JHM unites physicians and scientists of the Johns Hopkins University School of Medicine with the organizations, health professionals and facilities of The Johns Hopkins Hospital and Health System. JHM’s mission is to improve the health of the community and the world by setting the standard of excellence in medical education, research and clinical care. Diverse and inclusive, JHM educates medical students, scientists, health care professionals and the public; conducts biomedical research; and provides patient-centered medicine to prevent, diagnose and treat human illness. JHM operates six academic and community hospitals, four suburban health care and surgery centers, more than 38 primary health care outpatient sites and other businesses that care for national and international patients and activities. The Johns Hopkins Hospital, opened in 1889, was ranked number one in the nation for 21 years by U.S. News & World Report.

Johns Hopkins Medicine Media Relations and Public Affairs

Media Contact:

Stephanie Desmon 410-955-8665; sdesmon1@jhmi.edu

Helen Jones 410-502-9422, hjones49@jhmi.edu

Estrogen fuels autoimmune liver damage

Contact: Ekaterina Peshva epeshev1@jhmi.edu 410-502-9433 Johns Hopkins Medicine

Johns Hopkins research in mice unravels mystery behind sex disparities in drug-induced hepatitis

A life-threatening condition that often requires transplantation and accounts for half of all acute liver failures, autoimmune hepatitis is often precipitated by certain anesthetics and antibiotics. Researchers say these drugs contain tiny molecules called haptens that ever so slightly change normal liver proteins, causing the body to mistake its own liver cells for foreign invaders and to attack them. The phenomenon disproportionately occurs in women, even when they take the same drugs at the same doses as men.

Results of the new study, described in the April issue of the journal PLoS One, reveal that estrogen and a signaling molecule called interleukin-6 collude to form a powerful duo that leads to immune cell misconduct and fuels autoimmune liver damage.

The findings, the research team says, also suggest therapeutic strategies to curb damage in people who develop drug-induced liver inflammation.

“Our study shows that estrogen is not alone in its mischief but working with an accomplice to set off a cascade of events that leads to immune cell dysregulation and culminates in liver damage,” says Dolores Njoku, M.D., a pediatric anesthesiologist and critical care expert at Johns Hopkins Children’s Center.

In the study, led by Njoku, researchers induced liver inflammation in mice by injecting them with drug-derived haptens. Female mice developed worse liver damage than male mice, and castrated male mice fared worse than their intact brethren, likely due to loss of testosterone and altered estrogen-to-testosterone ratio, the researchers say. Female mice with missing ovaries — the chief estrogen-secreting organs — suffered milder forms of hepatitis than mice with intact ovaries.

Female mice produced more liver-damaging antibodies and more inflammation-triggering chemicals, specifically the inflammatory molecule interleukin-6, known to fuel autoimmunity. Liver damage was notably milder in female mice whose interleukin-6 receptors were blocked or missing compared with normal female mice. On the other hand, male mice and female mice with missing ovaries had nearly undetectable levels of interleukin-6, while castrated male mice showed simultaneous upticks in both estrogen and interleukin-6.

The research team further zeroed in on a class of cells known as regulatory T cells, whose main function is keeping tabs on other immune cells to ensure they don’t turn against the body’s own tissues. When researchers compared the number of regulatory T cells present in the spleens of male and female mice, they noticed far fewer regulatory T cells in the spleens of female mice. The spleen, the researchers explain, is the primary residence of mature immune cells.

“Deficiency of regulatory T cells effectively takes the reins off other immune cells, leading to overactive immunity,” Njoku says.

In a final, dot-connecting move, the researchers immersed spleen-derived immune cells in estrogen. What they observed proved beyond doubt that estrogen, interleukin and regulatory T cells form a powerful triangle. Estrogen induced the immune cells of female mice to express more interleukin-6, which in turn diminished the expression of inflammation-taming regulatory T cells.

When the researchers injected sick female mice with a booster dose of regulatory T cells, their liver inflammation subsided to levels seen in male mice.

This powerful response, the researchers say, suggests that therapy with regulatory T cells may reduce estrogen-related liver damage in patients with autoimmune hepatitis. Such treatment, however, remains years away from human application.

One reason, the researchers say, is that regulatory T cells maintain the fine equilibrium between overactive and underactive immunity. Because an overactive immune system can lead to autoimmune diseases and an underactive one can promote tumor growth, any therapy with regulatory T cells must be precisely calibrated to avoid tipping this precarious balance.

“We first must figure out where the golden mean lies,” Njoku says.

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Co-investigators on the study included Joonhee Cho, Lina Kim, Zhaoxia Li, Noel Rose and Monica Vladut Talor, all from Johns Hopkins.

The research was funded in part by the William R. Rienhoff Scholars Foundation, by the American Autoimmune Related Diseases Association, by the National Institute of Diabetes and Digestive and Kidney Diseases (grant number NIHR21DK075828) and by the Scoby Family Foundation.

Founded in 1912 as the children’s hospital of the Johns Hopkins Medical Institutions, the Johns Hopkins Children’s Center offers one of the most comprehensive pediatric medical programs in the country, with more than 92,000 patient visits and nearly 9,000 admissions each year. Hopkins Children’s is consistently ranked among the top children’s hospitals in the nation. Hopkins Children’s is Maryland’s largest children’s hospital and the only state-designated Trauma Service and Burn Unit for pediatric patients. It has recognized Centers of Excellence in dozens of pediatric subspecialties, including allergy, cardiology, cystic fibrosis, gastroenterology, nephrology, neurology, neurosurgery, oncology, pulmonary, and transplant. For more information, visit http://www.hopkinschildrens.org.

Johns Hopkins Medicine Media Relations and Public Affairs Media Contacts: Ekaterina Pesheva, epeshev1@jhmi.edu, 410-502-9433, 410-926-6780 cell Helen Jones, hjones49@jhmi.edu, 410-502-9422

ADHD symptoms persist for most young children despite treatment

Contact: Ekaterina Pesheva epeshv1@jhmi.edu 410-502-9433 Johns Hopkins Medicine

Nine out of 10 young children with moderate to severe attention-deficit hyperactivity disorder (ADHD) continue to experience serious, often severe symptoms and impairment long after their original diagnoses and, in many cases, despite treatment, according to a federally funded multi-center study led by investigators at Johns Hopkins Children’s Center.

The study, published online Feb. 11 in the Journal of the American Academy of Child & Adolescent Psychiatry, is the largest long-term analysis to date of preschoolers with ADHD, the investigators say, and sheds much-needed light on the natural course of a condition that is being diagnosed at an increasingly earlier age.

“ADHD is becoming a more common diagnosis in early childhood, so understanding how the disorder progresses in this age group is critical,” says lead investigator Mark Riddle, M.D., a pediatric psychiatrist at Johns Hopkins Children’s Center. “We found that ADHD in preschoolers is a chronic and rather persistent condition, one that requires better long-term behavioral and pharmacological treatments than we currently have.”

The study shows that nearly 90 percent of the 186 youngsters followed continued to struggle with ADHD symptoms six years after diagnosis. Children taking ADHD medication had just as severe symptoms as those who were medication-free, the study found.

Children with ADHD, ages 3 to 5, were enrolled in the study, treated for several months, after which they were referred to community pediatricians for ongoing care. Over the next six years, the researchers used detailed reports from parents and teachers to track the children’s behavior, school performance and the frequency and severity of three of ADHD’s hallmark symptoms—inattention, hyperactivity and impulsivity. The children also had full diagnostic workups by the study’s clinicians at the beginning, halfway through and at the end of the research.

Symptom severity scores did not differ significantly between the more than two-thirds of children on medication and those off medication, the study showed. Specifically, 62 percent of children taking anti-ADHD drugs had clinically significant hyperactivity and impulsivity, compared with 58 percent of those not taking medicines. And 65 percent of children on medication had clinically significant inattention, compared with 62 percent of their medication-free counterparts. The investigators caution that it remains unclear whether the lack of medication effectiveness was due to suboptimal drug choice or dosage, poor adherence, medication ineffectiveness per se or some other reason.

“Our study was not designed to answer these questions, but whatever the reason may be, it is worrisome that children with ADHD, even when treated with medication, continue to experience symptoms, and what we need to find out is why that is and how we can do better,” Riddle says.

Children who had oppositional defiant disorder or conduct disorder in addition to ADHD were 30 percent more likely to experience persistent ADHD symptoms six years after diagnosis, compared with children whose sole diagnosis was ADHD.

ADHD is considered a neurobehavioral condition and is marked by inability to concentrate, restlessness, hyperactivity and impulsive behavior. It can have profound and long-lasting effects on a child’s intellectual and emotional development, Riddle says. It can impair learning, academic performance, peer and family relationships and even physical safety. Past research has found that children with ADHD are at higher risk for injuries and hospitalizations.

More than 7 percent of U.S. children are currently treated for ADHD, the investigators say. The annual economic burden of the condition is estimated to be between $36 billion and $52 billion, according to researchers.

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Other Johns Hopkins investigators on the research included Elizabeth Kastelic, M.D., and Gayane Yenokyan, Ph.D.

The other institutions involved in the research were Columbia University Medical Center, Duke University, the Nathan Kline Institute, University of California—Irvine and University of California—Los Angeles.

The research was funded by the National Institute of Mental Health under grant numbers: U01 MH60642 (Johns Hopkins), U01MH60848 (Duke University Medical Center), U01MH60943 (New York University Child Study Center), U01MH60903 (Columbia University), U01 MH60833 (University of California–Irvine) and U01H60900 (University of California—Los Angeles).

Related

Journal of the American Academy of Child & Adolescent Psychiatry http://www.jaacap.com/article/S0890-8567%2812%2900993-8/abstract

Popular ADHD Drug Safe and Effective for Preschoolers http://www.hopkinschildrens.org/Popular-ADHD-Drug-Safe-and-Effective-for-Pre-Schoolers.aspx

Increasing Prevalence of Parent-Reported Attention-Deficit/Hyperactivity Disorder Among Children — United States, 2003 and 2007 http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5944a3.htm?s_cid=mm5944a3_w

Founded in 1912 as the children’s hospital at Johns Hopkins, the Johns Hopkins Children’s Center offers one of the most comprehensive pediatric medical programs in the country, treating more than 90,000 children each year. Hopkins Children’s is consistently ranked among the top children’s hospitals in the nation. Hopkins Children’s is Maryland’s largest children’s hospital and the only state-designated Trauma Service and Burn Unit for pediatric patients. It has recognized Centers of Excellence in dozens of pediatric subspecialties, including allergy, cardiology, cystic fibrosis, gastroenterology, nephrology, neurology, neurosurgery, oncology, pulmonary, and transplant. For more information, please visit

Diet may eliminate spasms for infants with epilepsy: Low Carbohydrate Diet

2008 re-post for filing

Contact: Sean Wagner swagner@wiley.com 781-388-8550 Wiley-Blackwell

Treatment shown to be effective without side effects in children before trying drugs

Baltimore, Md. – September 08, 2008 – Infantile spasms are a severe and potentially devastating epilepsy condition affecting children aged typically 4-8 months. In a new study appearing in Epilepsia, researchers have found that the ketogenic diet, a high fat, low carbohydrate diet more traditionally used for intractable childhood epilepsy, is an effective treatment for this condition before using drugs. The study is the first description of the ketogenic diet as a first-line therapy for infantile spasms.

ACTH and vigabatrin, medications that are the commonly-used first treatments worldwide, can have potentially-serious side effects such as hypertension, gastric ulceration, cortical atrophy, and visual field constriction. ACTH, though it is effective in 60-70 percent of cases, also costs more than $80,000 for a one-month supply and vigabatrin is not currently available in the U.S. Both drugs have about a 30-40 percent recurrence rate of spasms as well. Other therapies are not yet proven.

“We decided to review our experience at Johns Hopkins using the ketogenic diet to treat infantile spasms before medications were tried and compare this to our use of ACTH over the same time period,” says Eric Kossoff, M.D, a pediatric neurologist at Johns Hopkins Hospital and lead author of the study. “We knew that the ketogenic diet worked well for difficult-to-control infantile spasms, so we thought it would also be effective earlier.”

If the diet stopped the spasms, infants were kept on it for usually 6 months. The diet worked in 8-of-13 infants within approximately one week. Only 1-of-8 had recurring spasms, and that infant was controlled again with the addition of topiramate to the diet. Side effects were fewer than ACTH in this series and the recurrence rate was also lower with the diet. In the 5 patients in which the diet did not work, ACTH was started immediately; it worked quickly in 4 of the 5 infants. ACTH did lead to a normal EEG quicker, but long-term developmental outcomes were identical.

As a result of the findings, the ketogenic diet is now one of the typically-offered first-line therapies for new-onset infantile spasms at Johns Hopkins. Other hospitals are beginning to use the ketogenic diet similarly. The researchers hope this novel use of the ketogenic diet may be the first step in finding another treatment to control new-onset infantile spasms.

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This study is published in Epilepsia. Media wishing to receive a PDF of this article may contact medicalnews@bos.blackwellpublishing.net.

Eric Kossoff, M.D., is a pediatric neurologist at Johns Hopkins Hospital. To reach Dr. Kossoff for questions, please contact Ekaterina Pesheva, Senior Media Relations Representative at Johns Hopkins Hospital, at epeshev1@jhmi.edu or 410-516-4995.

Epilepsia is the leading, most authoritative source for current clinical and research results on all aspects of epilepsy. As the journal of the International League Against Epilepsy, subscribers every month will review scientific evidence and clinical methodology in: clinical neurology, neurophysiology, molecular biology, neuroimaging, neurochemistry, neurosurgery, pharmacology, neuroepidemiology, and therapeutic trials. For more information, please visit www.blackwell-synergy.com/loi/epi

Having a tonsillectomy can cause Obesity

Contact: David March
dmarch1@jhmi.edu
410-955-1534
Johns Hopkins Medicine

Age, not underlying diagnosis, key factor in weight gain in children after tonsillectomy

Potentially worrisome weight gains following tonsillectomy occur mostly in children under the age of 6, not in older children, a study by Johns Hopkins experts in otolaryngology- head and neck surgery shows.

Sudden increases in body mass index, or BMI, have been routinely observed for months after some of the more than half-million surgeries performed annually in the United States to remove the sore and swollen tissues at the back of the throat.

The Johns Hopkins study, in 115 children in the Baltimore region, is believed to be the first to dispel long-held beliefs that such weight gains occurred mostly in children whose tonsils were removed as primary treatment for diagnosed sleep apnea, when the swollen, paired tissues partially obstruct breathing and disrupt sleep. It is also believed to be the largest study to analyze weight gain specific to every child’s age group, from 1 through 17.

Although researchers have yet to pinpoint the underlying cause of the weight-gain phenomena, they did find that it happened at the same rate in the 85 children who had the surgery for obstructive sleep apnea as in the 30 who had it due to recurrent episodes of tonsil inflammation.

Senior study investigator, otolaryngologist and sleep medicine expert Stacey Ishman, M.D., M.P.H., says her team’s study findings, scheduled to be presented Sept. 12 at the annual meeting of the American Academy of Otolaryngology—Head and Neck Surgeons in Washington, D.C., should help alleviate rising concerns among many parents whose adolescent children are already overweight that tonsillectomy may aggravate the problem; or start one in normal weight kids. Recent surveys have shown that record numbers of American children, as many as one-third, are overweight or obese.

“Our study results show that parents’ current concerns about weight gain are serious, but only underweight or normal weight children between the ages of 2 and 6 are most likely to gain even more weight, not older children,” says Ishman, an assistant professor at the Johns Hopkins University School of Medicine.

“Parents with overweight adolescent children need not fear tonsillectomy, and those with younger, normal weight and overweight children just really need to closely watch their child’s diet following surgery, and make caloric adjustments,” says Ishman, who has performed hundreds of the roughly 30-minute procedures that typically require a general anesthetic.

In the study, researchers analyzed the medical records of children between the ages of 6 months and 18 years who had had their tonsils removed at the Johns Hopkins Outpatient Center between 2008 and 2011. Researchers looked only at those medical records for children who had been routinely examined for at least six months after their procedure, with detailed measurements of any possible weight gain, which were averaged and compared based on a formula involving age, gender and height. All also had a history of recurrent tonsillitis or obstructive sleep apnea, as strictly determined by an individual sleep study analysis.

Results showed an averaged post-surgical weight gain of 2 to 5 pounds – or a 1.0- to 1.2-point increase in averaged BMI scores—but the gains were not dependent on whether the underlying condition was inflammation or sleep apnea. Only age mattered, researchers say, after discounting gender and height.

Ishman says that while such weight gains might appear small, in these children’s small bodies, whose initial weight was between 22 and 60 pounds (or between 10 to 30 kilos), “a 10 percent weight gain can be quite worrisome.”

Results showed a normal weight, 5-year-old boy, weighing 40 pounds (or 18 kilos) and measuring 42 inches tall, who gained 3 pounds after tonsillectomy, would move from the 68th percentile to the 89th percentile in their age-weight group, and become overweight. For an underweight 5-year-old boy of similar height, originally weighing 34 pounds (15 kilos), the same 3-pound weight gain would shift them from the 24th percentile group to the 28th percentile, moving them closer to a normal weight.

However, she says, in an overweight 10-year-old boy, already weighing 90 pounds (41 kilos) and 55 inches tall, there was no weight gain post tonsillectomy, and he remained in the 92nd percentile group, meaning his poor condition did not worsen.

Ishman says her team’s next steps are to gain a better understanding of why and how children’s age affects weight gain post-tonsillectomy. She already has plans to monitor children immediately after surgery to find out what factors or interventions may help underweight children gain pounds, while helping those who are overweight to not get any bigger.

Since 2002 tonsillectomy has been recommended by the American Academy of Pediatrics as the primary treatment for obstructive sleep apnea, as sleeping aids and drug therapies are not as effective. Studies have shown that if left untreated, sleep apnea can lead to long-term health problems, including increased heart and lung diseases, even death.

 

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Funding support for this study was provided by The Johns Hopkins Hospital.

In addition to Ishman, other Johns Hopkins researchers involved in this study were David Smith, M.D., Ph.D., and Emily Boss, M.D., M.P.H. Other study co-investigators included Ami Vikani, B.S., at the George Washington University School of Medicine, in Washington, D.C.; and Fernando Aguirre-Amezquita, M.D., at Escuela de Medicina Ignacio A. Santos de Monterrey, in Mexico.

For more information, go to:
http://www.hopkinsmedicine.org/otolaryngology/our_team/faculty/ishman.html
http://www.entannualmeeting.org/12/