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History Taking
Published in Pudupakkam K Vedanthan, Harold S Nelson, Shripad N Agashe, PA Mahesh, Rohit Katial, Textbook of Allergy for the Clinician, 2021
Gabriel K Wong, Mamidipudi Thirumala Krishna
Atopic diseases such as eczema, asthma and rhinitis often occur in clusters within affected families with variable penetrance suggesting a genetic predisposition to these conditions. Moreover, the ‘allergic march’ hypothesis proposed a link between the development of eczema to food allergy to allergic rhinitis to asthma. Data from studying Australian siblings has provided strong evidence to support the causal effect of eczema in allergic rhinitis though the link between eczema and asthma is less evident (Hopper et al. 2012). Another recent study has observed that the highest risk for developing asthma is within the first few years after developing allergic rhinitis. In this study approximately 80% of children and 60% of adults develop asthma within 2 years after the onset of allergic rhinitis, whereas asthma is unlikely to develop in children or adults who have had allergic rhinitis for more than 10 years (Mahesh et al. 2009). These findings raise the debate of early immunological intervention for the prevention of asthma. It is therefore important during history taking to establish the duration of allergy symptoms to guide the decision on implementing secondary prevention of asthma; such as immunotherapy for allergic rhinitis.
Food allergies and eosinophilic gastrointestinal diseases
Published in Phillip D. Smith, Richard S. Blumberg, Thomas T. MacDonald, Principles of Mucosal Immunology, 2020
Cathryn Nagler, Glenn T. Furuta
Food allergy is clinically linked to other allergic diseases, including asthma. Thus, atopic dermatitis, food allergy, and asthma may be viewed as cutaneous, gastrointestinal, and pulmonary manifestations of atopy as a systemic allergic disorder. All three conditions are characterized by eosinophilia and elevated levels of IgE. The progression of allergic manifestations from cutaneous and gastrointestinal sites to the respiratory tract has been called the “allergic march” and describes the natural history of atopy as a systemic disorder, whose manifestations peak sequentially at different sites (Figure 35.5). Pediatric patients who develop food allergy are at a higher risk of developing asthma over time.
Allergic Diseases
Published in Stephan Strobel, Lewis Spitz, Stephen D. Marks, Great Ormond Street Handbook of Paediatrics, 2019
Adam Fox, George Du Toit, Stephan Strobel
The term ‘allergic march’ is used for description of the natural history of atopic manifestations, which develop during the first decade of life (Fig. 23.2). Although there exists a great variability, this period is characterised by increasing IgE antibody responses and clinical symptoms that occur in early life and can remit over time. Early eczematous changes and gastrointestinal (GI) symptoms (Fig. 23.3) within the first 3 years are followed from around 3–7 years by asthma and later by allergic rhinitis. It has to be noted that many children exhibit multiple symptoms simultaneously. Presence of early eczema in childhood is often associated with the development of IgE-mediated common food allergies. The term ‘food allergic march’ implies that children typically present with egg or milk allergy or both and then go on to develop additional food allergies followed in adolescence/adulthood by the oral allergy syndrome (OAS). The natural history of these ‘atopic marches’, including which determinants are modifiable and might become candidates for preventive intervention, is still very poorly understood.
Stress, mindfulness, and the allergic patient
Published in Expert Review of Clinical Immunology, 2018
Gailen D. Marshall, Matthew T. Tull
Recognition of the immunopathophysiological components, including IgE-mediated, of asthma and other allergic diseases has developed in recent years even though the clinical recognition has had a much longer history without any clear understanding of the term ‘allergy’ first used by von Pirquet at the beginning of the twentieth century [11]. For centuries before that, clinical sensitivities to a variety of substances including plants, foods, animals, and other acute exposures were linked to adverse clinical effects of both respiratory and non-respiratory origin, which we now call allergies. In many parts of our modern-day world, the incidence and prevalence of allergic diseases have increased in recent years, and there is little indication that this rate of increase is moderating. Indeed, some believe the incidence continues to increase as we see new onset allergic diseases such as food allergy, once only described in children, now more common in adult populations [12] and even in some geriatric adults [13]. The term ‘allergic march’ describes a genetically susceptible child (with strong family history of allergy representing genetic risk) who develops atopic dermatitis and/or allergic rhinitis with sensitivities to a variety of airborne allergens and/or foods. Overtime, the clinical condition ‘marches’ on until the child finally develops asthma [14]. The alarming observation is that this allergic march is no longer exclusively true of only pediatric populations, but also of adolescent and adult populations [15].
Association of delayed chronotype with allergic diseases in primary school children
Published in Chronobiology International, 2022
Yiting Chen, Anda Zhao, Jiajun Lyu, Yabin Hu, Yong Yin, Jiajie Qu, Shilu Tong, Shenghui Li
In today’s industrial societies, allergic diseases (including asthma, rhinitis, and eczema) have become increasingly prevalent (Asher et al. 2006; Silverberg et al. 2021), and it has been reported that one in four people suffers from allergies (Pawankar et al. 2013). Allergic diseases usually occur in early childhood and progress as an “allergic march” (Linneberg 2008). They become more hard to control during adolescence as a result of physical, emotional, and cognitive changes (de Benedictis and Bush 2017). Thus, before puberty, school-age could be a crucial period for allergy control, preventing irreversible or severe progressions (Zhang et al. 2018). Since the etiology of allergic diseases is elusive, identifying modifiable risk factors at primary school age could be crucial.
Atopic phenotypes and their implication in the atopic march
Published in Expert Review of Clinical Immunology, 2020
Adnan Custovic, Darije Custovic, Blazenka Kljaić Bukvić, Sara Fontanella, Sadia Haider
The age of onset, clinical presentation, and co-occurrence of different allergic diseases varies considerably over the life-course and between individual patients, and the extent to which this phenotypic variation is a consequence of differences in etiology remains unclear [4]. The term “atopic march” (also called “allergic march”) refers to the natural history of atopic diseases and is usually interpreted as a sequential development of symptoms (or diseases) from eczema in infancy to allergic airway disease (asthma, and then allergic rhinitis) in later childhood [6,7]. That there is an exclusive sequence of events is implied by the use of the term “march,” which indicates a forward movement, an advance in a stepwise, organized and deliberate manner. The origins of this framework are observations from epidemiological studies that the point prevalence of eczema is highest in early life (i.e. that eczema is more common in infants than in school-age children), which is followed by the highest period prevalence of asthma in mid-school age, which is in turn supplanted by an increase in allergic rhinitis in late childhood [8–10]. These population-level observations could be a consequence of the progression of symptoms within-individual children, and were used to propose that a natural progression of symptoms exists in individual patients, starting with eczema, advancing to asthma, and then finally rhinitis (with a resolution of the early eczema and asthma with increasing age in some patients) [6,7,11–13]. The concept of atopic march has been extended to suggest that clinicians in primary care “should inform parents that children with eczema may later develop asthma” [14]. A further extrapolation to daily clinical practice is found in suggestions that “effective eczema treatment may decrease the risk of asthma” [15], and that “effective atopic eczema control not only improves quality of life but may also prevent the atopic march” [14]. Furthermore, the framework of atopic march has been used to design intervention studies aiming to prevent the development of asthma in children who are deemed to be at risk by the virtue of having eczema in infancy [16–18]. Notably, however, studies using antihistamines [16], topical calcineurin inhibitor pimecrolimus [17], and probiotics (Lactobacillus paracasei and Bifidobacterium lactis) [18] among infants with eczema showed no benefits on the subsequent development of asthma.