As we all know, Ive had asthma Ive had severe asthma for decades. I’ve lived it, studied it, and written about it here. But my recent visit with Dr. Erin Gordon at UCSF, one of my favorite pulmonologist for over a decade, shifted something fundamental in how I understand my own disease.
Reconnecting with Dr. Gordon
This appointment came about after I asked my allergist if I could be followed more closely by the pulmonary team again—specifically by someone who truly understands asthma. For a while, I’d stepped back from regular pulmonology visits. Not out of frustration, but because I genuinely felt they didn’t have much more to offer. My asthma is complex, and after years of trial and error, I wasn’t sure what else could be done.
But this lingering exacerbation—now stretching into its fourth month—pushed me to reconsider. I wanted fresh eyes, and ideally, someone with a passion for asthma research. That’s when Dr. Erin Gordon came to mind. I’ve known her for years, but it had been over a decade since we’d had a private visit. I knew she was involved in research, but I had no idea her work focused on the airway epithelium—the very place she believes asthma truly begins. That revelation alone made this Zoom visit an eye-opener.
We spent time catching up—ten years is a long time—and then dove into the science. One thing I’ve always admired about Dr. Gordon is her optimism. She’s genuinely hopeful about finding better treatments, maybe even a cure, and she brings that energy into every conversation. She’s also deeply empathetic, which is rare in pulmonology. At one point, she paused and said, “I don’t know very many people with a baseline FEV1 of 0.8 liters who do what you do—marathon walks, pilgrimages, travel. It’s extraordinary.” That kind of affirmation means a lot when you’ve spent years navigating a disease that often feels invisible to others.
The Epithelium Revelation
About midway into the appointment, I told Dr. Gordon I was frustrated. This latest flare had dragged on for months requiring multiple steroid cycles, and unlike past episodes, there were no clear triggers—no colds ir flu, no environmental allergens, nothing I could point to. I’d done everything right to treat it, but I was still actively flaring. That’s when she leaned in and started talking about the epithelium.
Dr. Gordon believes asthma doesn’t just live in the lungs—it begins in the airway epithelium. She’s spent years researching how epithelial cells aren’t passive; they’re active players, capable of triggering inflammation even when classic markers like IgE or eosinophils are low. For someone like me, with extraordinary mast cell presence in the upper airways, this theory isn’t abstract—it’s personal. It reframes my symptoms not as failures of treatment, but as the result of an airway surface that’s constantly on edge, flaring up even when there’s no clear reason.
She also validated what I’ve long suspected—but really, what we’ve known for years: my asthma doesn’t fit neatly into textbook categories. It’s complex and stubborn. Still, hearing her say it out loud, backed by her research, landed differently.
My ACT score was 6 out of 25 according to this test, which indicates very poor asthma control. I’m using rescue meds multiple times a day. And yet, the usual biologics—Xolair, Dupixent, Tezepelumab—either failed or made things worse. Even Fasenra, which I’ve been on for three years and which has likely helped reduce my hospitalizations, hasn’t actually made me feel any better on a day-to-day basis.
You can view the full After Visit Summary from this appointment here,
The Clinical Trial Possibility
Dr. Gordon is exploring whether I might qualify for a UCSF-led trial involving Brensocatib, a pill targeting neutrophilic inflammation. She’s reaching out to Dr. Shaw, a researcher involved in the study. I may not know whether I’d receive the drug or placebo, but the opportunity to contribute to something bigger than myself feels meaningful.
We also discussed Brinsupri, a newer therapy for bronchiectasis-related exacerbations. My imaging shows mild bronchiectasis—no productive cough, but occasional mucus plugs. It’s not the headline diagnosis, but it’s part of the puzzle. If insurance approves, Brinsupri could be a preventive layer.
The Bronchiectasis Surprise
One unexpected twist from this visit was the diagnosis of mild bronchiectasis. It caught me off guard. I don’t cough much, and I don’t produce a lot of mucus—two hallmark symptoms I’ve always associated with the condition. But the CT scan told a different story. Dr. Gordon pointed out the telltale signs: airway dilation, subtle structural changes that don’t always show up in daily symptoms. It’s not the dominant issue in my case, but it’s part of the puzzle. And it’s a reminder that imaging can reveal what experience alone can’t. We discussed Brinsupri as a possible preventive therapy, pending insurance approval. It’s not a headline diagnosis, but it’s quietly reshaping how I think about my airways.
What This Visit Taught Me
Inflammation isn’t always visible on standard labs. Mast cells, epithelial stress, and non-T2 pathways may be the missing pieces in my asthma puzzle. After years of managing symptoms, this visit reminded me that understanding the “why” still matters.
Dr. Gordon didn’t just offer a plan—she offered perspective. She acknowledged the complexity, affirmed my resilience, and opened doors to research that might finally speak my language. And as she signed off with, “It was so nice to catch up with you today,” I felt something rare in medicine: seen.
Related Reading:
Before Dr. Gordon, my very first pulmonologist at UCSF was Dr. Stephen Lazarus. If you want a laugh—and a glimpse into the wild world of 1970s asthma care, check out this post about aminophylline injections, vintage news clips, and a full-circle moment that still makes me smile.
