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儿科学会2005年会热点(2005-5)

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摘要:Medscapeconferencecoveragewillincludeanupdateonmethicillin-resistantStaphylococcusaureus(MRSA),particularlycommunity-acquiredMRSA(CA-MRSA),abriefupdate......

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儿科学会2005年会热点

Highlights of the Pediatric Academic Societies 2005 Annual Meeting

2005年5月14-17日

美国华盛顿特区

May 14 - 17, 2005, Washington, DC

Community-Acquired MRSA: Evolving Pathogens

William T. Basco, Jr., MD

The Pediatric Academic Societies Annual Meeting was held May 14-17, 2005 at the Washington, DC, Convention Center. Over 5000 participants attended the meeting. Medscape conference coverage will include an update on methicillin-resistant Staphylococcus aureus (MRSA), particularly community-acquired MRSA (CA-MRSA), a brief update on immunizations, and an extensive review of research on the obesity epidemic in the United States and the metabolic syndrome.

Epidemiology Overview

A "Hot Topic" session sponsored jointly by the PAS and the Pediatric Infectious Diseases Society focused on the increasing difficulties posed by CA-MRSA. The epidemiology of MRSA was described by Daniel Jernigan,[1] Centers of Disease Control and Prevention, Atlanta, Georgia. He noted that when MRSA resistance began in the 1970 it was mostly a phenomenon of strains isolated within hospitals. However, by the late 1990s or certainly early 2000's, CA-MRSA had emerged.

Defining a strain as CA-MRSA is not as easy as it may seem. In the final analysis, it is more of a syndromic diagnosis. In order to consider an MRSA isolate as "community associated," the patient should not have had recent a hospitalization, recent in-dwelling catheters or other hardware, or have undergone any surgical procedure within the past year. In addition, CA-MRSA should have an antibiotic sensitivity profile that demonstrates sensitivity to most antibiotics, in contrast to the profile of healthcare associated MRSA (HA-MRSA).

Jernigan pointed out that the most commonly used definition for CA-MRSA is a clinical one, where any lesion typical of this bacterium, such superficial, small abscesses, is considered CA-MRSA by most clinicians until proven otherwise. In a recent publication, Fridkin and co-investigators demonstrated that CA-MRSA accounted for 9%-20% of the isolates from 3 survey areas in the United States.[2] The incidence for having CA-MRSA varied from a high of 25.7 per 100,000 population in Atlanta, Georgia, to a low of 18 cases per 100,000 population in Maryland. In this cohort of patients, 77% of the CA-MRSA isolated caused skin and other soft tissue infections. Wound infections comprised 10% of CA-MRSA disease; 4% were urinary tract infections or sinusitis. Only 3% of the patients were bacteremic and an additional 2% had pneumonia.

Several groups seem to be at increased risk for contracting S aureus of either variety. These groups include sports participants, daycare attendees, military recruits, and prisoners -- all groups with a higher number of people in a relatively restricted space. In addition, individuals with chronic skin conditions such as eczema also have higher rates of MRSA infection.

Conditions that raise the risk of staphylococcal disease include the 5 C's. These include: (1) crowding, (2) contact (usually skin to skin), (3) compromised skin, (4) contaminated surfaces, and (5) cleanliness, or lack of it. For example, Kasakova[3] evaluated an outbreak of skin abscesses in a professional sports team. It was determined that the players were contracting the MRSA infections from multiple fomites in the locker room. In addition, recent antibiotic use by a player raised the risk of contracting MRSA.

One of the major differences between CA-MRSA and HA-MRSA are their resistance patterns. The patterns result from differences in the resistance gene harbored by the 2 stain. Jernigan pointed out that just a few clonal variations of MRSA seem to cause the bulk of the disease that we are currently seeing. This has raised the question, "Did this new onslaught of CA-MRSA occur as a result of increased use of the pneumococcal conjugate vaccine?"

Because one might presume that pneumococcus and MRSA would normally compete in the nasopharynx, having so many young children immunized against pneumoccous might produce an environment where MRSA could become more dominate. Although this seems to be a plausible explanation, there are no data to definitely support this conclusion (see later comments by Dr. Kaplan).

The Molecular Basis for Resistance

The second presenter was Robert Daum,[4] University of Chicago, Illinois, who reviewed the molecular basis for the resistance of S aureus. He began his presentation by noting that 84% of skin infections in Illinois are currently caused by CA-MRSA.

The term "MRSA" really implies resistance to multiple drugs, not just methicillin. Even CA-MRSA can be resistant to several drugs. The overall resistance pattern of CA-MRSA is not nearly extensive as that of HA-MRSA. However, the overall resistance pattern of CA-MRSA is not as extensive as that of HA-MRSA. One possible explanation is that the resistant element or sequences harbored within CA-MRSA are actually smaller in size. This relatively smaller size of the resistance elements may ease the ability for different bacteria to exchange resistance elements, but it may also limit the amount of resistance that any given sequence can carry. This is a very plausible explanation for why CA-MRSA tends to be less multidrug-resistant.

One would logically would ask the question, "Where did CA-MRSA originate?" The differences in resistance patterns suggest that CA-MRSA is not HA-MRSA that "escaped" the hospital and invaded the community. Instead, it appears that methicillin sensitive S aureus have gained resistance patterns that are what is known today as CA-MRSA.

Clinical Experiences of CA-MSRA

Sheldon Kaplan,[5] Texas Children's Hospital, Baylor College of Medicine, Houston, was the third speaker in the MRSA session. He began by reviewing the experience with CA-MRSA at Texas Children's Hospital. In response to the question of whether the advent of pneumococcal conjugate vaccine has in part contributed to the rise in MRSA infection, Dr. Kaplan noted that the increases in CA-MRSA disease are not occurring in young children. Because young children are those who are primarily receiving the new 7-valent pneumococcal conjugate vaccine, he believes it is unlikely that the epidemiological increase in CA-MRSA observed has been due to CA-MRSA filling a niche vacated by pneumococcus.

At Texas Children's, 90% of the MRSA isolates are obtained from soft tissue infections. In addition, over 60% of those patients are admitted to the hospital, a phenomenon that has clearly resulted in increased cost. Kaplan noted that most of the CA-MRSA isolates are susceptible to vancomycin, gentamicin, rifampin, trimethoprim-sulfamethoxazole, clindamycin, doxycycline, and linezolid.

He also noted that although most strains are usually susceptible to clindamycin, some have inducible resistance to the drug. It is unclear whether this reducible resistance to clindamycin will become more widespread. At Texas Children's Hospital, there has been an increase in resistance to clindamycin from approximately 2% to 6% over the course of a 3-year study that will soon be published.[5] Therefore, therapeutic approaches in this area will likely need to change as a result of the onset of widespread resistance. However, It is important for clinicians in other communities to be aware of any local CA-MRSA resistance to clindamycin because this antibiotic is otherwise a good first-line drug of choice for treatment of CA-MRSA.

It was also emphasized that incision and drainage is often an effective initial therapy. Lee and co-investigators[6] published a series in 2004 revealing that even patients sent home on what was later determined to be an inactive antimicrobial agent (because the isolate was later found to be resistant) did well if incision and drainage had occurred in the Emergency Department. A take-home message was to culture more often and drain pus any time you can!

Another take home point was that it is acceptable to choose a non-MRSA antibiotic for initial treatment of cellulitis, but that one should consider switching treatment within 48 hours if the patient does not improve. This would only hold if the local prevalence of CA-MRSA for skin infections was not already high, in which case the patient should initially be treated for CA-MRSA.

Kaplan then reviewed the evidence suggesting that invasive CA-MRSA appears to be increasingly common. He cautioned that there are not much data available about this at present. However, there seems to be a trend for patients to have multiple sites of infection. In a 2004 publication by Martinez, Kaplan and other colleagues[7] reported on causative agents in a series of osteomyelitis patients. The subset of osteomyelitis patients who had CA-MRSA were more likely to have complications such as chronic osteomyelitis and a notable increase in deep venous thromboses.

In addition to this skin and soft tissue predisposition of CA-MRSA, Schultz and colleagues[8] also published data from Texas Children's Hospital showing that CA-MRSA now forms a larger percentage of empyemas complicating pneumonias. In this study, S aureus comprised 60% of the bacteria causing empyemas (compared with 18% in the pre-pneumococcal conjugate vaccine era), and over 70% of the S aureus isolates were MRSA.

Kaplan finished his presentation with additional warnings, reviewing the findings of a paper recently published by Gonzales, Kaplan, and colleagues[9] that reported on the experience with severe invasive CA-MRSA at Texas Children's Hospital. In this investigation, researchers reviewed 15 cases of severe invasive MRSA infection -- and 13 of the 15 cases were CA-MRSA. Eighty percent of the patients had no underlying chronic medical condition and had no social history that would place them at higher risk for CA-MRSA (eg, having a parent that is a healthcare worker). A majority (60%) of the patients had suffered a traumatic event and 30% required pressor support to maintain blood pressure. Most had bone or joint involvement, 4 out of the 15 had vascular complications, and 4 of the 15 patients died.

The take home messages from this case series and the other studies reviewed by Kaplan was that CA-MRSA has been shown to have multiple manifestations and should be added to the list of organisms considered in a patient with a picture of septic shock, osteomyelitis, and cellulitis. It should also be considered in the very ill child with pneumonia and empyema.

Approaches to CA-MRSA Prevention

The final session was presented by Don Goldmann,[10] Children's Hospital, Boston, Massachusetts, and Harvard Medical Center. He focused on potential control options for preventing CA-MRSA. However, he began his presentation with an overall disclaimer statement because he is actually fairly skeptical about whether we will obtain "control" of CA-MRSA, short of employing a vaccine. Nevertheless, he provided a review of some basic points that might help to diminish the spread of the organism.

MRSA is very durable, so multiple fomites can serve as reservoirs for the organism. These include hands, medical equipment, and even clothing. Factors associated specifically with increased risk of CA-MRSA disease were also reviewed. Begier and colleagues[11] found that body shaving, whirlpool bath use, and not using soap were all associated with increased incidence of skin abscesses in a group of athletes.

Goldmann reviewed the findings of the Berier article to illustrate his principal point -- that hygiene, and rigorous attention to it in the hospital setting, can be very effective in decreasing the rate of MRSA infections. He also emphasized that most of the variation in hospital rates of HA-MRSA infections revolve around basic antisepsis approaches and suggested that much of this variation is due to cultural issues. For example, some medical cultures do not tolerate hospital-acquired infections while others consider these unavoidable. It has been demonstrated that hospitals that view patient HA-MRSA infections as a "quality" issue tend to have fewer MRSA infections.[10]

Key strategies for controlling MRSA include:

Reviewer Comments

Any clinician seeing pediatric patients is aware of the striking increase in CA-MRSA. The most important points made by the presenters were the following:

References

  1. Jernigan DB, Centers for Disease Control and Prevention, Atlanta, GA. Epidemiology of Community-Acquired, Methicillin-Resistant Staphylococcus aureus. Program and abstracts of the Pediatrics Academic Societies Annual Meeting; May 14-17, 2005; Washington, DC. Course # 5102
  2. Fridkin S K, Hageman JC, Morrison M, et al. Methicillin-Resistant Staphylococcus aureus disease in three communities. N Engl J Med. 2005; 352: 1436-1444.
  3. Kazakova SV, Hageman JC, Matava M, et al. A clone of methicillin-resistant Staphylococcus aureus among professional football players. N Engl J Med. 2005;352:468-475.
  4. Daum RS. The molecular basis for epidemic community-onset MRSA. Program and abstracts of the Pediatrics Academic Societies Annual Meeting; May 14-17, 2005; Washington, DC. Course #5102
  5. Kaplan SL. Clinical implications of community-acquired methicillin-resistant Staphylococcus aureus. Program and abstracts of the Pediatrics Academic Societies Annual Meeting; May 14-17, 2005; Washington, DC. Course # 5102.
  6. Lee MC, Rios AM, Aten MF, et al. Management and outcome of children with skin and soft tissue abscesses caused by community-acquired methicillin-resistant Staphylococcus aureus. Pediatr Infect Dis J. 2004;23:123-127.
  7. Martinez-Aguilar G, Avalos-Mishaan A, Hulten K, Hammerman W, Mason EO Jr, Kaplan SL. Community-acquired, methicillin-resistant and methicillin-susceptible Staphylococcus aureus musculoskeletal infections in children. Pediatr Infect Dis J. 2004;23:701-706.
  8. Schultz KD, Fan LL, Pinsky J, et al. The changing face of pleural empyemas in children: epidemiology and management. Pediatr. 2004;113:1735-1740.
  9. Gonzalez BE, Martinez-Aguilar G, Hulten KG, et al. Severe staphylococcal sepsis in adolescents in the era of community-acquired methicillin-resistant staphylococcus aureus. Pediatr. 2005;115:642-648.
  10. Goldmann DA. Prevention and control of methicillin-resistant staphylococcus aureus. Program and abstracts of the Pediatrics Academic Societies Annual Meeting; May 14-17, 2005; Washington, DC. Course #5102.
  11. Begier EM, Frenette K, Barrett NL, et al. A high-morbidity outbreak of methicillin-resistant Staphylococcus aureus among players on a college football team, facilitated by cosmetic body shaving and turf burns. Clin Infect Dis. 2004;39:144614-53.
  12. Baker CJ, Frenck RW Jr. Change in management of skin/soft tissue infections needed. American Academy of Pediatrics News. September 2004. Available at : lcgcmag.mediwire.com/main/Content.aspx?ArticleID=156076.



Obesity and the Metabolic Syndrome

William T. Basco, Jr., MD   

Introduction

The PAS 2005 meeting had a plethora of presentations about obesity and the metabolic syndrome, both as invited science platform presentations and as original science abstracts presented as posters or platform presentations. This report covers a just a sampling of the obesity presentations, including a workshop reporting on the findings of a recent Institute of Medicine (IOM) report on childhood obesity, an invited science session on the metabolic syndrome, and selected original science abstracts reviewing the interactions of obesity and comorbid conditions.

Extent of the Obesity "Epidemic" and Recommendations to Address the Problem

One of the first events was the IOM-sponsored workshop on the extent of obesity in children and suggestions for prevention.[1] The session presenters included Thomas Robinson, Stanford University, Palo Alto, California; Dennis Bier, Baylor College of Medicine, Houston, Texas; and Vivica Kraak from IOM. This presentation was primarily an overview of the problem of obesity in the United States and a review of the suggested strategies for addressing this public health issue.

The IOM report, Preventing Childhood Obesity: Health in the Balance,[2] was released in September 2004 and is available for online preview and purchase. The executive summary of the document can also be viewed online.[3] The United States Congress requested this study be conducted in 2002; it was funded through a partnership of the Centers for Disease Control and Prevention (CDC), the National Institutes for Health, The Robert Wood Johnson Foundation and others. The task of the study was to develop a prevention-focused action plan to stem the rise in childhood obesity.

According to Dennis Bier,[1] who reviewed the epidemiology of obesity, over 9 million children age 6 and older are now considered obese. Since the 1970s, obesity has increased in all school age groups. The prevalence of obesity has doubled for children aged 2-5 years and for children aged 12-19 years. But even more significant is the fact that obesity has tripled in prevalence for those aged 6-11 years.

The IOM defines obesity as a body mass index (BMI) greater than the 95th percentile for age and gender.[2] In order to help clinicians identify these patients, the CDC produced BMI charts based on data from 1963 to 1994. It was determined that these older data should be used to try to capture the weights and heights of children before the clinical rise in obesity began in the late 1990s. A CDC primer on BMI and how to use growth charts is available in a CME/CE clinical update on Medscape.[4] BMI-for-age growth charts are also available online.[5]

There is a slight difference in the CDC and the IOM definitions for obesity. As mentioned previously, the IOM defines obesity as a BMI greater than 95th percentile for age and gender. The CDC would call those same children "overweight." The reason for this discrepancy is that the CDC reserves the term "obesity" for those children who are above the 95th percentile for age and gender but who are overweight due to excess body fat alone. The IOM classifies children as "obese" if they are above the 95th percentile, but admits that a small proportion of those are actually not in that percentile due to excess body fat alone.

Corresponding to the doubling of obesity rates, for 2- to 5-year-olds the current prevalence of obesity is 10%. For children aged 6-11 the prevalence is 15%, and for those aged 12-19 it is approximately 16%. All 3 of these age groups had an obesity prevalence of less than 5% from 1963-1970. Bier also emphasized that, according to data from Headley and colleagues,[6] the greatest rate of increase in prevalence was seen among minority individuals; approximately 25% of Mexican-American boys and 23% of black girls were classified as obese.

An "at risk" profile for obesity in childhood: individuals with parental obesity, low socioeconomic status, minorities, and individuals from the Southern region of the United States all appear to be at increased risk of becoming obese. However, it was noted that the root cause of the increased risk is unclear.

The biggest consequence of the obesity epidemic has been a large increase in the frequency and prevalence of type 2 diabetes mellitus (DM) in children. Children with type 2 DM now constitute an increasing proportion of patients in pediatric endocrinology clinics. There are many things that contribute to a child becoming obese, but the final common pathway is in an energy imbalance -- a difference between the calories taken in and the calories expended. Bier also emphasized that the current trends in obesity are almost certainly due to environmental rather than genetic factors. The time period from 1970 to 2005 is simply too short for genetic factors to produce such a large change in obesity prevalence. Genetic factors exert their effects over much longer time horizons.[1]

Vivica Kraak[1] reviewed some of the specifics of the IOM report. She emphasized that the full report provides a comprehensive review of the obesity prevention literature, and that any provider interested in determining what approaches to reducing overweight and obesity have been effective would find this report to be an invaluable resource. Key conclusions from the IOM report included:

The final point was most strongly emphasized in this presentation. Thomas Robinson reviewed the multilevel societal changes that will be needed to stem the obesity epidemic. The IOM committee, while preparing the report, struggled with the fact that rigorous evaluations of approaches to limit weight gain and encourage healthy lifestyles are sorely lacking from the existing obesity literature. Thus, the members felt that they were basing their recommendations on a dearth of published interventional studies. Such studies are emergently needed and absolutely essential to help guide policy.

Nevertheless, the IOM committee made the following suggestions for needed societal changes:

  1. Governmental involvement. Governmental agencies should provide clear guidance to corporations, communities, and individuals on healthy approaches to achieving energy balance.

  2. Marketplace and media. People in the United States need to be presented with healthier meals, and healthier eating must become a desired goal. Manufacturers should improve the labeling of products. For example, although a bag of potato chips may contain 3 servings, many individuals reading the label may not realize that they are reading the fat, sodium, and carbohydrate statistics for only 1 serving. Governmental agencies may need to institute new marketing guidelines. Finally, the media needs to clearly and forcefully incorporate healthy lifestyle messages into advertising.

  3. Communities. Multiple community agencies need to focus on the problem of obesity. Coalitions of groups will need to develop community-wide action plans to address the problem. Recommended changes include improving access to more healthy foods for low socioeconomic status individuals and improvements in the "built environment." In short, we all need to walk more and ride less.

  4. Schools. Schools need to get children to become more active. This may include increasing recess time, adding physical education back to school curricula, and redoubling the emphasis on health promotion classes. The committee suggested a goal of children having at least 30 minutes of cardiovascular activity per day as part of school curricula. The committee made a very strong statement that schools should get advertising, particularly for snack foods of all types, out of schools.

  5. Healthcare Providers. The authors in the report also have several recommendations for providers. These include:

    • Providers should routinely track BMI of their patients using the CDC charts.

    • When an individual is diagnosed as obese or at risk for becoming obese, the provider should provide relevant evidence-based counseling and guidance.

    • Providers should serve as role models, implementing or continuing their own healthy lifestyle, eating, and exercise habits.

    • Providers should provide community leadership and serve as a resource to communities. Many community-wide efforts will require the input of healthcare providers. In addition, providers can be a forceful voice in ensuring appropriate advertising, especially advertising in local schools.

  6. Health plans. Health plans should emphasize screening for obesity and pay for both screening and obesity-related interventions. This only seems to make sense given the exorbitant downstream costs of obesity related to cardiovascular problems and diabetes.

  7. Healthy homes. Although government and community efforts can be helpful, the home is the most influential environment for children. There is evidence that breastfeeding for 4-6 months exclusively can reduce the chance that a child will become obese.[7] In addition, greater emphasis should be placed on keeping healthful foods and healthful portions central in families' eating habits. The family should engage in regular physical activity. Families should also reduce "screen time" for children, including television and computers, to less than 2 hours per day. Finally, parents should be role models for their children in their own physical activities and eating habits, just as providers should be role models for their patients.

  8. Research. There is a pressing need for rigorous evaluation of potential interventions to reduce weight and improve healthy lifestyles in order to guide public policy. Behavioral intervention research is required to identify how to help individuals stick to the interventions determined to be effective. Additional community-based and population-based research on obesity is needed to help understand why certain ethnic groups and regions appear to be at increased risk for obesity.

Finally, the presenters described a resource that both clinicians and parents would find useful and user-friendly. It is a Web site created by the Children's Nutrition Research Center, a cooperative venture between Baylor College of Medicine Children's Hospital and the US Department of Agriculture/Agricultural Research Service.[8] This site has downloadable posters for parent education (eg, posters on serving sizes), brochures about weight management, news items, and nutrition calculators.

The Metabolic Syndrome

In addition to multiple presentations on the widespread prevalence of obesity, many presenters provided data about one of the most common results of obesity, the metabolic syndrome (MS). A Topic Symposium on metabolic syndrome was jointly sponsored by American Society of Pediatric Nephrology, the International Pediatric Hypertension Association, Lawson Wilkins Pediatric Endocrine Society, and PAS.

The first presentation, by Sonia Caprio,[9] Yale University, New Haven, Connecticut, began with a review of the current definition of metabolic syndrome, previously called "insulin resistance syndrome." In order to be classified as having metabolic syndrome, an individual should have 3 of the following conditions:

  1. Hypertension
  2. Altered glucose metabolism
  3. Dyslipidemia
  4. Obesity

Therefore, a person may be obese but not have full-blown MS. It is the full-blown MS that appears to have the greatest effect on increasing risk for cardiovascular disease.

Cook and colleagues[10] showed, in an analysis published in 2003, that the prevalence of MS in children was approximately 6% to 7%. Using data from the Third National Health and Nutrition Examination Survey (1988-1994), the investigators found that black males appeared to have a much lower rate of MS, and that there was a great deal of variation among ethnic groups and between genders. These data demonstrated that 28% of all obese children have MS. Data from de Ferranti and colleagues[11] published in 2004 demonstrated similar rates of MS in children, again finding that black children were less likely to have MS.

Although the definition of MS is better established in adults, there is also a building consensus for a definition in children. Cook's definition for MS included the following components:

Even though other researchers have used slightly different variations of these components, it is notable that all investigations to date have found a fairly similar prevalence of MS.

The prevalence of MS appears to increase with increasing degrees of obesity. Weiss and colleagues[12] demonstrated that 30% of moderately obese children suffered from MS. The prevalence rose to 50% in children with severe obesity. There are 2 other notable findings of the Weiss study. First, these data demonstrated clearly that insulin resistance is perhaps the central problem in MS. Second, the study showed that children with obesity have an elevated baseline C-reactive protein (CRP) level.

Caprio concluded that the definition of MS still has room for evolution. For example, fasting glucose may be an inaccurate predictor of whether someone actually has impaired glucose tolerance. Patients may have a normal fasting glucose but have markedly abnormal and elevated 2-hour postprandial glucose. In addition, much more research needs to be conducted to determine whether insulin resistance is the critical component in producing the pathologic outcomes seen in patients with MS.

The structural vascular changes that occur in patients with MS were reviewed by Albert Rocchini,[13] University of Michigan, Ann Arbor. His central thesis was that obesity in children is associated with endothelial dysfunction, even in youth. There were several studies published in 2003, including research by Sorof and colleagues[14] demonstrating that obesity and hypertension in children are associated with vascular effects. In the Sorof study, children with obesity had a thickening of the intimal-media of the common carotid artery demonstrated on carotid artery ultrasound.

Although intimal-media thickness has not been directly linked to later cardiovascular disease, measuring it may prove to be a good noninvasive method for assessing future risk of atherosclerosis. The exact cause of intimal-media thickening is not known, but it may be related to the phenomenon of insulin resistance. The thickening leads to increased vascular resistance and contributes to elevated blood pressure levels. Rocchini's own study,[15] published in 1992, demonstrated that as obese children lose weight, their vascular resistance decreases along with decreasing insulin resistance. So while it seems clear that insulin resistance and vascular resistance are related, the direction of the association (which is the cause and which is the effect) remains undetermined.

There are other factors that may contribute to endothelial dysfunction in obesity, including changes in the renin-angiotensin-aldosterone system, the sympathetic nervous system, dyslipidemia, increased endothelin levels, and even chronic inflammation. In fact, future studies may look at whether blocking inflammatory pathways can help prevent the vascular outcomes that occur in MS.

Obesity and Asthma

In addition to invited science presentations about obesity and MS, other investigators presented original abstracts evaluating associations between obesity and asthma, another chronic medical condition often associated with obesity. Frintner and colleagues[16] presented an abstract sponsored by the American Academy of Pediatrics describing outcomes of a study that evaluated the degree of asthma symptoms among patients with increased BMI. Their findings were part of the Child Health Information Reporting Project, a 3-year study funded by the National Heart, Lung, and Blood Institute.

The data were obtained in urban and suburban Ohio; 414 children and their parents completed the study. The investigators asked the research question, "Do overweight children experience more asthma symptoms compared to normal weight peers?" They used CDC definitions, classifying children whose BMI for age was equal to the 95th percentile as overweight, children with a BMI between the 85th-95th percentile as at risk for overweight, and children whose BMI was less than the 85th percentile as normal weight. The parents in the sample completed questionnaires assessing the child's asthma symptoms and limitations of activity during the 2 previous weeks.

The sample included 406 children with a mean age of 11 years. The sample was 58% male, 45% black, 38% white and 11% Hispanic. Of the 406 children, 27% met the CDC definition for overweight; an additional 15% were at risk for overweight. Only 46% of the parents of overweight children reported that their child's health was "excellent/very good" compared with 50% of at-risk children and 70% of parents of children whose weight was normal. Overweight children were more likely to experience asthma symptoms, with 62% of them experiencing 1 or more asthma symptoms at least some of the time compared with only 48% of the normal-weight children. Thirty-two percent of the overweight children experienced limitations of strenuous activity compared with only 18% of the normal weight children.

The investigators concluded that overweight children and children at risk for overweight may experience more asthma symptoms and have greater limitations on their activities than children of normal weight. They contended that further efforts should help to delineate the exact relationship between overweight and asthma, and that asthma interventions may need to include weight reduction components for children who are overweight.

Susan Woolford and colleagues,[17] University of Michigan, evaluated the role of obesity in increasing the charges for patients experiencing inpatient asthma admissions. Their investigation analyzed information from the Agency for Healthcare Research and Quality's Kids Inpatient Database, which contains a nationally representative sample of pediatric hospital discharges from the year 2000. Length of stay and charges for children aged 1-18 years were included in the sample. Comparisons of the length of stay for asthma admissions for patients with obesity and without, as well as differences for pneumonia admissions for patients who were and were not obese, were made.

Children with asthma admissions complicated by obesity had a mean length of stay of 3.26 days compared with 2.32 days for children who were not obese (95% CI 2.97-3.54). In a similar fashion, obese children admitted for pneumonia stayed in the hospital 1 full day longer (at 4.4 days) than those who were not obese. Longer stays were associated with increased charges, with obese children admitted for asthma incurring an average of $8784.00 in charges compared with an average of only $5,724.00 in nonobese asthmatic patients. Similar excess costs were noted for obese children admitted for pneumonia. The investigators conclude that obesity in children with asthma is a problematic comorbid condition associated with increased hospitalization length and increased total charges.

Finally, findings from a study by Philomena Asante and colleagues[18] provided some guidance for providers regarding what parental behaviors targeting the obesity problem might be malleable with office-based counseling. This study, conducted by the Children's Hospital of Boston and the Center for Child Health Care Studies, Harvard Medical School, Massachusetts, included 300 parents of children aged 3-13 years. The children presented to a single clinic during 2004.

The investigators evaluated parental willingness to institute behavioral and nutritional changes that would help children who are overweight. These changes included: decreasing meal portion sizes, exercising as a family, watching less TV, eating less fast food, drinking less soda, eating more vegetables, eating together as a family, and eating more fruits. Parents were able to respond that they either planned to implement the change, might implement the change, or that they did not plan to implement the change. The sample was 54% black and 20% Hispanic.

The proactive behaviors that were best accepted by parents were drinking less soda, eating more vegetables and fruits, and eating more together as a family. Of particular note: 93% of the parents of overweight children agreed to drinking less soda. The lowest planned implementation rates (at 58% and 71%, respectively) were for decreasing meal portion sizes and for exercising as a family. Parents of normal-weight children drove the relatively low acceptance of these 2 changes. When looking at responses by parents of only the overweight children, 77% of those same parents agreed to decrease meal portion sizes. The investigators concluded that parents are in need of counseling on healthier lifestyle choices, but cautioned that parental readiness to change is low in areas that might be most beneficial such as decreasing meal sizes and increasing physical activity.

Reviewer comment:

Obesity, and its downstream effects such as hypertension and other components of MS, will be a central part of pediatric practice for many years to come. We will all need to accept the problem as a significant one; learn the components of MS, how to screen for them and the abnormal "cutoff" values; and how to find local resources and perhaps establish within-practice resources to help obese patients.

References

  1. Robinson TN, Bier DM, Kraak VA. Institute of Medicine Committee on Prevention of Obesity in Children and Youth: recommendations and assessment. Program and abstracts of the Pediatrics Academic Societies Annual Meeting; May 14-17, 2005; Washington, DC. PAS Educational workshop,
  2. Koplan JP, Liverman CT, Kraak VA. (Eds) Preventing Childhood Obesity: Health in the balance. Committee on the Prevention of Obesity in Children and Youth, Institute of Medicine. National Academy of Sciences, 2004. Available at: http://www.iom.edu/report.asp?id=22596 (Accessed June 11, 2005)
  3. Committee on the Prevention of Obesity in Children and Youth. Institute of Medicine. Executive summary. Available at: http://www.iom.edu/report.asp?id=22596
  4. Polhamus B, Thompson D, Benton-Davis SL, Reinold CM, Grummer-Strawn LM, Dietz W. Using the BMI-for-Age growth charts. Medscape 2004. Available at: http://www.medscape.com/viewprogram/2640 (Accessed June 10, 2005)
  5. Centers for Disease Control and Prevention. 2000 CDC growth charts: United States. Clinical growth charts. Available at: http://www.cdc.gov/growthcharts (Accessed June 11, 2005)
  6. Hedley AA, Ogden CL, Johnson CL, Carroll MD, Curtin LR, Flegal KM. Prevalence of overweight and obesity among US children, adolescents, and adults, 1999-2002. JAMA. 2004;291:2847-2850.
  7. Owen CG, Martin RM, Whincup PH, Smith GD, Cook DG. Effect of infant feeding on the risk of obesity across the life course: a quantitative review of published evidence. Pediatrics. 2005;115:1367-1377.
  8. Baylor College of Medicine and the US Department of Agriculture/Agricultural Research Service. Children's Nutrition Research Center. Available at: http://www.kidsnutrition.org/ (Accessed June 9, 2005)
  9. Caprio SK. Can we agree on a definition of the metabolic syndrome in children?. PAS/ASPN/IPHA/LWPES Topic Symposium: Consequences of Metabolic Syndrome in Children: Hypertension, Diabetes and Renal Disease. Program and abstracts of the Pediatrics Academic Societies Annual Meeting; May 14-17, 2005; Washington, DC. Course # 5520
  10. Cook S, Weitzman M, Auinger P, Nguyen M, Dietz WH. Prevalence of a metabolic syndrome phenotype in adolescents: findings from the third National Health and Nutrition Examination Survey, 1988-1994. Arch Pediatr Adolesc Med. 2003;157:821-827.
  11. de Ferranti SD, Gauvreau K, Ludwig DS, Neufeld EJ, Newburger JW, Rifai N. Prevalence of the metabolic syndrome in American adolescents: findings from the Third National Health and Nutrition Examination Survey. Circulation. 2004;110:2492-2497.
  12. Weiss R, Dziura J, Burgert TS, et al. Obesity and the metabolic syndrome in children and adolescents. N Engl J Med. 2004;350:2362-2374.
  13. Rocchini AP. Pathogenesis of structural vascular changes in patients with hypertension and the metabolic syndrome. PAS/ASPN/IPHA/LWPES Topic Symposium: Consequences of Metabolic Syndrome in Children: Hypertension, Diabetes and Renal Disease. Program and abstracts of the Pediatrics Academic Societies Annual Meeting; May 14-17, 2005; Washington, DC. Course #5520.
  14. Sorof JM, Alexandrov AV, Cardwell G, Portman RJ. Carotid artery intimal-medial thickness and left ventricular hypertrophy in children with elevated blood pressure. Pediatrics. 2003;111:616-616.
  15. Rocchini,AP, Moorehead C, Katch V, Key J, Finta KM. Forearm resistance vessel abnormalities and insulin resistance in obese adolescents. Hypertension. 1992;19:615-620.
  16. Frintner MP, Radecki L, Olson LM. Relationships between BMI, asthma symptom report & activity limitations: findings from the Child Health Information Reporting Project (CHIRP). Program and abstracts of the Pediatrics Academic Societies Annual Meeting; May 14-17, 2005; Washington, DC. PAS Poster Session I, May 14, 2005, Course # 4902.
  17. Woolford SJ, Gebremariam A, Clark SJ, Davis MM. The incremental costs of obesity as a comorbidity in pediatric asthma hospitalizations. Program and abstracts of the Pediatrics Academic Societies Annual Meeting; May 14-17, 2005; Washington, DC. Poster Symposium: Obesity and Metabolism II, May 16, 2005, Course # 6734.
  18. Asante P, Cox J, Rein J, Hannon C, Samuels R, Taveras E. Childhood obesity prevention: which behaviors are parents ready to change? Program and abstracts of the Pediatrics Academic Societies Annual Meeting; May 14-17, 2005; Washington, DC. PAS Poster Session I, May 14, 2005. Course #



Influenza Vaccination: A Look at Barriers and Facilitators

William T. Basco, Jr., MD   

Introduction

The 2003-2004 influenza season began relatively early and was characterized by the widely reported deaths of children, especially in Colorado, and complicated by periodic local shortages of vaccine. Given the public interest in receiving influenza vaccine created by that season, it is understandable that many immunization investigators sought to answer questions related to influenza vaccine acceptance, receipt, and delivery. As a result, a large proportion of the immunization abstracts presented at the 2005 PAS meeting focused on influenza.

Evaluations of Barriers and Facilitators

The Immunization Delivery Poster Symposium contained presentations of original science abstracts. Gnanasekaran and colleagues[1] evaluated parental beliefs, the media, and the media's effects on parental willingness to accept influenza immunization. Their study evaluated children aged 5-18 years with asthma. The participants were randomly divided into 1 of 3 different vaccine reminder approaches to determine factors influencing whether parents would accept influenza vaccination.

In the sample, 44% of the children received influenza vaccine during the 2003-2004 season compared with only 27% during the previous winter season. The investigators demonstrated that the weekly influenza vaccination rates in 2003-2004 increased during times when media attention focused on the influenza deaths of children in Colorado. However, the factor most strongly correlated with children receiving the vaccine was physician recommendation, with an odds ratio of 2.6 (95% CI 1.5-4.5). The researchers concluded that media coverage and physician recommendation both influenced parents to increase the chances of their child receiving influenza immunization.

These findings were echoed in a similar evaluation of 862 Denver Colorado area children presented by Daley and colleagues.[2] In this study, parents surveyed after the 2003-2004 influenza season were more likely to view their child as at risk for catching influenza and were more likely to consider influenza infections to be severe compared with parental responses to same survey items before the beginning of the 2003-2004 influenza season. In addition, the parents felt that there were fewer risks associated with influenza vaccine than there were prior to the beginning of that flu season.

In the Daley study, a physician's recommendation that a child receive influenza vaccine increased the odds that a parent would get the child vaccinated by 3.8 (95% CI 1.81-7.95). As in the Gnanasekaran study,[1] the researchers concluded that a physician recommendation for a child to receive influenza vaccine exerted a strong influence on the parental acceptance of the vaccine.

Data from the New Vaccine Surveillance Network, a Centers for Disease Control and Prevention (CDC)-sponsored multisite monitoring network, were presented by Poehling.[3] This investigation evaluated whether mothers vaccinated during pregnancy were less likely to have an infant diagnosed with influenza during the subsequent influenza season. Pregnant women are considered to be a high-risk population, and it was therefore recommended they receive inactivated influenza vaccine so they would be "covered" during the second and third trimesters.[4]

Maternal vaccination history was available for 337 children born during the 2 most recent influenza seasons. Of these 337 infants, 11% experienced an influenza infection during 1 of the 2 seasons. By contrast, only 15% of the mothers reported receiving influenza vaccine during their pregnancies.

The number of women followed in the investigation was actually small, making statistical comparison difficult. However, there was the suggestion that infants born to women who received the vaccine were less likely to be admitted to the hospital for treatment of their influenza. Most disappointingly, Poehling and co-investigators found that less than 20% of pregnant women actually received the vaccine.

The researchers concluded that vaccination rates of pregnant women were very low. Although data from this study suggested that vaccination of pregnant mothers can reduce the rate of admission for influenza in infants, larger participant numbers are needed to answer this question adequately. In the meantime, clinicians should remember to encourage expectant mothers to be immunized with the influenza vaccine.

Clark, from the University of Michigan, Ann Arbor, and co-investigators from the CDC presented data on pediatric provider factors that might influence the delivery of influenza vaccine.[5] They surveyed a national random sample of 500 pediatricians in 2004. The focus was on evaluating whether the providers adopted the influenza vaccination recommendations for healthy children between 6 and 23 months of age. Provider influences and barriers to adoption of the recommendation were also assessed.

Data were collected from 258 eligible respondents and showed that approximately 56% were "adopters" of the recommendation to give influenza vaccine to healthy 6- to 23-month-olds. The adopters were more likely to list the American Academy of Pediatrics recommendation as a strong influence.[6] However, 2 particular differences between adopters and non-adopters were evident in their perceptions of barriers to delivery of the vaccine. Non-adopters were twice as likely to list vaccine purchase cost, limited amount of vaccine without thimerosal, and parental acceptance as barriers. Sadly, more than 70% of both adopters and non-adopters also listed vaccine shortage as a barrier.

The researchers concluded that vaccine shortages and parental concerns were both barriers to implementation. However, they noted that additional financial barriers that could limit provider adoption of the influenza vaccine recommendation should also be remedied.

Dombkowski and co-investigators,[7] University of Michigan Child Health Evaluation and Research Unit, presented an abstract at a poster session based on their evaluation of the role of missed influenza vaccination opportunities for children with asthma. They analyzed 2001-2003 Michigan Medicaid data from 5000 children aged 5-18 years with asthma to determine rates of influenza vaccine receipt and the frequency of missed opportunities to vaccinate. They found that 79% of the children had at least 1 office visit during the respective influenza seasons, but only 14% to 18% of the asthmatic children received the vaccine during the respective season. In addition, 77% of the asthmatic children who did not receive influenza vaccine had at least 1 office visit (a missed opportunity) during the 2001-2002 season and 75% had a missed opportunity in the 2002-2003 season. The researchers concluded that in this cohort, the influenza vaccination rates in general were low, and a large majority of the children had office visits where they could have receive the influenza vaccine. They maintained that interventions focusing on missed opportunities for influenza vaccine administration are needed.

References

  1. Gnanasekaran SK, Finkelstein JA, Hohman K, O'Brien M, Kruskal B, Lieu TA. Improving influenza vaccination rates among children with asthma: parental beliefs, provider factors and the media. Program and abstracts of the Pediatrics Academic Societies Annual Meeting; May 14-17, 2005; Washington, DC. PAS Original Science Abstract Poster Symposium: Immunization Delivery, Abstract 57-1681. 2. Daley MF, Crane LA, Chandramouli V, et al. Influenza immunization in healthy young children: changes in parental perceptions and predictors of immunization during the 2003-2004 influenza season. Program and abstracts of the Pediatrics Academic Societies Annual Meeting; May 14-17, 2005; Washington, DC. PAS Original Science Abstract Poster Symposium: Immunization Delivery, Abstract 57-1682.
  2. Poehling KA, Griffin MR, Edwards KM, et al. Influenza vaccine for pregnant mothers -- important but underutilized. Program and abstracts of the Pediatrics Academic Societies Annual Meeting; May 14-17, 2005; Washington, DC. PAS Original Science Abstract Poster Symposium: Immunization Delivery, Abstract 57-1683.
  3. Englund JA. Maternal immunization with inactivated influenza vaccine: rationale and experience. Vaccine. 2003;21:3460-3464. 5. Clark SJ, Cowan AE, Rickert DL, Allred NJ, Woolford SJ, Freed GL. Pediatricians' approaches to influenza vaccination of healthy children 6-23 months during the 2003-04 influenza season. Program and abstracts of the Pediatrics Academic Societies Annual Meeting; May 14-17, 2005; Washington, DC. PAS Original Science Abstract Poster Symposium: Immunization Delivery, Abstract 57-1685.
  4. American Academy of Pediatrics, Committee on Infectious Diseases. Recommendations for influenza immunization of children. Pediatrics. 2004;113:1441-1447. 7. Dombkowski KJ, Davis MM, Cohn LM, Clark SJ. Missed opportunities for influenza vaccination among children with asthma. Program and abstracts of the Pediatrics Academic Societies Annual Meeting; May 14-17, 2005; Washington, DC. Poster Session I.

 


作者: 2006-12-9
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