Journal: Current allergy and asthma reports
The avoidance of wheat- and gluten-containing products is a worldwide phenomenon. While celiac disease is a well-established entity, the evidence base for gluten as a trigger of symptoms in patients without celiac disease (so-called ‘non-celiac gluten sensitivity’ or NCGS) is limited. The problems lie in the complexity of wheat and the ability of its carbohydrate as well as protein components to trigger gastrointestinal symptoms, the potentially false assumption that response to a gluten-free diet equates to an effect of gluten withdrawal, and diagnostic criteria for coeliac disease. Recent randomized controlled re-challenge trials have suggested that gluten may worsen gastrointestinal symptoms, but failed to confirm patients with self-perceived NCGS have specific gluten sensitivity. Furthermore, mechanisms by which gluten triggers symptoms have yet to be identified. This review discusses the most recent scientific evidence and our current understanding of NCGS.
Peanut seeds are currently widely used as source of human food ingredients in the United States of America and in European countries due to their high quality protein and oil content. This article describes the classification and molecular biology of peanut seed allergens with particular reference to their cross-reactivities. Currently, the IUIS allergen nomenclature subcommittee accepts 12 peanut allergens. Two allergens belong to the cupin and four to the prolamin superfamily, and six are distributed among profilins, Bet v 1-like proteins, oleosins, and defensins. Clinical observations frequently report an association of peanut allergy with allergies to legumes, tree nuts, seeds, fruits and pollen. Molecular cross-reactivity has been described between members of the Bet v 1-like proteins, the non-specific lipid transfer proteins, and the profilins. This review also addresses the less well-studied cross-reactivity between cupin and prolamin allergens of peanuts and of other plant food sources and the recently discovered cross-reactivity between peanut allergens of unrelated protein families.
Vaping is gaining popularity in the USA, particularly among teens and young adults. While e-cigs are commonly represented as safer alternatives to tobacco cigarettes, little is known regarding the health effects of their short- or long-term use, especially in individuals with pre-existing respiratory diseases such as asthma. Flavored e-cig liquids (e-liquids) and e-cig aerosols contain airway irritants and toxicants that have been implicated in the pathogenesis and worsening of lung diseases. In this review, we will summarize existing data on potential health effects of components present in e-cig aerosols, such as propylene glycol, vegetable glycerin, nicotine, and flavorings, and discuss their relevance in the context of asthma.
Although rodent allergy has long been recognized as an occupational disease, it has only been in the past decade that it has been recognized as a community-based disease that affects children. Most homes in the US have detectable mouse allergen, but the concentrations in inner-city homes are orders of magnitude higher than those found in suburban homes. Home mouse allergen exposure has been linked to sensitization to mouse, and children with asthma who are both sensitized and exposed to high mouse allergen concentrations at home are at greater risk for symptoms, exacerbations and reduced lung function. Rat allergen is found primarily in inner-city homes and has also been linked to asthma morbidity among sensitized children. The objective of this review is to summarize the scientific literature on rodents and their allergens, the effects of exposure to these allergens on allergic respiratory disease, and to make recommendations, based on this evidence base, for the evaluation and management of mouse allergy in the pediatric population.
Anaphylaxis is a severe allergic reaction that can be rapidly progressing and fatal. In instances where the triggering allergen is not known, establishing the etiology of anaphylaxis is pivotal to long-term risk management. Our recent work has identified a novel IgE antibody (Ab) response to a mammalian oligosaccharide epitope, galactose-alpha-1,3-galactose (alpha-gal), that has been associated with two distinct forms of anaphylaxis: (1) immediate onset anaphylaxis during first exposure to intravenous cetuximab, and (2) delayed onset anaphylaxis 3-6 h after ingestion of mammalian food products (e.g., beef and pork). The results of our studies strongly suggest that tick bites are a cause, if not the only significant cause, of IgE Ab responses to alpha-gal in the southern, eastern and central United States. Patients with IgE Ab to alpha-gal continue to emerge and, increasingly, these cases involve children. This IgE Ab response cross-reacts with cat and dog but does not appear to pose a risk for asthma; however, it may impair diagnostic testing in some situations.
Clinical practice always necessitates proper diagnosis and correct treatment. For most clinical fields, determining the cause of the illness is irrelevant to the intervention. An oncologist, for example, has no need to explore the “cause” of the patient’s lymphoma. Allergists, by contrast, have tools and the need to examine the relevant allergen which is the putative “cause” of the patient’s allergic symptomatology. In the context of a legal claim, the “cause” of the symptoms or disorder is central, because it determines financial responsibility. However, in the case of an allergic disorder and identified allergen, a claim requires more. Whose allergen? Where did it come from? These are crucial questions that must be answered. This paper explores the approaches to causal assessment which are important for the clinical allergist as he/she navigates the interface between clinical practice and legal proceedings. Its purpose is to help the allergist understand that interface, and to be prepared to enter an unfamiliar legal arena.
Food allergies are estimated to affect as many as 8 % of children with 2.5 % being allergic to peanut products. Based on the results of recent surveys, this prevalence has been increasing over the last few decades for unknown reasons. As children with food allergies reach school age, the issue is becoming more common in schools. For that reason, schools are now required to be prepared to take responsibility for the safety of food-allergic students. This review discusses the common problems surrounding management of food allergies in the school setting along with reasonable recommendations for addressing those problems. The most important component of food allergy management is for the student to get an accurate diagnosis and to then discuss development of an anaphylaxis action plan with their health-care provider. Each school should insist that a copy of such a plan be provided for each student with food allergy and that epinephrine is readily available should a student have an anaphylactic reaction. In addition to epinephrine, it is essential that school personnel be properly trained to recognize and treat allergic reactions should they occur. Known deficiencies in school preparedness have been documented in previous literature, and consequently, both state and the federal government have begun to implement policies to help with school preparedness.
This review aims to highlight the latest advance on epigenetics in the development of food allergy (FA) and to offer future perspectives. FA, a condition caused by an immunoglobulin (Ig) E-mediated hypersensitivity reaction to food, has emerged as a major clinical and public health problem worldwide in light of its increasing prevalence, potential fatality, and significant medical and economic impact. Current evidence supports that epigenetic mechanisms are involved in immune regulation and that the epigenome may represent a key “missing piece” of the etiological puzzle for FA. There are a growing number of population-based epigenetic studies on allergy-related phenotypes, mostly focused on DNA methylation. Previous studies mostly applied candidate-gene approaches and have demonstrated that epigenetic marks are associated with multiple allergic diseases and/or with early-life exposures relevant to allergy development (such as early-life smoking exposure, air pollution, farming environment, and dietary fat). Rapid technological advancements have made unbiased genome-wide DNA methylation studies highly feasible, although there are substantial challenge in study design, data analyses, and interpretation of findings. In conclusion, epigenetics represents both an important knowledge gap and a promising research area for FA. Due to the early onset of FA, epigenetic studies of FA in prospective birth cohorts have the potential to better understand gene-environment interactions and underlying biological mechanisms in FA during critical developmental windows (preconception, in utero, and early childhood) and may lead to new paradigms in the diagnosis, prevention, and management of FA and provide novel targets for future drug discovery and therapies for FA.
Increasing evidence suggests that intake of long-chain polyunsaturated fatty acids (LCPUFA), especially omega-3 LCPUFA, improves respiratory health early in life. This review summarizes publications from 2009 through July 2012 that evaluated effects of fish, fish oil or LCPUFA intake during pregnancy, lactation, and early postnatal years on allergic and infectious respiratory illnesses. Studies during pregnancy found inconsistent effects in offspring: two showed no effects and three showed protective effects of omega-3 LCPUFA on respiratory illnesses or atopic dermatitis. Two studies found that infants fed breast milk with higher omega-3 LCPUFA had reduced allergic manifestations. Earlier introduction of fish improved respiratory health or reduced allergy in four studies. Three randomized controlled trials showed that providing LCPUFA during infancy or childhood reduced allergy and/or respiratory illness while one found no effect. Potential explanations for the variability among studies and possible mechanisms of action for LCPUFA in allergy and respiratory disease are discussed.
Rhinitis is a multifactorial disease characterized by symptoms of sneezing, rhinorrhea, postnasal drip, and nasal congestion. Non-allergic rhinitis is characterized by rhinitis symptoms without systemic sensitization of infectious etiology. Based on endotypes, we can categorize non-allergic rhinitis into an inflammatory endotype with usually eosinophilic inflammation encompassing at least NARES and LAR and part of the drug induced rhinitis (e.g., aspirin intolerance) and a neurogenic endotype encompassing idiopathic rhinitis, gustatory rhinitis, and rhinitis of the elderly. Patients with idiopathic rhinitis have a higher baseline TRPV1 expression in the nasal mucosa than healthy controls. Capsaicin (8-methyl-N-vanillyl-6-nonenamide) is the active component of chili peppers, plants of the genus Capsicum. Capsaicin is unique among naturally occurring irritant compounds because the initial neuronal excitation evoked by it is followed by a long-lasting refractory period, during which the previously excited neurons are no longer responsive to a broad range of stimuli. Patients with idiopathic rhinitis benefit from intranasal treatment with capsaicin. Expression of TRPV1 is reduced in patients with idiopathic rhinitis after capsaicin treatment. Recently, in a Cochrane review, the effectiveness of capsaicin in the management of idiopathic rhinitis was evaluated and the authors concluded that given that many other options do not work well in non-allergic rhinitis, capsaicin is a reasonable option to try under physician supervision. Capsaicin has not been shown to be effective in allergic rhinitis nor in other forms of non-allergic rhinitis like the inflammatory endotypes or other neurogenic endotypes like rhinitis of the elderly or smoking induced rhinitis.