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Immunoglobulin E Associated Respiratory Diseases: Part 2 FOCUSED REVIEW Immunoglobulin E associated respiratory diseases: Part 2 Amr Ismail MD, Kenneth C. Iwuji MD, James A. Tarbox MD ABSTRACT Multiple pulmonary pathologies have been associated with elevated levels of Immunoglobulin E (IgE). Since its discovery in 1966, its role in multiple diseases has become clearer. This has allowed for the emergence of new medications that target IgE. In this review, we will summarize some of the most common pulmonary pathologies in which IgE has a role in their etiology. Keywords: Immunoglobulin E, asthma, allergic rhinitis, acute eosinophilic pneumonia, chronic eosinophilic pneumonia, parasitic lung infection, allergic bronchopulmonary aspergillosis INTRODUCTION these effects by its dual interactions with specific anti- gens and two receptors, FcεRI and CD23, present Immunoglobulin E (IgE) is one of the five human on effector cells, most notably mast cells, basophils, immunoglobulins: IgG, IgA, IgM, IgD, and IgE. It is pro- eosinophils, and monocytes. duced by B-cells after they undergo isotype switching In this review♦, we will summarize some of the to produce IgE instead of the default IgM. This is usu- most common pulmonary pathologies in which IgE ally achieved by DNA recombination events within the has a role in their etiology (Table 1). immunoglobulin heavy chain locus. B-cells produced in the bone marrow produce heavy chains for both IgM and IgD. Later in the B-cell life cycle, after stimu- ASTHMA lation by specific cytokines and T-cell interaction, the B-cell undergoes class-switch recombination and can Asthma, according to the National Asthma produce different immunoglobulin classes, including Education and Prevention Program, is defined as a IgE.1 chronic inflammatory disorder of the airways in which many cells and cellular elements have a role; these The role of IgE in humans is not fully understood. include mast cells, eosinophils, neutrophils (especially It is the least abundant isotype in the serum and has in sudden onset, fatal exacerbations, occupational the shortest serum half-life (~2 days) among human asthma, and patients who smoke), T lymphocytes, 2 immunoglobulin types. It has an obvious role in macrophages, and epithelial cells. In susceptible indi- defense against parasitic infections and inactivation viduals, this inflammation causes recurrent episodes of certain venoms. It also has a major role in the pro- of wheezing, breathlessness, chest tightness, and cess of immune regulation and, therefore, is involved coughing, particularly at night or in the early morn- 1 in the pathogenesis of allergic disease. IgE exerts ing. These episodes are associated with widespread Corresponding author: Amr Ismail Contact Information: [email protected] ♦ Part 1 of this review was published in July 2019 in DOI: 10.12746/swrccc.v7i31.593 The Southwest Respiratory and Critical Care Chronicles 2019;7(31):29–35. 34 The Southwest Respiratory and Critical Care Chronicles 2019;7(31):34–43 Immunoglobulin E Associated Respiratory Diseases: Part 2 Ismail et al. Table 1. Summary of IgE related pulmonary conditions Disease Characteristics Diagnosis Treatment Asthma Chronic inflammatory Suggestive history and SABA are used for mild symptoms disorder of the airways symptoms Inhaled corticosteroids and LABA Episodic wheezing, chest Reduced FEV1 and are added for maintenance therapy tightness, SOB, and cough reduced FEV1/FVC Other medications: leukotriene Airflow limitation is the Reversibility is positive receptor antagonists, long-acting hallmark of the disease when FEV1 (or FVC) muscarinic receptor antagonists, increase ≥12% or >200 ml and biologics (anti-IgE, anti-IL-5, after bronchodilator anti-IL-5Rα, and anti-IL-4α) Allergen immunotherapy is used when a strong association with allergens exists Allergic rhinitis Chronic inflammatory Chronicity, seasonality, Mild/episodic symptoms are disorder of the nasal mucosa and pattern of symptoms treated with second-generation suggest diagnosis antihistamines Associated with rhinosinusitis, allergic Pale, boggy nasal Moderate/severe symptoms conjunctivitis, and asthma turbinates; nasal crease; are treated with intranasal allergic shiners corticosteroids Congestion, rhinorrhea, sneezing, itching, upper Combination sprays (intranasal airway obstruction, and corticosteroids with nasal watery eyes are common antihistamines) and short courses of oral steroids for severe cases and/or nasal polyps Allergen immunotherapy is used when a strong association with allergens exists Acute eosinophilic Idiopathic, hypothesized Inspiratory crackles and Responds well to corticosteroids pneumonia to be a hypersensitivity possible wheezes IV methylprednisolone 125 mg reaction Peripheral eosinophilia not every 6 hours for initial dose Temporal relation with common Switch to oral prednisone of exposure to different CXR: bilateral opacities 40–60 mg daily once symptoms allergens/irritants, especially of alveolar, interstitial, or improve tobacco smoke mixed pattern Taper over 2–6 weeks Fever, dyspnea, and cough >25% eosinophils on BAL Respiratory distress can or eosinophilic pneumonia be present and progress to on lung biopsy respiratory failure Absence of other causes of pulmonary eosinophilia The Southwest Respiratory and Critical Care Chronicles 2019;7(31):34–43 35 Ismail et al. Immunoglobulin E Associated Respiratory Diseases: Part 2 Table 1. Summary of IgE related pulmonary conditions (Continued) Disease Characteristics Diagnosis Treatment Chronic Insidious course Wheezes/crackles present High dose corticosteroids eosinophilic for more than 2 weeks 0.5 mg/kg/day continued for Eosinophilic infiltration pneumonia 2 weeks after resolution of leads to tissue damage Alveolar eosinophilia symptoms and radiologic findings 40% on BAL; blood Not associated with ≥ eosinophilia 1000/ l Taper steroids to the lowest effective environmental exposures ≥ µ dose to control the symptoms CXR: Predominantly Productive cough, weight peripheral pulmonary High rate of relapse loss, fever, night sweats, and infiltrates dyspnea Occasional need of long term Absence of other causes of steroids pulmonary eosinophilia Steroid-sparing drugs: anti-IgE and anti-IL-5 monoclonal antibodies Parasitic lung Hydatid cystic lung disease, Travel history and exam are Hydatid cysts may require surgical infections Amoebiasis, Ascariasis, paramount resection and albendazole and Schistosomiasis cause CXR and CT are helpful Amoebiasis is treated with parasitic lung infections tinidazole or metronidazole for Amoebiasis: stool positive Stimulate a TH2 response: trophozoites, then paromomycin for for trophozoites and eosinophilia, IL-4, IL-5, IL- intestinal cysts serum positive for parasite 13, and antigen-specific IgE specific antibodies Surgical treatment may be needed in pleuropulmonary disease Allergic Hypersensitivity reaction to Supported by clinical Long-term corticosteroids: bronchopulmonary Aspergillus fumigatus picture, radiological prednisolone 0.5–1 mg/kg/day for aspergillosis findings, and immunologic 2 weeks, then 0.5 mg/kg every other Commonly seen in cystic findings day for 6–8 weeks, then a slow taper fibrosis and asthma over 3–5 months Peripheral eosinophilia, Recurrent cough, wheezing, elevated total IgE ( 1000 Itraconazole 200 mg twice daily for pleuritic chest pain, > IU/mL), and Aspergillus 16 weeks dyspnea, blood tinged specific IgE sputum, and brown mucus Omalizumab may be used as a plugs Positive Aspergillus steroid sparing drug or adjunct intradermal skin testing in patients who fail to respond to steroids CXR: parenchymal infiltrates and bronchiectasis usually in upper lobes, better defined by HRCT 36 The Southwest Respiratory and Critical Care Chronicles 2019;7(31):34–43 Immunoglobulin E Associated Respiratory Diseases: Part 2 Ismail et al. but variable airflow obstruction that is often reversible ordered. These tests should show a reduced FEV1 either spontaneously or with treatment. The inflam- and reduced FEV1/FVC in patients with asthma, mation also causes an increase in bronchial hyper- which suggests obstruction. Reversibility is present responsiveness to a variety of stimuli. Reversibility of when FEV1 (or FVC) increases by ≥12% or >200 ml airflow limitation may be incomplete in some patients. after bronchodilator administration. The presence of Asthma was reported to affect 22 million people in the a consistent history and symptoms, obstructive PFTs, US in 2007.3 and the exclusion of other possible diagnoses are generally adequate to make a diagnosis of asthma.3 Airflow limitation is the hallmark of asthma. It is When patients present with symptoms strongly sug- usually caused by airway hyperresponsiveness, gesting asthma but have normal PFTs, provocation which is an exaggerated response to stimuli leading tests using methacholine, histamine, or exercise can to bronchoconstriction. This can be allergen induced be done. Further workup could include skin testing to when antigen specific IgE crosslinks on the surface evaluate for environmental triggers of asthma.3 of mast cells and releases mediators (e.g., histamine, prostaglandins, leukotrienes, and tryptase) resulting After the diagnosis is made, asthma severity in airway smooth muscle contraction. Patients with should be assessed by checking symptom sever- high levels of IgE are more likely to have asthma ity, effect on daily activities, nighttime awakenings, than those with normal IgE levels; however, there impact on quality of life, and lung function with PFTs.3 is no absolute cutoff for IgE levels in patients with Treatment
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