A task force made up of 33 experts from multiple disciplines present updated recommendations for the diagnosis and management of eosinophilic esophagitis (EoE) in this month’s issue (J Allergy Clin Immunol 2011;128:3-20). Liacouras and colleagues performed an exhaustive literature review to inform new clinical recommendations (CR) for 5 categories: diagnostics, genetics, allergy evaluation, therapies, and complications. They also offer recommendations for future critical research areas. Importantly, they provide a concept definition to assist clinicians with framing the clinical presentation of EoE. Liacouras et al. state this concept definition: “Eosinophilic esophagitis represents a chronic, immune/ antigen-mediated esophageal disease characterized clinically by symptoms related to esophageal dysfunction and histologically by eosinophil-predominant inflammation.”
Overview of diagnostic recommendations: The task force makes recommendations in the diagnostic areas of history and physical exam, endoscopy, histology, pH monitoring, and laboratory findings. Among these are a thorough H & P, with emphasis on eating and swallowing symptoms, proximal and distal endoscopic biopsies, and gastric pH and pH impedance testing. Additionally, Liacouras et al. recommend that any and all histological findings be reported until EoE-specific findings are identified. The authors note that very few laboratory tests have been demonstrated to be informative, with the exception of peripheral esosinophil count and skin prick testing.
Overview of genetic studies and recommendation: Noting that the previous consensus report, published in 2007 (Gastroenterology 2007;133:1342–1363), presented a single genotype study, Liacouras et al. provides a substantial review of recent genetic research. Two important genetic findings are the description of an EoE transcriptome with increased expression of eotaxin-3 and IL-13, and the report of a single susceptibility locus, 5q22, for EoE that contains genes encoding thymic stromal lymphopoetin (TSLP), a critical cytokine in TH2 cell commitment. An X-linked variant of TSLP and a common deletion mutation in the filaggrin gene family have also been identified.
Overview of allergic evaluation: Atopic conditions including food allergy, asthma and eczema are known to associate with EoE and the task force emphasizes allergist/immunologist consultation for management of comorbid allergic symptoms. Skin prick testing is necessary to identify reactive allergens and eliminate or mitigate them. Liacouras et al. recommend assessment of allergen-specific IgE to document sensitivity prior to initiating desensitization/tolerance protocols.
Overview of therapeutic options: Liacouras et al. review and recommend a multifocal treatment strategy that includes proton-pump inhibitors (PPI), dietary restrictions, and topical corticosteroids. Oral steroids are recommended only for severe symptom presentations. They also state that alternative therapies, such as cromolyn sodium, LTR antagonists and immunosuppressive drugs, are not recommended based on lack of efficacy data.
Overview of complications: Liacouras et al. point out the common complications, namely, emergent food impaction, esophageal stricture, and non-interventional (“spontaneous”) esophageal perforation. They go on to discuss esophageal dilation for mitigation, but advise that it is best applied as an “add-on” intervention to the recommended clinical management.
Liacouras et al. provide recommendations for the focus of future studies for each of the 5 areas they cover and conclude that the most pressing need is for research to distinguish EoE from gastric esophageal reflux disease (GERD), with several other priorities, such as translational analysis to describe EoE phenotypes, and idenfication of EoE biomarkers and unique histological findings.
We asked lead author Chris Liacouras, from the Children’s Hospital of Philadelphia, to tell us more about our current understanding of EoE and where the research will go from here:
JACI: How has our understanding of EoE changed since the 2007 consensus recommendations were published?
Liacouras: We have been been extremely fortunate that the number of physicians and scientists interested in EoE has grown tremendously since the original Consensus Report in 2007 as noted by the number of additional authors included in the 2011 Updated Guidelines. The most important component of the Updated recommendations continues to be the understanding of the definition which attempts to explain that EoE is an antigen/immune medicated disease process different from acid induced or PPI-responsive esophageal eosinophilia. Additionally, the other most significant advances since 2007 have been made in genetics and with the identification of specific esophageal biochemical tissue markers.
JACI: In your opinion, what is the next priority area in EoE research after the need to distinguish it clinically and pathologically from GERD?
Liacouras: Currently, EoE has become one of the interesting and confusing disorders for both gastroenterologists and allergists. Apart from the need for physicians to identify and accurately diagnose patients with EoE, there are many areas of ongoing research that need to be explored. Clinically, it is essential that we continue to pursue the natural history, non-invasive testing, best treatment options and which patients are likely to develop complications. In addition, scientifically, we need to identify the etiology, pathophysiology, and development of esophageal fibrosis in patients with EoE. We also need to continue to explore the genetics of the disease.
Friday, July 1, 2011
Eating baked cow’s milk products may facilitate resolution of cow’s milk allergy
Kim et al. (J Allergy Clin Immunol 2011;128:125-131.e2) investigate the clinical implications of the empirical observation that 75% of milk-allergic children tolerate extensively heated milk in foods such as baked goods. These children have been observed to have milk-specific IgE directed at conformational epitopes rather than sequential epitopes. Heating (such as baking) disrupts the tertiary structure and consequently, reduces the allergenicity of milk proteins to which these children are sensitive. In contrast, children who are reactive to heated milk products have milk-specific IgE to heat-stable, sequential epitopes.
Kim et al. report on their findings from a clinical study of baked milk tolerant and baked milk reactive subjects, wherein baked milk tolerant subjects were advised to include baked milk food products in their diet on a daily basis, while baked milk reactive subjects were advised to practice complete strict avoidance. A comparison group, not initially challenged to baked milk products, was also observed over the study period.
Overall, Kim et al. report that initially baked milk tolerant subjects were 28 times more likely to become unheated milk tolerant than those initially baked milk reactive subjects, as compared to those subjects who observed strict avoidance. Baked milk tolerant subjects that received active treatment (that is, were able to include baked milk products into their diets) were significantly more likely to develop tolerance to unheated milk compared to the comparison group.
The authors demonstrate two important outcomes of their study: 1) baked milk tolerance is a marker of mild, transient cow’s milk allergy; baked milk reactivity implies a more persistent, severe form of cow’s milk allergy and, 2) the majority of children with baked milk tolerance that routinely eat baked milk food products will develop unheated milk tolerance at an accelerated rate compared to children prescribed a strict avoidance diet.
Kim et al. suggest that ingestion of baked milk products by tolerant patients is a safer, more convenient and cost-effective method of immunotherapy. They also comment that their results might be extrapolated to children with egg allergy in light of reports on heat-related changes in allergenicity of egg proteins.
We asked first author Jennifer Kim, from Mt. Sinai School of Medicine, to tell us about the implications of this work for future research. According to Dr. Kim, “These findings have provided the impetus for a more rigorously designed study that has been developed by our group to determine whether more rapid introduction of increasingly allergenic forms of baked-milk products in baked-milk non-reactive participants shortens the time until they tolerate higher doses of less heated milk and ultimately unheated milk.”
Tell us what you think. Please feel free to post your comments below.
Kim et al. report on their findings from a clinical study of baked milk tolerant and baked milk reactive subjects, wherein baked milk tolerant subjects were advised to include baked milk food products in their diet on a daily basis, while baked milk reactive subjects were advised to practice complete strict avoidance. A comparison group, not initially challenged to baked milk products, was also observed over the study period.
Overall, Kim et al. report that initially baked milk tolerant subjects were 28 times more likely to become unheated milk tolerant than those initially baked milk reactive subjects, as compared to those subjects who observed strict avoidance. Baked milk tolerant subjects that received active treatment (that is, were able to include baked milk products into their diets) were significantly more likely to develop tolerance to unheated milk compared to the comparison group.
The authors demonstrate two important outcomes of their study: 1) baked milk tolerance is a marker of mild, transient cow’s milk allergy; baked milk reactivity implies a more persistent, severe form of cow’s milk allergy and, 2) the majority of children with baked milk tolerance that routinely eat baked milk food products will develop unheated milk tolerance at an accelerated rate compared to children prescribed a strict avoidance diet.
Kim et al. suggest that ingestion of baked milk products by tolerant patients is a safer, more convenient and cost-effective method of immunotherapy. They also comment that their results might be extrapolated to children with egg allergy in light of reports on heat-related changes in allergenicity of egg proteins.
We asked first author Jennifer Kim, from Mt. Sinai School of Medicine, to tell us about the implications of this work for future research. According to Dr. Kim, “These findings have provided the impetus for a more rigorously designed study that has been developed by our group to determine whether more rapid introduction of increasingly allergenic forms of baked-milk products in baked-milk non-reactive participants shortens the time until they tolerate higher doses of less heated milk and ultimately unheated milk.”
Tell us what you think. Please feel free to post your comments below.
Thursday, June 2, 2011
Psoriasis and atopic dermatitis: The same, only different
In the May issue of JACI, Guttman-Yassky et al. (J Allergy Clin Immunol 2011;127:1110-1118), in part 1 of a 2-part review, covered the clinical and pathological similarities and differences between psoriasis and atopic dermatitis (AD) with AD as the point of reference. They finish up in this month’s issue (J Allergy Clin Immunol 2011;127:1420-1432) with a broad discussion comparing the immune phenotypes and therapies for AD and psoriasis.
In part 1, Guttman-Yassky et al. pointed out that psoriasis and AD both present with defects in skin barrier function, skin lesions infiltrated by increased numbers of T cells and dendritic cells and upregulation of epidermal proliferation genes. They note that the chronic phase of AD is more similar to psoriasis than the acute phase. There are distinct differences though. AD patients are susceptible to bacterial and viral skin infections, which is not true for psoriasis patients. Also, AD skin is characterized by decreases in keratinocyte differentiation, cornification, moisture and lipid content. Though lipid depletion is also observed for psoriasis, it is characterized by increased differentiation and cornification. Cytokine milieu in AD is dominated by TH2 cells, while psoriasis is associated with TH1 and TH17 cytokines. Additionally, AD is associated with structural protein anomalies (e.g., filaggrin dysfunction) that are not observed in psoriasis.
The authors discuss in part 2 how the disorders were thought to be mediated by polarized T helper cell responses with TH2 dominance seen in AD; however, this simple dichotomy did not account for all observations, such as hyperkeratinization, seen in chronic AD. They point out that the discovery that TH17 and T22 cells affected epidermal activation eventually led to a new working model wherein psoriasis is mediated by TH1 and TH17 immunity, and AD is mediated by TH2 and T22 cell effects. Production of anti-microbial peptides (AMP) is known to be compromised in AD compared to psoriasis. This was originally attributed to the TH2 environment, but the authors comment that IL-17 deficiency as well as excessive TH2 cytokines can explain the decreased AMP production found in AD. Guttman-Yassky et al note that the impaired AMP production would explain increased susceptibility to skin infections in AD. In contrast, psoriasis is characterized by increased AMP production. The authors also discuss basic differences between AD and psoriasis with regard to differences in dendritic cell populations, AD-associated eosinophilia, barrier defects and inflammation, and mast cell production of interferon gamma (IFN-γ) in psoriasis.
Guttman-Yassky et al. finish up part II with a discussion of the prognosis and intervention for psoriasis and AD. Unlike AD, they note that active psoriasis can be completely resolved and treatment time is short. The authors comment that, in spite of their differences, both AD and psoriasis share epidermal hyperplasia, aberrant immunity, and skin barrier anomalies. This would suggest that immune-based strategies to correct barrier defects that have been developed for psoriasis might be effective for AD. Guttman-Yassky et al. detail current AD treatments and make a case for psoriasis therapies as intervention for AD.
Tell us what you think. Please feel free to post your own comments and/or predictions below.
In part 1, Guttman-Yassky et al. pointed out that psoriasis and AD both present with defects in skin barrier function, skin lesions infiltrated by increased numbers of T cells and dendritic cells and upregulation of epidermal proliferation genes. They note that the chronic phase of AD is more similar to psoriasis than the acute phase. There are distinct differences though. AD patients are susceptible to bacterial and viral skin infections, which is not true for psoriasis patients. Also, AD skin is characterized by decreases in keratinocyte differentiation, cornification, moisture and lipid content. Though lipid depletion is also observed for psoriasis, it is characterized by increased differentiation and cornification. Cytokine milieu in AD is dominated by TH2 cells, while psoriasis is associated with TH1 and TH17 cytokines. Additionally, AD is associated with structural protein anomalies (e.g., filaggrin dysfunction) that are not observed in psoriasis.
The authors discuss in part 2 how the disorders were thought to be mediated by polarized T helper cell responses with TH2 dominance seen in AD; however, this simple dichotomy did not account for all observations, such as hyperkeratinization, seen in chronic AD. They point out that the discovery that TH17 and T22 cells affected epidermal activation eventually led to a new working model wherein psoriasis is mediated by TH1 and TH17 immunity, and AD is mediated by TH2 and T22 cell effects. Production of anti-microbial peptides (AMP) is known to be compromised in AD compared to psoriasis. This was originally attributed to the TH2 environment, but the authors comment that IL-17 deficiency as well as excessive TH2 cytokines can explain the decreased AMP production found in AD. Guttman-Yassky et al note that the impaired AMP production would explain increased susceptibility to skin infections in AD. In contrast, psoriasis is characterized by increased AMP production. The authors also discuss basic differences between AD and psoriasis with regard to differences in dendritic cell populations, AD-associated eosinophilia, barrier defects and inflammation, and mast cell production of interferon gamma (IFN-γ) in psoriasis.
Guttman-Yassky et al. finish up part II with a discussion of the prognosis and intervention for psoriasis and AD. Unlike AD, they note that active psoriasis can be completely resolved and treatment time is short. The authors comment that, in spite of their differences, both AD and psoriasis share epidermal hyperplasia, aberrant immunity, and skin barrier anomalies. This would suggest that immune-based strategies to correct barrier defects that have been developed for psoriasis might be effective for AD. Guttman-Yassky et al. detail current AD treatments and make a case for psoriasis therapies as intervention for AD.
Tell us what you think. Please feel free to post your own comments and/or predictions below.
Chronic mucocutaneous candidiasis associated with impaired TH17 cell differentiation
In this month’s issue, Hanna and Etzoni (J Allergy Clin Immunol 2011;127:1433-1437) shed light on the primary players in the pathogenesis of chronic mucosal candidiasis (CMC). They review current knowledge of CMC as it is most commonly observed; namely, as secondary to other clinical conditions, particularly those that cause immunocompromise, such as HIV, diabetes mellitus, and T-cell deficiency disorders. Hanna and Etzoni then discuss CMC as a primary symptom in immunodeficiency disease, such as in hyper-IgE syndrome (HIES) and autoimmune polyendocrinopathy with candidiasis and ectodermal dysplasia (APECED), or, more rarely, with no other related clinical presentation.
The authors review the primary innate immune defense against Candida albicans, noting that activation of the Dectin-1 and -2 receptors mediate host response through spleen tyrosine kinase (Syk) and caspase recruitment domain member 9 (CARD9) to initiate T cell differentiation to produce multiple cytokines, particularly those associated with TH17 differentiation, IL-17 and IL-22. T regulatory cells are also mobilized and critical for containing the TH17 inflammatory response to C. albicans.
Hanna and Etzoni move on to discuss CMC as the primary clinical feature of HIES and point to research that has shown that a heterozygous mutation in the transcription factor, STAT3, is the cause of this syndrome. Impaired STAT3 signaling negatively impacts RORγt function, which is required for TH17 cell development. The authors point out that this is supported by clinical findings of very low circulating markers for TH17 cell lineage in patients with HIES.
They also review severe CMC as a major feature of the autoimmune disease, APECED. Unlike the transcription dysregulation in HIES, CMC in APECED results from high titers of neutralizing autoantibodies against IL-17 and IL-22. Finally, Hanna and Etzoni describe less common presentations of non-syndromic CMC, some of which are idiopathic, while others have autosomal inheritance associations. In the latter, the authors discuss a genetic analysis of familial CMC in 5 generations of an Iranian family, which revealed a loss-of-function mutation in CARD9.
The authors conclude noting that in most non-syndromic CMC cases the genetic defects are still unknown, though abnormal TH17 function or production was observed.
Tell us what you think. Please feel free to post your own comments and/or predictions below.
The authors review the primary innate immune defense against Candida albicans, noting that activation of the Dectin-1 and -2 receptors mediate host response through spleen tyrosine kinase (Syk) and caspase recruitment domain member 9 (CARD9) to initiate T cell differentiation to produce multiple cytokines, particularly those associated with TH17 differentiation, IL-17 and IL-22. T regulatory cells are also mobilized and critical for containing the TH17 inflammatory response to C. albicans.
Hanna and Etzoni move on to discuss CMC as the primary clinical feature of HIES and point to research that has shown that a heterozygous mutation in the transcription factor, STAT3, is the cause of this syndrome. Impaired STAT3 signaling negatively impacts RORγt function, which is required for TH17 cell development. The authors point out that this is supported by clinical findings of very low circulating markers for TH17 cell lineage in patients with HIES.
They also review severe CMC as a major feature of the autoimmune disease, APECED. Unlike the transcription dysregulation in HIES, CMC in APECED results from high titers of neutralizing autoantibodies against IL-17 and IL-22. Finally, Hanna and Etzoni describe less common presentations of non-syndromic CMC, some of which are idiopathic, while others have autosomal inheritance associations. In the latter, the authors discuss a genetic analysis of familial CMC in 5 generations of an Iranian family, which revealed a loss-of-function mutation in CARD9.
The authors conclude noting that in most non-syndromic CMC cases the genetic defects are still unknown, though abnormal TH17 function or production was observed.
Tell us what you think. Please feel free to post your own comments and/or predictions below.
Friday, May 6, 2011
Dietary fat intake linked directly to airway inflammation
What you eat determines how you breathe whether or not you have asthma. Wood et al. (J Allergy Clin Immunol 2011;127:1133-1140) present first-ever findings on the local inflammatory effects of high fat food, in this month’s issue.
The authors examine the effect of single high-fat or low-fat meals on non-obese subjects with asthma. Then, healthy, non-obese subjects and obese subjects with asthma were administered a single high-fat meal. All groups that consumed a high fat meal showed increased neutrophilic airway inflammation as measured by sputum induction and IL-6 levels, decreased % predicted FEV1 post-bronchodilator, and increased TLR4 expression and TNF-α levels. Wood et al. report that increased total plasma fatty acid levels were correlated significantly to increases in TNF-α and neutrophil percentage in sputum. Additionally, increased fatty acid levels were inversely correlated to change in % FEV1, %FVC, and FEV1/FVC.
They also examined the effect of meals containing trans-fatty acids as compared to meals with no trans-fatty acids. Subjects consuming trans-fatty acids demonstrated increased sputum neutrophilia compared to those that consumed no trans-fatty acids, which is consistent with other research reporting the pro-inflammatory properties of trans-fat.
Wood et al. state in conclusion that consumption of a high fat meal causes local airway inflammation and asthma worsening through activation of the innate immune response. They recommend that future research on this subject should focus on the effects of chronic consumption of high fat food in patients with asthma.
Have a comment? Tell us what you think. Please feel free to post your own comments and/or predictions below.
The authors examine the effect of single high-fat or low-fat meals on non-obese subjects with asthma. Then, healthy, non-obese subjects and obese subjects with asthma were administered a single high-fat meal. All groups that consumed a high fat meal showed increased neutrophilic airway inflammation as measured by sputum induction and IL-6 levels, decreased % predicted FEV1 post-bronchodilator, and increased TLR4 expression and TNF-α levels. Wood et al. report that increased total plasma fatty acid levels were correlated significantly to increases in TNF-α and neutrophil percentage in sputum. Additionally, increased fatty acid levels were inversely correlated to change in % FEV1, %FVC, and FEV1/FVC.
They also examined the effect of meals containing trans-fatty acids as compared to meals with no trans-fatty acids. Subjects consuming trans-fatty acids demonstrated increased sputum neutrophilia compared to those that consumed no trans-fatty acids, which is consistent with other research reporting the pro-inflammatory properties of trans-fat.
Wood et al. state in conclusion that consumption of a high fat meal causes local airway inflammation and asthma worsening through activation of the innate immune response. They recommend that future research on this subject should focus on the effects of chronic consumption of high fat food in patients with asthma.
Have a comment? Tell us what you think. Please feel free to post your own comments and/or predictions below.
A look at commensal gut bacteria, probiotics and atopy and obesity
In a clinical review in this month’s issue, Ly et al. (J Allergy Clin Immunol 2011;127:1087-1094) pull together what is known currently about gut microbiota influence on immunity, the association of abnormal microflora with eczema, asthma and obesity, the usefulness of probiotics for normalizing commensal gut bacteria, and newer information about vitamin D interactions with intestinal flora.
The authors begin commenting on how infants achieve gut colonization peri- and post-natally and note that vaginal delivery results in different gut flora in the infant than cesarean delivery. In particular, infants delivered by cesarean establish gut flora dominated by Klebsiella and Clostridum species, and enterobacteria other than E. coli, with later and less colonization by Bacteroides sp. and Bifidobacterium sp. Ly et al. point out that hospitalized neonates have gut flora similar to infants delivered by cesarean, suggesting that standard of care antibiotic use could be related to the decreased colonization by healthy bacteria.
They continue with a review of current knowledge of differential gut microbial populations between atopic and non-atopic infants, noting that atopic infants have lower fractions of lactobacilli, bifidobacteria, and Bacteroides sp. than their non-atopic counterparts. Ly et al. comment that current studies on neonatal gut commensalism and atopy are inconclusive, then discuss the design variability and limitations that result in contradictory findings.
The authors move to the evidence supporting a relationship between disturbance of the gut microflora and diet-related obesity, linking it to inflammation and impaired energy metabolism. They further note that gut flora composition shifts toward healthier bacteria dominance in obese subjects on dietary restriction for weight loss.
Ly et al. wrap up with a discussion of the equivocal findings from studies employing probiotics as prevention or mitigation of atopic diseases and a short note on the requirement of vitamin D for healthy gut microbial effects on inflammation. They conclude stating that evidence suggests early diversity of microbiota is pivotal to healthy gut-immune dynamics and that future research must comprise data on maternal flora-neonate flora interactions, vitamin D’s role and dietary confounders.
Have a comment? Tell us what you think. Please feel free to post your own comments and/or predictions below.
The authors begin commenting on how infants achieve gut colonization peri- and post-natally and note that vaginal delivery results in different gut flora in the infant than cesarean delivery. In particular, infants delivered by cesarean establish gut flora dominated by Klebsiella and Clostridum species, and enterobacteria other than E. coli, with later and less colonization by Bacteroides sp. and Bifidobacterium sp. Ly et al. point out that hospitalized neonates have gut flora similar to infants delivered by cesarean, suggesting that standard of care antibiotic use could be related to the decreased colonization by healthy bacteria.
They continue with a review of current knowledge of differential gut microbial populations between atopic and non-atopic infants, noting that atopic infants have lower fractions of lactobacilli, bifidobacteria, and Bacteroides sp. than their non-atopic counterparts. Ly et al. comment that current studies on neonatal gut commensalism and atopy are inconclusive, then discuss the design variability and limitations that result in contradictory findings.
The authors move to the evidence supporting a relationship between disturbance of the gut microflora and diet-related obesity, linking it to inflammation and impaired energy metabolism. They further note that gut flora composition shifts toward healthier bacteria dominance in obese subjects on dietary restriction for weight loss.
Ly et al. wrap up with a discussion of the equivocal findings from studies employing probiotics as prevention or mitigation of atopic diseases and a short note on the requirement of vitamin D for healthy gut microbial effects on inflammation. They conclude stating that evidence suggests early diversity of microbiota is pivotal to healthy gut-immune dynamics and that future research must comprise data on maternal flora-neonate flora interactions, vitamin D’s role and dietary confounders.
Have a comment? Tell us what you think. Please feel free to post your own comments and/or predictions below.
Tuesday, April 5, 2011
Severity of human rhinovirus infection in infants linked to maternal atopy
Human rhinoviruses (HRV) are known to be associated with asthma exacerbations in both children and adults. Additionally, bronchiolitis, which is usually associated with respiratory syncytial virus (RSV), is being associated with HRV as well. Typically, HRV is a viral infection associated with older children and has not been closely examined in infants with low risk for atopy.
Miller and colleagues in this month’s issue (J Allergy Clin Immunol 2011;127:883-891) examine the HRV burden in upper respiratory infections (URI) and bronchiolitis among children that had participated in the Tennessee Children’s Respiratory Initiative. They collected atopy risk information, clinical severity from hospital admission records, and performed type testing on the three HRV strains, A, B, and C.
Miller et al find that both URI and bronchiolitis in healthy infants are commonly caused by HRV. Maternal atopy and asthma were associated significantly with risk of more severe bronchiolitis, with maternal atopy conferring more than double the severity risk. Of the three strains of HRV, the newly described group, HRVC was very common and occurred more often in black infants thnt HRVA and HRVB. Infants infected with HRVB had higher severity scores and were more likely to require oxygen supplementation and have longer hospital stays.
The authors conclude that an infant’s susceptibility to severe HRV illness is significantly correlated to asthma and atopy susceptibility in the mother.
Tell us what you think. Please feel free to post your own comments below.
Miller and colleagues in this month’s issue (J Allergy Clin Immunol 2011;127:883-891) examine the HRV burden in upper respiratory infections (URI) and bronchiolitis among children that had participated in the Tennessee Children’s Respiratory Initiative. They collected atopy risk information, clinical severity from hospital admission records, and performed type testing on the three HRV strains, A, B, and C.
Miller et al find that both URI and bronchiolitis in healthy infants are commonly caused by HRV. Maternal atopy and asthma were associated significantly with risk of more severe bronchiolitis, with maternal atopy conferring more than double the severity risk. Of the three strains of HRV, the newly described group, HRVC was very common and occurred more often in black infants thnt HRVA and HRVB. Infants infected with HRVB had higher severity scores and were more likely to require oxygen supplementation and have longer hospital stays.
The authors conclude that an infant’s susceptibility to severe HRV illness is significantly correlated to asthma and atopy susceptibility in the mother.
Tell us what you think. Please feel free to post your own comments below.
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