Allergy & Immunology
Expert discussions on allergic conditions, immunodeficiencies, drug hypersensitivity, and immunotherapy approaches.
Recent Discussions
Which patient factors drive you to pursue patch testing in the workup of chronic hand eczema?
Seasonal hand eczema occurring only during the cold season is usually irritant and best addressed by minimizing hand washing and using cotton under occlusive gloves with frequents changes for wet work. Careful examination for signs of psoriasis and anti-synthetase syndrome is important. Next step is...
Where in the current treatment algorithm for CHE do you feel delgocitinib best fits?
Given the cost of delgocitinib, I have difficulty justifying it unless there has been an inadequate response to high-potency topical steroids and calcineurin inhibitors. I expect there to be significant improvement with these, and consider an inadequate response to be the inability to decrease to a ...
How often do you rely on using the C1 inhibitor functional assay versus the quantitative level alone to diagnose HAE?
We have seen a significant increase in lab costs billed to well-insured patients for some of the more "esoteric", detailed testing associated with immune/inflammatory disorders such as HAE. The cheapest screen is a C4 level, which, if normal during an active angioedema episode, makes C1 inhibitor de...
What literature do you recommend for reviewing lymphocyte panels for the workup of immunodeficiency?
The literature I would recommend is the following: Bonilla et al., PMID 26371839 Bousfiha et al., PMID 36198931 Tangye et al., PMID 35748970 Puck et al., PMID 33551023
Do patients with low C4 and known hereditary angioedema need an immunodeficiency/complement deficiency evaluation even if there is no infection history?
In most cases of HAE, the C4 is depressed and not absent, and the CH50 would be normal. For this reason, the complement pathway can still generate C3a, C5a, and induce cell lysis.
How do you approach performing a food challenge in a patient with CSU who is dependent on their H1 blockers?
We will perform food challenges for patients with CSU using 2 approaches depending on the patient and clinical history. Stop H1 blocker and start prednisone at the same time, continue until the day of the oral challenge, use that as a bridge to block the hives, do the challenge, then resume H1 block...
When should we suspect ‘climate-amplified’ rhinitis/asthma versus poor control from other causes?
Before labeling rhinitis or asthma as “climate-amplified,” we must first exclude common causes of poor control: adherence issues, suboptimal controller dosing, inhaler technique, indoor allergen exposure, occupational triggers, and comorbidities (GERD, CRS, OSA, obesity). These remain far more commo...
Can autoimmune thyroiditis present with recurrent angioedema and bronchospasm?
There is an association between angioedema and autoimmune thyroid disease, although the incidence is not known. Activated CD4+ T lymphocytes, monocytes, and eosinophils. The incidence of thyroid autoimmunity in chronic urticaria is similar to the background population, but there is a cluster of angi...
Should a patient with breakthrough urticaria, on maximal dosing of second generation H1 antihistamines with elevated CRP and anti-TPO antibodies, be treated with omalizumab to protect the thyroid from autoantibodies and improve urticaria control?
This patient likely has chronic autoimmune (Type IIB) urticaria. Would obtain a CU index. It is likely based on data that OMA would be less effective at the currently approved doses. There is data that increasing the dose or frequency of administration of OMA may be effective in those patients with ...
Does MCAS cause early closure of growth plates?
I am not aware of or encountered this complication in my mastocytosis patients some of whom also have mast cell activation episodes.