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Biomedical subjects

J O Hourihane

Publications and source records attributed to J O Hourihane.

At least 19 recordsLinked to original sources
PubMed2002

Food allergy in children.

Food allergies are increasing in prevalence and as a disease burden throughout the world, however they seem to increasingly affect countries with a formerly low prevalence. Consideration and diagnosis of food allergies are important as it has ramifications that affect a child's diet, care at school and home and is recognised to be associated with anxiety of parents, family and care takers. Food allergies vary significantly between countries, however nut allergies appear to be widely associated with serious reactions and death. The value of specific food immunoglobulin E (IgE) and skin prick tests (SPT) has been extensively analysed in children in recent years and can provide very useful information in an appropriately selected population. Diagnosis may require formal challenges to confirm a genuine allergic reaction condition rather than an intolerance reaction due to other mechanisms. The medical care of a food allergic child requires concurrent dietary advice and management, risk avoidance and emergency management plans. Reintroduction of foods occurs when the risk profile is appropriate based mainly on the predictive information obtained by SPTs and specific IgE levels. Fortunately allergies to egg and milk resolve by 3-5 years in about 80% of children. There have been some recent advances in immunotherapeutic approaches to food allergy although this has not translated to success in human treatment to date.

Child↗
PubMed2001

A revised nomenclature for allergy. An EAACI position statement from the EAACI nomenclature task force.

This report has been prepared by an EAACI task force representing the five EAACI Sections and the EAACI Executive Committee composed of specialists that reflect the broad opinion on allergy expressed by various clinical and basic specialties dealing with allergy. The aim of this report is to propose a revised nomenclature for allergic and related reactions that can be used independently of target organ or patient age group. The nomenclature is based on the present knowledge of the mechanisms which initiate and mediate allergic reactions. However, the intention has not been to revise the nomenclature of nonallergic hypersensitivity.

Humans↗
PubMed2000

Autosomal recessive lissencephaly with cerebellar hypoplasia is associated with human RELN mutations.

Normal development of the cerebral cortex requires long-range migration of cortical neurons from proliferative regions deep in the brain. Lissencephaly ("smooth brain," from "lissos," meaning smooth, and "encephalos," meaning brain) is a severe developmental disorder in which neuronal migration is impaired, leading to a thickened cerebral cortex whose normally folded contour is simplified and smooth. Two identified lissencephaly genes do not account for all known cases, and additional lissencephaly syndromes have been described. An autosomal recessive form of lissencephaly (LCH) associated with severe abnormalities of the cerebellum, hippocampus and brainstem maps to chromosome 7q22, and is associated with two independent mutations in the human gene encoding reelin (RELN). The mutations disrupt splicing of RELN cDNA, resulting in low or undetectable amounts of reelin protein. LCH parallels the reeler mouse mutant (Reln(rl)), in which Reln mutations cause cerebellar hypoplasia, abnormal cerebral cortical neuronal migration and abnormal axonal connectivity. RELN encodes a large (388 kD) secreted protein that acts on migrating cortical neurons by binding to the very low density lipoprotein receptor (VLDLR), the apolipoprotein E receptor 2 (ApoER2; refs 9-11 ), alpha3beta1 integrin and protocadherins. Although reelin was previously thought to function exclusively in brain, some humans with RELN mutations show abnormal neuromuscular connectivity and congenital lymphoedema, suggesting previously unsuspected functions for reelin in and outside of the brain.

Animals↗
PubMed1998

Resolution of peanut allergy: case-control study.

OBJECTIVES: To determine whether there are any differences between children who remain mildly or moderately allergic to peanut and children with similar histories but a negative reaction on challenge with peanut. DESIGN: Case-controls matched for age and sex. SETTING: Children's day wards in two teaching hospitals. INTERVENTION: Open food challenge with peanut. SUBJECTS: 15 children with resolved peanut allergy (resolvers) and 15 with persistent allergy (persisters). MAIN OUTCOME MEASURE: Reaction on challenge with peanut, serum total and peanut specific IgE concentrations. RESULTS: The groups had a similar median age at first reaction to peanut (11 months, range 5-38) and similar symptoms. Allergy to other foods was less common in resolvers (2/15) than persisters (9/15) (P=0.02). On skin prick testing with peanut all 13 resolvers tested but only 3/14 persisters had a weal of <6 mm (P<0.0001). Total and peanut specific IgE concentrations did not differ much between the groups. CONCLUSION: Appropriately trained clinicians must be prepared to challenge preschool children with peanut as some will be tolerant despite a history of reactions to peanut and a positive skin prick test with peanut. Preschool children whose apparent peanut allergy is refuted by food challenge show allergy to other foods less often than those in whom peanut allergy persists. The size of weal on skin prick testing to peanut predicts reactivity but not severity on peanut challenge.

Arachis↗
PubMed1998

Immunogenetic analysis of the heavy chain variable regions of IgE from patients allergic to peanuts.

Peanuts are one of the most allergenic of the foods, and hypersensitivity responses to peanut allergens can be fatal. Although the nature of the antigenic components of peanuts is being defined at the molecular level, there is little information on the induced IgE antibodies, which are central to the allergic reaction. Recognition sites of IgE antibody molecules arise from the variable regions of heavy and light chains (VH and VL). By using nested polymerase chain reactions with specific primers for the available repertoire of VH genes, together with primers in the constant epsilon region, we have amplified VH sequences of IgE from blood lymphocytes of two patients with peanut allergy. After cloning and sequencing the products, we found a predominance of VH1 family use in both patients, which was not found in control IgM-specific primers. The IgE VH sequences were highly somatically mutated, but in only six of 17 cases was there clear evidence for clustering of amino acids indicative of antigen selection. Previous results from patients with allergy to house dust mites have indicated predominance of VH5 use and little evidence for antigen selection. Although results from two patients allergic to peanuts must be regarded as preliminary, they do suggest that the IgE response to peanuts may have a different VH bias, with a similar mutational pattern.

Adolescent↗
PubMed1998

Peanut allergic subjects' peripheral blood mononuclear cell proliferative responses to crude peanut protein.

BACKGROUND: Peanut allergy is characterized by a high frequency of severe and occasionally fatal reactions. OBJECTIVE: To determine if there are features of the in vitro cellular response that may account for the observed severity of peanut allergy. METHODS: Skin-prick testing (SPT), RAST assay of serum peanut-specific and total IgE and mixed peripheral blood mononuclear cells (PBMC) proliferative responses to crude peanut protein were measured in 44 peanut allergics with varying severity of clinical reactions. PBMC responses of 13 non-peanut allergic controls (six atopic) were also studied. RESULTS: Subjects' PBMCs proliferated more than controls', even without stimulation. Subjects' PBMC proliferative responses did not correlate with clinical severity, SPT weal size or peanut-specific IgE levels. Controls' PBMCs did not respond to peanut. There was no correlation between PBMC response and time since last reaction to peanut. Subjects' PBMCs responded more than controls, to mitogen as well as allergen. Proliferation increased with increasing concentration of peanut protein (P < 0.0001). CONCLUSION: PBMCs of peanut allergics demonstrate a dose-dependent response to peanut which does not correlate with clinical severity, SPT reaction or levels of peanut specific IgE. The response is antigen-specific. Peanut protein is not mitogenic and is not acting as a superantigen. While there are non-specific differences in the PBMC responses of peanut allergic individuals compared with atopic and non-atopic controls, these differences do not explain the unique severity of peanut allergy.

Adolescent↗
PubMed1998

HLA class II DRB1, DQB1 and DPB1 genotypic associations with peanut allergy: evidence from a family-based and case-control study.

BACKGROUND: Peanut is one of the most common foods provoking allergic reactions and is the most frequent cause of fatal and near-fatal food-induced anaphylaxis. However, as yet, little is known of the genetic and immunological mechanisms which underly peanut allergy. OBJECTIVE: Based on findings in other allergic diseases, we have investigated whether particular human leucocyte antigen (HLA) class II genetic polymorphisms contribute to the development of peanut allergy. METHODS: All individuals from 37 families each containing one or more peanut allergic individuals, plus nine unrelated patients (161 individuals in total, defined as the study group) were typed for the HLA class II DRB1, DQB1 and DPB1 loci, by PCR-based techniques. Genotype frequencies were compared with those found in 293 unrelated controls. RESULTS: Four class II genotypes (DRB1*08 (13.7% vs 4.8%; Pc = 0.026), DRB1*08/12 tyr 16 (22.4% vs 8.2%; Pc = 0.021), DQB1*04 (12.2% vs 2.7%; Pc = 0.0026) and DPB1*0301 (49.1 vs 22.5%; Pc = 0.00062)) were present at a significantly higher frequency in the study group compared with controls. Three of these genotypes (DRB1*08 (18.0%; Pc = 0.027), DRB1*08/12 tyr16 (24.0%; Pc = 0.029) and DQB1*04 (16.7%; Pc = 0.0029)) were also significantly increased in peanut allergic individuals compared with controls. In addition, two genotypes (DPB1*0101 and 0201) were significantly decreased in frequency in the overall study group, but not specifically in peanut allergic individuals. CONCLUSION: While other genetic factors may be important, results from this study indicate that HLA class II genetic polymorphism may play a role in determining susceptibility to peanut allergy.

Arachis↗
PubMed1998

Serological characteristics of peanut allergy.

BACKGROUND: Peanut is the most common cause of severe or fatal food-associated anaphylaxis. Studies indicate that peanut extracts contain many allergenic proteins. The identification of major and minor allergenic components is necessary for standardization of experimental and diagnostic extracts. OBJECTIVE: To identify further major and minor allergenic components of peanut extract using a large population of peanut allergics, and to relate serological findings to clinical parameters. METHODS: The crude peanut extract was fractionated by fast protein liquid chromatography and the IgE binding proteins identified by sodium dodecyl sulphate polyacrylamide gel electrophoresis followed by western blotting. Serum from 89 peanut allergics with a positive history of peanut allergy and elevated specific IgE and control serum from four atopic and four non-atopic, non-peanut allergics were used. RESULTS: Nineteen peanut proteins were found to bind IgE from peanut allergic sera. Over 70% of subjects reacted to protein bands of 63 and 17 kDa (consistent with Ara h 1 and Ara h 2, respectively), confirming the importance of these two proteins as major allergens. A high proportion of patient sera also bound proteins at 15, 10, 30, 18 and 51 kDa in decreasing order. The percentage of cases with sensitivity to a 15 kDa protein was found to be higher in patient groups with severe reactions to peanut. CONCLUSION: This study highlights the diversity of peanut allergens. Diagnostic extracts containing a high proportion of the 15 kDa component may aid in diagnosis.

Adolescent↗
PubMed1998

Prevalence and severity of food allergy--need for control.

Food allergy is an increasingly recognized manifestation of atopy. Patient and public awareness of food allergy is also increasing. Justifiable demands are being made for better medical guidance of the practice of food labelling for industry and catering businesses. Such advice must bear in mind the relative frequency and severity of allergies to certain foods. Some commonly allergenic foods (milk, egg, soya, wheat) are staple components of the diets of populations, used widely in prepared foods. The frequency of the allergies to these foods and their widespread uses means they and their derivatives must be declared on food labels. Less commonly used foods such as fish, shellfish, peanut, and tree nuts demand declaration due to the severity of reactions induced in the admittedly more rare, but increasingly common, sufferers of these allergies. Reactions to more unusual foods are increasingly being identified, and the "minimum" list is likely to be extended in the future.

Arachis↗
PubMed1997

Randomised, double blind, crossover challenge study of allergenicity of peanut oils in subjects allergic to peanuts.

OBJECTIVE: To determine the in vivo allergenicity of two grades of peanut oil for a large group of subjects with proved allergy to peanuts. DESIGN: Double blind, crossover food challenge with crude peanut oil and refined peanut oil. SETTING: Dedicated clinical investigation unit in a university hospital. SUBJECTS: 60 subjects allergic to peanuts; allergy was confirmed by challenge tests. OUTCOME MEASURES: Allergic reaction to the tested peanut oils. RESULTS: None of the 60 subjects reacted to the refined oil; six (10%) reacted to the crude oil. Supervised peanut challenge caused considerably less severe reactions than subjects had reported previously. CONCLUSIONS: Crude peanut oil caused allergic reactions in 10% of allergic subjects studied and should continue to be avoided. Refined peanut oil did not pose a risk to any of the subjects. It would be reasonable to recommend a change in labelling to distinguish refined from crude peanut oil.

Adolescent↗
PubMed1997

Clinical characteristics of peanut allergy.

BACKGROUND: Current clinical advice regarding peanut allergy is based on small series of patients. OBJECTIVE: To determine, in a large group of peanut allergic subjects, the patterns of clinical severity, symptom progression and availability and use of rescue medications. METHODS: Questionnaire study of 622 self-reported allergic subjects. RESULTS: A total of 406 patients (66%) reported symptoms on contact with peanut. Only 121 (19%) had been knowingly exposed to peanut before the first documented reaction, implying a high frequency of occult sensitization. Severe symptoms were more common in adults. Abdominal symptoms were significantly associated with collapse. Fifty per cent reported reactions in the previous year. Only 82 (13%) had been admitted to hospital because of a reaction. Adrenaline was carried in some form by 65% though only 78 subjects (12.5%) had ever received injected adrenaline. Only 18/43 subjects (41%) who collapsed were given adrenaline. Skin-prick test weal size correlated weakly with severity but there were large overlaps between the groups. Peanut-specific IgE peaked in the teenage group, but did not correlate with severity. CONCLUSIONS: Peanut allergy is characterized by more severe symptoms than other food allergies and by high rates of symptoms on minimal contact. Skin-prick testing and peanut-specific IgE levels do not predict clinical severity. Avoidance of peanut is difficult. Many people suffering severe relations are inadequately treated. Sufferers need education and training in the use of rescue medication.

Adolescent↗