Researchers examined 619 exclusively breast-fed 3-month-old infants for AD, scored any AD for severity, and screened for common mutations of the filaggrin FLG gene (which encodes the epidermal barrier protein filaggrin). They also performed skin-prick testing for allergy to six foods (cow's milk, egg, cod fish, wheat, sesame, and peanut).

About 25% had AD at examination. About 12% carried at least one FLG mutation (93% heterozygous, 7% either homozygous or compound heterozygous); in children with AD, the incidence of FLG mutation was 24%. Infants with FLG mutations were more likely than others to have AD at 3 months. Roughly 6% were sensitized to one or more of the six foods (egg 24/619, cow's milk 10/619, peanuts 8/619, wheat 2/619, sesame and cod fish 0/619). FLG mutations were not associated with food sensitization, but having AD was strongly associated with having food allergy (P<0.001). More-severe AD was associated with increased food allergy incidence.

Comment

Exclusive breast-feeding did not prevent atopic dermatitis.Food sensitization may occur through affected skin. The filaggrin gene FLG mutation does not predispose to food allergy unless AD is present. The results surprised me, until I remembered that food allergens are proteins too big to penetrate intact skin even if FLG mutations are present. They can, however, penetrate the damaged barrier in AD skin. It seems counterintuitive that inflamed skin of exclusively breast-fed babies would come into contact with food. Perhaps sensitization occurs to food allergens in breast milk, or perhaps, via transplacental transport in utero.

Lower exposure to food allergens may inadequately stimulate immunoregulatory networks, just as the hygiene hypothesis proposes that decreased bacterial exposure results in increased predisposition to infection. These investigators are now testing whether early introduction of allergenic foods might better protect against AD than breast-feeding alone (http://www.eatstudy.co.uk).

Editor Disclosures at Time of Publication

Disclosures for Mark V. Dahl, MD at time of publication Consultant / Advisory board Genentech; Makucell, Inc.; Mayo Clinic Equity Elorac, Inc.; Johnson & Johnson; Pfizer Speaker's bureau Los Angeles Dermatological Society; University of Southern California Editorial boards UpToDate

Citation(s):

Flohr C et al. Atopic dermatitis and disease severity are the main risk factors for food sensitization in exclusively breastfed infants. J Invest Dermatol 2013 Jul 18; [e-pub ahead of print]. (http://dx.doi.org/10.1038/jid.2013.298)

Swimming has been recommended for patients with asthma because the warm humidified air might lessen exercise-induced bronchoconstriction, but several studies suggest that exposure to chlorine byproducts (especially trichloramine) might actually be asthmogenic. Researchers followed 5738 children in the U.K. from birth to age 10 years and prospectively collected data by questionnaire on swimming and respiratory status. Lung function, bronchial hyperresponsiveness, and skin tests were measured at age 7 to 8 years.

After adjustment for confounding variables, swimming frequency did not increase the prevalence of asthma, eczema, atopy, or rhinoconjunctivitis symptoms. On the contrary, swimming was associated with increased lung function and decreased prevalence of current asthma symptoms at age 10 years in children with previous wheezing. Swimming had a protective effect in children who wheezed before age 3.5 years.

Comment: In an accompanying pro/con exchange, editorialists debate these findings in light of studies showing increased rates of atopy and allergic disease in recreational swimmers, higher rates of occupational asthma in indoor swimming-pool workers, and increased bronchial hyperresponsiveness and asthmalike symptoms in competitive swimmers. The study results are reassuring for recreational swimmers. I believe that we should encourage all patients with asthma to exercise regularly but still caution them that prolonged exposure to chlorine products (e.g., in elite swimmers) could cause lung injury.

- David J. Amrol, MD

David J. Amrol, MD, is an Associate Professor of Clinical Internal Medicine and Director of the Division of Allergy and Immunology at the University of South Carolina School of Medicine in Columbia.

"Epinephrine in appropriate doses is safe, and there are no absolute contraindications for its use in treating anaphylaxis," according to a consensus statement prepared by an expert panel of emergency physicians and allergists.

"Delay in administration of epinephrine may lead to more severe and treatment resistant anaphylaxis," the authors report in an article published online August 6 in the Annals of Allergy, Asthma and Immunology.

"It is not necessary for the [National Institute of Allergy and Infectious Disease and the Food Allergy and Anaphylaxis Network] criteria to be met to administer epinephrine," they stress.

The panel was convened in 2014 to discuss the limitations of current knowledge and barriers to emergency management of anaphylaxis, focusing specifically on three primary barriers to improved care: the complexity of diagnosing anaphylaxis, the underuse of epinephrine, and inadequate post discharge follow-up.

In addition to patients with anaphylaxis, those identified as being at risk for anaphylaxis are candidates for epinephrine administration, Stanley M. Fineman, MD, from Emory University School of Medicine and Atlanta Allergy and Asthma Clinic, Atlanta, Georgia, and colleagues report. At-risk patients include those with a history of previous severe reaction, as well as those who have had a known or suspected exposure to their allergic trigger, with or without the development of symptoms.

Antihistamines and glucocorticoids do not work fast enough to be an appropriate first-line treatment for a severe reaction, but they may be administered after epinephrine at the discretion of the treating physicians, the authors write.

The panel also recommends providing a prescription for epinephrine autoinjectors to patients treated for anaphylaxis or for severe allergic reactions in emergency settings, and to those considered at risk for a future event. It is imperative that these individuals also be provided with an action plan for autoinjector use before discharge, they write.

Postdischarge protocol should also include referral to an allergist "to assist with diagnosis confirmation, trigger identification, and continued outpatient management," the authors write.

Breaking down barriers to optimal emergency management of anaphylaxis "should be a joint effort of all who have a stake in improving anaphylaxis care, including emergency physicians, emergency medical services practitioners, allergists, and patient advocacy groups," the authors write, noting the need for widespread education efforts for emergency medical services practitioners and emergency department clinicians to improve the diagnosis and management of anaphylaxis.

In addition, "allergists should be proactive in seeking collaborations with emergency practitioners in their community," the authors conclude.

This research was supported by an educational grant from Mylan Specialty LP. The authors have disclosed no relevant financial relationships.

Ninety-six infants with symptomatic congenital CMV disease were randomized to receive oral valganciclovir, 16 mg per kg orally twice daily, either for 6 months or for 6 weeks, plus placebo for an additional 4.5 months. All had a gestational age of ?32 weeks, were aged ?30 days, and weighed ?1800 g at initiation of therapy.

The primary endpoint - change in "best-ear" hearing between baseline and 6 months - was similar between groups. However, in assessments of changes in best- or total-ear hearing between baseline and 12 and 24 months, 6-month-group participants were more likely to show improvement or to have maintained normal hearing. The 6-month group also had better Bayley III language-composite and receptive-communication scale scores at 24 months. Viral load was lower in 6-month-group participants only during the period when they were receiving the drug and the others were receiving placebo. Rates of adverse events were similar between groups.

Comment

Among infants with symptomatic congenital CMV disease, 6 months of oral valganciclovir therapy had a moderately favorable effect on long-term audiologic and neurodevelopmental outcomes and was not associated with an excess risk for adverse events such as neutropenia. Both regimens avoid the need to maintain intravenous access.

In conducting the study, researchers at King's College London and colleagues examined the amount of peanut protein to which 577 babies were exposed during their first year of life. This was done by measuring the amount of peanut protein in the dust collected by vacuum from the living room sofa in their home. The children were tested for peanut allergy years later when they were 8 and 11 years old. Their DNA was also checked for a specific skin barrier defect, known as an FLG mutation.

Previous studies identified a specific gene that codes for the skin barrier protein, filaggrin. Mutations to this gene, known as the FLG gene, lead to a skin barrier impairment, which is thought to make the body more vulnerable to an allergic reaction.

The study, published this month in the Journal of Allergy and Clinical Immunology, found that one in five children with peanut allergy had an FLG mutation.

The researchers found that a threefold increase in exposure to peanut protein in dust in the first 12 months of life was associated with a threefold increase in risk for a later peanut allergy. They said, however, exposure to peanut protein in household dust had no effect on children who did not have a skin barrier defect from an FLG mutation.

"Our findings provide evidence that peanut allergy may develop via the skin in children with mutations in the gene that codes for filaggrin which damage the function of this important skin protein," said the study's first author, Dr. Helen Brough, from the department of pediatric allergy at King's College London. "These findings are also an example of how an individual's response to their environment can be modified by their genes," Brough said in a university news release.

"Our study raises the possibility of being able to identify a group of children with FLG mutations through genetic testing in the future, and altering their environmental exposure to peanut early in life to reduce the risk of developing peanut allergy," she added.

The study offers further evidence for the dual-allergen-exposure theory, said the study's senior author, Gideon Lack, also from the King's College London pediatric allergy department. This theory "suggests food allergies develop through exposure to allergens via the skin, likely through a disrupted skin barrier, [and that] consumption of these food proteins early in life builds up tolerance in the body," he said in the news release.

"Previous guidelines recommending that mothers should avoid peanuts during pregnancy and breastfeeding have now been withdrawn. Ongoing studies at King's aim to find if exposure to solids in early infancy might actually help to prevent allergies," Lack said. "It may be that the timing and balance of skin and oral exposure to a particular food early in life determines whether a child develops an allergy or tolerance to that food."

To determine the incidence and etiologies of pediatric community-acquired pneumonia requiring hospitalization since the introduction of vaccines for Haemophilus influenzae type b and Streptococcus pneumoniae, the Centers for Disease Control conducted an active-surveillance study. From 2010 to 2012, 2358 children (<18 years) with radiographic evidence of pneumonia were enrolled at children's hospitals in three cities. Extensive testing for pathogens was performed, including polymerase chain reaction assays for viruses in respiratory swab specimens, serologic testing for viruses, and multiple blood and pleural fluid (when available) tests for bacteria.

Most patients (70%) were younger than 5 years and had at least one underlying condition, such as asthma (33%) or prematurity (21%). A pathogen was isolated in 81% of patients: viruses in 66%, bacteria in 8%, and both in 7%. Respiratory syncytial virus (28%) and rhinovirus (27%) were the most commonly detected viruses, followed by human metapneumovirus (13%), adenovirus (11%), and parainfluenza and influenza viruses (both 7%). Mycoplasma pneumoniae was identified in 8% of children (more commonly in those aged 5 and older), Streptococcus pneumoniae in 4%, and Staphylococcus aureus in 1%. Only 30% of eligible children had received influenza vaccine; 87% of children aged 19 months to 12 years had received at least three doses of pneumococcal conjugate vaccine. Hospital stays were short (median length, 3 days), however, 21% of children required intensive care, 7% were intubated, and 3 (<1%) died. The estimated annual incidence of hospitalization for pneumonia was 15.7 cases per 10,000 children.

Comment

This surveillance study provides extensive information about the causes of community-acquired pneumonia in children. Viruses were overwhelmingly implicated, yet 88% of children received antibiotics. Aggressive efforts and improved diagnostics to identify viral etiologies in children with pneumonia will curb unnecessary antibiotic use.

Citation

Jain S et al. Community-acquired pneumonia requiring hospitalization among U.S. children. N Engl J Med 2015 Feb 26; 372:835. (http://dx.doi.org/10.1056/NEJMoa1405870)

The three main allergy associations commissioned a practice parameter update on food allergy, diagnosis, and management. The 13-member task force considered results of impactful studies, guidelines, clinical reports, and meta-analyses. They graded each reference for overall strengths of recommendation (SOR) and level of evidence (LOE). Food allergy was defined as adverse health effects arising from specific immune responses occurring reproducibly on exposure to a given food. Some relevant summary statements for dermatologists were:

• A high proportion of food allergy is caused by relatively few allergens (cow's milk, hen's egg, soy, wheat, peanuts, tree nuts, fish, shellfish). (SOR strong; LOE B)
• Evaluate patients with latex allergy for possible cross-reactivity to banana, avocado, kiwi, chestnut, potato, green pepper, and other fruits and nuts. (SOR strong, LOE C)
• For infants with family history of atopy, consider partially or extensively hydrolyzed infant formula to prevent atopic dermatitis. (SOR moderate, LOE B)
• Do not routinely recommend that patients with chronic idiopathic urticaria avoid foods containing additives. (SOR strong, LOE B)
• Use prick tests and/or serum tests for specific immunoglobulin E (IgE) to diagnose food allergy; testing should be focused on suspected foods and test results alone should not be considered diagnostic. (SOR strong, LOE B)
• Do not routinely obtain total IgE levels to diagnose food allergy. (SOR strong, LOE C)
• Unproved tests (allergen-specific IgG measurement, cytotoxicity assays, applied kinesiology, provocation neutralization, hair analysis) should not be used to diagnose food allergy. (SOR strong, LOE C)
• Routine use of atopy patch tests to diagnose food allergy is not recommended, except in conjunction with pediatric eosinophilic esophagitis evaluation. (SOR moderate, LOE C)
• Recommend a nutritionist consult for growing children, as elimination diets might affect growth. Be aware of nutritional consequences of elimination diets, including deficiencies of vitamins C and D. (SOR strong, LOE B)

Comment

Self-reported food allergy is more common than proven food allergy. Food allergy is more common in children than adults, and among children, more common in those with other atopic diseases (atopic dermatitis, asthma, allergic rhinitis). Cutaneous reactions to foods include IgE-mediated reactions (urticaria, angioedema, flushing, pruritus), cell-mediated reactions (contact dermatitis, dermatitis herpetiformis), and mixed reactions (atopic dermatitis). The authors cite evidence that food allergy may be a “significant trigger” for atopic dermatitis in 30% to 40% of infants and children. In my view, this number is too high.

Mark V. Dahl, MD Reviewing Sampson HA et al., J Allergy Clin Immunol 2014 Nov 134:1016

Methods
We performed a multicenter, randomized, double-blind, placebo-controlled dietary-intervention study involving 944 children who were positive for HLA-DQ2 or HLA-DQ8 and had at least one first-degree relative with celiac disease. From 16 to 24 weeks of age, 475 participants received 100 mg of immunologically active gluten daily, and 469 received placebo. Anti-transglutaminase type 2 and antigliadin antibodies were periodically measured. The primary outcome was the frequency of biopsy-confirmed celiac disease at 3 years of age.

Results
Celiac disease was confirmed by means of biopsies in 77 children. To avoid underestimation of the frequency of celiac disease, 3 additional children who received a diagnosis of celiac disease according to the 2012 European Society for Pediatric Gastroenterology, Hepatology, and Nutrition diagnostic criteria (without having undergone biopsies) were included in the analyses (80 children; median age, 2.8 years; 59% were girls). The cumulative incidence of celiac disease among patients 3 years of age was 5.2% (95% confidence interval [CI], 3.6 to 6.8), with similar rates in the gluten group and the placebo group (5.9% [95% CI, 3.7 to 8.1] and 4.5% [95% CI, 2.5 to 6.5], respectively; hazard ratio in the gluten group, 1.23; 95% CI, 0.79 to 1.91). Rates of elevated levels of anti-transglutaminase type 2 and antigliadin antibodies were also similar in the two study groups (7.0% [95% CI, 4.7 to 9.4] in the gluten group and 5.7% [95% CI, 3.5 to 7.9] in the placebo group; hazard ratio, 1.14; 95% CI, 0.76 to 1.73). Breast-feeding, regardless of whether it was exclusive or whether it was ongoing during gluten introduction, did not significantly influence the development of celiac disease or the effect of the intervention.

Conclusions
As compared with placebo, the introduction of small quantities of gluten at 16 to 24 weeks of age did not reduce the risk of celiac disease by 3 years of age in this group of high-risk children. (Funded by the European Commission and others; PreventCD Current Controlled Trials number, ISRCTN74582487.).

Because many symptoms and illnesses could be wrongly blamed on "food allergies," it is important for parents to know the usual symptoms. The following is information from the American Academy of Pediatrics (AAP) about food allergies and how to recognize and treat the symptoms. There is also important information about how to keep your child safe and healthy at home and in school if he has a food allergy.

Symptoms of a food allergy
When the body's immune system overreacts to certain foods, the following symptoms may occur:

• Skin problems
  • Hives (red spots that look like mosquito bites)
  • Itchy skin rashes (eczema, also called atopic dermatitis)
  • Swelling
• Breathing problems
  • Sneezing
  • Wheezing
  • Throat tightness
• Stomach symptoms
  • Nausea
  • Vomiting
  • Diarrhea
• Circulation symptoms
  • Pale skin
  • Light-headedness
  • Loss of consciousness

If several areas of the body are affected, the reaction may be severe or even life-threatening. This type of allergic reaction is called anaphylaxis and requires immediate medical attention.

Not a food allergy
Food can cause many illnesses that are sometimes confused with food allergies. The following are not food allergies:

• Food poisoning — Can cause diarrhea or vomiting, but is usually caused by bacteria in spoiled food or undercooked food.
• Drug effects — Certain ingredients, such as caffeine in soda or candy, can make your child shaky or restless.
• Skin irritation — Can often be caused by acids found in such foods as orange juice or tomato products.
• Diarrhea — Can occur in small children from too much sugar, such as from fruit juices.

Some food-related illnesses are called intolerance, or a food sensitivity, rather than an allergy because the immune system is not causing the problem. Lactose intolerance is an example of a food intolerance that is often confused with a food allergy. Lactose intolerance is when a person has trouble digesting milk sugar, called lactose, leading to stomachaches, bloating, and loose stools. Sometimes reactions to the chemicals added to foods, such as dyes or preservatives, are mistaken for a food allergy. However, while some people may be sensitive to certain food additives, it is rare to be allergic to them.

Foods that can cause food allergies
Any food could cause a food allergy, but most food allergies are caused by the following:

• Cow milk
• Eggs
• Peanuts
• Soy
• Wheat
• Nuts from trees (such as walnuts, pistachios, pecans, cashews)
• Fish (such as tuna, salmon, cod)
• Shellfish (such as shrimp, lobster)
• Peanuts, nuts, and seafood are the most common causes of severe reactions. Allergies also occur to other foods such as meats, fruits, vegetables, grains, and seeds such as sesame.

The good news is that food allergies are often outgrown during early childhood. It is estimated that 80% to 90% of egg, milk, wheat, and soy allergies go away by age 5 years. Some allergies are more persistent. For example, 1 in 5 young children will outgrow a peanut allergy and fewer will outgrow allergies to nuts or seafood. Your pediatrician or allergist can perform tests to track your child's food allergies and watch to see if they are going away.

Among the 530 infants in the intention-to-treat population who initially had negative results on a skin-prick test, the prevalence of peanut allergy at 60 months of age was 13.7% in the avoidance group and 1.9% in the consumption group.

Among the 98 participants in the intention-to-treat population who initially had positive test results, the prevalence of peanut allergy was 35.3% in the avoidance group and 10.6% in the consumption group (P=0.004).

There was no significant between-group difference in the incidence of serious adverse events. Increases in levels of peanut-specific IgG4 antibody occurred predominantly in the consumption group; a greater percentage of participants in the avoidance group had elevated titers of peanut-specific IgE antibody. A larger wheal on the skin-prick test and a lower ratio of peanut-specific IgG4:IgE were associated with peanut allergy.

Conclusions
The early introduction of peanuts significantly decreased the frequency of the development of peanut allergy among children at high risk for this allergy and modulated immune responses to peanuts. Visit Food Allergy and Food Intolerance Network at:Click Here

Presented by the American Academy of Allergy Asthma and Immunology.

Series of Instructional Videos
Click on any of the images below to visit the website where these very useful instructional videos are available courtesy of The Royal Children's Hospital, Melbourne, Australia.

On that web page you will also find a short URL (www.sn.im/rch-puffers) that you can give to families to watch the videos at home. The videos play really well on mobile devices like smartphones and iPads. I have used them in clinic in just this way. The parent and child can watch the video on their phone in the room and then bookmark it for future reference. They can then always refresh their memory or show it to other family members, childcare, school etc.

On the web page there is a QR code they can scan to go to the site on their mobile phone. They will need a QR code reader app on their phone but many people have these now.