Linda Zhu
Clinical Assistant Professor, Medicine - Pulmonary, Allergy & Critical Care Medicine
Clinical Focus
- Allergy and Immunology
Academic Appointments
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Clinical Assistant Professor, Medicine - Pulmonary, Allergy & Critical Care Medicine
Professional Education
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Residency: University of Chicago Hospitals Internal Medicine Residency (2017) IL
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Board Certification: American Board of Allergy and Immunology, Allergy and Immunology (2021)
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Fellowship: Stanford University Allergy and Immunology Fellowship (2021) CA
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Board Certification: American Board of Internal Medicine, Internal Medicine (2017)
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Internship: University of California Davis (2015) CA
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Medical Education: Case Western Reserve School of Medicine (2014) OH
All Publications
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Referral Patterns and Uptake of Penicillin Delabeling in Pregnancy
MOSBY-ELSEVIER. 2024: AB164
View details for Web of Science ID 001267526000508
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Asian American Patients With Allergic Diseases: Considerations for Research and Clinical Care.
The journal of allergy and clinical immunology. In practice
2022; 10 (4): 950-952
View details for DOI 10.1016/j.jaip.2022.01.031
View details for PubMedID 35397816
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Road Less Traveled: Drug Hypersensitivity to Fluoroquinolones, Vancomycin, Tetracyclines, and Macrolides.
Clinical reviews in allergy & immunology
1800
Abstract
While fluoroquinolones, vancomycin, macrolides, and tetracyclines are generally safe antibiotics, they can induce both immediate and delayed hypersensitivity reactions (HSRs). Historically, less has been published on allergies to these antibiotics compared to beta lactams, but the prevalence of non-beta lactam HSRs is increasing. To fluoroquinolones, immediate HSRs are more common than delayed reactions. Both IgE and non-IgE mechanisms, such as the mast cell receptor Mas-related G protein-coupled receptor X2 (MRGPRX2), have been implicated in fluoroquinolone-induced anaphylaxis. Skin testing for fluoroquinolones is controversial, and the gold standard for diagnosis is a graded dose challenge. To vancomycin, the most common reaction is vancomycin infusion reaction (previously called "red man syndrome"), which is caused by infusion rate-dependent direct mast cell degranulation. Severity can range from flushing and pruritis to angioedema, bronchospasm, and hypotension that mimic type I HSRs. MRGPRX2 has been implicated in vancomycin infusion reactions. IgE-mediated HSRs to vancomycin are rare. Vancomycin skin testing yields high false positive rates. Thus, direct provocation challenge with slower infusion rate and/or antihistamine pre-treatment is preferred if symptoms are mild to moderate, and desensitization can be considered if symptoms are severe. To tetracyclines, non-IgE-mediated and delayed HSRs predominate with cutaneous reactions being the most common. There is no standardized skin testing for tetracyclines, and avoidance is generally recommended after a severe reaction because of the paucity of data for testing. Graded dose challenges and desensitizations can be considered for alternative or index tetracyclines if there are no alternatives. With macrolides, urticaria/angioedema is the most common immediate HSR, and rash is the most common delayed HSR. The predictive value for skin testing to macrolides is similarly poorly defined. In general, HSRs to fluroquinolones, vancomycin, macrolides, and tetracyclines are challenging to diagnose given the lack of validated skin testing and in vitro testing. Direct provocation challenge remains the gold standard for diagnosis, but the benefits of confirming an allergy may not outweigh the risk of a severe reaction. Skin testing, direct provocation challenge, and/or desensitization to the index non-beta lactam antibiotic or alternatives in its class may be reasonable approaches depending on the clinical context and patient preferences.
View details for DOI 10.1007/s12016-021-08919-5
View details for PubMedID 35092578
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Elexacaftor/Tezacaftor/Ivacaftor Outpatient Desensitization.
Annals of allergy, asthma & immunology : official publication of the American College of Allergy, Asthma, & Immunology
2021
View details for DOI 10.1016/j.anai.2021.08.010
View details for PubMedID 34391901
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Electronic Medication Monitoring vs. Self-Reported Use of Inhaled Corticosteroids and Short Acting Beta2 Agonists in Adult Patients with Uncontrolled Asthma
MOSBY-ELSEVIER. 2020: AB59
View details for Web of Science ID 000517092700180
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A Randomized Controlled Trial of Electronic Medication Monitoring (EMM), Patient Mobile App and Health Care Provider Feedback compared to EMM alone on Inhaled Corticosteroids (ICS) and Short Acting Beta2 Agonists (SABA) Utilization and Asthma Control in Adult Patients with Uncontrolled Asthma
MOSBY-ELSEVIER. 2020: AB58
View details for Web of Science ID 000517092700178
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Potential new targets for drug development in severe asthma
WORLD ALLERGY ORGANIZATION JOURNAL
2018; 11: 30
Abstract
In recent years there has been increasing recognition of varying asthma phenotypes that impact treatment response. This has led to the development of biological therapies targeting specific immune cells and cytokines in the inflammatory cascade. Currently, there are two primary asthma phenotypes, Type 2 hi and Type 2 lo, which are defined by eosinophilic and neutrophilic/pauci- granulocytic pattern of inflammation respectively. Most biologics focus on Type 2 hi asthma, including all four biologics approved for treatment of uncontrolled asthma in the United States - omalizumab, mepolizumab, reslizumab, and benralizumab. Potential new targets for drug development are being investigated, such as IL-13, IL-4α receptor, CRTH2, TSLP, IL-25, IL-13, IL-17A receptor, and CXCR2/IL-8. This review will discuss the role of these molecules on the inflammatory response in uncontrolled asthma and the emerging biologics that address them. Through the delineation of distinct immunological mechanisms in severe asthma, targeted biologics are promising new therapies that have the potential to improve asthma control and quality of life.
View details for DOI 10.1186/s40413-018-0208-1
View details for Web of Science ID 000448509900001
View details for PubMedID 30386455
View details for PubMedCentralID PMC6203275