What is the magic bullet of medical treatment? How about a biological that treats two or more diseases at one time? Dupilumab (Dupixent) is one such medication and I agree with Dr. Castro’s interpretation of the data on dupilumab–after all, he wrote the study. Here’s what I like about Dupixent:
Blocks 2 cytokines, both IL-4 and IL-13
Treats 3 different diseases: asthma, nasal polyps, and atopic dermatitis.
If you can’t get approved through your insurance, the company has a very good patient assistance program that makes Dupixent affordable for most patients.
Xolair, xolair, xolair. This biological has been around since my days back in Kansas. I have to admit, when Xolair was first released 20 years ago, I thought “who would use this type of medication?” Not only was I wrong, but Xolair has now set the standard for the use of monoclonal treatment of allergic disease, asthma, and urticaria. But I can’t compete with the video on Xolair….enjoy!
The last biological I mention is one that wasn’t the first on the scene, but has made it’s impression with a unique mechanism for getting rid of allergic inflammation: why not block the eosinophil IL-5 receptor directly? What do I like about Fasenra?
Gets rid of eosinophils quickly–you notice within several weeks many times when Fasenra makes you feel better.
After the first 3 doses, you only have to use Fasenra every OTHER month–pretty cool schedule compared to a daily inhaler.
Reduces both exacerbations of asthma AND the need for corticosteroids.
Ok..it’s time we learn the “why” of using spacers, because most patients don’t use them on a regular basis. Spacers do several things for your pocketbook and your asthma:
This spacer below can be purchased for < $10 on-line at Amazon. That’s almost better than a used toilet roll cardboard! Yes, we used to use and recommend I might add this “makeshift” spacer for patients because the others were too expensive.
Your asthma inhaler is much more effective when you use a spacer, because the aerosol is delivered deep into the lungs where you need it–in the small airways. Make sure you don’t use a spacer with dry powder –not needed here. For example, Advair has both dry powder and aerosol; the choice is yours, but no spacer for the dry powder.
If you’re using an aerosol or MDI, you may find that only 1 puff is needed–you save money with similar results, but check with your doctor first before making that kind of switch.
Now you know why we harp on you to use your spacer–saves money and better results.
Go out (or order from home) and get you one today! Leave me a note on how it works. Happy breathing–Dr. Wiens
Allergic bronchopulmonary aspergillosis is a pulmonary disorder caused by hypersensitivity to Aspergillus fumigatus, and rarely other Aspergillus species, and is characterized by chronic asthma, recurrent pulmonary infiltrates, and bronchiectasis.
An ABPA-like syndrome called allergic bronchopulmonary mycosis is indistinguishable from ABPA but is caused by other fungi.
The condition occurs almost exclusively in patients with cystic fibrosis (CF) or asthma.
The global prevalence of allergic bronchopulmonary aspergillosis is reported to be 2.5% (range 0.7%-3.5%) among adults with asthma and reported to be 2%-15% in patients with cystic fibrosis.
Suspect allergic bronchopulmonary aspergillosis (ABPA) in patients with asthma or cystic fibrosis who have symptoms consistent with ABPA, such as:
new or worsening cough
increased sputum production
expectoration of brown-black mucus plugs
ABPA may also be suspected in patients with computed tomography (CT) findings of bronchiectasis, especially central bronchiectasis.
Multiple sets of diagnostic criteria exist, all of which include a combination of clinical signs, imaging findings, and serologic features.
Rosenberg-Patterson diagnostic criteria for patients without cystic fibrosis (most commonly used):
major criteria for diagnosis (at least 6 required for diagnosis):
transient pulmonary opacities on imaging (fleeting shadows)
positive skin test for Aspergillus (type 1 immediate hypersensitivity)
peripheral blood eosinophilia (> 1,000 cells/mcL)
precipitating antibodies (immunoglobulin [Ig] G) against Aspergillus fumigatus in serum
elevated total IgE > 1,000 units/mL
central/peripheral bronchiectasis with normal tapering of distal bronchi
elevated A. fumigatus-specific IgG and IgE
Aspergillus in sputum
brownish black mucus plugs in expectorate
delayed type III skin reaction to Aspergillus
Cystic Fibrosis Foundation diagnostic criteria for patients with cystic fibrosis:
classic case (all criteria required):
acute or subacute clinical deterioration (cough, wheeze, exercise intolerance, increased sputum, decrease in pulmonary function, exercise-induced asthma) not attributable to other cause
serum total IgE > 1,000 units/mL (2,400 ng/mL) in patient not on corticosteroids
immediate skin reaction to Aspergillus (wheal > 3 mm diameter with erythema in patient not on antihistamines) or positive serum IgE antibody to A. fumigatus
precipitating antibodies to A. fumigatus or serum IgG antibody to A. fumigatus
recent or new infiltrates or mucus plugging on chest x-ray or bronchiectasis on chest computed tomography (CT) that does not clear with antibiotics or chest physiotherapy
minimal diagnostic criteria:
acute or subacute clinical deterioration not attributable to other cause
serum total IgE > 500 units/mL (1,200 ng/mL) (if disease suspected and serum total IgE is 200-500 units/mL, repeat testing in 1-3 months)
immediate skin reaction to Aspergillus or positive serum IgE antibody to A. fumigatus
1 of following:
precipitins to A. fumigatus or IgE antibody to A. fumigatus
recent or new infiltrates or mucus plugging on chest x-ray or bronchiectasis on chest CT that does not clear with antibiotics and standard chest physiotherapy
diagnosis of ABPA in cystic fibrosis should not be based in serology and skin tests only(2)
prevention or treatment of pulmonary exacerbations of allergic bronchopulmonary aspergillosis (ABPA)
reducing or remitting pulmonary inflammation
avoiding progression to end-stage fibrotic or cavitary disease
No large randomized trials have evaluated efficacy of various treatment options as of September 20, 2017.
Refer patients with suspected or known ABPA to a pulmonologist or an allergist-immunologist.
Systemic corticosteroids are considered the cornerstone of therapy for ABPA.
In patients with asthma:
typical initial therapy is prednisone 0.5 mg/kg/day (or equivalent) with tapering dose as symptoms improve
for patients with mild exacerbation – inhaled corticosteroids and bronchodilators may help control symptoms
for patients with acute exacerbation – prednisone 0.5-1 mg/kg/day for 1-2 weeks, then 0.5 mg/kg every other day for 6-12 weeks following remission, then tapering dose to preexacerbation dose
for patients with refractory disease with multiple asthmatic exacerbations – chronic corticosteroid therapy suggested, usually > 7.5 mg/day
dosing may be increased based on findings from routine monitoring of serum immunoglobulin E (IgE) levels, pulmonary function tests, and chest imaging, such as:
significant increase of IgE levels (such as doubling of baseline IgE level)
imaging evidence of infiltrates, mucoid impaction, fibrosis, worsening bronchiectasis, or worsening physiology
In patients with cystic fibrosis:
oral corticosteroids indicated for all patients except those with corticosteroid toxicity
typical initial dose prednisone (or equivalent) is 0.5-2 mg/kg/day orally to maximum 60 mg/day for 1-2 weeks, tapering to 0.5-2 mg/day every other day for 1-2 weeks with attempt to taper completely within 2-3 months
in patients with relapse, increase corticosteroid dose, add itraconazole, and taper corticosteroids when clinical status improves
fungi produce substances that contain pathogen-associated molecular patterns (pamps) and damage-associated molecular patterns (damps) which bind to pattern recognition receptors, stimulating innate immune responses in humans. they also produce allergens that induce production of specific ige. Areas covered: In this review we cover both innate and adaptive immune responses to fungi. Some fungal products can activate both innate and adaptive responses and in doing so, cause an intense and complex health effects. Methods of testing for fungal allergy and evidence for clinical treatment including environmental control are also discussed. In addition, we describe controversial issues including the role of Stachybotrys and mycotoxins in adverse health effects. Expert commentary: Concerns about long-term exposure to fungi have led some patients, attorneys and fungus advocates to promote fears about a condition that has been termed toxic mold syndrome. This syndrome is associated with vague symptoms and is believed to be due to exposure to mycotoxins, though this connection has not been proven. Ultimately, more precise methods are needed to measure both fungal exposure and the resulting health effects. Once that such methods become available, much of the speculation will be replaced by knowledge.
Yes, it’s true that foods go past your lips in order to be swallowed, but that may not have anything to do with food allergy or fixing your problem.
Let’s get it on with those not so strawberry lips….
Cheilitis is an acute or chronic inflammation of the lips, which may extend to include the vermilion border. Cheilitis may occur in isolation or associated with perioral involvement depending on the cause of the inflammation.
Patients with irritant or allergic cheilitis may present with dryness, scaliness and/or fissuring, with or without erythema or edema of the vermillion border.
Ask about common allergens, such as lipsticks, cosmetics, nail polishes, and oral hygiene products; and common irritants, such as wind or cold weather exposure, irritative topicals (lip cosmetics, antiseptics), repeated lip-licking behaviors, and musical instrument contact.
For allergic contact cheilitis, consider patch testing if the culprit allergen is not identified by history.
Angular cheilitis (also called perleche) may occur in young children or in adults with dentures or dental appliances. Erythema, scaling, fissuring, bleeding, or ulceration is seen at the angle (corner) of the lip, and may be unilateral or bilateral.
We’ve been so caught up with the #Coronavirus pandemic, that we’ve missed two important developments in the field of allergy:
The FDA has now approved the use of Palforzia for taking care of peanut allergy. Guess when this was released? January 2020, about one month prior to the outbreak of COVID-19; the affect on our practice and most other medical clinics across the country was predictable. Nothing happened except to try and avoid COVID-19 as long as possible. Hopefully, our efforts will pay off, but the viral pandemic isn’t over yet, even though the panic has appeared to lessen.
I won’t talk more about COVID-19 because many of us (including myself) are suffering from Corona fatigue and plenty of good information about COVID exists on YouTube channels such asMedCram and ZDogg. Be prepared to devote some time to listen to these experts, because they won’t give you just a brief summary. They drill down to the ever evolving truth about COVID-19. (definitely worth your time)
Back to the peanut story. #Palforzia is designed to give minute (very small) powder of peanut protein a little bit at a time so you don’t develop anaphylaxis with every ingestion. The company making this product spent large amounts of money to train professionals such as allergists with Zoom! conferences and field representatives to make sure we launched the program of desensitization without a hitch. Then came Coronavirus and knocked that one out of the park. So where does that leave us:
Palforzia or peanut desensitization still works and is available to those patients who make good candidates. And who wouldn’t be a good candidate?
Palforzia is associated with some risk and a consultation just to focus on this new treatment is required before starting the process. Can you believe, patients have to pass a certification as well?
For more information, call our office at 918-495-2636 to schedule a consultation for peanut desensitization.
In years past, everyone lived their life (or especially free time) outdoors because we live in Tulsa for the Spring & Fall, right? Well, this year, it was hard to live outside when you’re quarantined. Hopefully, you avoided exposure to the Coronavirus, but you also avoided exposure to the outdoor Spring allergens (good for you). What you’ll find when we relax the “stay-at-home” rules is more sneezing, runny nose, and typical allergy symptoms. Just a great case in point at how exposure really plays a significant role in your allergy symptoms. So don’t make fun of me when I tell you to cover your mattress and pillows with a substance that isolates the dust mites! Let’s review how allergies work, because a “pollen grain” and IgE look a lot like COVID-19. the video below is a pollen grain that attaches to IgE and the process of “allergy” begins. Notice that whatever process happens in the body occurs because a receptor (suction cup on the cell) binds to a virus or IgE. Every reaction (both good and bad) happens because of this union between body cells and external molecules. Listen to the video below to see how this actually works–and BTW, infection with COVID-19 works the same way.
So how do I tell if I’m having allergy or a nasty virus?
As is usual for me, I like to give you academic information on topics that I really want you to understand–don’t just take my word for it. Too many hits come up searching for “corona virus or allergy,” so I will make it simple and give you the best video to watch.
Patients with allergy are always sneezing and coughing, and many stories this year involve allergy patients who were suspected of having “the virus”. One patient said, “the isle cleared at Wal-Mart when I sneezed”. Another patient found she was ostracized at a friendly get together because of her runny nose and cough–it wasn’t Corona, only spring allergies. She told me later, that she felt embarrassed and wanted to leave the party immediately. You shouldn’t have to experience this rejection and embarrassment if you know what separates virus (any type) from allergy.
Viral infections will often have fever, sore muscles/joints, and in the case of COVID-19, significant shortness of breath. Most likely, this is your first experience with rhinitis, whereas allergy patients have sneezing, coughing, and runny nose year after year.
If you have any questions, please ask your doctor if you need further testing. Testing for both allergies and viral infections (not just Corona) are readily available and you should take advantage of knowing how best to treat your symptoms by correctly diagnosing your problem. Now, don’t show up at your allergists’ office if you think you have COVID-19 before calling first! Don’t take my word alone, watch the video from Dr. Skoner at West Virginia — 3 minutes long and will give you the peace of mind to know “is this allergy or virus.” Your health depends on it!
Jane (fictitious name, of course because of HIPPA regulations) is now 56 years old and just last year was diagnosed with #asthma. She thought, “no big deal, there are plenty of inhalers for me to use so I don’t wheeze”. Little did she know that 2019 would put her in the hospital 3 times and multiple visits to the emergency room because of asthma. In fact, she even missed her grandson’s graduation from kindergarten because of her asthma. Now if that doesn’t motivate you, nothing will! Continue reading →