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Book: Allergy and Asthma – The Basics to Best Practices


Editors Massoud Mahmoudi (Editor-in-Chief), Timothy Craig, Dennis K. Ledford


Allergy is a unique area of medicine that is not taught as a single subject in medical or allied health schools. Therefore learning the fundamentals of this distinctive area of medicine requires gathering information from various disciplines. This is because the allergic diseases affect various organ systems and the practice of a wide range of physicians such as Ear, Nose, and Throat (ENT) specialists, pulmonologists, gastroenterologists, dermatologists, and ophthalmologists, among others; all encounter patients with such problems. As knowledge in this area of medicine grows, clinicians and trainees need a resource to learn the basics as well as intermediate and advanced concepts and strategies. This title is intended to serve as a single comprehensive reference covering all needed knowledge of allergic diseases.

The authors of this work will be comprised of some of the foremost experts in the field, coming primarily from the United States. They will cover their topics using a structured, consistent format from chapter to chapter to provide continuity and uniformity to the work. This reference will not only provide basic knowledge on diagnosing and treating allergies, but will go beyond the basics and also emphasize using a systematic approach to working up and treating a patient. Ample numbers of tables and illustrations for better visualization of the complicated areas will be provided in each chapter. Discussion about trends, current research, and future research directions for each disorder will be incorporated as warranted. Summary sections will be used. Following initial publication, new information to the existing chapters, or entirely new chapters, will be added as necessary via continuous updating.

The audience for this reference work includes physicians and residents in allergy and immunology, pulmonology, ENT, gastroenterology, dermatology, ophthalmology and other specialties; physician assistants, nursing professionals, allergy fellows (in-training), primary care providers, and allied health personnel are also part of the audience. Medical students will also find the work of value, as will researchers in a range of areas especially immunology and food science.

Table of contents

Acute and Chronic Urticaria

William J. Lavery, Jonathan A. Bernstein

Allergic Contact Dermatitis

John Havens Cary, Howard I. Maibach

Allergic Ocular Diseases

Satoshi Yoshida

Allergic Rhinitis

Niharika Rath, Salman Aljubran

Allergy from Ants and Biting Insects

Karla E. Adams, John F. Freiler, Theodore M. Freeman, Dennis Ledford

Allergy Skin Testing

Vivian Wang, Fonda Jiang, Anita Kallepalli, Joseph Yusin

Anaphylaxis and Systemic Allergic Reactions

Jocelyn Celestin

Aspirin or Nonsteroidal Drug-Exacerbated Respiratory Disease (AERD or NERD)

Mario A. Sánchez-Borges

Asthma in Athletes

John D. Brannan, John M. Weiler

Asthma in Pregnancy

Devi Kanti Banerjee

Atopic Dermatitis

Neeti Bhardwaj

Biologic and Emerging Therapies for Allergic Disease

Christina G. Kwong, Jeffrey R. Stokes

Bronchodilator Therapy for Asthma

Joseph D. Spahn, Ryan Israelsen

Chemotherapy and Biologic Drug Allergy

Schuman Tam

Chronic Rhinosinusitis and Nasal Polyposis

Leslie C. Grammer

Cough and Allergic Diseases

Helen Wang, Zachary Marshall, Nicholas Rider, David B. Corry

Drug Allergy and Adverse Drug Reactions

Faoud T. Ishmael, Ronaldo Paolo Panganiban, Simin Zhang

Eosinophilic Esophagitis

Gisoo Ghaffari

Epidemiology of Allergic Diseases

Rayna J. Doll, Nancy I. Joseph, David McGarry, Devi Jhaveri, Theodore Sher, Robert Hostoffer

Hereditary Angioedema

Saumya Maru, Timothy Craig

IgE Food Allergy

Sebastian Sylvestre, Doerthe Adriana Andreae

Inhaled Corticosteroid Therapy for Asthma

Jennifer Padden Elliott, Nicole Sossong, Deborah Gentile, Kacie M. Kidd, Christina E. Conte, Jonathan D. Skoner et al.

Latex Allergy

Massoud Mahmoudi

Non-IgE Food Immunological Diseases

Brian Patrick Peppers, Robert Hostoffer, Theodore Sher

Occupational Asthma

Justin Greiwe, Jonathan A. Bernstein

Penicillin Allergy and Other Antibiotics

Thanai Pongdee, James T. Li

Primary and Secondary Environmental Control Measures for Allergic Diseases

Wilfredo Cosme-Blanco, Yanira Arce-Ayala, Iona Malinow, Sylvette Nazario

Pulmonary Function, Biomarkers, and Bronchoprovocation Testing

Mark F. Sands, Faoud T. Ishmael, Elizabeth M. Daniel

Subcutaneous Immunotherapy for Allergic Rhinitis and Asthma

Chen Hsing Lin

Keywords: allergic diseases allergy allergy diagnosis allergy treatment immunology

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Case Report: A Successful Opioid-Free Anesthetic in a Patient Undergoing Cardiac Surgery


Journal of Cardiothoracic and Vascular Anesthesia, Available online 28 November 2018

Elizabeth LandryMD, Stacey Burns MD, Marc P. Pelletier MD, Jochen Daniel Muehlschlegel MDMMSc


The negative side effects of opioids have been well documented, and as our nation faces an opioid addiction crisis, the morbidity and mortality associated with opioids continues to rise dramatically. However, the majority of anesthesiologists are continuing to administer high doses of opioids to patients undergoing both non-cardiac and cardiac surgery. Opioid-free anesthesia (OFA) is a technique in which non-opioid multimodal analgesics are used to provide adequate pain control both during surgery and postoperatively. While there are several studies that demonstrate the effectiveness of OFA in patients undergoing non-cardiac surgery, it has not been studied in patients undergoing cardiac surgery. The authors present a case of successful implementation of an OFA regimen in a patient with opioid-induced mastocytosis undergoing an open aortic valve replacement (AVR).


Opioids Opioid-free anesthesia Cardiac surgery

Published by Elsevier Inc.

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Rethinking of the concepts: Migraine is an autoimmune disease?


Neurology, Psychiatry and Brain Research, Volume 31, February 2019, Pages 20-26

Murugesan Arumugam, Sunil K. Narayan


• Exact etiology of migraine uncertain, none of the hitherto postulated mechanisms sufficiently explain the pathogenesis of migraine.

• Recent studies have suggested that immunological dysfunction or autoimmunity could play an integral role in the pathophysiology of migraine.

• Our recent experiments showed decreased CD4+CD25+ cell population in peripheral blood of migraineurs compared to the healthy volunteers.

• One clinical trial has illustrated that immunotherapy would significantly decrease the headache frequency in migraine patients.

• First time in literature, this review advocate s immunological dysfunction could be a powerful mechanism setting off migraine.


Background: For more than a century, scientists have investigated the pathophysiology of migraine and debated on various mechanisms of pathogenesis, ranging from the vascular theory to cortical spreading depression. For some time now, there has been a debate on the role of autoimmunity in migraine pathophysiology.

Objective: Our earlier clinical studies had revealed intriguingly but convincingly that migraine patients had reduced regulatory T cells in peripheral blood, which is a strong evidence for autoimmunity. Therefore we wished to look for further evidences available literature to probe deeper into this postulate.

Methods: We searched pubmed, Embase, Scopus and web of science for further support /refute this postulate. This is not a metaanalysis or systematic review but an exploration for evidence to substantiate a novel hypothesis.

Results: Very recently, Nurkhametova et al, have suggested that immunological dysfunction and/or autoimmunity could play a role in the pathophysiology of migraine. Migraine like headaches are also common in several dyscollagenoses. There is also a comorbid association of migraine with atopic disorders incriminating an exaggerated immune response in migraine pathophysiology. Martin and his co-workers have illustrated through elegant studies that immunotherapy would significantly decrease the headache frequency in migraine patients. Further, migraine has been reported to affect women more commonly than men, especially in the young, which is consistent with its association with oestrogens, a hormone which enhances the humoral immunity in the body.

Conclusion: From these compelling evidences, authors further advocate that immunological dysfunction and/or autoimmunity is a plausible pathophysiology in migraine.

 Keywords

Migraine pathophysiology Migraine aetiology Autoimmunity Regulatory T cells Migraine prevalence Adaptive immunity

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Persistent fatigue induced by interferon-alpha: a novel, inflammation-based, proxy model of Chronic Fatigue Syndrome


Russell, Alice, Hepgul, Nilay, Nikkheslat, Naghmeh, Borsini, Alessandra, Zajkowska, Zuzanna, Moll, Natalie, Forton, Daniel, Agarwal, Kosh, Chalder, Trudie, Mondelli, Valeria, Hotopf, Matthew, Cleare, Anthony, Murphy, Gabrielle, Foster, Graham, Wong, Terry, Schütze, Gregor A, Schwartz, Markus J, Harrison, Neil, Zunszain, Patricia A and Pariate, Carmine M (Brighton and Sussex Medical School, Sackler Centre for Consciousness Science)

Psychoneuroendocrinology. ISSN 0306-4530 (Accepted). 29 Nov 2018


The role of immune or infective triggers in the pathogenesis of Chronic Fatigue Syndrome (CFS) is not yet fully understood. Barriers to obtaining immune measures at baseline (i.e., before the trigger) in CFS and post-infective fatigue model cohorts have prevented the study of pre-existing immune dysfunction and subsequent immune changes in response to the trigger.

This study presents interferon-alpha (IFN-α)-induced persistent fatigue as a model of CFS. IFN-α, which is used in the treatment of chronic Hepatitis C Virus (HCV) infection, induces a persistent fatigue in some individuals, which does not abate post-treatment, that is, once there is no longer immune activation. This model allows for the assessment of patients before and during exposure to the immune trigger, and afterwards when the original trigger is no longer present.

Fifty-five patients undergoing IFN-α treatment for chronic HCV were assessed at baseline, during the 6-12 months of IFN-α treatment, and at six-months post-treatment. Measures of fatigue, cytokines and kynurenine pathway metabolites were obtained. Fifty-four CFS patients and 57 healthy volunteers completed the same measures at a one-off assessment, which were compared with post-treatment follow-up measures from the HCV patients.

Eighteen patients undergoing IFN-α treatment (33%) were subsequently defined as having ‘persistent fatigue’ (the proposed model for CFS), if their levels of fatigue were higher six-months post-treatment than at baseline; the other 67% were considered ‘resolved fatigue’. Patients who went on to develop persistent fatigue experienced a greater increase in fatigue symptoms over the first four weeks of IFN-α, compared with patients who did not (Δ Treatment Week (TW)-0 vs. TW4; PF: 7.1±1.5 vs. RF: 4.0±0.8, p = 0.046). Moreover, there was a trend towards increased baseline interleukin (IL)-6, and significantly higher baseline IL-10 levels, as well as higher levels of these cytokines in response to IFN-α treatment, alongside concurrent increases in fatigue. Levels increased to more than double those of the other patients by Treatment Week (TW)4 (p = 0.011 for IL-6 and p = 0.001 for IL-10). There was no evidence of an association between persistent fatigue and peripheral inflammation six-months post-treatment, nor did we observe peripheral inflammation in the CFS cohort. While there were changes in kynurenine metabolites in response to IFN-α, there was no association with persistent fatigue. CFS patients had lower levels of the ratio of kynurenine to tryptophan and 3-hydroxykynurenine than controls.

Future studies are needed to elucidate the mechanisms behind the initial exaggerated response of the immune system in those who go on to experience persistent fatigue even if the immune trigger is no longer present, and the change from acute to chronic fatigue in the absence of continued peripheral immune activation.

Keywords: Chronic Fatigue Syndrome; inflammation; fatigue; cytokines; kynurenine; tryptophan

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The new tool “KIT” in advanced systemic mastocytosis


ASH Education Book November 30, 2018 vol. 2018 no. 1 127-136

William Shomali and Jason Gotlib (Divisions of Hematology and Medical Oncology, Stanford University School of Medicine/Stanford Cancer Institute, Stanford, CA)


Mastocytosis is a rare disease characterized by KIT-driven expansion and accumulation of neoplastic mast cells in various tissues. Although mediator symptoms related to mast cell activation can impose a symptom burden in cutaneous disease and across the spectrum of systemic mastocytosis subtypes, the presence of an associated hematologic neoplasm and/or organ damage denotes advanced disease and the potential for increased morbidity and mortality. In addition to the revised 2016 World Health Organization classification of mastocytosis, a new diagnostic and treatment toolkit, tethered to enhanced molecular characterization and monitoring, is poised to transform the management of patients with advanced systemic mastocytosis (advSM). Although the efficacy of midostaurin and novel selective KIT D816V inhibitors, such as avapritinib (BLU-285), have validated KIT as a therapeutic target, the clinical and biologic heterogeneity of advSM requires that we reimagine the blueprint for tackling these diseases and use tools that move beyond KIT-centric approaches.

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Chondroitin sulfate inhibits secretion of TNF and CXCL8 from human mast cells stimulated by IL-33


Biofactors. 2018 Dec 6. doi: 10.1002/biof.1464. [Epub ahead of print]

Gross AR, Theoharides TC (Tufts University School of Medicine and Tufts Medical Center, Boston, MA, USA)


Glycosaminoglycans (GAGs) are linear, highly negatively charged carbohydrate chains present in connective tissues. Chondroitin sulfate (CS) and heparin (Hep) are also found in the numerous secretory granules of mast cells (MC), tissue immune cells involved in allergic and inflammatory reactions. CS and Hep may inhibit secretion of histamine from rat connective tissue MC, but their effect on human MC remains unknown. Human LAD2 MC were pre-incubated with CS, Hep, or dermatan sulfate (DS) before being stimulated by either the peptide substance P (SP, 2 μM) or the cytokine IL-33 (10 ng/mL). Preincubation with CS had no effect on MC degranulation stimulated by SP, but inhibited TNF (60%) and CXCL8 (45%) secretion from LAD2 cells stimulated by IL-33. Fluorescein-conjugated CS (CS-F) was internalized by LAD2 cells only at 37 °C, but not 4 °C, indicating it occurred by endocytosis. DS and Hep inhibited IL-33-stimulated secretion of TNF and CXCL8 to a similar extent as CS. None of the GAGs tested inhibited IL-33-stimulated gene expression of either TNF or CXCL8. There was no effect of CS on ionomycin-stimulated calcium influx. There was also no effect of CS on surface expression of the IL-33 receptor, ST2. Neutralization of the hyaluronan receptor CD44 did not affect the internalization of CS-F. The findings in this article show that CS inhibits secretion of TNF and CXCL8 from human cultured MC stimulated by IL-33. CS could be formulated for systemic or topical treatment of allergic or inflammatory diseases, such as atopic dermatitis, cutaneous mastocytosis, and psoriasis.

© 2018 BioFactors, 2018.

KEYWORDS: CXCL8; TNF; chondroitin sulfate; glycosaminoglycans; inflammation; mast cells

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Anaphylactic shock with methylprednisolone, Kounis syndrome and hypersensitivity to corticosteroids: a clinical paradox


Nicholas G. Kounis, Ioanna Koniari, George D. Soufras and Emmanouil Chourdakis

Italian Journal of Pediatrics 2018 44:143. https://doi.org/10.1186/s13052-018-0579-5. Published: 28 November 2018


Corticosteroids are widely used for the treatment of allergic reactions but paradoxically themselves may induce acute, delayed, local or systemic allergic reactions and even anaphylaxis with Kounis syndrome. They can suppress the release of arachidonic acid from mast cell membranes, via phospholipase A2 and eicosanoid biosynthesis inhibition. Corticosteroids can promote cell apoptosis and mediate in annexin or lipocortin synthesis, substances that modulate inflammatory cell activation, adhesion molecule expression, transmigratory and phagocytic functions. Antigen-antibody reaction, hapten formation, and medication contaminants are some of the incriminated causes. Patients with atopic diathesis are particularly vulnerable. Complete and thorough previous history of drug reactions or allergies is necessary before administration of any particular medication including corticosteroids.

© The Author(s). 2018

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