The article by Astapczyk et al,¹ published in the current issue of Polish Archives of Internal Medicine, evaluates an important and common problem encountered in clinical practice: the attribution of troublesome symptoms to gastroesophageal reflux disease (GERD). The findings of the study are both precise and disquieting. Among the patients who had failed or only partially responded to proton pump inhibitor (PPI) therapy and were referred for ambulatory pH‑impedance monitoring, nearly 4 out of 5 individuals with isolated atypical symptoms (eg, cough, belching, globus, bitter taste, throat pain) had acid exposure time (AET) below 4%, a threshold that excludes pathological reflux.² Even among the individuals presenting exclusively with canonical symptoms of reflux, such as heartburn and regurgitation, around half had AET below 4%. The clinical implication is clear: symptoms alone are insufficient to diagnose GERD.

The discrepancy between symptom presentation and objective evidence of reflux matters because the differential diagnosis for PPI‑refractory complaints is wide and carries real consequences. Reflux hypersensitivity, functional heartburn, supragastric belching, rumination syndrome, eosinophilic esophagitis, and laryngeal or cardiopulmonary disorders unrelated to acid exposure are common, and each of them requires distinct management strategies.^3,4 Conflating these conditions with GERD does not merely delay appropriate treatment—it actively perpetuates a diagnostic error, exposing patients to unnecessary long‑term therapy, while leaving the true underlying disorder unaddressed. In the study by Astapczyk et al,¹ functional heartburn accounted for 41.6% of all patients reporting heartburn, and this is a stark reminder that the cardinal symptom of GERD is frequently unrelated to acid exposure in the PPI‑refractory population.⁵

Two additional findings of the study deserve attention. First, the results of endoscopy, available in 92% of the patients, showed no objective evidence of GERD in 84% of the cases, and the addition of endoscopic findings to pH‑impedance monitoring increased the overall rate of GERD diagnosis by only 2.6%—from 27% to 29.6%.¹ This underscores that endoscopy alone is insufficient to confirm or exclude GERD, particularly when performed during PPI therapy, which induces mucosal healing, reducing the possibility of detecting erosive esophagitis.⁶ Second, mean nocturnal baseline impedance (MNBI), a validated surrogate marker of esophageal mucosal integrity,^2,5 correlated inversely with acid burden and was the primary driver of GERD diagnosis in the patients with inconclusive AET values and atypical symptoms. Two‑thirds of the patients with isolated atypical symptoms had normal MNBI values,¹ which objectively supports the absence of acid‑related mucosal damage and reinforces the case against empirical acid suppression in this group.

Typical GERD symptoms are very common.⁷ However, the presence of heartburn or regurgitation does not establish GERD,² just as their improvement on PPIs does not confirm it, as part of the observed benefit may be attributable to a placebo effect.⁸ More strikingly, approximately 1 in 2 patients receiving PPIs continues to experience troublesome symptoms⁷; a statistic that challenges the durability of empirical acid suppression as a diagnostic and therapeutic strategy. Symptoms speak loudly, but they do not always speak truthfully about the underlying mechanism.

Extraesophageal manifestations deserve particular scrutiny. Patients with laryngeal or respiratory complaints are frequently evaluated first by otolaryngology or pulmonology specialists, and referrals to gastroenterologists due to symptoms assumed to be reflux‑related are commonplace. However, laryngoscopy findings attributed to GERD are nonspecific and can be observed in asymptomatic individuals.^6,9 Beyond the diagnostic challenge, the economic consequences are substantial: costs associated with the evaluation and treatment of extraesophageal symptoms considerably exceed those incurred by typical GERD, and these patients frequently require multiple specialist consultations and diagnostic procedures before receiving a coherent diagnosis.¹⁰

The Lyon Consensus 2.0 provides an objective and reproducible framework for establishing conclusive GERD.² Endoscopic evidence of Los Angeles grade B, C, or D erosive esophagitis, histologically proven Barrett esophagus, or peptic stricture constitutes definitive proof of disease. On ambulatory reflux monitoring performed off antisecretory therapy, AET exceeding 6% over 24 hours on pH‑impedance monitoring, or AET above 6% on at least 2 days during prolonged wireless pH monitoring is also conclusive.²

In patients with typical symptoms without alarm features, an 8‑week empirical PPI trial remains applicable.^2,6 However, in those without adequate symptomatic relief, the appropriate next step is diagnostic endoscopy performed 2–4 weeks after PPI withdrawal, followed by ambulatory reflux monitoring off antisecretory therapy, if endoscopy fails to demonstrate established GERD.⁶ This stepwise approach has both clinical and economic justification: in patients with heartburn unresponsive to PPIs, the combination of endoscopy and off‑therapy pH monitoring is more cost‑effective than empirical PPI escalation without objective testing.¹¹

Establishing a correct diagnosis is useful for another purpose: it creates the conditions for safe and rational PPI deprescribing. Long‑term PPI therapy requires periodic assessment, and continuation without a clear indication is difficult to justify.¹² Although the causality of many adverse effects reported in observational studies remains uncertain,^6,13,14 a large randomized controlled trial¹⁵ demonstrated that patients receiving PPIs had a modest but significant increase in the risk of enteric infections, as compared with those receiving placebo. A further underrecognized obstacle to deprescribing is rebound acid hypersecretion: upon discontinuation of PPIs, patients may develop acid‑related symptoms that sometimes persist for several weeks, a phenomenon demonstrated even in healthy volunteers.¹⁶ Unless the patients are forewarned, these rebound symptoms are readily misinterpreted as evidence of underlying GERD, creating a self‑reinforcing cycle of unnecessary prescription.

Taken together, the data presented by Astapczyk et al¹ and the broader evidence summarized here converge on a single imperative: objective confirmation of GERD should precede, not follow, long‑term therapeutic commitment. Symptoms are the starting point of clinical reasoning, not its conclusion.