Toothpaste instead of allergy shots? Oral mucosal immunotherapy (OMIT) for allergic rhinitis

Oral mucosal immunotherapy (OMIT) via a toothpaste has been in the works since 2012 but it is still not FDA-approved as of 2019. The toothpaste base is called Allerdent (R). Most insurances do not pay for oral mucosal immunotherapy (OMIT) as of 2019 (see below). The cost is approximately $400 for 3 months. The recommended duration of treatment is 3 years. Several allergens can be mixed together.

Dr. William Reisacher, ENT, an associate professor of otolaryngology at Weill Cornell, is a co-founder and chief medical officer of Allovate, the company takes makes the Allerdent (R) oral mucosal immunotherapy (OMIT) toothpaste. In the video below he shows how to mix the allergens in the toothpaste base and load the dispenser:

In 2016, Dr. Reisacher published a review of alternative routes to allow IT: intralymphatic immunotherapy (ILIT), epicutaneous immunotherapy (EPIT), local nasal immunotherapy (LNIT), oral immunotherapy (OIT), and oral mucosal immunotherapy (OMIT) (

From BC/BS website info:

The following allergy treatments are not covered because they are considered investigational including, but not limited to:

1) Provocative and neutralization therapy for food allergies, by sublingual, intradermal, and subcutaneous routes. Provocative and neutralization therapy involves administering neutralizing doses rather than standard doses of allergens either under the tongue or into the skin;
2) Sublingual immunotherapy (SLIT) except for the following FDA approved products: Oralair®, Grastek®, Ragwitek®, and Odactra.
3) Urine autoinjections (autogenous urine immunization) - (a substance from the urine is injected into the skin);
4) Repository emulsion therapy;
5) Low dose immunotherapy also known as the "Rinkel" technique;
6) Enzyme-Potentiated Desensitization;
7) Acupuncture for allergies;
8) Homeopathy for allergies;
9) Rhinophototherapy.
10). Oral mucosal immunotherapy, including Allerdent® compounded toothpaste.

Subcutaneous immunotherapy performed in the home setting is considered investigational.

Allergy sufferers find relief in immunotherapy toothpaste - Fox News:

Related reading:

In 2017, Pediatric Allergy Solutions (“PAS”) and Allovate Therapeutics (“Allovate®”) announced that they have signed an exclusive agreement to combine PAS’s fingerstick allergy test and Allovate’s Allerdent®, a patented toothpaste-based system for the delivery of allergy immunotherapy to enable primary care physicians to offer personalized allergy care:

PPD-free hair dyes: Alternative hair dyes for patients allergic to para-phenylenediamine (PPD)

Para-phenylenediamine is an azo dye, most commonly used in permanent hair dyes as a black dye. It is also used in black rubbers, photographic developers, fabric dyes, epoxy resin curing agents, oils and greases, and gasoline. Potential cross-reactions include preservatives of the paraben family, para-aminobenzoic acid, sulfonamides (including diuretics and diabetes agents), and benzoic acid ester group anesthetics. Even if the hair product is "PPD free", other phenylenediamine variants may cause reactions.

Pure, uncontaminated Lawsonia inermis (henna tree) should not cause reactions in PPD-allergic patients and may be a reasonable alternative as a hair dye. Pure henna is an extremely rare cause of allergic contact dermatitis (ACD).

The vast majority of reactions to hair-dye products are caused by para-phenylenediamine (PPD). As of 2019, PPD has been used in most permanent, demipermanent, and semipermanent hair-dye products. PPD was the contact allergen of the year in 2006.

Some manufacturers produce permanent and demipermanent dyes using para-toluenediamine sulfate (PTDS) instead of PPD (see below), 57% of patients allergic to PPD will tolerate hair dyes based on PTDS.

Practical recommendations for 3 patch tests:

1. TRUE patch test. Test for PPD with TRUE patch test.

2. Hair dye series patch test. If contact allergy to PPD is confirmed: test with a complete hair dye series. If that series is unavailable, at least do a patch test for PTDS. Patients who are allergic to PPD but test negative for allergy to PTDS will very likely tolerate the PPD-free hair-dyes based on PTDS.

3. Specific hair dye patch test. Although patients who are patch test negative to PTDS will likely tolerate the PTDS-based hair-dyes, the recommendation is to do a patch-test for any proposed PTDS-based hair dye. If the test is negative, then use the product.

In patients allergic to hair dye: do not use a hair dye without a patch test.  

Alternative to PPD-hair dyes

PPD-Free Hair Dyes Based on PTDS:

- Wella Koleston Perfect (permanent), Wella Color Charm (demipermanent) - The Wella Corporation, Richimond, VA

- Schwarzkopf Igora Royal (permanent) - Schwarzkopf & Dep, Rancho Dominguez, CA

- Goldwell Color Chic (permanent), Goldwell ReShade for Men (demipermanent)

- Sanotint Light (demipermanent) - Sanotint, Cosval Arese, Italy, PSS, Iinthicum Heights, MD

- L'Oréal Paris Excellence To-Go 10-Minute Cre`me Colorant (demipermanent) - IL'Oreal USA Inc, Clark, NJ

Pure henna is an alternative hair dye. Uncontaminated Lawsonia inermis (henna tree) is an extremely rare cause of allergic contact dermatitis (ACD).

PPD cross-reactions

In PPD-allergic patients, cross-reactions may occur with other chemicals such blue disperse clothing dyes. Cross-reactions have also been reported to para-aminobenzoic acid-containing sunscreens and topical sulfonamides.

Hair dye-induced allergic contact dermatitis (click here to enlarge the image).

UpToDate, 2019.

Xylitol nasal spray (XLEAR) and irrigation for treatment of chronic rhinitis and sinusitis

Xylitol nasal spray (XLEAR) is commercially available OTC for treatment of rhinitis:

However, most of the published studies focused on xylitol nasal irrigation rather than nasal spray. The studies with small with 20 to 50 patients each and the results were mixed. The references are below.

As of year 2019, xylitol nasal spray (XLEAR) and irrigation are not the standard of treatment for chronic rhinitis and sinusitis.


PubMed search:

Can Microbes Protect from Asthma? Twitter summary from the 2019 WSAAI meeting

Donata Vercelli spoke on "Can Microbes Protect from Asthma? Studies with Amish & Hutterite Gut Microbiota".

Asthma & allergy are to a large extent environmental diseases that can be treated but not cured.

Erika von Mitius showed a "farm effect" in Alpine Europe, where exposure to cows, hay and unpasteurized milk lead to protection from allergies and asthma. Since then we have been asking and answering why this occurs with relations to genetics, specific farm exposures, and what other components of the farm environments are responsible for protection.

Recent NEJM article addressed two genetic similar populations from a specific region in Europe who settled in different areas of the US - the Amish and Hutterites. Their origins are only 800 km apart in Europe. But while they are very similar in origins (genetics), diet, religion, etc., their farming is very different. Amish non-mechanized single-family farms. Hutterites: large, industrial farming. So for asthma and allergic sensitization Amish are 3-4x lower than Hutterites. While there are differences in cell types (eosinophils, neutrophils, etc) there are no major difference in T regulatory cells.

Asthma protection requires innate immunity. Inflammation appears to generate a neutrophilic response as opposed to eosinophilic responses. This appears to depend on type of exposures and suggests that microbiome plays a strong relationship with risk of childhood asthma.

Gene expression patterns in PBLs of Amish and Hutterite children differ especially in innate immune pathways. Endotoxin much higher in Amish homes, a proxy for microbial load in these homes:

Dust collectors suggested inhalation of Amish, but not Hutterite, dust extract is sufficient to block allergen-induced airway hyperreactivity and eosinophilia in mice- important because even this dust was enough to create this phenotype. Found asthma protection in “Amish mice” requires innate immunity, most notably in MyD88-TRif.

Farm effect involved environmental microbiome:

This relationship of the risk of asthma and the gut microbiome happens very early:

Amish but not Hutterite fecal microbiota are sufficient to suppress allergen-induced AHR and OVA-specific IgE. Profiles of BAL eosinophilia in germ-free mice associated with Amish fecal microbiota showed regulatory eosinophils with regulatory transcription signatures (Prg3) in Amish mice (inflammatory eos in Hutterites).

What is happening between gut and environment? May be "pioneer taxa" are transferred from mother to infant, then the pioneers create a micro-environment for beneficial microbiota to come from the environment (dust) during the 1st year of life.

Dr. Lozupone talked on gut microbiome and how it affects health and inflammation:

Gut microbes affect your health by competitively excluding pathogens, metabolically transforming your diet and drugs, and modulating your immune system. Excellent summary!

Factors that influence microbiome: age, diet, location. Early microbe exposures influence allergy and asthma likely from epigenetic changes. Different approaches using microbiome therapeutics - transplant ecosystem, prebiotics, probiotics.

Dr. Laidlaw mentioned that they have good success with single day protocols.

Commensal micro-derived butyrate induces differentiation of colonic regulatory T Cells, driving the colon away from inflammation.

Age is associated with the most pronounced differences in the gut microbiome.

This is a Twitter summary from the 2019 WSAAI meeting. This summary was compiled from the tweets posted by Matthew Bowdish @MatthewBowdish and Ray Firszt @RayFirszt, who attended the 2019 Western Society of Allergy, Asthma and Immunology (WSAAI) meeting. The tweets were labeled #WSAAI. The text was edited by me.

What have we learned from aspirin desensitization in AERD? Twitter summary from the 2019 WSAAI meeting

Katherine Woessner presented on "What have we learned from aspirin desensitization in AERD: How can the methods be improved."

AERD is chronic eosinophilic (Type 2) inflammation of sinuses +/- the lungs with sensitivity to all COX-1 inhibiting NSAIDS with age of onset in 3rd or 4th decade. No obvious genetic signature that is associated with AERD.

AERD always has chronic sinus disease but not always with asthma, although it usually develops 1-5 years after onset of rhinitis. Asthma is not necessary to make dx of AERD. It needs CRS and NSAID sensitivity.

Known baseline abnormalities in AERD - decreased PGE2 is main one:

“All you need to know about AERD” in one slide:

Diagnosing AERD is difficult. History can be problematic. Small amounts of aspirin can often be tolerated, sometimes small amounts of alcohol can augment symptoms. Only way to diagnose AERD is with ASA/NSAID challenge.

83% of AERD patients will react to alcohol (nasal congestion, even wheeze). Patients with AERD appear to be sensitive to all alcohol. Mechanism is unclear.

Reactions to oral Aspirin Challenge:

Addition of a Leukotriene Receptor Antagonist (LTRA) does not change the outcome of oral aspirin desensitizations.

Treatment of AERD:

1. Avoid COX-1 inhibitor NSAIDs
2. Highly-selective COX-2 inhibitors and Acetaminophen are generally well-tolerated
3. ASA Desens if needed

Q: Who should get ASA Desens?

A: Pts with recurrent chronic sinusitis/polyps, all AERD pts except those well-controlled on ICS, ICS/LABA & LTMDs, those who require antiplatelet therapy w/ASA or other COX-1 inhibitors.

Optimization of ASA Desensitization: FEV1 over 60% (or 1.5 L).

Try to increase FEV1 at baseline. If unable, it may be OK to start since patients might have irreversible airway obstruction.

ASA Desensitization Protocol:

Safety of ASA Desensitization:

- Scripps have done more than 1400 challenges with only 3 systemic reactions (all responded to 1 Epi)
-Average time to reaction is 102 minutes
-Typical provoking dose is 45-100 mg ASA

Safety of asa desensitization: note expedited protocols don’t seem to be safe. Reactions can be severe. Need another blocking drug before single day desensitizations:

Cross desensitization to other NSAIDS occurs. However, you can only use ASA for desensitization purposes.

Nasal congestion improves immediately during asa desensitization. However, airway irritability remains unchanged.

Aspirin Dosing after ASA Desensitization:

-81mg ok for cardiovascular diz prevention
-325mg ok to be cross-desensitized to any doses of all NSAIDs
-650mg BID initial starting dose for AERD; about 50% can decrease to 325 mg BID after 1-6 months

Biologics targeting TH2 inflammation seem to be effective in AERD. Biologics like omalizumab and others (anti-IL5, anti-IL4/13) may have a role in AERD but there have not been big enough studies to show that it works or helps in polyps or ASA challenges, some studies are ongoing as we speak.

“In an ideal world, it would be great to have a clinical test to confirm AERD other than desensitization.”

Salicylates are not COX inhibitors and have no effect in AERD. There is some evidence that low salicylate diet might be helpful.

Bits of Wisdom from the front lines of ASA Desensitization:

This is a Twitter summary from the 2019 WSAAI meeting. This summary was compiled from the tweets posted by Matthew Bowdish @MatthewBowdish and Ray Firszt @RayFirszt, who attended the 2019 Western Society of Allergy, Asthma and Immunology (WSAAI) meeting. The tweets were labeled #WSAAI. The text was edited by me.

Drug allergy management in 5 steps (click to enlarge the image).

Bacteriotherapy of eczema: host microbe interactions in pathogenesis of atopic dermatitis - Twitter summary from the 2019 WSAAI meeting

Richard Gallo presented on "Host Microbe Interactions in the pathogenesis of atopic dermatitis."

The size of the skin surface area for microbiota interface is 25 square meters when your take into account the hair follicles. Not only the general size of the hair follicle surface area, but there are also nerve fibers and blood vessels in the hair follicle:

The immune system exerts pressure for beneficial interactions but driving microbiota towards commensalism and mutualism and away from competition, amensalism and predation/parasitism. Skin produces antimicrobial peptides (AMPs) that are essential for defense of the skin. AMPS in host control of microbial growth:

Another way the skin protects is Reactive Adipogenesis, where AMPs produced by fat cells causes expansion of adipose layer in response to local infections with S aureus. Evidently GI surgeons have used this phenom to find areas of colitis for a century. When they open patients up, they look for the area of the bowel wrapped in more fat..

Pathophysiology of Atopic Dermatitis involves deficiency of AMP. Patients with AD have deficiencies in AMP that lead to susceptibility to Staph aureus. S. aureus seems to trigger AD also. They are both interdependent on each other. Moisturizers improve barrier repair which leads to a decrease in IL4, while increasing AMP. Blocking IL4 reduces Staph. aureus colonization and correlates with improved disease.

Atopic dermatitis promotes Staph aureus but does Staph aureus cause Atopic Dermatitis? In a couple of recent studies, it's been shown that S aureus preceded development of atopic dermatitis - JACI 2017 139(1):166 and J Invest Dermatol 2017 137(12):2497.

Topical and systemic antibiotics are not effective in atopic dermatitis. Antibiotics did not kill Staph. aureus. Antibiotics only worked if impetigo was present clinically. Bleach baths don’t seem to be more effective than regular baths. Bacteria do not seem to be changed by adding bleach.

Plausible molecular explanations for causal association between S aureus and atopic dermatitis:

How can we treat atopic dermatitis related to Staph. aureus without use of antibiotics which seem to be ineffective?

Applying topical bacteriotherapy in a small trial completely eliminated Staph. aureus - this is an exciting application of skin microbiome. There were no adverse events from topical application of microbiome therapy. Effective anti Staph. aureus agent. Microbiome transcriptome diversity improved with the application. Skin inflammation improved only after 1 week of application.

This is a Twitter summary from the 2019 WSAAI meeting. This summary was compiled from the tweets posted by Matthew Bowdish @MatthewBowdish and Ray Firszt @RayFirszt, who attended the 2019 Western Society of Allergy, Asthma and Immunology (WSAAI) meeting. The tweets were labeled #WSAAI. The text was edited by me.

Atopic dermatitis maintenance (click to enlarge the image).

Immunotherapy Basics - COLA Video Lectures by Jay Portnoy, MD (held in 2012)

Immunotherapy Basics - COLA Video Lectures by Jay Portnoy, MD:

Dr. Jay Portnoy reviews the basics of allergen immunotherapy (allergy shots) starting with its history and the extracts used to administer it. Held on August 13, 2012:

Dr. Jay Portnoy describes the process for writing a prescription for allergen immunotherapy (allergy shots). Held on August 13, 2012:

HAE with normal C1 inhibitor (HAE-nl-C1INH) - Twitter summary from the 2019 WSAAI meeting

Dr Zuraw talked about HAE with normal C1 inhibitor.

Women are more commonly affected by HAE with normal C1 than men. HAE with normal C1 can skip generations unlike normal HAE, mainly because it has low penetrance.

UCSD only has two families with Factor XII in their registry, showing just how rare that is. Impact of Factor XII on HAE-nl-C1INH:

HAE classification is getting more complicated - 4 types of HAE-nl-C1INH, and counting:

Current classification of Angioedema:

You cannot separate HAW-nl-C1INH from non-histaminergic bradykinin angioedema except by family history +/- genes.

Clinical findings that help distinguish between HAE and HAE-nl-C1INH:

Differentiating HAE normal and deficient C1 inh - note facial swelling:

Current treatment approach for HAE-nl-c1INH:

Treatment for HAE n C1inh: progestin and TXA are effective. C1inh can help during active attacks in HAE n C1inh because of deficiency that occurs during angioedema. C1inh cannot be used for prophylaxis. Lanadelumab is a monoclonal Ab against kallikrein. It should work in HAE w normal C1inh.

Phase 2 trial: Factor XIIa monoclonal ab - CSL312. It should work since kallikrein activation goes through factor XII.

Biomarker development for angioedema: measuring kallikrein activity can distinguish between histaminergic and non histaminergic angioedema. 93% PPV and 86% NPV. Patient can’t be on treatment for 1 week prior to test.

Biomarkers for HAE using kallikrein activity:

This is a Twitter summary from the 2019 WSAAI meeting. This summary was compiled from the tweets posted by Matthew Bowdish @MatthewBowdish and Ray Firszt @RayFirszt, who attended the 2019 Western Society of Allergy, Asthma and Immunology (WSAAI) meeting. The tweets were labeled #WSAAI. The text was edited by me.

Different causes of bradykinin-related angioedema. Click here to enlarge the image.

What’s new in food allergy? Twitter summary from the 2019 WSAAI meeting

Dr. Sicherer discussed important papers from the JACI-In Practice on food allergies and anaphylaxis. March 2019 issue will be food allergy centric.

Food allergy themed issue 2018:

Wasserman et al on Real World Experience with Peanut OIT:

Goals of families doing OIT - 62% wanted to reduce risk of fatal reaction, most thought the risk of death was 1:1,000 to 1:10,000, when data actually suggests risk is 1 in 325,000 over 10 years. An increased threshold from 100 mg to 300 mg peanut in OIT reduces the risk of a reaction by 95%.

Survey for undergoing OIT - motivations include reduce risk of fatal reaction, reduce hassle of avoidance, decrease risks of reaction. This was greater than desire to incorporate foods into diet. QOL: improved after completion of OIT. Low dose OFC to 1.5 mg of peanut likely would allow patients to not worry about precautionary labeling.

Avoidance of peanut precautionary labeling carries individual burdens and costs ($182M per death prevented) - Shaker and Greenhawt.

Baked Potpourri:

Baked milk challenges: passing occurs in pts who are younger, with lower IgE. About 70% pass. SPT was not reflective of outcome. If sIGE to milk is less than 8, patients are more likely to pass. They can have serious reactions, more respiratory reactions. Egg allergy leads to more GI reactions.

Dupixent may lead to passing OFCs to foods that were previously not tolerated. Dupilumab and Food Allergy:

Any food allergy is a risk factor for asthma with a relative risk of 1.7 to 2.9 depending on specifics.

If you get anaphylactic reactions after VIT, rule out a mast cell disorder, including full workup, beyond just tryptase. Need for lifelong treatment of VIT. Study of 19 patients with severe sting reaction post stopping Venom IT, 18 had clonal mast cell disease, 8 had normal tryptase. Contrary to popular belief, you can get an increase in tryptase during food anaphylaxis, but it's usually 25% rise from baseline rather than over the cut-off of 11ng/ml.

Tryptase and food anaphylaxis: tryptase rose above baseline in 60% of pts. Median rise of 25%. Rise related to severity. Peak is at 2 hrs.

Beta blockers do not seem to block Epi effects in anaphylaxis.

EIA: omega 5 gliadin IgE testing can be helpful in diagnosis. It’s the best predictor of reactivity. You can do an exercise challenges with the suspecting food. You can also do a higher dose food challenge at rest. Cofactors can be exercise and alcohol. sIgE to wheat can be negative.

EoE is prevalent in milk allergic patients. 40% had EoE. 30% were asymptomatic. Risk of EoE in Cow's Milk Allergy:

EoE: lots of comorbidities: allergies, immune disorders. EoE Potpourri:

EoE: it is rare to outgrow food sensitivity triggering EoE. It occurred only in 9/1,812 patients. EoE was linked to OAS and it improved after removing raw birch-related foods, some patients developed IgE allergies after avoiding foods for EoE. It’s complicated!

Antihistamine allergies: case report to Benadryl, rare event!! But possible. Two papers of allergy/anaphylaxis to antihistamines. It's a rare but it can occur.

There are no detectable food proteins in any common childhood vaccines.

Fructose induced anaphylaxis reported after drinking Coca Cola. Super rare.

FPIES to peanut - there are growing cases with the early introduction following the LEAP study.

There are reported cases of delayed anaphylaxis to shellfish.

Sometimes you need to duplicate SPT, since there can be significant variability, especially when making clinically important decisions.

Milk allergic patients: if they’re severe, 10% can also be allergic to beef and lamb. Especially with undercooked beef. You can do OFCs with well cooked beef. They likely should avoid undercooked meat.

Studies suggest that 26-41% of those with cold-induced urticaria experience systemic reactions, consider epinephrine auto-injector.


Mastering Food Allergy Diagnosis

Scott Sicherer presented on "Mastering Food Allergy Diagnosis".

Recommended Food Allergy Testing: history, physical exam, skin prick test, allergen specific serum IgE, elimination diet, oral food challenge. Have to get a good history before ordering tests, don't test foods that are clearly tolerated.

Not recommended food allergy testing: atopy patch test, intradermal test, "combination of tests," unproven tests (IgG, kinesiology, VEGA, etc).

IgE levels in isolation are difficult to interpret. For example, wheat sIGE tends to run high, even sometimes higher than 100, in patients that tolerate wheat, while cashew sIgE tends to run low and you might be worried about low positive levels. 5% of patients with peanut allergies cross react to legumes. Cow milk allergy cross reacts with goat milk in 92%.

What are the challenges to food allergy diagnosis: chronic symptoms, multiple possible triggers, definite outcomes needed, masqueraders (eg Frey's Syndrome), imperfect tests. Dr Sicherer presented a case of Blepharochalasis masquerading as food allergy.

Frey's Syndrome is a rare neurological disorder (fewer than 20,000 cases in US) that may result from injury or surgery near the parotid glands (which manufacture saliva), damaging the facial nerve. Sx: Sweating and flushing of a patch of skin near the ear that occurs when someone is eating.

Different pathophysiologies for different adverse food reactions:’

Epidemiology - Child with peanut allergy who has not eaten tree nuts has a 35% risk of tree nut allergy.

Epidemiology - Sibling of child with peanut allergy who has not eaten peanut has 7% risk of peanut allergy.

Child who has atopic derm has 35% risk of having a food involved if eczema is moderate to severe.

10% of patients with milk allergy are also allergic to beef, especially if undercooked.

Sesame seeds don’t have a lot of protein. Sesame allergic patients can tolerate sesame seeds and still be allergic to sesame, so be careful.

Predictive values but must be taken with grain of salt (at arrow):

Component testing with risk:

Asamoj JACI 2012 130(2):469-72. Shows isolated Ara h8 patients - 144 Swedish pts, 143 passed OFC, 10% had oral symptoms even to cooked peanut but no systemic rxn.

Those with egg IgE less than 2kU/l likely to do well with baked egg challenge. Those with egg sIgE higher than 10kU/L not likely to do well with baked egg challenge. Those with milk IgE less than 5kU/l likely to do well with baked milk challenge. Those with milk sIgE higher than 35 kU/L not likely to do well with baked milk challenge.

Future food allergy diagnostics and prognostics: Basophil activation, ratios (specific IgE to total IgE), epitopes, more components, calculators, DNA methylation patterns.

Food specific IgE to Total IgE: has a predictive calculator for outgrowing egg and milk allergy.

This is a Twitter summary from the 2019 WSAAI meeting. This summary was compiled from the tweets posted by Matthew Bowdish @MatthewBowdish and Ray Firszt @RayFirszt, who attended the 2019 Western Society of Allergy, Asthma and Immunology (WSAAI) meeting. The tweets were labeled #WSAAI. The text was edited by me.

Adverse Food Reactions (click to enlarge the image).

What’s New in Asthma and Drug Allergy? Twitter summary from the 2019 WSAAI meeting

Michael Schatz discussed Asthma and Drug Allergy in this year's JACI-In Practice.

92% of patients with difficult to control asthma had at least one medical comorbidity. What were those comorbidities? Obesity, anxiety/depression, GERD, cardiovascular disease. Asthma: 90% of pts with severe asthma have at least one comorbidity, 70% have more than 2. Many co-morbidities are bi-directional, ie if you treat one, you get improvement in the other and vice versa.

Non pharma management of asthma: exercise - high intensity, diet - high protein/low glycemic diet - you need both to improve asthma control.

Step down RX for asthma who are well controlled for 3 months: stopping LABA was associated with greater decline in lung function and more hospitalizations, maybe we need longer than 3 months of control.

Pts who cough and failed ICS/LABA combo inhaler improved with Spiriva. Likely through modulating cough reflex sensitivity, despite no difference in FEV1.

Only 22% of large group of health care providers used asthma inhalers correctly (JACI-IP 2018;6:987). Most common specific errors of healthcare professionals with not using their inhalers correctly:

Check our JACI-IP 2018;6:1246 for interesting article on skin testing for suspected iodinated contrast media hypersensitivity.

For contrast reactions: consider SPT :prick undiluted, ID 1:10 dilution - not irritating. Pretreatment for contrast reactions does not appear to be helpful. Approach to RCM reactions:

Controversies in beta-lactam allergy covered in JACI-IP:

1. Role of skin testing vs direct challenge
2. Length of challenge (single dose vs multiple day)
3. Cephalosporin cross-reactivity with PCN and other cephalosporins

Optimal length of penicillin challenge is unclear. 5 days seems reasonable to rule out delayed non severe reactions.

Current Kaiser San Diego approach:

Cross-Reactions between PCN and Cephalosporins mainly related to side-chain similarity JACI-IP 2018;6:1662 - Avoid aminocephalosporins in PCN allergic pts?

This is a Twitter summary from the 2019 WSAAI meeting. This summary was compiled from the tweets posted by Matthew Bowdish @MatthewBowdish and Ray Firszt @RayFirszt, who attended the 2019 Western Society of Allergy, Asthma and Immunology (WSAAI) meeting. The tweets were labeled #WSAAI. The text was edited by me.

Drug allergy management in 5 steps (click to enlarge the image).