Singular/Montelukast: Not Just For Asthma (Part 1)
Early on in my asthma journey, when we were throwing everything possible at my asthma—which, at that point, didn’t get things even under a semblance of control, because it turns out we were not throwing the right things at my asthma—I was on Singulair. For years.
Trying Singulair (Montelukast)
Eventually, one day my then-allergist and I discussed Singulair, and determined it likely was not doing much if anything for me. I had no side effects, thus, why I stayed on it for years. But when I pulled off of it, nothing happened either. My doctor said she finds a third of her patients have a noticeable response, a third have side effects (with no/little result) that make them discontinue, and a third were like me: no noticeable response, no side effects.
When researching allergic rhinitis earlier, I thought again about Singulair. I never read my Singulair leaflets closely, and this may be a new addition, but it turns out, Singulair is FDA-approved to treat allergic rhinitis.1
In my next post, I’ll look at the research on Singulair for allergic rhinitis specifically—for now, here’s a refresher on what, exactly, montelukast does.
What is Montelukast?
Singulair is in the class of drugs known as Leukotriene Receptor Antagonists (LTRAs) or Leukotriene Modifiers. Leukotrienes are long thought to contribute to asthma2,3, released from inflammatory cells and contributing to changes in airway constriction and eosinophil levels.3,4 If you paid attention in English class, you’ll remember that antagonists work against the main character—in medicine, it’s basically the same deal: a leukotriene receptor antagonist will work against the ability of leukotrienes to bind to receptor sites in the airway, thus preventing or decreasing the level of response (bronchoconstriction, in this case).5
This is basically the opposite of how, for instance, a bronchodilator, known as a beta-2 adrenergic agonist, works. The antagonist blocks a response from occurring in the first place, acting specifically on targeted cells to prevent a response (bronchoconstriction), rather than to perform one as an agonist would (bronchodilation).7
If your brain hurts now, here’s a Fun Fact from this Canadian: Montelukast is named after Montreal, the city in Québec where the drug was developed
Why Montelukast? For asthma and beyond.
Typically, physicians take an “entire airway” or “one airway” approach to asthma management8, which is why many asthmatics are identified as having co-occurring sinus disease or allergic/non-allergic rhinitis. The thought is that the inflammatory process must be addressed throughout the airway for optimal results from treatment.8 Allergic rhinitis is one of the approved uses for Singulair, but one you likely don’t hear about very often, as it’s a “second line” treatment.9
Keeping treatment localized, by way of intranasal corticosteroids (nasal sprays), is preferred to cut down on potential side effects, which explains why—since intranasal steroids are effective and safe—Singulair hasn’t hit the mainstream for rhinitis treatment. However, leukotrienes are also found to be present in those with exercise-induced asthma—montelukast is sometimes prescribed for prophylaxis (prevention) of EIA symptoms (bonus!).5
In addition, emerging research is looking at the roles of montelukast on Parkinson disease sup>10, menstrual-related pain11, and more—so it doesn’t just go beyond asthma in terms of working upward to upper-airways disease in the sinuses!
After learning more about the potential role of montelukast in rhinitis treatment, and based on my lack of “compliance" with my nasal steroids, I figured looking more into this research could be interesting. Now that we’ve got the basics of montelukast down, we’ll tackle that topic in my next post.
Have you tried Singulair (montelukast) for your asthma? Did it work for you?
Do you get muscle cramps caused by your asthma medicine?