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Year of Publication
1.  Reviewer acknowledgement 2014 
Contributing reviewers
The editors of Allergy, Asthma & Clinical Immunology would like to thank all of our reviewers who have contributed to the journal in Volume 10 (2014).
doi:10.1186/s13223-015-0070-4
PMCID: PMC4320480  PMID: 25663841
5.  Reviewer acknowledgement 2013 
Contributing reviewers
The editors of Allergy Asthma & Clinical Immunology would like to thank all of our reviewers who have contributed to the journal in Volume 9 (2013).
doi:10.1186/1710-1492-10-5
PMCID: PMC3911797  PMID: 24490702
6.  Reviewer acknowledgement 2012 
Contributing reviewers
The editors of Allergy, Asthma & Clinical Immunology would like to thank all of our reviewers who have contributed to the journal in Volume 8 (2012).
doi:10.1186/1710-1492-9-3
PMCID: PMC3649928  PMID: 23659583
8.  An introduction to immunology and immunopathology 
In basic terms, the immune system has two lines of defense: innate immunity and adaptive immunity. Innate immunity is the first immunological, non-specific (antigen-independent) mechanism for fighting against an intruding pathogen. It is a rapid immune response, occurring within minutes or hours after aggression, that has no immunologic memory. Adaptive immunity, on the other hand, is antigen-dependent and antigen-specific; it has the capacity for memory, which enables the host to mount a more rapid and efficient immune response upon subsequent exposure to the antigen. There is a great deal of synergy between the adaptive immune system and its innate counterpart, and defects in either system can provoke illness or disease, such as autoimmune diseases, immunodeficiency disorders and hypersensitivity reactions. This article provides a practical overview of innate and adaptive immunity, and describes how these host defense mechanisms are involved in both health and illness.
doi:10.1186/1710-1492-7-S1-S1
PMCID: PMC3245432  PMID: 22165815
9.  Drug allergy 
Drug allergy encompasses a spectrum of immunologically-mediated hypersensitivity reactions with varying mechanisms and clinical presentations. This type of adverse drug reaction (ADR) not only affects patient quality of life, but may also lead to delayed treatment, unnecessary investigations, and even mortality. Given the myriad of symptoms associated with the condition, diagnosis is often challenging. Therefore, referral to an allergist experienced in the identification, diagnosis and management of drug allergy is recommended if a drug-induced allergic reaction is suspected. Diagnosis relies on a careful history and physical examination. In some instances, skin testing, graded challenges and induction of drug tolerance procedures may be required.
The most effective strategy for the management of drug allergy is avoidance or discontinuation of the offending drug. When available, alternative medications with unrelated chemical structures should be substituted. Cross-reactivity among drugs should be taken into consideration when choosing alternative agents. Additional therapy for drug hypersensitivity reactions is largely supportive and may include topical corticosteroids, oral antihistamines and, in severe cases, systemic corticosteroids. In the event of anaphylaxis, the treatment of choice is injectable epinephrine. If a particular drug to which the patient is allergic is indicated and there is no suitable alternative, induction of drug tolerance procedures may be considered to induce temporary tolerance to the drug.
This article provides a backgrounder on drug allergy and strategies for the diagnosis and management of some of the most common drug-induced allergic reactions, such allergies to penicillin, sulfonamides, cephalosporins, radiocontrast media, local anesthetics, general anesthetics, acetylsalicylic acid (ASA) and non-steroidal anti-inflammatory drugs.
doi:10.1186/1710-1492-7-S1-S10
PMCID: PMC3245433  PMID: 22165859
10.  Primary immunodeficiency 
Primary immunodeficiency disorder (PID) refers to a heterogeneous group of over 130 disorders that result from defects in immune system development and/or function. PIDs are broadly classified as disorders of adaptive immunity (i.e., T-cell, B-cell or combined immunodeficiencies) or of innate immunity (e.g., phagocyte and complement disorders). Although the clinical manifestations of PIDs are highly variable, most disorders involve at least an increased susceptibility to infection. Early diagnosis and treatment are imperative for preventing significant disease-associated morbidity and, therefore, consultation with a clinical immunologist is essential. PIDs should be suspected in patients with: recurrent sinus or ear infections or pneumonias within a 1 year period; failure to thrive; poor response to prolonged use of antibiotics; persistent thrush or skin abscesses; or a family history of PID. Patients with multiple autoimmune diseases should also be evaluated. Diagnostic testing often involves lymphocyte proliferation assays, flow cytometry, measurement of serum immunoglobulin (Ig) levels, assessment of serum specific antibody titers in response to vaccine antigens, neutrophil function assays, stimulation assays for cytokine responses, and complement studies. The treatment of PIDs is complex and generally requires both supportive and definitive strategies. Ig replacement therapy is the mainstay of therapy for B-cell disorders, and is also an important supportive treatment for many patients with combined immunodeficiency disorders. The heterogeneous group of disorders involving the T-cell arm of the adaptive system, such as severe combined immunodeficiency (SCID), require immune reconstitution as soon as possible. The treatment of innate immunodeficiency disorders varies depending on the type of defect, but may involve antifungal and antibiotic prophylaxis, cytokine replacement, vaccinations and bone marrow transplantation. This article provides a detailed overview of the major categories of PIDs and strategies for the appropriate diagnosis and management of these rare disorders.
doi:10.1186/1710-1492-7-S1-S11
PMCID: PMC3245434  PMID: 22165913
11.  Urticaria and angioedema 
Urticaria (hives) is a common disorder that often presents with angioedema (swelling that occurs beneath the skin). It is generally classified as acute, chronic or physical. Second-generation, non-sedating H1-receptor antihistamines represent the mainstay of therapy for both acute and chronic urticaria. Angioedema can occur in the absence of urticaria, with angiotensin-converting enzyme (ACE) inhibitor-induced angioedema and idiopathic angioedema being the more common causes. Rarer causes are hereditary angioedema (HAE) or acquired angioedema (AAE). Although the angioedema associated with these disorders is often self-limited, laryngeal involvement can lead to fatal asphyxiation in some cases. The management of HAE and AAE involves both prophylactic strategies to prevent attacks of angioedema (i.e., trigger avoidance, attenuated androgens, tranexamic acid, and plasma-derived C1 inhibitor replacement therapy) as well as pharmacological interventions for the treatment of acute attacks (i.e., C1 inhibitor replacement therapy, ecallantide and icatibant). In this article, the authors review the causes, diagnosis and management of urticaria (with or without angioedema) as well as the work-up and management of isolated angioedema, which vary considerably from that of angioedema that occurs in the presence of urticaria.
doi:10.1186/1710-1492-7-S1-S9
PMCID: PMC3245442  PMID: 22165855
12.  Assessment of epicutaneous testing of a monovalent Influenza A (H1N1) 2009 vaccine in egg allergic patients 
Background
H1N1 is responsible for the first influenza pandemic in 41 years. In the fall of 2009, an H1N1 vaccine became available in Canada with the hopes of reducing the overall effect of the pandemic. The purpose of this study was to assess the safety of administering 2 different doses of a monovalent split virus 2009 H1N1 vaccine in egg allergic patients.
Methods
Patients were skin tested to the H1N1 vaccine in the outpatient paediatric and adult allergy and immunology clinics of the Health Sciences Centre and Children's Hospital of Winnipeg, Manitoba Canada. Individuals <9 years of age were administered 1.88 μg's of hem-agglutinin antigen per 0.25 ml dose and individuals ≥9 years were administered 3.75 μg's of hemagglutinin antigen per 0.5 ml dose. Upon determination of a negative skin test, the vaccine was administered with a 30 minute observation period.
Results
A total of 61 patients with egg allergy (history of an allergic reaction to egg with either positive skin test &/or specific IgE to egg >0.35 Ku/L) were referred to our allergy clinics for skin testing to the H1N1 vaccine. 2 patients were excluded, one did not have a skin prick test to the H1N1 vaccine (only vaccine administration) and the other passed an egg challenge during the study period. Ages ranged from 1 to 27 years (mean 5.6 years). There were 41(69.5%) males and 18(30.5%) females. All but one patient with a history of egg allergy, positive skin test to egg and/or elevated specific IgE level to egg had negative skin tests to the H1N1 vaccine. The 58 patients with negative skin testing to the H1N1 vaccine were administered the vaccine and observed for 30 minutes post vaccination with no adverse results. The patient with the positive skin test to the H1N1 vaccine was also administered the vaccine intramuscularly with no adverse results.
Conclusions
Despite concern regarding possible anaphylaxis to the H1N1 vaccine in egg allergic patients, in our case series 1/59(1.7%) patients with sensitization to egg were also sensitized to the H1N1 vaccine. Administration of the H1N1 vaccine in egg allergic patients with negative H1N1 skin tests and observation is safe. Administering the vaccine in a 1 or 2 dose protocol without skin testing is a reasonable alternative as per the CSACI guidelines.
doi:10.1186/1710-1492-7-3
PMCID: PMC3045365  PMID: 21314925
13.  2010 International consensus algorithm for the diagnosis, therapy and management of hereditary angioedema 
Background
We published the Canadian 2003 International Consensus Algorithm for the Diagnosis, Therapy, and Management of Hereditary Angioedema (HAE; C1 inhibitor [C1-INH] deficiency) and updated this as Hereditary angioedema: a current state-of-the-art review: Canadian Hungarian 2007 International Consensus Algorithm for the Diagnosis, Therapy, and Management of Hereditary Angioedema.
Objective
To update the International Consensus Algorithm for the Diagnosis, Therapy and Management of Hereditary Angioedema (circa 2010).
Methods
The Canadian Hereditary Angioedema Network (CHAEN)/Réseau Canadien d'angioédème héréditaire (RCAH) http://www.haecanada.com and cosponsors University of Calgary and the Canadian Society of Allergy and Clinical Immunology (with an unrestricted educational grant from CSL Behring) held our third Conference May 15th to 16th, 2010 in Toronto Canada to update our consensus approach. The Consensus document was reviewed at the meeting and then circulated for review.
Results
This manuscript is the 2010 International Consensus Algorithm for the Diagnosis, Therapy and Management of Hereditary Angioedema that resulted from that conference.
Conclusions
Consensus approach is only an interim guide to a complex disorder such as HAE and should be replaced as soon as possible with large phase III and IV clinical trials, meta analyses, and using data base registry validation of approaches including quality of life and cost benefit analyses, followed by large head-to-head clinical trials and then evidence-based guidelines and standards for HAE disease management.
doi:10.1186/1710-1492-6-24
PMCID: PMC2921362  PMID: 20667127
14.  AACI is now an open access journal 
It is our pleasure to welcome you to the new website of Allergy, Asthma & Clinical Immunology (AACI).
doi:10.1186/1710-1492-5-1
PMCID: PMC2776231
15.  Is Obesity Associated with an Increased Risk for Airway Hyperresponsiveness and Development of Asthma? 
We investigated the association between airway hyperresponsiveness (AHR) and obesity in adults referred for confirmation of asthma diagnosis. Data were analyzed for obesity class I (body mass index [BMI] 30-34.9 kg/m2), class II (BMI ≥ 35-39.9 kg/m2), and class III (BMI ≥ 40 kg/m2). Of 861 subjects, 401 demonstrated AHR; the mean dose of methacholine was 4.16 ± 2.55 mg/mL. A significant association between obesity and AHR was evident for all subjects: the odds ratio was 1.37 (95% CI 1.02-1.82; p = .0317). One unit of increased BMI (1 kg/m2) was associated with a 3.1% increase in AHR risk (95% CI 1.01-1.05, p < .005). The odds ratio increased from 1.86 (95% CI 1.27-1.76; p = .0012) for class I to 2.61 (95% CI 1.48-4.60; p = .0006) for class III. Obesity was found to be associated with AHR and appears to be a risk factor for asthma.
doi:10.1186/1710-1492-4-2-51
PMCID: PMC2868882  PMID: 20525125
airway hyperresponsiveness; asthma; obesity

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