What Is Severe Asthma? Part 2: Decoding My Phenotype
As I wrote in my previous post, What is Severe Asthma?, my asthma specialist, AKA Dr. Smartypants, recently described my asthma as "moderate-to-severe [well-controlled] asthma with a mild atopic component”.
How I viewed severe asthma
The word “severe” conjured my curiosity, as I’ve characterized my asthma as weird and not fitting into boxes nicely, but not exactly as all that severe. At least not based on all the severity classification pages I’d dug up online circa 2008-2010, many of which focused around airflow obstruction (decreased FEV1) of under 60%.
After all, I have friends with what I consider bonafide severe asthma—with accompanying decreased FEV1 (lung function), steroid-dependence, and significant impact of asthma on their daily life. These things are not part of my own equation; these things are why the greyness of “moderate-to-severe”, in context, sort of made sense to me early on.
However, this is me, so I needed more information. Obviously. It’s not like I doubted Dr. Smartypants’ assessment -- that woman went to Harvard. One night, the curiosity surrounding the word “severe” lead me to reading the entirety of the International ERS/ATS Guidelines on Definition, Evaluation and Treatment of Severe Asthma document (for this process I was forced to find a digital PDF note-taking/highlighting chrome extension, even!). I gleaned insight into both my doctor's process of determining this, as well as connected some dots of the nuances within my own asthma.
Meeting the threshold: Indications from treatment
I started an inhaled steroid six months after my asthma diagnosis, after I’d finally gained access to a family doctor. High dose Flovent made little difference for me. Above-maximum dose Symbicort helped, but clearly that’s not ideal.2 Three years, three specialists, seven different meds and a half dozen or so different combinations, and a few appointments with Dr. Smartypants later, “control” happened.
What did the useful, even if not ideal, combinations have in common? High-dose inhaled steroids — which make a difference in severe asthma, but have less a clinical impact at increased doses in mild-to-moderate asthma — coupled with long-acting bronchodilators.1 (17) Within these combinations, some steroid types just worked better for me than others — namely, mometasone (as in Zenhale/Dulera) and beclomethasone (Qvar).
For adults, the “high dose inhaled corticosteroid” threshold varies based on which ICS drug a person is on. I take both Qvar (beclomethasone) and mometasone (a component of Zenhale/Dulera).
For simplicity in conversion since only dry powder mometasone made the chart and I take the metered dose—pressurized—inhaler (MDI), we can either equate this as follows1 (72):
- I take 3 puffs 100 mcg MDI Qvar (beclomethasone) and 3 puffs 200 mcg MDI Zenhale (mometasone) daily.
- Equivalent to 6 puffs Qvar = 600 mcg HFA MDI - anything over 500 mcg is “high”1 (72)
- Equivalent to 6 puffs mometasone = 1200 mcg DPI - anything over 800 is considered high.
I was going to do another conversion there with some attempts at fancy math, but whichever way you slice it, it’s still above the “high dose” threshold.
Additional treatment methods
In addition, I’m also on a long acting beta agonist bronchodilator, and Atrovent, an anti-cholinergic bronchodilator daily. My positive response to Atrovent has been a curiosity among my well-read or respiratory therapist friends with asthma, as it does work quite well as an add-on for me—interestingly, Atrovent is described as being used to attempt “to reduce daily use or overuse of [beta 2] agonists [short acting bronchodilators], particularly in those demonstrating intolerant side effects of [beta 2] agonists such as tremor and [heart] palpitations.”1 (41)
Look, between asthma and ADHD I got enough meds that can increase my heart rate. The more I can reduce my beta-2 agonists (and keep breathing decently), the better.
A matter of control
Dr. Smartypants described me as “well-controlled” — this makes sense for a few reasons. It has been several years since I last required prednisone (yay!), I require my rescue inhaler more than GINA asthma control guidelines recommend, and more than most mild-to-moderate asthmatics, sometimes daily, but seldom multiple times per day unless in an exacerbation.
However, each time I attempt to decrease my ICS lower than the above dose, I experience a loss of control and worsening of symptoms, and thus, require remaining in the “high dose” threshold to maintain control. Per the Guidelines, this is classified as “controlled severe asthma”.1 (68)
And that “slightly atopic” bit.
I’ve long considered myself “barely allergic to anything” or “just allergic to dust mites like half the world”.
And here’s what’s interesting in the context of severe asthma. A direct quote from the authors of the Guidelines:
"Atopy and allergy have long been associated with asthma and, to some degree, with severe asthma. However, most large epidemiological studies are reporting that severe asthma is less associated with atopy/allergy than milder asthma, with a lower proportion of patients with positive skin testing."1 (33)
Huh. Well then! Maybe my lack of atopy is somewhat significant.
Interesting notes on FEV1 (lung function) and severe asthma
As written above, I previously had read airflow obstruction of <60% FEV1 was indicative of severe asthma.3 In the literature, this exact specification is hard to find outside of the basis of the ERS-ATS guidelines specifying that severe asthma is uncontrolled if FEV1 is under 80% predicted, and is classified as “severe obstructive asthma” if FEV1 is <60%1 (18, 64). No other mention of severity classification of severe asthma based on FEV1 was provided in the Guidelines. Upon digging further, I did not come across any significant notes regarding FEV1 in regard to classifying severe asthma.
Given my FEV1 is typically around normal, but did drop significantly during my 2010 methacholine challenge, my circa 2009 reading lead me to believe my FEV1 was incongruous with severe asthma—my reading of more literature has lead me to believe FEV1 may be independent of asthma severity in some cases.
Interestingly, per a PLOS One article (2009—where’s that been hiding?) on asthma severity in young adults, this may be more typical of presentation of severe asthma in women—“In our study, moderate-to-severe asthma was more particularly characterized by a decrease in FEV1 (<60% [predicted]) in men whereas in women it was associated with more intensive treatment.”4
Intensive treatment? Yeah, I think 16-20+ puffs of various inhalers a day over here, let’s call it that.
There’s probably more.
I highlighted lots of stuff in the ERS/ATS Guidelines, so there’s probably more. I’ve covered here the most interesting points in my opinion. (And look, we’re at over 1000 words here, so if you’re still with me, thanks for being interested in lung weirdness, particularly my lung weirdness). The reality is, that there is a lot we don’t know about asthma, a lot we don’t know about severe asthma, and research like this lays the groundwork for much more discovery—scientific and self—to come.
Understanding my own asthma is important to me: I want to know what the heck is going on in these goofy lungs I cannot see, and I am aware that there’s a lot more to theorize on, speculate on, and study. But, reading what’s out there is a good place to start decoding those phenotypic questions I have of myself.
Have you ever gotten "moon face" as a side effect of prednisone?