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Showing posts with label allergy. Show all posts
Showing posts with label allergy. Show all posts

Sunday, November 29, 2015

WAO Secretariat FOOD ALLERGY SYMPOSIUM. December 5th, 6th; MIAMI. EE.UU.


Comprehensive genomic sequencing requires a different skill set for clinical geneticists and other medical professionals using genetic data. The genomic data from patients, collected in a standardized format all over the globe, will be enormously valuable to improve our understanding of variant pathogenicity and disease susceptibility. Data sharing on a global scale is therefore essential to improved understanding of genotype–phenotype correlations [6]. Global data sharing is not just a lofty goal but rather a requirement for understanding human biology and deviations from homeostasis or health; it transcends geographic, political and religious boundaries that can sometimes divide the human race. These genomic data are, however, useful only if combined with phenotypic information collected in a standardized manner as well. It is remarkable to think that genome sequencing itself may soon turn out to be the easy part of the equation. Standardized phenotyping all over the world is likely to be a major challenge required for maximizing the medical knowledge acquisition from personal genomic variant information. This requires clinicians to adapt their clinical practice and potentially adopt and incorporate novel phenotyping tools.

From Global Medical Genome.  University of Texas at Baylor College of Medicine.




WAO Secretariat. Food Allergy Symposium. December 5th and 6th, Miami. EE.UU



Carlos E. Mijares ha compartido el vídeo de ILoveKLOVE.
10 min
El Hospital Bambino Jesu de Roma, is ready to conquer Miami, EE.UU December 5th and 6th 2015 with the Omic´s sciences developed by its Scholars, The Hygiene Hypothesis and the Bionomenclature and Genomics. Epigenomics, Proteomics, Metabolomics, Microbiomics, Macrobiomics, Chromosomics; even the Vaticonomics or Catholicomics - are just "suffixes" not a core or medical code, brought as a new Allergy Field (Allergonomics or Immunologomics) ready to create a Holistic Allergy Medicine; as asserted by its Scholars and Priests. For the Omic-endings satisfy the stress of so many overtures and tones of the immunoallergic mechanisms of the human body.On the contrary, a divine medium or holistic aproach to medicine is out of question regarding the Medical Sciencies.As a matter of fact, Aquinas and Luther were displaced by the Higgs-Englert boson discovery - and what is waiting ahead...For instance, the Climate Summit Plan proposed by the United States and president Barack Obama wants to intervene to regulate and climatize the Environment; as clean as possible to Breathe a cleaner air...and help the underdeveloped regions worldwide.

According to the GlobalMed Genome paragraph written above, and this paragraph we try to say that Holistic Medicine is a misnomer phrase, for Mind and Body are the same matter or the same body or the same anatomical structure; we do not think and then exist; we do not exist and then, think...we live as we dream - alone; as said by Joseph Conrad in Heart of Darkness. 

Carlos E. Mijares, MD is a former Fellow in Allergy / Immunologic, pediatrics.


Please, translate! University of Kansas. USA.



34 249 891 reproducciones
ILoveKLOVE ha subido un vídeo nuevo.

Tuesday, November 24, 2015

ANAFILAXIA INDUCIDA POR EJERCICIO EN ALERGIA ALIMENTARIA / PRESENTACION DE UN CASO




Allergy & Clinical Immunology

Food-Dependent Exercise-Induced Anaphylaxis to Chickpea in a 17-Year-Old Female: A Case Report

Hannah Roberts; Moshe Ben-Shoshan
Disclosures
J Med Case Reports. 2015;9(186) 

Abstract and Introduction

Abstract

Introduction: Food-dependent exercise-induced anaphylaxis is a subtype of anaphylaxis and, although rare, it is an important condition to be familiar with as it can ultimately lead to death.
Case presentation: We present a case of food-dependent exercise-induced anaphylaxis in a 17-year-old white girl due to chickpea. She had a history of anaphylaxis after eating crackers and hummus before exercising. Skin prick testing and serum-specific immunoglobulin E level confirmed chickpea to be the causative allergen.
Conclusions: This case demonstrates the challenge in identifying specific causative food allergens when foods are eaten in combination, when the food is processed, and when cross-reactivity is possible. These challenges add complexity to a condition that is already rare and unfamiliar to some health care providers. We hope that this case will serve as an important reminder that although rare, food-dependent exercise-induced anaphylaxis exists and making a diagnosis can lead to life-saving preventative strategies. As legumes are not a common food associated with food-dependent exercise-induced anaphylaxis, this will add to our current knowledge base in the field of allergy.

Introduction

Anaphylaxis is a systemic allergic reaction that is rapid in onset and has the potential to cause death.[1] Once diagnosed, avoidance of allergen and carrying an epinephrine auto-injector is recommended.[2] Most anaphylactic reactions are immunoglobulin E (IgE) mediated and the major triggers include food, medication, venom, latex, exercise, and transfusions.[3] It is reported that anaphylaxis affects at least 1.6% of the general population.[4]
Food-dependent exercise-induced anaphylaxis (FDEIA) is a subtype of anaphylaxis and is rare.[5] FDEIA is more commonly described in adolescents and adults versus younger children.[6] The condition is characterized by anaphylaxis that develops in association with physical exertion and ingestion of a causative food within a certain timeframe. In an analysis of 167 Japanese cases of FDEIA, 80% of the patients developed symptoms within 2 hours of eating the causative food.[7] Neither the food allergen nor exercise alone triggers anaphylaxis. Typical symptoms seen in FDEIA include skin manifestations (urticaria, erythema, edema, and pruritus), dyspnea, abdominal pain, and fatigue.[8] The pathogenesis is not fully understood yet. Based on skin prick testing (SPT) and specific IgE results for causative foods, an IgE mechanism is likely. The exact mechanism that results in a transient disruption in immune tolerance to causative foods is not known and different theories exist.[9] It is thought that exertion triggers physiological change that enhances absorption of undigested, immunoreactive forms of allergen from the gastrointestinal tract. Specific co-triggers such as non-steroidal anti-inflammatory drugs (NSAIDS), aspirin, extreme temperatures, a second food, menstruation, and stress, have also been theorized to aid in the development of FDEIA.[5], [6] The primary foods reported to trigger FDEIA are wheat and shellfish,[10] although in Europe tomatoes appear to be more common in FDEIA than wheat.[6] A variety of other foods have been identified in FDEIA including vegetables, fruits, nuts, egg, mushrooms, rice, and meat.[7]
Diagnosis relies on a thorough history to identify food allergen exposure, along with the combination of exercise and possible co-triggers. SPT and specific IgE levels can reveal the food allergen(s) and exclude other suspected allergens. A positive oral-food exercise challenge would further confirm a diagnosis, but is unnecessary if the history is suggestive and SPT and/or IgE levels are consistent.[5]
We present a case of FDEIA to chickpea in a 17-year-old girl with a convincing clinical history, positive SPT to fresh chickpea and hummus extract, along with an elevated serum-specific IgE level to chickpea. To the best of our knowledge, this is the first case demonstrating FDEIA to chickpea in an adolescent. This case describes the challenge in identifying specific causative food allergens when foods are eaten in combination, when the food is processed, and when cross-reactivity is possible.
1 of 5

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Monday, November 23, 2015

WHEAT GENOME PUZZLE / SECOND STAPLE IN FOOD ALLERGY, WORLDWIDE

Wheat Allergy as treated by Carlos E Mijares MD, former fellow in Allergy / Immunology, pediatrics  at University of Kansas, USA.
Currently, practicing at www.centromedicodecaracas.com,ve
carlosmixares@gmail.com

Elimination Diet Sheet : Wheat, Oats, Rice, Barley, Rye. All breads and baked goods, flour, cake,crackers, doughnuts, cookies, waffles, pancakes, pretzels, icecream cones, pie crust, macaroons, rolls, buns, cereals, macaroni, spaghetti, noodles, gravy.

Common Food Relationships:
Family or Class     Important Members      Usual Manifestations                Cross reactivity

Buckwheat            Buckwheat, rhubarb      Rare offenders;                          Probably strong
                                                                    buckwheat useful
                                                                    in wheat-sensitive
                                                                    children




Insights and opinion from BioMed Central on the latest biology research and developments in the field. About this blog »



Durum roll please: updated genome a huge milestone for designing high-yield sustainable wheat

The updated wheat genome sequence, released today, is a new step toward generating improved wheat varieties. Here, Genome Biology's Dominique Morneau outlines the challenges and opportunities that accompany the sequencing of the wheat genome.
Bread wheat (Triticum aestivum) is the second most highly produced cereal worldwide, grown on more than 215 million hectares, and the leading source of vegetable protein in human food. It was first domesticated in western Asia around 11,700 years ago, after which it spread to North Africa, Europe, and East Asia. Scientists are currently trying to figure out how to feed a growing population; in the next 50 years, we will need to grow more wheat than has been produced since the dawn of agriculture.
The key to improving wheat lies in identifying genes that can be exploited to meet the increased demand for high quality food. Unfortunately, sequencing the wheat genome is proving to be quite difficult.

The complexity of the wheat genome

Bread wheat is an allohexaploid, meaning that it has six sets of seven chromosomes derived from three different progenitor species (Triticum uratru, Aegilops speltoides, and Aegilops tauschii). The wheat genome is divided into three subgenomes: A, B, and D, each of which is almost twice as large as the human genome.
The wheat genome itself isn’t any harder to sequence than smaller genomes. What researchers have been struggling with is putting all the letters together in the right order. The wheat genome contains 17 gigabases (compared to the 3 gigabase human genome), and 80% of it is repetitive sequences. Using whole-genome shotgun sequencing methods thus becomes unattractive, since they generate reads of 500-1000 bases.
To understand why this problem is so complex, imagine a jigsaw puzzle with 17 million small pieces, 80% of which are very similar to each other. An international consortium of 1,100 researchers from 55 countries has been working on sequencing and assembling the wheat genome for the last 10 years!

The wheat genome – spelt out here

The wheat genome is currently being sequenced chromosome by chromosome. In July 2014, a draft of the full genome was published in the journal Science along with a reference sequence for chromosome 3B. Because of the complexity of the genome, the draft genome has lower accuracy, with segments either missing or in the wrong order or orientation.
Since then, work has focused on producing reference-quality assemblies for the remaining chromosomes – filling in the gaps with high accuracy and removing ambiguity in the order of segments – and mapping specific genes and genomic features. Other researchers have used the draft genome to study the evolution of wheat and other cereals, and to find variability in loci encoding agronomically important traits.
Today, The Genome Analysis Centre (TGAC) in Norwich, UK, has made a more complete and accurate wheat genome assembly available to the research community. The updated genome is now assembled into fewer, larger sections of DNA covering regions that were previously not sequenced. These regions include many of the large and complex groups of genes in wheat that contribute to the nutritional and bread-making quality of the grain.
wheat 2
Photo: The Genome Analysis Centre

Flour power

Here at Genome Biology, we’re big fans of wheat genomics, and have put together a collection of articles that we’ve published in the last year. Highlights include a more in-depth understanding of the structure, evolution, and expression of genes from chromosome 3B, a new method for assembling the wheat genome, finding sequence variations across the genome, and identifying genes that produce important traits that we may want to exploit, like grain dormancy.
But there’s more to wheat genomics than meets the eye. Growing wheat also means dealing with a slew of pathogens that affect yield. As interest in wheat genomics grows, so too does work in pathogenomics to prevent productivity losses, like those caused by the wheat yellow rust pathogen (Puccinia striiformis f. sp. tritici).

Never miss a triticum

The updated wheat genome is another step toward a chromosome-based complete genome in this important crop species. With this information, plant breeders will have high quality tools at their disposal to identify specific genes affecting agronomically important traits, such as yield, grain size and weight, nutritional quality, and stress tolerance. This will enable farmers and breeders to produce new wheat varieties better adapted to increasing demand in a changing climate.


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Wednesday, November 18, 2015

AN OVERVIEW OF ASTHMA MANAGEMENT / Translate!

Asthma as treated by Carlos E Mijares, MD

Former Allergy Fellow and resident at University of Kansas, USA

Currently. headquarted at www.centromedicodecaracas,com.ve

carlosmixares@gmail.com

An overview of asthma management
Disclosures: Christopher H Fanta, MD Nothing to disclose. Robert A Wood, MD Grant/Research/Clinical Trial Support: DBV [Food allergy]. Consultant/Advisory Boards: Sanofi [Food allergy (Epinephrine)]; Stallergenes [Allergic rhinitis (Sweet vernal/orchard/perennial rye/timothy/kentucky blue grass mixed pollen allergen extract - sublingual route)]. Bruce S Bochner, MD Grant/Research/Clinical Trial Support: NIAID; NHLBI; GSK [Siglec-8, Siglec-9, asthma, COPD, anaphylaxis, imaging; eosinophilic granulomatosis with polyangiitis]. Consultant/Advisory Boards: TEVA; Sanofi; Merck; GlycoMimetics; Allakos; Biogen; Svelte Medical Systems. Patent Holder: Siglec-8 and its ligand; anti-Siglec-8 antibodies [Held by Johns Hopkins University]. Employment: Northwestern University Feinberg School of Medicine. Equity Ownership/Stock Options: GlycoMimetics; Allakos. Other Financial Interest: Elsevier [Publication royalties]. Helen Hollingsworth, MD Nothing to disclose.
Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these are addressed by vetting through a multi-level review process, and through requirements for references to be provided to support the content. Appropriately referenced content is required of all authors and must conform to UpToDate standards of evidence.
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Oct 2015. | This topic last updated: Jul 08, 2014.
INTRODUCTION — This overview topic presents the components and goals of asthma management. It is applicable to both children and adults. The information herein is consistent with "The National Asthma Education and Prevention Program: Expert Panel Report 3, Guidelines for the Diagnosis and Management of Asthma – Full Report 2007" [1]. Similar guidelines have been published by the Global Initiative for Asthma (GINA) [2].
The diagnosis of asthma and more detailed management issues are reviewed elsewhere. (See "Diagnosis of asthma in adolescents and adults" and "Asthma in children younger than 12 years: Initial evaluation and diagnosis" and "Asthma in children younger than 12 years: Treatment of persistent asthma with controller medications" and "Treatment of intermittent and mild persistent asthma in adolescents and adults" and "Treatment of moderate persistent asthma in adolescents and adults".)
COMPONENTS OF ASTHMA MANAGEMENT — The successful management of patients with asthma includes four essential components:
Routine monitoring of symptoms and lung function
Patient education to create a partnership between clinician and patient
Controlling environmental factors (trigger factors) and comorbid conditions that contribute to asthma severity
Pharmacologic therapy
GOALS OF ASTHMA TREATMENT — The goals of chronic asthma management may be divided into two domains: reduction in impairment and reduction of risk [1].
Reduce impairment — Impairment refers to the intensity and frequency of asthma symptoms and the degree to which the patient is limited by these symptoms. Specific goals for reducing impairment include:
Freedom from frequent or troublesome symptoms of asthma (cough, chest tightness, wheezing, or shortness of breath)
Minimal need (≤2 days per week) of inhaled short acting beta agonists (SABAs) to relieve symptoms
Few night-time awakenings (<2 nights per month) due to asthma
Optimization of lung function
Maintenance of normal daily activities, including work or school attendance and participation in athletics and exercise
Satisfaction with asthma care on the part of patients and families
Reduce risk — The 2007 NAEPP guidelines introduced the concept of risk to encompass the various adverse outcomes associated with asthma and its treatment [1]. These include asthma exacerbations, suboptimal lung development (children), loss of lung function over time (adults), and adverse effects from asthma medications. Proper asthma management attempts to minimize the patient's likelihood of experiencing these outcomes. Specific goals for reducing risk include:
Prevention of recurrent exacerbations and need for emergency department or hospital care
Prevention of reduced lung growth in children, and loss of lung function in adults
Optimization of pharmacotherapy with minimal or no adverse effects
MONITORING PATIENTS WITH ASTHMA — Currently, the majority of medical visits for asthma are for urgent care. Effective asthma management, however, requires a proactive, preventative approach, similar to the treatment of hypertension or diabetes. Routine follow-up visits for patients with active asthma are recommended, at a frequency of every one to six months, depending upon the severity of asthma. These visits should be used to assess multiple aspects of the patient's asthma [3]. The aspects of the patient's asthma that should be assessed at each visit include the following: signs and symptoms, pulmonary function, quality of life, exacerbations, adherence with treatment, medication side effects, and patient satisfaction with care.
Well-controlled asthma is characterized by daytime symptoms no more than twice per week and nighttime symptoms no more than twice per month. SABAs for relief of asthma symptoms should be needed less often than twice weekly, and there should be no interference with normal activity (preventative use of a SABA, such as prior to exercise, is acceptable even if used in this way on a daily basis). Peak flow should remain normal or near-normal. Oral glucocorticoid courses and/or urgent care visits should be needed no more than once per year [4]. Assessment of control in patients of different ages is summarized in the tables (table 1A-C).
Symptom assessment — Symptoms over the past two to four weeks should be assessed at each visit. Assessment should address daytime symptoms, nighttime symptoms, use of short acting inhaled beta agonists to relieve symptoms, and difficulty in performing normal activities and exercise. Several quick and validated questionnaires, like the Asthma Control Test, have been published (form 1 and figure 1) [5-15].
Assessment of impairment — The following questions are representative of those used in validated questionnaires to assess asthma control:
Has your asthma awakened you at night or in the early morning?
How often have you been needing to use your quick-acting relief medication to relieve symptoms of cough, shortness of breath, or chest tightness?
Have you needed any unscheduled care for your asthma, including calling in, an office visit, or an emergency department visit?
Have you been able to participate in school/work and recreational activities as desired?
If you are measuring your peak flow, has it been lower than your personal best? Home monitoring of peak flow measurements is reviewed in detail separately. (See "Peak expiratory flow rate monitoring in asthma".)
Have you had any side effects from your asthma medications?
Assessment of risk — The following questions address the most important risk factors for future exacerbations [1]. A discussion of the risk factors for fatal and near-fatal asthma is provided separately. (See "Identifying patients at risk for fatal asthma", section on 'Identifying high-risk patients'.)
Have you taken oral glucocorticoids ("steroids") for your asthma in the past year?
Have you been hospitalized for your asthma? If yes, how many times have you been hospitalized in the past year?
Have you been admitted to the intensive care unit or been intubated because of your asthma? If yes, did this occur within the past five years?
Do you currently smoke cigarettes?
Have you ever noticed an increase in asthma symptoms after taking aspirin or a nonsteroidal antiinflammatory agent (NSAID)?
Monitoring pulmonary function — Peak expiratory flow rate (PEFR) (performed in the office and/or at home) and spirometry (performed in the office) are the two most commonly employed modalities for monitoring pulmonary function in children older than five years of age and in adults. The 2007 NAEPP guidelines state a preference for use of spirometry in medical offices, when available [1]. Children older than five years of age are usually able to perform the peak flow or spirometric maneuver.
Office monitoring — Measurement of PEFR can be a useful indicator of airflow obstruction, the hallmark finding of asthma. PEFR can be measured with handheld peak flow meters in settings not equipped with a spirometer. Average normal values for men, women, and children are listed in the tables (table 2A-C). Adolescents have values closer to children than to adults [1].
It is important to understand the limitations of PEFR. A reduced peak flow is not synonymous with airway obstruction; spirometry is needed to distinguish conclusively an obstructive from restrictive abnormality [16]. Also, the accuracy of a single peak flow measurement to detect the presence of airflow obstruction is limited, given the large variability of PEFR among healthy individuals of the same age, height, and gender (±20 percent) [17-19]. Nonetheless, repeated measurements of PEFR in an individual patient are useful for determining relative changes or trends in asthma control [17,20-24]. PEFR monitoring is best used in patients in whom the diagnosis of asthma has been previously established with a more complete evaluation. The use of PEFR monitoring and its limitations are presented in more detail elsewhere. (See "Peak expiratory flow rate monitoring in asthma".)
Spirometry, which additionally measures forced expiratory volume in one second (FEV1) and forced vital capacity (FVC), can be used to document airflow obstruction (by demonstration of a reduced FEV1/FVC ratio) and provides additional information that is useful in monitoring asthma, such as risk for exacerbations [16,25]. Spirometry has greater sensitivity for detecting airflow obstruction in the presence of a normal peak expiratory flow. As mentioned previously, the 2007 NAEPP guidelines recommend the use of spirometry in practices that are regularly caring for patients with asthma. (See "Office spirometry".)
Home monitoring — Home monitoring of the peak expiratory flow rate (PEFR) may be helpful in patients with moderate to severe asthma. It is also useful in patients who poorly perceive limitations in airflow. These individuals cannot be easily identified at the outset of care, although over time they display a lack of awareness of increasing impairment, and typically seek care for exacerbations only after symptoms have become severe [26,27].
Peak flow meters for individual use are widely available, inexpensive (approximately $20), and easy to use. However, the resulting measurements are highly dependent upon the patient's technique. It is therefore important that the clinician periodically checks the patient's use of the meter, and corrects any mistakes in technique. Instructions for patients are provided. (See "Patient information: How to use a peak flow meter (Beyond the Basics)".)
The patient should be instructed in how to establish a baseline measure of peak flow when feeling entirely well: the "personal best" peak flow value. The personal best PEFR is then used to determine the normal PEFR range, which is between 80 and 100 percent of the patient's personal best. Readings below this normal range indicate airway narrowing, a change that may occur before symptoms are perceived by the patient. (See 'Asthma action plan' below.)
Novel forms of monitoring — Measurements of lung function such as peak flow and spirometry assess asthma control based on airway diameter. However, it would also be desirable to measure airway inflammation directly. Quantitative analysis of expectorated sputum for eosinophilia and concentration of nitric oxide in exhaled breath are two modalities currently being explored for this purpose. Studies have reached conflicting conclusions about whether regularly measuring these markers could help optimize asthma management. Neither technique is currently in routine use outside of investigational settings. The use of expectorated sputum eosinophilia and exhaled nitric oxide analysis in the management of asthma are discussed in more detail separately. (See "Evaluation of severe asthma in adolescents and adults", section on 'Airway inflammation' and "Exhaled nitric oxide analysis and applications".)
PATIENT EDUCATION — Clinicians should enable patients to become active partners in managing their asthma. Ideally, this would occur through direct education in the office, as well as adjunctive education through other members of the health care team, emergency department providers, pharmacists, and organized programs [3]. The effectiveness of direct one-on-one education by the primary clinician, in particular, is well supported by evidence [1].
Patient education decreases hospitalizations due to asthma, improves daily function, and improves patient satisfaction [28-30]. A well-informed and motivated patient can assume a large measure of control over his or her asthma care.
Patients must learn how to monitor their symptoms and pulmonary function; they must understand what triggers their asthma attacks and how to avoid or decrease exposure to these triggers; and they must understand what medicine to take and how to use inhalers properly (table 3 and table 4 and table 5 and table 6). If they have difficulty taking the medications regularly, they need help devising methods to improve compliance. The specific information that should be conveyed to the patient is reviewed in detail separately. (See "What do patients need to know about their asthma?".)
Asthma action plan — The patient's normal PEFR value can be used to construct a personalized "asthma action plan" (form 2). Symptom-based plans appear to be equally effective. The asthma action plan provides specific directions for daily management and for adjusting medications in response to increasing symptoms or decreasing PEFR. Instructions and forms for asthma action plans are presented elsewhere. (See "What do patients need to know about their asthma?".)
CONTROLLING TRIGGERS AND CONTRIBUTING CONDITIONS — The identification and avoidance of asthma "triggers" is a critical component of successful asthma management, and successful avoidance or remediation may reduce the patient's need for medications. Directed questions can identify specific triggers and contributing conditions (table 7).
Adults should be questioned about symptoms not only in the home, but also in the workplace, as asthma can be exacerbated by both irritant and allergen exposures in occupational settings. Patterns of symptoms that suggest occupational triggers are presented in the table (table 8) [1]. (See "Occupational asthma: Definitions, epidemiology, causes, and risk factors".)
Some triggers are mostly unavoidable, such as upper respiratory tract illnesses, physical exertion, hormonal fluctuations, and extreme emotion, and patients should be taught to adjust their management accordingly.
Other triggers, however, should be identified and specifically addressed or treated [5,31]:
Inhaled allergens – The patient should be questioned about symptoms triggered by common inhaled allergens, at home, daycare, school, or work (table 7 and table 8). Indoor allergens, such as dust mites, animal danders, molds, mice, and cockroaches, are of particular importance. Food allergy rarely causes isolated asthma symptoms, although wheezing and cough can be symptoms of food-induced anaphylaxis.

If the history suggests the patient has allergic triggers, basic avoidance measures can be advised, and evaluation by an allergy specialist should be considered. The assessment and management of allergen exposure in patients with asthma are reviewed in detail separately. (See "Allergen avoidance in the treatment of asthma and allergic rhinitis".)
Respiratory irritants – Inhaled irritants include tobacco smoke, wood smoke from stoves or fireplaces, strong perfumes and odors, chlorine-based cleaning products, and air pollutants. Patients should be cognizant of avoiding irritants, and avoid exertion outdoors on days when levels of air pollution are elevated. (See "Trigger control to enhance asthma management".)

Smoking cessation and avoidance of environmental tobacco smoke are reviewed in detail elsewhere. (See "Control of secondhand smoke exposure" and "Secondhand smoke exposure: Effects in adults" and "Secondhand smoke exposure: Effects in children" and "Overview of smoking cessation management in adults".)
Comorbid conditions – Clinicians should be vigilant for comorbid conditions in patients with poorly-controlled asthma. In adults, these conditions include chronic obstructive pulmonary disease/emphysema (COPD), allergic bronchopulmonary aspergillosis, gastroesophageal reflux, obesity, obstructive sleep apnea, rhinitis/sinusitis, vocal cord dysfunction, and depression/chronic stress. These conditions are reviewed separately. (See "Clinical manifestations and diagnosis of allergic bronchopulmonary aspergillosis" and "Gastroesophageal reflux and asthma" and "Clinical presentation and diagnosis of obstructive sleep apnea in adults" and "An overview of rhinitis" and "Chronic rhinosinusitis: Clinical manifestations, pathophysiology, and diagnosis".)

In young children, potential alternative or comorbid conditions include respiratory syncytial virus infection, foreign body aspiration, bronchopulmonary dysplasia, cystic fibrosis, and obesity [1].
Medications – Non-selective beta-blockers can trigger severe asthmatic attacks, even in the minuscule amounts that are absorbed systemically from topical ophthalmic solutions. Selective beta-1 blockers can also aggravate asthma in some patients, especially at higher doses. (See "Treatment of hypertension in asthma and COPD".)

Aspirin and non-steroidal anti-inflammatory drugs can trigger asthma symptoms in approximately 3 to 5 percent of adult asthmatic patients. The incidence of aspirin-exacerbated respiratory disease is higher among asthmatic patients with nasal polyposis (constituting "triad asthma" or Samter's triad). Aspirin-sensitive asthma is uncommon in children. (See "Aspirin-exacerbated respiratory disease".)
Complications of influenza – Annual administration of influenza vaccine is recommended for patients with asthma because they are particularly at risk for complications of influenza infection. However, vaccination does not reduce the number or severity of asthma exacerbations during the influenza season, and providers should ensure that patients understand this distinction. Indications for vaccination against influenza are reviewed separately. (See "Seasonal influenza vaccination in adults" and "Seasonal influenza in children: Prevention with vaccines", section on 'Indications'.)
Complications of pneumococcal infection – Administration of pneumococcal vaccination is recommended for adults whose asthma is severe enough to require controller medication and for children with asthma who require chronic oral glucocorticoid therapy (table 9 and table 10) [32]. (See "Pneumococcal (Streptococcus pneumoniae) conjugate vaccines in children", section on 'Indications' and "Pneumococcal (Streptococcus pneumoniae) polysaccharide vaccines in children", section on 'Indications' and "Pneumococcal vaccination in adults", section on 'Indications'.)
Dietary sulfites – Sulfite compounds are used in the food industry to prevent discoloration. As many as 5 percent of patients with asthma may note significant and reproducible exacerbations following ingestion of sulfite-treated foods and beverages, such as beer, wine, processed potatoes, dried fruit, sauerkraut, or shrimp.
PHARMACOLOGIC TREATMENT — Pharmacologic treatment is the mainstay of management in most patients with asthma [33]. The 2007 National Asthma Education and Prevention Program (NAEPP) Expert Panel Report presented a stepwise approach to pharmacologic therapy, which is reflected in this review [1]. These guidelines were intended to support, rather than dictate, care that is based upon the clinician's clinical judgment.
The stepwise approach to pharmacotherapy is based on increasing medications until asthma is controlled, and decreasing medications when possible to minimize side effects. The patient's management should be adjusted, if needed, at every visit.
The first step in determining appropriate therapy for patients who are not already on a controller medication is classifying the severity of the patient's asthma. For patients already taking one or more controller medications, treatment options are guided by an assessment of asthma control rather than asthma severity.
Categories of asthma severity — Asthma severity is determined by considering the following factors [1]:
Reported symptoms over the previous two to four weeks
Current level of lung function (FEV1 and FEV1/FVC values)
Number of exacerbations requiring oral glucocorticoids per year
The use of these three elements to determine severity in adolescents over the age of 12 years and in adults is graphically presented in the figure (table 11).
The classification of severity in children aged 5 to 11 years is similar to that in adults (table 12). Severity in children under the age of four years, however, is classified somewhat differently (table 13). Initiating long-term controller medications in children under the age of 12 years is reviewed separately. (See "Asthma in children younger than 12 years: Treatment of persistent asthma with controller medications".)
Intermittent — Intermittent asthma is characterized by the following (table 11). The criteria for adolescents and adults are utilized in this discussion [1]:
Daytime asthma symptoms occurring two or fewer days per week
Two or fewer nocturnal awakenings per month
Use of short-acting beta agonists to relieve symptoms fewer than two times a week
No interference with normal activities between exacerbations
FEV1 measurements between exacerbations that are consistently within the normal range (ie, ≥80 percent of predicted normal)
FEV1/FVC ratio between exacerbations that is normal (based on age-adjusted values)
One or no exacerbations requiring oral glucocorticoids per year
If any of the features of a patient’s asthma is more severe than those listed here, their asthma should be categorized as having persistent asthma, with its severity based on the most severe element. Patients experiencing two or more exacerbations of asthma requiring oral glucocorticoids in the past year are considered to have persistent asthma.
In addition, a person using a SABA to prevent exercise-induced asthmatic symptoms might fit into this category of intermittent asthma even if exercising more than twice per week. Others in whom asthmatic symptoms arise only under certain infrequently occurring circumstances (eg, upon encountering a cat or during viral respiratory tract infections) are also considered to have intermittent asthma. (See "Exercise-induced bronchoconstriction".)
Equivalent schema for classifying asthma in children 0 to 4 years and 5 to 11 years are provided (table 13 and table 12).
Mild persistent — Mild persistent asthma is characterized by the following (table 11):
Symptoms more than twice weekly (although less than daily)
Approximately three to four nocturnal awakenings per month due to asthma (but fewer than every week)
Use of short-acting beta agonists to relieve symptoms more than two times a week (but not daily)
Minor interference with normal activities
FEV1 measurements within normal range (≥80 percent of predicted normal) and normal FEV1/FVC ratio (based on age-adjusted values)
Two or more exacerbations requiring oral glucocorticoids per year
If any of the features of a patient’s asthma is more severe than those listed here, their asthma should be categorized according to the most severe element.
Equivalent figures for asthma in children 0 to 4 years and 5 to 11 years are provided (table 13 and table 12).
Moderate persistent — The presence of any of the following is considered an indication of moderate disease severity (table 11):
Daily symptoms of asthma
Nocturnal awakenings more than once per week
Daily need for short-acting beta agonists for symptom relief
Some limitation in normal activity
FEV1 between 60 and 80 percent of predicted and FEV1/FVC below normal (based on age-adjusted values)
Equivalent figures for asthma in children 0 to 4 years and 5 to 11 years are provided (table 13 and table 12).
Severe persistent — Patients with severe persistent asthma experience one or more of the following (table 11):
Symptoms of asthma throughout the day
Nocturnal awakenings nightly
Need for short-acting beta agonists for symptom relief several times per day
Extreme limitation in normal activity
FEV1 <60 percent of predicted and FEV1/FVC below normal (based on age-adjusted values)
Equivalent figures for asthma in children 0 to 4 years and 5 to 11 years are provided (table 13 and table 12).
Initiating therapy during an acute exacerbation — Patients with acute exacerbations of asthma often require systemic glucocorticoids. Treatment of asthma exacerbations is reviewed separately. (See "Treatment of acute exacerbations of asthma in adults" and "Acute asthma exacerbations in children: Emergency department management".)
Initiating therapy in previously untreated patients — The initiation of asthma therapy in a stable patient who is not already receiving medications is based upon the severity of the individual's asthma.
Initiating long-term controller medications in young children is reviewed separately. (See "Asthma in children younger than 12 years: Treatment of persistent asthma with controller medications".)
Intermittent (Step 1) — Patients with mild intermittent asthma are best treated with a quick-acting inhaled beta-2-selective adrenergic agonist, taken as needed for relief of symptoms (figure 2 and figure 3 and figure 4) [34-36]. Patients for whom triggering of asthmatic symptoms can be predicted (eg, exercise-induced bronchoconstriction) are encouraged to use their inhaled beta agonist approximately 10 minutes prior to exposure in order to prevent the onset of symptoms. (See "Beta agonists in asthma: Acute administration and prophylactic use" and "Exercise-induced bronchoconstriction".)
The pharmacologic management of mild intermittent asthma is discussed in more detail separately. (See "Treatment of intermittent and mild persistent asthma in adolescents and adults" and "Asthma in children younger than 12 years: Rescue treatment for acute symptoms".)
Mild persistent (Step 2) — The distinction between intermittent and mild persistent asthma is important, because current guidelines for mild persistent asthma call for initiation of daily long-term controller medication. For mild persistent asthma, the preferred long-term controller is a low dose inhaled glucocorticoid (GC) (figure 2 and figure 3 and figure 4 and table 14). Regular use of inhaled glucocorticoids reduces the frequency of symptoms (and the need for SABAs for symptom relief), improves the overall quality of life, and decreases the risk of serious exacerbations [37-39]. Regular use of inhaled glucocorticoids has not been shown to prevent progressive loss of lung function over time.
Alternative strategies for treatment of mild persistent asthma include leukotriene receptor antagonists, theophylline, and cromoglycates (figure 2). Among these alternatives, we favor the leukotriene blockers. Patients receiving long-term controller therapy should continue to use their short-acting beta agonist as needed for relief of symptoms and prior to exposure to known triggers of their symptoms.
The pharmacologic management of mild persistent asthma is presented in greater detail elsewhere. (See "Treatment of intermittent and mild persistent asthma in adolescents and adults" and "Asthma in children younger than 12 years: Treatment of persistent asthma with controller medications".)
Moderate persistent (Step 3) — For moderate persistent asthma, the preferred therapies are either low-doses of an inhaled glucocorticoid plus a long-acting inhaled beta agonist, or medium doses of an inhaled glucocorticoid (figure 2 and figure 3 and figure 4 and table 14). The former combination has proven more effective in controlling asthmatic symptoms than an increased dose of inhaled GCs, although it entails the potential risk of adverse outcomes that have been reported in association with long-acting inhaled beta agonists [40,41]. (See "Beta agonists in asthma: Controversy regarding chronic use", section on 'Long–acting beta-agonists'.)
Alternative strategies include adding a leukotriene modifier (leukotriene receptor antagonist or lipoxygenase inhibitor) or theophylline to low-dose inhaled GCs. The pharmacologic management of moderate asthma is presented in more detail elsewhere. (See "Treatment of moderate persistent asthma in adolescents and adults".)
Severe persistent (Step 4 or 5) — For severe persistent asthma, the preferred treatments are medium (Step 4) or high (Step 5) doses of an inhaled glucocorticoid, in combination with a long-acting inhaled beta-agonist (figure 2 and figure 3 and figure 4 and table 14).
In addition, for patients who are inadequately controlled on high-dose inhaled GCs and LABAs, the anti-IgE therapy omalizumab may be considered if there is objective evidence of sensitivity to a perennial allergen (by allergy skin tests or in vitro measurements of allergen-specific IgE) and if the serum IgE level is within the established target range. (See "Anti-IgE therapy".)
Step 6 therapy for the management of severe asthma involves the addition of oral glucocorticoids on a daily or alternate-day basis. Severe asthma is reviewed in more detail elsewhere. (See "Treatment of severe asthma in adolescents and adults".)
Assessing control to adjust therapy — Assessment of asthma control rather than severity is used to adjust therapy in returning patients, or in patients being evaluated for the first time who are already taking a long-term controller medication. Control is assessed based on impairment over the past two to four weeks (as determined by history or a validated questionnaire), current FEV1 or peak flow, and estimates of risk (table 15) [1,42]. Adjusting therapy in children younger than 12 years is reviewed in more detail separately. (See 'Monitoring patients with asthma' above and "Asthma in children younger than 12 years: Treatment of persistent asthma with controller medications".)
Using the information gathered, the clinician should determine whether the patient's asthma is well-controlled or not. If the asthma is not well-controlled, therapy should be "stepped-up." If the asthma is well-controlled, therapy can be continued or possibly "stepped-down" to minimize medication side effects. Therapy should be reassessed at each visit, because asthma is an inherently variable condition, and the management of asthma is a dynamic process that changes in accordance with the patient's needs over time.
EFFICACY OF ASTHMA MANAGEMENT — A prospective, randomized trial applied the management recommendations of previous NAEPP guidelines to approximately 1500 patients with all severities of asthma over the course of one year [43]. Guideline-based management resulted in significant improvement in health-related quality of life in most patients, regardless of disease severity. In this study, subjects who required inhaled GCs were randomly assigned to receive either fluticasone propionate (FP) alone or the combination of fluticasone propionate and salmeterol (FP + S). Subjects were evaluated every three months and medications were stepped up as needed (although the protocol did not allow for stepping down of therapy). With both treatments, the majority of patients achieved well-controlled or totally-controlled asthma; control was slightly better with FP + S. The greatest improvements occurred in the first few months of therapy. This study validated a stepwise approach to asthma management as effective in reducing symptoms and improving health-related quality of life. The current guidelines have expanded upon this same basic approach [1,2].
WHEN TO REFER — Both pulmonologists and allergists/immunologists have specialty training in asthma care. Referral for consultation or comanagement is recommended when any of the following circumstances arise [1]:
The patient has experienced a life-threatening asthma exacerbation
The patient has required hospitalization or more than two bursts of oral corticosteroids in a year
The adult and pediatric patient older than five years requires step 4 care or higher or a child under five requires step 3 care or higher
Asthma is not controlled after three to six months of active therapy and appropriate monitoring
The patient appears unresponsive to therapy
The diagnosis of asthma is uncertain
Other conditions are present which complicate management (nasal polyposis, chronic sinusitis, severe rhinitis, allergic bronchopulmonary aspergillosis, COPD, vocal cord dysfunction, etc)
Additional diagnostic tests are needed (skin testing for allergies, bronchoscopy, complete pulmonary function tests)
Patient may be a candidate for allergen immunotherapy (see "Subcutaneous immunotherapy for allergic disease: Indications and efficacy")
Other possible indications for referral include [1]:
The adult and pediatric patient older than five years who requires step 3 care or higher or a child under five who requires step 2 care or higher
There appear to be occupational triggers
Patients in whom psychosocial or psychiatric problems are interfering with asthma management and in whom referral to other appropriate specialists may be required
INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, “The Basics” and “Beyond the Basics.” The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on “patient info” and the keyword(s) of interest.)
SUMMARY AND RECOMMENDATIONS
The four essential components of asthma management are: routine monitoring of symptoms and lung function, patient education, control of trigger factors and amelioration of comorbid conditions, and pharmacologic therapy. (See 'Components of asthma management' above.)
The goals of asthma treatment are to reduce impairment from symptoms, minimize risk of the various adverse outcomes associated with asthma (eg, hospitalizations, loss of lung function), and minimize adverse effects from asthma medications. (See 'Goals of asthma treatment' above.)
Effective asthma management requires a preventative approach, with regularly scheduled visits during which symptoms are assessed, pulmonary function is monitored, medications are adjusted, and ongoing education is performed. (See 'Monitoring patients with asthma' above.)
Patients should learn to monitor asthma control at home (eg, frequency and severity of dyspnea, cough, chest tightness, and albuterol use). Patients with moderate to severe asthma and those with poor perception of increasing asthma symptoms may also benefit from assessment of their peak expiratory flow rate at home. A personalized asthma action plan should be provided with detailed instructions on how to adjust asthma medications based upon changes in symptoms and/or lung function (form 2). (See 'Patient education' above.)
Environmental triggers and co-existing conditions that interfere with asthma management should be identified and addressed for each patient. (See 'Controlling triggers and contributing conditions' above.)
Pharmacologic therapy varies according to asthma severity and asthma control. Asthma control can be judged, irrespective of medication use, based on the current level of symptoms, FEV1 or PEFR values, and number of exacerbations requiring oral glucocorticoids per year (table 11 and table 12 and table 13). (See 'Categories of asthma severity' above and "Asthma in children younger than 12 years: Treatment of persistent asthma with controller medications".)
A stepwise approach to therapy is recommended, in which the dose of medication, the number of medications, and/or the frequency of administration are increased as necessary and decreased when possible (figure 2 and figure 3 and figure 4). (See 'Initiating therapy in previously untreated patients' above.)
At each return visit, the patient's asthma control is evaluated (table 15). If the asthma is not well-controlled, therapy should be "stepped-up." If the asthma is well-controlled, therapy can be continued or possibly "stepped-down" to minimize medication side effects. (See 'Assessing control to adjust therapy' above and "Asthma in children younger than 12 years: Treatment of persistent asthma with controller medications".)
Guidelines for when to refer a patient to a pulmonologist or an allergist/immunologist are provided. (See 'When to refer' above.)
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