PPI-Refractory Non-Erosive Reflux: Baclofen or an Alginate Add-On
Confirmed non-erosive reflux disease that hasn't responded to a properly optimized PPI raises a genuine add-on question — baclofen, which targets the transient relaxations actually driving her reflux events, against a simpler alginate barrier her own pH-impedance data may not fully support.
Grace L., 45, has coached her son's travel hockey team for four seasons, spending most weekends in rinks where the concession-stand food is the only option for hours at a stretch — a routine she says she can't easily change without giving up something she genuinely loves doing. She has had heartburn and regurgitation for three years, confirmed on ambulatory pH-impedance monitoring while off medication as acid-predominant NERD with a normal endoscopy. Twelve weeks on omeprazole 40mg twice daily, taken correctly (30 minutes before breakfast and dinner, confirmed directly with her rather than assumed), has cut her symptom frequency by less than a third.
Repeat pH-impedance testing on therapy shows persistent reflux episodes clustering around meals and lying down, with a symptom-association probability that still meets the threshold for a genuine reflux-symptom link — not a functional-heartburn pattern, where add-on acid suppression would be the wrong move entirely. That distinction is what makes baclofen a real option here rather than a reflexive add-on. The ACG reflux guideline (Katz and colleagues) lists it precisely for this situation — persistent symptoms despite optimized PPI therapy with objective evidence of ongoing reflux — because it reduces the frequency of transient lower esophageal sphincter relaxations, the actual mechanical event behind most of her breakthrough episodes, rather than suppressing acid further in a patient whose acid suppression is already adequate on impedance testing.
Baclofen is a GABA-B receptor agonist acting centrally and at the vagal reflex arc that governs TLESR frequency — the very event her on-therapy impedance study keeps recording, which is a genuinely different target than an alginate's local, physical raft-barrier effect — two add-ons that could, in principle, be complementary rather than competing, though the group here chose to trial one at a time specifically so a clear response could be attributed to a single change rather than confounded by starting both together. Her own account of the breakthrough pattern — worse specifically after concession-stand meals and on the drive home reclined in the passenger seat — matched the on-therapy impedance data closely enough that the team felt confident attributing it to a real, describable mechanism rather than an unexplained residual symptom.
What breakthrough reflux on adequate acid suppression actually means
Her on-therapy pH-impedance is the piece that actually settles what we're treating. She still has genuine reflux episodes despite adequate acid suppression — this isn't functional heartburn, where adding more reflux-targeted therapy would be the wrong move. Baclofen reduces the frequency of transient LES relaxations, which is the actual mechanical event driving those breakthrough episodes. That's a more direct fit than adding another layer of acid control to a system where acid suppression is already adequate.
I'd start with an alginate before baclofen. Her breakthrough pattern is meal- and recumbency-associated, which is exactly the physical scenario an alginate raft is designed for — it forms a barrier that sits on top of the gastric contents specifically after meals and when lying down. It's better tolerated, has essentially no CNS side-effect profile, and she's on her feet coaching for hours most weekends.
I take the TLESR mechanism seriously, but a mechanically-simpler option deserves a real trial first when it fits her specific symptom pattern this well.
Both mechanisms are real, but I want to be honest about the evidence base behind baclofen specifically — the trials showing benefit in GERD are smaller and shorter than what backs alginate use, and sedation and dizziness are genuine, common side effects, not rare ones. For someone standing rink-side most weekends, that's a real cost to weigh against a moderate symptom-frequency benefit. I'd try the alginate first, precisely because it fits her meal- and recumbency-timed pattern and carries far less systemic burden, and hold baclofen in reserve if it isn't enough.
Agreed: alginate-antacid combination added after meals and at bedtime, PPI unchanged, with a symptom diary and a planned four-week follow-up rather than an open-ended trial.
Not agreed: whether baclofen should have gone first given the gastroenterologist's read of her on-therapy impedance data as the more direct mechanistic match. That disagreement wasn't resolved — it was deferred to the four-week follow-up, with baclofen named explicitly as the next step if the alginate underperforms rather than requiring a fresh argument to reach it.