Medical Journal Review
WAO Reviews – Editors' Choice
Articles are selected for their importance to clinicians who care for patients with asthma and allergic and immunologic diseases by WAO Reviews Editors Juan Carlos Ivancevich, MD, and John J. Oppenheimer, MD, FACAAI, FAAAAI.
NSAID-exacerbated respiratory disease: a population study
Andersén H, Ilmarinen P, Honkamäki J et al
ERJ Open Research 2022; 8(1):00462-2021 (24 Jan)
In this study, Andersén et al attempt to determine the prevalence of NSAID-exacerbated respiratory disease (N-ERD) as well as identify factors associated with N-ERD, by performing a cross-sectional questionnaire survey of a random adult population of 16 000 subjects aged 20–69 years in Helsinki and Western Finland. The response rate was 51.5 % and they found a prevalence of 1.4% for N-ERD, and 0.7% for aspirin-exacerbated respiratory disease (AERD). Furthermore, the prevalence of N-ERD was 6.9% among subjects with asthma and 2.7% among subjects with rhinitis. Risk factors for N-ERD were older age, family history of asthma or allergic rhinitis, long-term smoking, and exposure to environmental pollutants. Subjects with N-ERD had a higher risk of respiratory symptoms, severe hypersensitivity reactions, and hospitalizations than asthmatic subjects without N-ERD.
Type 2 inflammation in eosinophilic esophagitis: From pathophysiology to therapeutic targets
Racca F, Pellegatta G, Cataldo G et al
Frontiers in Physiology 2022; 12:815842 (12 January)
While there is broad consensus regarding first-line therapy for eosinophilic esophagitis (EoE), a subset of patients are non-responders to standard therapy. The pathogenesis of EoE is multifactorial and results from the complex, still mostly undefined, interaction between genetics and intrinsic factors, environment, and antigenic stimuli. A deep understanding of the pathophysiology of this disease is pivotal for the development of new therapies. This comprehensive review explores the pathophysiology of EoE, starting from major pathogenic mechanisms (genetics, type 2 inflammation, epithelial barrier dysfunction, gastroesophageal reflux, allergens, infections, and microbiota) and subsequently focusing on the single protagonists of type 2 inflammation (involved cells, cytokines, soluble effectors, surface proteins, and transcription factors) that could represent present and future therapeutic targets.
The adverse reactions to vaccines practice parameter 10 years on – What have learned?
Annals of Allergy Asthma and Immunology 2022; In press (28 January)
This is a wonderful review that examines the evaluation and management of adverse reactions to vaccines. The author stresses that the risk of reactions to vaccination should be weighed against the risk of suffering a vaccine preventable disease if the vaccine is withheld. The literature demonstrates that there is no need to ask about egg allergy prior to the administration of influenza vaccines, including on screening forms. In most cases, an allergy to a vaccine constituent is not a contraindication to the vaccine containing it. Patients who have had possible anaphylactic reactions to vaccines should be evaluated by an allergist rather than simply being labeled allergic, because most can go on to receive subsequent doses. It is important to note that most immediate reactions to COVID-19 vaccines are not allergic, and care should be taken to not label such reactions as anaphylactic. Finally the role, if any, of polyethylene glycol (PEG) in these reactions has yet to be demonstrated.
Hypersensitivity to non-β-lactam antibiotics
Merk HF, Bickers DR
Allergologie select 2022; 6(1):11-17
This review is focused on recent findings regarding the pathogenesis of allergic reactions to non-β-lactam antibiotics. While most allergic reactions to antibiotics are caused by β-lactam antibiotics, non-β-lactam antibiotics are also capable of causing both immediate allergic reactions as well as late-type reactions to these drugs. This is especially true for fluoroquinolones and sulfonamides. Of these, the combination of sulfamethoxazole with trimethoprim (Cotrimoxazol, eg, Bactrim) is most important. However, there are certain types of reactions to non-β-lactam antibiotics that are not associated with β-lactam antibiotics. These include photosensitivity to sulfonamides, tetracyclines, and fluoroquinolones as well as different patterns of drug metabolism and associations with human leukocyte antigen (HLA) alleles that may influence their prevalence.
Good’s Syndrome: Time to move on from reviewing the past
Kabir A, Alizadehfar R, Tsoukas CM
Frontiers in Immunology 2022; 12:815710 (12 January)
In this review, the authors examine the current literature and identify research gaps regarding Good’s syndrome (GS). In order to resolve controversies and fill knowledge gaps, they propose a coordinated paradigm shift from incidence reporting to robust investigative studies, addressing mechanisms of disease, hoping this novel approach sets a clear direction to solve the current controversies. For seven decades, the pathophysiology of GS has remained a mystery, with few attempts to solve it. While initially described as an association between hypogammaglobulinemia and thymoma, controversy exists whether this is a subgroup of Common Variable Immune Deficiency (CVID) or a unique disease. Recently, some distinguishing aspects of both syndromes have come to light reflecting fundamental differences in their underlying pathophysiology. GS and CVID differ in demographic features and immune phenotype. GS is found almost exclusively in adults and is characterized by a significantly reduced or absence of peripheral B cells. In CVID, which also occurs in children, most patients have normal or slightly reduced peripheral B cells, with a distinguishing feature of low memory B cells. Similarly, differences in T cell dysregulation and manifestations of hematologic cytopenias may further distinguish GS from CVID. Knowledge of the clinical phenotype of this rare adult immune deficiency stems from individual case reports, retrospective, and cross-sectional data on a few cohorts with a limited number of well characterized patients. The authors note that understanding of pathophysiology in GS is hampered by the incomplete and inconsistent reporting of clinical and laboratory data, with a limited knowledge of its natural history.