Self-Management of Reflux-Like Symptoms: A Patient-Centered Decision-Making Approach

Abstract

Background

Guidelines for the management of reflux-like symptoms (primarily heartburn and regurgitation) offer limited guidance to support decision-making in the nonprescription setting. This review aimed to summarize and compare nonprescription treatment options within the context of reflux-like symptom pathophysiology and provide a practical evidence-based tool to help guide tailored treatment selection.

Summary

A patient-centered approach should consider the requirement for reactive versus preventative therapies and each product’s unique characteristics. Antacids neutralize refluxed acid in the esophagus, providing temporary relief from occasional heartburn. Raft-forming alginate formulations provide relief of heartburn and regurgitation after meals by forming a viscous gel near the gastroesophageal junction, neutralizing the postprandial acid pocket and coating the esophagus when refluxed. Histamine-2 receptor antagonists reduce gastric acid secretion within 30 min, lasting for up to 12 h, making them useful for treatment and prevention of heartburn, but tachyphylaxis is a limitation. Nonprescription proton pump inhibitors are most effective for preventing frequent acid-related symptoms. They are packaged as a 2-week course for daily use, achieving maximum effect after a few days.

Key Messages

Important differences exist among self-management treatment options for reflux-like symptoms. A standardized algorithm is proposed to help tailor treatment selection according to symptom profile.

Introduction

Reflux-like symptoms, primarily heartburn and regurgitation, are highly prevalent and frequently managed using nonprescription (or “over the counter” [OTC]) medicines in unsupervised settings [1, 2]. Despite the range of products available (e.g., antacids, alginates, mucosal protectants, histamine-2 receptor antagonists [H₂RAs], and proton pump inhibitors [PPIs]), clinical guidelines offer minimal guidance on how to use them appropriately or tailor their use to specific patient needs [3–5]. The distinction between alginates and antacids is poorly understood, and concepts such as “on-demand” treatment are poorly defined in the context of PPIs, leading to potential misuse and suboptimal outcomes.

Concerns about PPI overprescribing and long-term safety have led to initiatives to limit continuous treatment in favor of self-management and a more patient-centered approach to care [4, 6–8]. In the UK, 41% of heartburn and dyspepsia consultations in 2023 advised the use of nonprescription medicine [9] and, in the USA, a third of PPI users for reflux-like symptoms now obtain them without a prescription [10]. In Germany, while most PPI units are still dispensed by prescription, the nonprescription market has grown consistently, with a 14% annual increase over a 3-year period [11].

Given the lack of practical guidance to support decision-making in the nonprescription setting, this review aimed to summarize and compare the main nonprescription treatment options. Product characteristics and mechanisms of action are discussed, as well as clinical evidence and safety considerations. The goal was to help health professionals support individuals in making well-informed and effective self-care decisions and provide a practical evidence-based tool to guide tailored treatment selection.

Pathophysiology of Reflux-Like Symptoms

Reflux-like symptoms have a complex, multifactorial pathophysiology that may involve a combination of anatomical, physiological, and perceptual components (Fig. 1). The lower esophageal sphincter functions as a reflux barrier through its interaction with the crural diaphragm [12, 13]. Widening of the diaphragmatic hiatus, hiatus hernia development, and weak esophageal contractility (commonly associated with advancing age) may compromise this barrier, leading to increased reflux frequency and volume [12, 14]. Pathological esophageal acid exposure can provoke retrosternal burning and greater reflux volume and proximal extent can result in regurgitation and chest pain. However, these symptoms can also be experienced when esophageal reflux exposure is defined as “normal” by ambulatory pH+/− impedance measurements, termed “reflux hypersensitivity” or “functional heartburn” depending on symptom-reflux association [15–17]. While reduced function of the anti-reflux barrier and esophageal clearance usually dominates in reflux esophagitis, modulators such as stress, cognitive-affective, and behavioral factors (e.g., hypervigilance and avoidance behavior) play a major role in symptoms that are not necessarily associated with pathological acid exposure (Fig. 1) [18]. Without specialist investigation, the physiological or perceptual nature of symptoms remains uncertain; hence, we refer to uninvestigated symptoms universally as “reflux-like” symptoms.

Fig. 1.

Reflux-like symptom pathophysiology is complex and multifactorial. DGIB, disorder of gut-brain interaction; IBS, irritable bowel syndrome.

Postprandial Reflux

Reflux events typically occur within 3 h of eating [19], especially after large refluxogenic (fatty/fried) meals, carbonated beverages, or alcohol [8, 20]. While food has a buffering effect when mixed with gastric acid, a layer of newly secreted acid, known as the acid pocket, pools on top of the meal in the proximal stomach within 15 min of eating [21]. It persists for up to 90 min and, together with pepsin and bile, acts as a reservoir for postprandial reflux [21]. The acid pocket is frequently located above the diaphragm in patients with large hiatus hernias [22] and may extend into the distal esophagus, even without a reflux event, especially during recumbency [21].

On-Demand Self-Management Treatment Options: Antacids and Alginates

The pharmacodynamic profiles of antacids and alginates allow them to be dosed as symptoms arise. Since most alginate formulations contain acid-neutralizing ingredients, they are often considered synonymous with antacids. However, their mechanism of action and clinical profile are markedly different (Fig. 2). Understanding this distinction may be important for tailoring products to individual needs.

Fig. 2.

Mechanism of action of the major types of nonprescription treatments available for self-management of reflux-like symptoms. H₂RA, histamine-2 receptor antagonist; H⁺K⁺ATPase, hydrogen potassium ATPase; PPI, proton pump inhibitor *Raft-forming alginate products only. Alginate formulations differ in their acid-neutralizing capacity and raft-forming capabilities.

Antacids

Clinical Use

Antacids are salts of weak bases (e.g., sodium bicarbonate, aluminum hydroxide) available as chewable tablets, liquids, and gum. Antacids have a rapid onset of action, making them ideal for treatment of ongoing reflux-like symptoms or PPI breakthrough symptoms [23–25], but the transient neutralizing effect (due to rapid esophageal and gastric emptying) limits effectiveness for prolonged or frequent symptom episodes [25]. Owing to their temporary effect, product labeling generally allows for numerous doses per day (up to 16 tablets per day for some products!) [26]. Antacids have relatively well-characterized safety profiles and are considered safe to use during pregnancy when lifestyle changes alone are not sufficient (although sodium-containing antacids should be avoided, see safety section) [27, 28].

Mechanism of Action

Antacids act through direct neutralization of hydrochloric acid to form chloride salts and water, which reduces the hydrogen ion concentration, raising the pH [29]. Evidence suggests they act primarily to neutralize refluxed acid within the esophageal lumen (Fig. 2), having only a minimal effect on intragastric acidity [30–32]. The onset of neutralization occurs rapidly [32, 33], but the scale and duration of neutralizing effect depends on the specific formulation [30–33]. For example, the chewing and repeated swallowing associated with antacid chewable tablets and gum prolongs the neutralization effect by exposing the esophagus to multiple small doses over a somewhat longer period, as well as stimulating bicarbonate-rich salivary secretion to promote esophageal acid clearance [25].

Efficacy

In terms of symptom relief, patients report meaningful heartburn improvement within 10–20 min of taking antacid [34–36]. A meta-analysis to assess the efficacy of OTC treatments for reflux-like symptoms found the quantity and quality of studies for antacids inferior to those for the other products [37], most likely because the bulk of antacid research was conducted long ago. Using data from randomized controlled trials (RCTs), the therapeutic gain relative to placebo was 11% (0.11 [95% CI: 0.03–0.20]) [37]. The effectiveness and duration of response of each antacid is influenced by the formulation and its acid-neutralizing capacity. However, guidelines have concluded that there is a lack of evidence to favor one antacid over another [38]. Selection will most likely depend on local availability and an individual’s subjective response to the palatability of the product, which can vary considerably [39].

Safety

Antacids are quickly eliminated from the stomach and side effects are rare. Magnesium salts can cause diarrhea and aluminum salts constipation, so they are often combined to minimize these adverse effects [29, 40]. Magnesium has slow absorption and is rapidly excreted in the urine, putting individuals with chronic renal failure at risk of hypermagnesemia, especially elderly at-risk patients [40]. Sodium-containing antacids should be avoided in patients on a strict low-sodium diet (e.g., hypertension, cirrhosis, congestive heart failure) [41] and pregnancy, owing to risk of fluid overload and metabolic alkalosis in the mother and fetus [28]. Prolonged use of calcium-containing antacids may increase the risk of hypercalcemia or alkalosis [42]. Some antacids may affect the absorption of concurrently administered medicines including antibiotics (e.g., tetracyclines, quinolones) and antifungals (itraconazole, ketoconazole), so allowing a 2–4 h window between taking antacids and other medicines is advisable [43–45].

Alginates

Clinical Use

Alginate-based formulations are available as tablets or liquids for on-demand use after meals and at bedtime. Updated guidelines suggest empirical alginate treatment as an alternative to empirical PPI treatment for patients with typical symptoms, without risk factors for complications or family history of upper digestive tract malignancies and without alarm symptoms [46], as well as for add-on therapy for PPI breakthrough symptoms [46] and rescue therapy during PPI tapering [46, 47].

Mechanism of Action

Most alginate-based formulations have an antacid component (e.g., sodium bicarbonate, calcium carbonate) to facilitate the primary mechanism of action, which is the formation of an alginate foam raft interface between gastric contents and the esophageal mucosa (Fig. 2) [48–50]. After entering the stomach, three simultaneous chemical reactions take place on contact with gastric acid: (i) alginate is converted to alginic acid; (ii) calcium carbonate releases free calcium ions which bind to alginic acid, cross-linking the polymers to provide raft strength; and (iii) sodium carbonate reacts to form carbon dioxide which becomes trapped with antacid within the matrix of the raft, causing the raft to float on top of the gastric contents [50, 51]. When taken postprandially, the alginate raft co-localizes with the acid pocket [52, 53] and refluxes in place of gastric contents (Fig. 2) [48, 49, 54]. The buoyant raft remains in place while the meal empties from the stomach [55] and in patients with hiatus hernia, it promotes subdiaphragmatic positioning of the acid pocket [52]. Studies have consistently shown that the acid pocket is longer in patients with hiatus hernia [22]. In small hiatus hernia, the acid pocket typically remains below the diaphragm, whereas in approximately 40% of patients with a large hiatus hernia, it extends above the diaphragm and is associated with increased esophageal acid exposure [22]. Promoting a subdiaphragmatic position of the acid pocket may therefore help reduce reflux. Accordingly, alginate-antacid therapy positioned the acid pocket below the diaphragm in 71% of patients compared with 21% receiving antacid alone (p = 0.08) and there was an inverse correlation between a subdiaphragm position of the acid pocket and acid reflux (r = −0.76, p < 0.001) [52]. Magnetic resonance imaging has been used to visualize the disposition of the alginate raft versus an antacid of equivalent acid-neutralizing capacity when taken after a meal [53]. An alginate raft developed at the air-meal interface within 15 min, whereas antacid sank to distal stomach [53]. Gastric acidity and pepsin measured at the esophagogastric junction after 30 min were lower with alginate use compared with patients taking an antacid [53]. Alginates have also demonstrated bioadhesive properties, adhering to the esophageal mucosa and providing protection by minimizing contact with gastric reflux (Fig. 2) [56–59].

Alginate-Based Products Are Not All the Same

Alginate is a structural polysaccharide derived from various species of brown algae (seaweed) [60]. Formulations are complex, varying in the type and amount of alginate and antacid components, resulting in markedly different weights, volumes, raft strength, resilience, porosity, pepsin-binding capacity, and acid-neutralizing capacity (Table 1) [50, 60–62]. Thus, clinical evidence derived from one alginate formulation may not translate to others. While the general term “alginates” is used throughout this review, the reader should refer to individual studies to ascertain the formulation to which the evidence applies. Caution is also required because a brand name can represent different formulations in different countries. For example, “Gaviscon” sold in the USA (Haleon US Holdings LLC., NJ, USA) is a non-raft-forming antacid containing aluminum hydroxide and magnesium carbonate (sodium alginate listed as an inactive ingredient), whereas the range of chewable tablets and liquid formulations sold under the same brand name in other countries contain sodium alginate as the active ingredient (Table 1). Among the Rennie brand (Bayer, Leverkusen, Germany), some products (e.g., Rennie Liquid/Rennie Dual action) contain alginate/alginic acid, whereas other “Rennie” products do not; differences that may not be apparent to the consumer.

Table 1.

Comparison of alginate products and their raft and acid-neutralizing characteristics

Product	Alginate	Antacid(s)	ANC	Raft characteristics
				acid trapping	duration of simulated reflux neutralization	alginate content* within the raft at pH 1.0
​	mg/max dose	mg/max dose	mEq/dose	yes/no	minutes	mg
GDA	Sodium alginate 1000	Calcium carbonate 650	7.9	Yes (absorbent)	93	550
		Sodium bicarbonate 426
GO	Sodium alginate 1000	Sodium bicarbonate 534	3.6	Yes (absorbent)	61	515
		Calcium carbonate 320
Peptac	Sodium alginate 1000	Sodium bicarbonate 534	3.3	No (nonabsorbent)	16	205
		Calcium carbonate 320
Algycon	Alginic acid 600	Aluminum hydroxide 90	1.3	No (no structure)	0	215
		Magnesium carbonate 120
Maalox	Sodium alginate 500	Calcium carbonate 164	1.7	No (nonabsorbent)	21	175
Mylan	Sodium alginate 1000	Sodium bicarbonate 534	2.2	No (nonabsorbent)	5	235
Rennie Duo	Sodium alginate 300	Calcium carbonate 1200	12.8	No (highly porous)	27	185
		Magnesium carbonate 140

Table adapted from Dettmar et al. [50].

ANC, acid-neutralizing capacity; AUC, area under the curve; GDA, Gaviscon Double Action; GO, Gaviscon Original.

*Estimates derived from plotted data [50]. GDA and GO liquid (Reckitt, Slough, UK), Peptac liquid (Pinewood Laboratories Limited, Clonmel, Ireland), Algycon tablets (American Taiwan Biopharma, Bangkok, Thailand), Maalox RefluRAPID (Sanofi-Aventis, Gentilly, France) liquid suspension, Mylan liquid suspension (Mylan, Pennsylvania, USA), and Rennie Duo (Bayer, Leverkusen, Germany) liquid suspension. All measurements relate to the maximum recommended dose of alginate product.

Efficacy

As monotherapy, meta-analyses have shown alginates to be more effective than placebo and antacids and statistically non-inferior to PPI and H₂RAs for improvement in reflux-like symptoms [37, 63]. Significant acid reflux reduction and/or symptom control has been demonstrated in patients with late night/night time symptoms [64, 65], with hiatus hernia [52, 66], during PPI tapering [67, 68] or PPI wash-out (in patients referred for investigation) [69], and in pregnancy [70]. Alginates have also demonstrated symptomatic benefit as add-on to PPI therapy in patients with breakthrough reflux symptoms [64, 71], although one RCT with an unusually large placebo response failed to demonstrate statistical significance [72]. A network meta-analysis of treatments for patients with heartburn and/or regurgitation found that the combination of alginate with omeprazole (20 mg) was more effective than either preparation alone after ≥4 weeks of treatment in patients without erosive esophagitis or evidence of severe gastroesophageal reflux disease [73]. By contrast, a study testing a pure non-bicarbonate-containing (i.e., non-raft forming) alginate formulation found no clinical benefit when added to PPI [74].

Safety

Owing to their nonsystemic mode of action, alginate-based formulations have a favorable safety profile [60], but caution is required regarding the sodium content (e.g., in some cases of congestive heart failure or renal impairment), calcium content (e.g., in patients with hypercalcemia, nephrocalcinosis, and recurrent calcium containing renal calculi), and potassium content (e.g., in some patients with kidney failure on a controlled potassium diet) [75]. As with antacids, a 2-h time interval is advisable before taking other medicines [75]. Clinical studies and post-marketing experience in pregnant women suggests no adverse effects during pregnancy or breastfeeding [75].

Nonprescription Gastric Acid Suppressants: H₂RAs and PPIs

Gastric acid suppressants are systemic medicines that target gastric parietal cells to inhibit acid secretion (Fig. 2), making them effective for prevention of acid-related symptoms, rather than providing immediate relief of existing symptoms. While several H₂RAs were approved for nonprescription use, concerns regarding contamination with N-nitrosodimethylamine (a potent human carcinogen) led to the withdrawal of all except famotidine, which is now the only nonprescription H₂RA available in many countries. In a survey of more than 800 gastroenterologists in the USA, half recommended nonprescription PPI for typical acid reflux, whereas only 13% recommended an H₂RA [76].

H2RAs

Clinical Use

Nonprescription H₂RAs are available as tablets or liquids taken either at the onset of heartburn or 30 min prior to eating food or drink that is expected to trigger heartburn. Product labeling allows 14 days of continuous, twice-daily dosing. However, owing to tachyphylaxis, H₂RAs may be best used as a one-off or short-term treatment for reducing gastric acidity to treat or prevent infrequent episodes of heartburn (e.g., when expected owing to planned overindulgence of food or drink) [25].

Mechanism of Action

H₂RAs block one of three pathways of acid secretion from gastric parietal cells by competitively and reversibly binding to the histamine H₂ receptor (Fig. 2) [25, 42]. By blocking this process, H₂RAs suppress gastric acid secretion under both stimulated and basal conditions, including nocturnal acid secretion [42, 77]. The antisecretory effect of H₂RAs is partly meal-dependent, reflecting differences in the physiological drivers of acid secretion. Basal (interdigestive) secretion is largely histamine-mediated, and H₂RAs are therefore most effective under these conditions, particularly at night (∼70% inhibition). In contrast, meal-stimulated secretion involves gastrin release, vagal cholinergic stimulation (acetylcholine), and histamine; consequently, selective histamine blockade yields only partial suppression of acid output (generally ≤50%) [78]. After famotidine administration, gastric pH begins to rise within 30 min [25], with pH >3 achieved within approximately 70 min [79], lasting for up to 12 h [80]. However, a comparative study found that the initial rise in gastric pH with nonprescription famotidine (10 mg or 20 mg twice daily) had diminished by day 3 owing to tachyphylaxis, and mean percentage time pH >4 was superior with nonprescription PPI (omeprazole 20 mg once daily) compared with famotidine after day 1 [81].

Efficacy

While PPIs are more potent gastric acid suppressants, H₂RAs have a faster onset of action, with most patients gaining meaningful heartburn relief within 1–2 h [34, 35]. On the other hand, while antacids have an immediate effect, H₂RAs exhibit greater and more durable symptomatic improvement [34, 37]. A 2007 meta-analysis comparing OTC therapies showed therapeutic gain of up to 41% with H₂RAs versus placebo, compared with 60% with alginate/antacid combinations, and 11% with antacids (nonprescription PPI not included in analysis) [37]. The addition of H₂RA to a PPI has been shown to reduce night symptoms, but this benefit diminished after day 1 [82, 83], emphasizing tachyphylaxis with H₂RA use for ≥2 consecutive days [84].

Safety

Nonprescription H₂RAs are generally well tolerated, with common adverse effects including headache, dizziness, diarrhea, and constipation [85]. Famotidine does not interact with the cytochrome P450-linked drug-metabolizing enzyme system, although the absorption of some medicines may be reduced, including ketoconazole, itraconazole, rilpivirine, cyanocobalamin, and most of tyrosines kinase inhibitors (excluding vandetanib, imatinib) [85]. Owing to a lack of sufficient safety data, they are generally not recommended in pregnant or breastfeeding women [85].

PPIs

Clinical Use

Nonprescription, low dose PPI formulations have been developed for esomeprazole, lansoprazole, pantoprazole, rabeprazole, and omeprazole (availability varies by country) [3]. Nonprescription PPIs are an “intermittent” therapy, usually sold as a 14-day course for once-daily oral dosing, with no more than 3 courses recommended within a 12-month period. They are appropriate for treating individuals experiencing frequent reflux-like symptoms (≥2 days per week) [86–88].

Mechanism of Action

PPIs are prodrugs that require activation by acid to be converted into the active sulphenamide, which binds covalently to exposed cysteine residues on activated gastric H⁺K⁺ ATPase (“proton pump”) (Fig. 2) [89, 90]. Although PPIs have relatively short serum half-lives (<2 h), they continue to inhibit acid secretion after clearance from the serum [89]. After PPI dosing, the resumption of acid secretion is based on multiple physiological mechanisms including de novo pump synthesis, trafficking of inactive proton pumps to the canalicular membrane, reversal of the covalent disulfide bond leading to reactivation of the pump, and pharmacokinetic decline in systemic drug levels [78, 91]. Only a fraction of pumps are active at any given time so repeated doses are required for maximal effect (∼3–5 days to reach steady state) [89]. Further, PPIs are most effective when taken ∼30 min before a meal, thereby facilitating synchrony between optimal blood concentrations of the drug- and meal-induced activation of proton pumps [89]. An analysis of RCT data of PPIs at OTC doses showed that maintenance of intragastric pH >4 was variable among PPIs, with esomeprazole 20 mg performing best by maintaining pH >4 for more than half of the 14-h daytime period when dosed 30 min before breakfast [92]. If a patient experiences symptoms mostly at night, dosing before the evening meal may be preferable [87]. Alternatively, alginate could be taken at bedtime to suppress symptoms related to acid exposure that often occurs on lying down, especially in patients with obesity/hiatus hernia [64, 65].

Efficacy

Nonprescription PPIs are effective at reducing typical reflux-like symptoms versus placebo, with the greatest treatment benefit observed during days 5–14 of the treatment period [93]. They are the most effective self-management treatment option for the prevention of acid-related symptoms [87]. Nonprescription PPIs are proven more effective than H₂RAs at suppressing gastric acid and provide significantly greater symptom relief from day 2 [81, 94]. Patients with typical symptoms (and no evidence of erosive reflux disease) report high rates of satisfaction, with no rebound symptoms and therapeutic benefit that can last for weeks after completing the 14-day course [87, 95].

Safety

Nonprescription PPIs are at the lower end of dosing and are considered safe for intermittent use [88]. Specific safety data for nonprescription use of PPI are lacking, but a consensus panel concluded that there is a low risk of adverse effects potentially associated with long-term use, e.g., changes in micronutrient absorption (iron, calcium, magnesium, vitamin B₁₂), osteoporosis, community-acquired pneumonia, or Clostridioides difficile infection [88]. However, nonprescription PPIs are often not taken optimally (30–60 min before a meal) [10] and individuals should be reminded that PPIs are not effective when taken “on-demand” for existing symptoms [96]. Idiosyncratic PPI side effects include headache, rash, dizziness, nausea, abdominal pain, constipation, and diarrhea [24, 88]. PPIs may interact with co-administered medicines by changing their solubility or absorption (by reducing gastric acidity), by modifying metabolism (mostly through the cytochrome P450 enzyme system), or by inhibiting renal proton pumps (altering drug excretion) [88]. Some drug-drug interactions are well documented including atazanavir, ketoconazole, digoxin, and methotrexate [96]. In pregnancy, while most PPIs are considered safe, their use is generally reserved for women with complicated reflux disease or troublesome symptoms not responding to nonsystemic treatments [28].

Other OTC Treatment Options/Active Ingredients for Reflux-Like Symptoms

Agents with bioadhesive properties, including alginates, may provide an alternative mechanism of action for patients with reflux hypersensitivity (who are less responsive to acid reduction/neutralization). Bioadhesive agents form a long-lasting film over the esophageal mucosa, creating a protective barrier that prevents transepithelial penetration of toxic refluxate components [97]. In addition to alginates, mucosal protectants, such as hyaluronic acid-based bioadhesive formulations [97–99] and Poliprotect (NeoBianacid, Aboca, Sansepolcro, Italy) [100] are available in some countries. Clinical studies have shown symptomatic benefits with hyaluronic acid-based bioadhesive formulations versus placebo when used alone [98] or as add-on to PPIs in patients with nonerosive reflux disease [99]. Poliprotect (NeoBianacid, Aboca, Sansepolcro, Italy) proved non-inferior to omeprazole (20 mg) in symptomatic patients with heartburn/epigastric burning over a 2-week treatment period [100]. A pilot study has also shown that a herbal preparation, STW5 (Iberogast, Bayer, Leverkusen, Germany), may have benefits for patients with pH-metry-confirmed reflux disease [101]. Simethicone, an anti-foaming agent, is sometimes combined with antacids to facilitate belching and reduce bloating/flatulence [40], and bismuth subsalicylate is used for dyspeptic symptoms, gastric discomfort, diarrhea, and nausea [102]. Other “natural” remedies, such as aloe vera, ginger, or apple cider vinegar, are popular, but published efficacy and safety data are lacking.

Tailored Approach to the Self-Management of Reflux-Like Symptoms

Based on the findings of this review, we propose a tailored approach to support decision-making for patients with reflux-like symptoms. The proposed algorithm (Fig. 3), integrating referral criteria (alarm symptoms), evidence-based lifestyle advice, symptom assessment, and individualized treatment selection, could be incorporated into digital tools, adapted for pharmacy or primary care, to support wider implementation in everyday practice. The algorithm directs appropriate treatment choice through assessment of the individual’s symptom pattern, frequency, and treatment priorities. For example, an individual whose symptoms are clearly related to dietary triggers may benefit from a recommendation of alginate dosed after meals with reinforcement of lifestyle advice about not reclining after eating and avoiding large meals. Other individuals whose symptoms wax and wane, with periods of increased frequency, may benefit from a 14-day course of nonprescription PPI, with advice about daily dosing ∼30 min before a meal (not “on demand” as symptoms arise).

Fig. 3.

Algorithm for tailored self-management of reflux-like symptoms in treatment-naïve patients. H₂RA, histamine-2 receptor antagonist; PPI, proton pump inhibitor.

Use of a protocol-based approach has previously been shown to improve real-world outcomes in patients with reflux-like/epigastric symptoms [103]. Implementation of an algorithm across 134 pharmacies provided significant improvements in patients’ symptoms and quality of life and gained more than 99% satisfaction among recipients of the pharmacist-led care [103]. These findings underscore the potential of structured, protocol-based approaches to improve care and patient outcomes in frontline settings.

Conclusion

The management of reflux-like symptoms is evolving based on a greater understanding of reflux-like symptom pathophysiology [6, 16, 104, 105]. The traditional acid-targeted approach to symptom management, involving widespread diagnosis of gastroesophageal reflux disease and liberal long-term prescribing of gastric acid suppressants, is being replaced with a patient-centered model of care which places greater emphasis on low-harm and pragmatic approaches to self-management, including dietary, lifestyle, and behavioral interventions, as well as OTC treatments [8, 106]. A previous evidence-based consensus developed statements of advice to help individuals recognize and manage their individual risk factors [8]. However, guidance on nonprescription treatment selection is generally lacking. Individuals may need help understanding the different modes of action and discriminating between available treatments which fall into 2 broad categories: on-demand treatments for rapid relief of existing symptoms and sustained gastric acid suppression for prevention of frequent or anticipated symptoms. Ultimately, effective self-management of reflux-like symptoms relies on collaborative efforts across pharmacy, primary care, and gastroenterology to ensure consistency in advice, appropriate use of treatments, and optimal outcomes. A standardized algorithm can help tailor treatments to an individual’s symptom profile to minimize the impact of symptoms on their quality of life.

Acknowledgments

The authors would like to thank Lisa O’Rourke, PhD (for Lumanity, UK) for editorial assistance.

Conflict of Interest Statement

A.P.S.H., C.S., A.J.B., M.F., E.L-P., J.M.M., E.S., and P.J.K attended online meetings funded by Reckitt Benckiser Healthcare Ltd., which formed the basis for this work. A.P.S.H. has served as a consultant and an advisory board member and has been involved in the development of educational materials for Reckitt and the UK and European Primary Care Societies for Gastroenterology. C.S. has served as a speaker, consultant, and/or advisory board member for Alfasigma, Pfizer, Takeda, Reckitt Benckiser, and Dicofarm and has in the past received funding from Giuliani Pharmaceuticals and Pfizer. A.J.B. has received research funding from Sanofi/Regeneron, Uniquity, Aqilion, SST, Laborie, and Dr. Falk Pharma and received speaker and/or consulting fees from AlfaSigma, Uniquity, Laborie, BMS, Dr. Falk Pharma, Calypso Biotech, Eupraxia, Aqilion, Alimentiv, Sanofi/Regeneron, Uniquity, Reckitt, Domain, and AstraZeneca. M.F. has served as a consultant and has been involved in the development of educational materials and events for Medtronic, Laborie, Diversatek, Jinshan, FAN, Kibion, Sanofi/Regeneron, Reckitt, and Weleda. He has served as a speaker for the same companies and for Schwabe. He has received research funding and/or equipment from Medtronic, Laborie, Jinshan, FAN, Chocosuisse, and Weleda. E. L-P. has served as a consultant and an advisory board member and has been involved in the development of educational materials for Reckitt and the Spanish and Ibero-American Society of Community Pharmacy. J.M.M. has served as a consultant and an advisory board member and has been involved in the development of educational materials for Reckitt, Novo Nordisk, and Boehringer Ingelheim. E.V.S. has served as speaker for AbbVie, Aboca, Abivax, Agave, AG Pharma, Alfasigma, Apoteca, Bios Line, CadiGroup, Celltrion, Dr. Falk, EG STADA Group, Eli Lilly, Fenix Pharma, Galapagos, Giuliani, Johnson & Johnson, JB Pharmaceuticals, Innovated/Adacyte, Lionhealth, Malesci, Mayoly Biohealth, Montefalco, Novartis, Omega Pharma, Pfizer, Rafa, Reckitt Benckiser, Recordati, Sandoz, Sanofi/Regeneron, SILA, Takeda, Tillotts, and Unifarco. He has served as consultant for AbbVie, Alfasigma, Apogee, AstraZeneca, Biogen, Bristol Myers Squibb, Celltrion, Dr. Falk, Eli Lilly, Fenix Pharma, Ferring, Giuliani, Grunenthal, Johnson & Johnson, JB Pharmaceuticals, Merck & Co, Nestlè, Pfizer, PRO.MED.CS Praha a.s., Reckitt Benckiser, Recordati, Sanofi/Regeneron, SILA, Takeda, and Unifarco. He received research support from Bonollo, Difass, Pfizer, Reckitt Benckiser, Sanofi/Regeneron, SILA, Unifarco, and Zeta Farmaceutici. P.J.K. has served as a consultant and an advisory board member for Reckitt and Implantica, as a speaker for Phathom Pharmaceuticals, and shares ownership of the patent for Medtronic FLIP Panometry methods and technology.

Funding Sources

The online meetings were organized by Lumanity, UK, and funded by Reckitt Benckiser Healthcare Ltd. Writing support was provided by Lisa O’Rourke, PhD, for Lumanity, UK, and funded by Reckitt Benckiser Healthcare Ltd. The funder had no role in manuscript conception, planning, writing, and decision to publish.

Author Contributions

A.P.S.H., C.S., A.J.B., M.F., E.L-P., J.M.M., E.S., and P.J.K. meet the International Committee of Medical Journal Editors (ICMJE) authorship criteria and analyzed the literature and developed the manuscript content and algorithm, critically reviewed and revised the manuscript, and approved the final version, including the authorship list. A.P.S.H. made substantial contributions to the conceptualization of the project and, with P.J.K., drafted the original manuscript.

Funding Statement

The online meetings were organized by Lumanity, UK, and funded by Reckitt Benckiser Healthcare Ltd. Writing support was provided by Lisa O’Rourke, PhD, for Lumanity, UK, and funded by Reckitt Benckiser Healthcare Ltd. The funder had no role in manuscript conception, planning, writing, and decision to publish.