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Meal-induced heartburn appears to follow two distinct GERD phenotypes, suggesting that esophageal hypersensitivity, rather than acid exposure alone, may influence symptom severity and treatment response.
Not all heartburn follows the same pattern, even among people with gastroesophageal reflux disease (GERD). An exploratory analysis of a randomized clinical trial suggests that patients develop one of two distinct meal-induced heartburn phenotypes, with differences in symptom persistence linked more closely to esophageal sensitivity than to acid exposure.
The analysis included 26 adults with symptomatic GERD who consumed a standardized meal and subsequently received either placebo or a ranitidine–antacid combination. Researchers assessed heartburn severity using a visual analog scale (VAS) and measured esophageal and gastric pH every 15 minutes to examine the relationship between symptoms and acid levels. Tracking heartburn over time revealed two clear symptom trajectories. One group, termed persistent heartburn, experienced continuously high symptom severity throughout the observation period.
The second group, non-persistent heartburn, showed an initial rise in heartburn severity that gradually subsided. Surprisingly, those with persistent heartburn phenotype reported more severe overall heartburn despite having lower esophageal acid exposure than those in the non-persistent heartburn group. Gastric acidity remained comparable between the two phenotypes, indicating that excess gastric acid alone did not explain the persistent symptoms. Another notable finding was that both phenotypes experienced clinically significant heartburn even when esophageal pH remained above 4.0, a level generally considered non-acidic.
This observation points to esophageal hyperalgesia, or increased sensitivity of the esophagus, as a fundamental contributor to symptom generation. The degree of hypersensitivity was more pronounced in the persistent heartburn phenotype, suggesting that heightened sensory responses may amplify symptoms independently of acid reflux. The two phenotypes also illustrated different responses to placebo and ranitidine–antacid treatment, reinforcing the possibility that factors beyond acid suppression influence symptom persistence in a subset of patients.
Hence, GERD is not a single clinical entity but may encompass distinct heartburn phenotypes with different underlying mechanisms. Recognizing these phenotypes could help explain why some patients continue to experience troublesome symptoms despite acid-suppressive therapy and may support the development of more personalized treatment strategies targeting esophageal hypersensitivity alongside acid control.
Physiological Reports
Exploratory analyses of meal-induced heartburn identify distinct clinical phenotypes of gastroesophageal reflux disease
Jerry D Gardner et al.
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