Karen S Tuano MD Neha Seth MD Javier Chinen MD PhD Ann Allergy Asthma Immunol November 20211276617626 Secondary Immunodeficiencies Key Messages Secondary immunodeficiencies may be defined as an impairment of the immune response resulting from conditions or factors extrinsic to the i ID: 935755
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Slide1
Slide2Secondary Immunodeficiencies
Karen S. Tuano, MD
Neha Seth, MD
Javier Chinen, MD, PhD
Ann Allergy Asthma Immunol. November 2021;127(6):617-626
Slide3Secondary Immunodeficiencies
Key Messages
Secondary immunodeficiencies may be defined as an impairment of the immune response resulting from conditions or factors extrinsic to the immune system.
Secondary immunodeficiencies are more frequently diagnosed than primary immunodeficiencies.
The immune response depends on the integrity of other systems, such as the skin and the gastrointestinal system.Immunodeficiency can occur as a consequence of malnutrition, metabolic disorders, use of immunosuppressive medications, chronic infections, malignancies, and severe trauma.The neonate and the elderly may have decreased immune responses relative to healthy adults.Optimal management of the secondary immunodeficiencies focuses on the improvement of the primary condition and their manifestations and provides recommendations to reduce the risk of infections.
Tuano, et al. Ann Allergy Asthma Immunol. November 2021;127(6):617-626
Slide4Secondary Immunodeficiencies
Tuano, et al. Ann Allergy Asthma Immunol. November 2021;127(6):617-626
Slide5Basic Principles of the Management of Secondary Immunodeficiencies
Tuano, et al. Ann Allergy Asthma Immunol. November 2021;127(6):617-626
Slide6Strategies for Choosing a Biologic for Your Patient with Allergy or Asthma
Tara Saco, MD
Israel C. Ugalde, DO
Juan Carlos Cardet, MD
Thomas B. Casale, MD
Ann Allergy Asthma Immunol. November
2021;127(6):627-637
Slide7Strategies for Choosing a Biologic for Your Patient with Allergy or Asthma
Key Messages
Approved biologics for the treatment of asthma include omalizumab, mepolizumab,
reslizumab
, benralizumab, and dupilumab. Possible future therapies include tezepelumab and astegolimab.The only currently approved biologic for urticaria is omalizumab. Possible future therapies include ligelizumab, dupilumab, lirentelimab
, mepolizumab,
benralizumab
,
tezepelumab
, and
Celldex
.
Approved biologics for nasal polyps include dupilumab, omalizumab, and mepolizumab.
Benralizumab
is a possible future therapy.
The only currently approved biologic for atopic dermatitis is dupilumab. Possible future therapies include interleukin (IL)-13 blockers,
tezepelumab
,
fezakinumab, and nemolizumab.
There are currently no biologics which the Food and Drug Administration approved for the treatment of food allergy. Possible future therapies include omalizumab,
ligelizumab
, dupilumab, and
etokimab
.
There are currently no biologics approved by the Food and Drug Administration for the treatment of eosinophilic esophagitis. Possible future therapies include dupilumab,
lirentelimab
, mepolizumab,
reslizumab
,
benralizumab
, IL-13–blocking agents, anti–IL-15 agents, and anti–tumor necrosis factor alpha agents.
Saco, et al. Ann Allergy Asthma Immunol. November 2021;127(6):627-637
Slide8Cellular and Molecular Targets for Biologics Used
in the Treatment of Allergic Diseases
Saco, et al. Ann Allergy Asthma Immunol. November 2021;127(6):627-637
Slide9Clinical Relevance of Inherited Genetic Differences
in Human Tryptases
Sarah C. Glover, DO
Melody C. Carter, MD
Peter Korošec, PhD
Patrizia Bonadonna, MD
Lawrence B. Schwartz, MD, PhD
Joshua D. Milner, MD
George H. Caughey, MD
Dean D. Metcalfe, MD
Jonathan J. Lyons, MD
Ann Allergy Asthma Immunol. November 2021;127(6
):638-647
Slide10Clinical Relevance of Inherited Genetic Differences
in Human Tryptases
Key Messages
Alpha- and beta-tryptases exhibit variability in copy number with the number of
α-tryptase–encoding gene copies ranging from 0 to many; this is likely owing in part to their recent evolution, making them essentially unique to human mast cells.Hereditary α-tryptasemia (HαT) is a common autosomal dominant genetic trait caused by increased TPSAB1 copy number–encoding α-tryptase and is the cause for a significant majority (approximately 90%) of individuals with elevated basal serum tryptase in the general population.
Increased α-
tryptase–encoding copy number resulting in H
α
T is associated with formation of mature
α/β-
tryptase
heterotetramers
that have unique biological functions and may contribute to associated symptoms.
H
α
T modifies clonal and nonclonal mast cell–associated disorders, increasing the prevalence or severity of systemic hypersensitivity reactions and mast cell mediator-associated symptoms.
H
α
T is associated with other multisystem complaints that require validation in future studies, though up to two-thirds of carriers may have few symptoms.
Given the clinical evidence that not only increased
α-
tryptase–encoding copy number modifies certain clinical phenotypes and/or reactions but also a relative increase in active
β-
tryptase copies may affect different clinical presentations, we envision increased use of tryptase genotyping in evaluation and risk stratification of patients and in clinical trial design in the future.
Glover, et al. Ann Allergy Asthma Immunol. November 2021;127(6):638-647
Slide11Reported Tryptase Haplotypes and Genotypes in Healthy Individuals
and in those with H
α
T
Glover, et al. Ann Allergy Asthma Immunol. November 2021;127(6):638-647
Slide12Putative effects of mature tryptases in H
α
T
Glover, et al. Ann Allergy Asthma Immunol. November 2021;127(6):638-647