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This study aims to evaluate the acid inhibition and clinical improvement of the addition of bedtime lafutidine to esomeprazole in comparison with esomeprazole only in Gastroesophageal reflux disease (GERD) patients with nocturnal symptoms. We conducted a single-center, observer-blinded, randomized, clinical trial. Forty-eight consecutive GERD patients with nocturnal symptoms were randomized to take twice daily esomeprazole, 20 mg (ESO Group, n = 24) or twice daily esomeprazole, 20 mg, with bedtime lafutidine, 10 mg (LAF & ESO Group, n = 24) for one week. The 24-h impedance-pH monitoring, and high-resolution manometry were measured on the seventh day during the treatment. The symptoms and sleep quality were assessed both at baseline and following treatment. Intragastric pH > 4 holding time ratios were significantly higher in the LAF & ESO Group compared to the ESO Group, both overall (85.4% vs. 77.7%, P = 0.003) and specifically during nighttime (92.6% vs. 77.2%, P = 0.006). Furthermore, the incidence of nocturnal acid breakthrough (NAB) was markedly reduced in the LAF & ESO Group (29.2% vs. 75.0%, P = 0.001). Esophageal acid exposure times, however, were comparable between the two groups (P > 0.05). Although both groups experienced symptom improvement, patients in the LAF & ESO Group demonstrated superior enhancement in sleep quality, as measured by the Pittsburgh Sleep Quality Index. Notably, patients without NAB exhibited a more substantial improvement in sleep quality from baseline after treatment. Therefore, adding bedtime lafutidine to esomeprazole effectively inhibits nocturnal gastric acid secretion and reduces the incidence of NAB. GERD patients who received lafutidine in addition to esomeprazole achieved a more significant improvement in sleep quality correlated with NAB reduction.

Gastroesophageal reflux disease (GERD) is a chronic relapsing disorder often inadequately controlled with proton pump inhibitors (PPIs), particularly in patients with nocturnal acid breakthrough (NAB) or non‐erosive reflux disease (NERD). Tegoprazan, a potassium‐competitive acid blocker (PCAB), offers rapid, potent, and CYP2C19‐independent acid suppression. This systematic review and meta‐analysis evaluated randomized controlled trials comparing Tegoprazan with PPIs in adults with GERD and related disorders. Databases searched included PubMed, Cochrane, Wiley, and ClinicalTrials.gov (2015–2026). Eighteen studies met inclusion criteria. In erosive esophagitis, Tegoprazan 50 mg once daily achieved mucosal healing rates of 91.1%–99.1%, non‐inferior to PPIs (93.5%–98.9%; pooled RR = 1.01, 95% CI 0.98–1.05). Pharmacodynamic and clinical studies demonstrated faster acid suppression and improved nocturnal pH control versus PPIs, achieving pH ≥ 4 within 30–60 min and maintaining levels throughout the 12‐h period. In nocturnal symptom analyses, Tegoprazan achieved earlier relief (1.5 vs. 3 days to first heartburn‐free night) and higher proportions of heartburn‐free nights (57.8% vs. 43.1%), with significantly greater complete (p = 0.038) and partial (p = 0.034) nighttime symptom resolution than Esomeprazole. In NERD, symptom resolution ranged from 42.5% to 48.9% versus 24.2% with placebo. In open‐label functional dyspepsia cohorts, improvements ranged from 74.6% to 86.7% in open‐label cohorts. Seven trials (n = 2492) showed higher Helicobacter pylori eradication with Tegoprazan‐based therapy (RR = 1.05, 95% CI 1.01–1.09; p = 0.006; I2 = 0%). Adverse events were mild and comparable to PPIs. Tegoprazan provides rapid, sustained acid suppression, effective nocturnal symptom control, and a modest but statistically significant improvement in H. pylori eradication, representing a potential alternative to PPIs for patients with persistent or CYP2C19‐related variable response.

Esomeprazole, a proton pump inhibitor (PPI), is widely used to treat acid-related disorders, but it has short plasma half-life which can cause insufficient gastric acid suppression, such as nocturnal acid breakthrough. A new dual delayed-release (DR) formulation of esomeprazole (Esomezol DR), was developed to extend the duration of gastric acid suppression. This study aimed to evaluate the pharmacokinetics (PKs) and pharmacodynamics (PDs) of esomeprazole for the DR formulation compared to a conventional enteric-coated (EC) formulation (Nexium) in healthy male subjects. Two randomized, open-label, multiple-dose, two-way crossover studies with esomeprazole 20 mg and 40 mg were conducted. Subjects received the DR formulation or the EC formulation once daily for 7 days in each period with a 7-day washout. Serial blood samples were collected up to 24 hours after the 1st dose, and 24-hour intragastric pH was continuously monitored before the 1st dose as baseline and after the 1st and the 7th dose. In 20 mg and 40 mg dose groups, 38 and 44 subjects completed the study, respectively. The DR formulation exhibited the dual-release pattern of esomeprazole, resulting in more sustained plasma concentration-time profiles compared to the EC formulation. The systemic exposure of esomeprazole for the DR formulation was comparable to that for the EC formulation, showing the similar area under the plasma concentration-time curve. The 24-hour gastric acid suppression was also similar between the two formulations, while the inhibition during night-time (22:00-06:00) showed a better tendency in the DR formulation. The sustained exposure of esomeprazole in the DR formulation led to well-maintained and higher acid inhibition compared to the EC formulation, especially during the night-time. These results suggest that the DR formulation can be an alternative formulation to the conventional EC formulation, expecting the potential of relieving nocturnal acid-related symptoms.

Nocturnal gastric acid breakthrough (NAB) is defined as nocturnal intragastric pH less than 4 for more than 1 h during proton pump inhibitor (PPI) administration. A bedtime dose of an H2 receptor antagonist (H2RA) inhibites NAB, but the efficacy of the H2RA decreases with continuous administration. We carried out the present study to investigate the effect of 14-day H2RA administration on NAB. Ten male volunteers without Helicobacter pylori infection received four different 14-day regimens of rabeprazole and ranitidine (study a, morning dose of 20 mg rabeprazole; study b, morning dose of 20 mg rabeprazole with a single bedtime dose of 150 mg ranitidine only on the last day; study c, continuous 20 mg morning dose of rabeprazole and 150 mg at bedtime; study d, morning and evening doses of 10 mg rabeprazole). Ambulatory 24-h gastric pH monitoring was conducted on the last day of each regimen. NAB in studies a, b, c, and d was observed in 9, 1, 4, and 4 subjects, respectively, and the longest periods of nocturnal gastric pH at less than 4.0 were 102.5, 14.0, 37.5, and 52.5 min, respectively (study b vs study c, P<0.05). The continuous inhibitory effect of ranitidine combined with rabeprazole on nocturnal gastric acid secretion declined during 14-day-long administration in H. pylori-negative subjects. Split dosing of rabeprazole was more effective than the single morning dose for inhibiting nocturnal gastric acid secretion.