Dyspepsia medical therapy

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Fahad Hasan, M.D.[2] Ajay Gade MD[3]]

Overview

Medical therapy for dyspepsia is stepwise, empiric, and symptom-directed. The same treatment sequence applies to uninvestigated dyspepsia and to functional dyspepsia (FD) once organic disease has been excluded: Helicobacter pylori test-and-treat, then a time-limited proton pump inhibitor (PPI) trial, then a central neuromodulator, then a prokinetic, with psychological therapy for non-responders. H. pylori eradication and empiric PPI therapy both carry strong ACG/CAG recommendations; eradication is the only therapy that is potentially disease-modifying, since sustained benefit reclassifies the patient as having H. pylori-associated dyspepsia. Effect sizes across all effective therapies are modest.[1][2]

Medical Therapy

General Principles

  • Therapy is empiric and sequential. Each therapeutic trial should be time-limited (typically 4–8 weeks) with explicit discontinuation if there is no meaningful improvement, rather than indefinite accumulation of agents.[2]
  • An empathetic physician–patient relationship, with explanation of the disordered gut–brain interaction underlying symptoms, is itself part of therapy and should precede drug escalation.[3]
  • Subtype-directed therapy (postprandial distress syndrome [PDS] vs epigastric pain syndrome [EPS]) is a heuristic, not a validated stratification; no trial data exist for the large EPS–PDS overlap group.[2]
  • Review and withdraw or substitute dyspepsia-provoking drugs at first contact: NSAIDs, aspirin, bisphosphonates, oral potassium and iron preparations, and opioids.
  • Longest studied duration for neuromodulators in FD is 12 weeks; long-term efficacy is unknown.[2]

Step 1: Helicobacter pylori Eradication

Non-invasive H. pylori test-and-treat is first-line in patients aged <60 years without alarm features and without other endoscopy indications; a threshold of 50 years may be applied in populations at higher gastric cancer risk. Regimen selection follows the 2024 ACG guideline.[1][4]

Efficacy. In 29 RCTs, eradication was superior to control for symptom cure and for symptom improvement. Benefit was substantially larger when eradication was actually achieved. Adverse events and withdrawals due to adverse events were significantly more frequent with eradication therapy and should be raised in shared decision-making.[5] Head-to-head, eradication therapy has not shown a significant symptomatic advantage over empirical PPI therapy, so the Step 1 → Step 2 ordering rests on the durability of eradication benefit rather than on superior short-term symptom control.[6]

Within functional dyspepsia specifically, eradication is the only therapy graded high-quality evidence (PPIs are graded moderate in FD, and high only in uninvestigated dyspepsia), and it is the only therapy whose benefit may be permanent. Sustained benefit beyond 6 months reclassifies the patient as having H. pylori-associated dyspepsia, an organic diagnosis, rather than FD.[2][5][7] A meta-analysis of 23 studies found that eradication conferred significant symptomatic benefit at >6 months but not at <6 months, which both supports the reclassification concept. One trial reported benefit on epigastric pain and burning but not on early satiety or postprandial fullness, suggesting the effect may be greater in EPS than PDS.[8][7]

Regimen (2024 ACG): Optimized bismuth quadruple therapy for 14 days is the preferred empiric regimen. PPI–clarithromycin triple therapy is no longer recommended empirically. Rifabutin triple therapy and vonoprazan-based regimens are conditional alternatives. Vonoprazan is FDA-approved for H. pylori eradication both as dual therapy with amoxicillin and as triple therapy with amoxicillin and clarithromycin.[4][9] Confirm eradication ≥4 weeks after completing therapy and ≥2 weeks off PPI, using urea breath test or stool antigen test.[4]

For full regimen in detail, see Helicobacter pylori infection medical therapy.

Step 2: Acid Suppression

PPIs are first-line for H. pylori-negative patients and for those still symptomatic after documented eradication.[1]

Dosing

Standard once-daily dose (e.g., omeprazole 20 mg or lansoprazole 30 mg) taken before the first meal for 4–8 weeks. Dose escalation is not effective and is explicitly recommended against by the 2025 Italian joint consensus and the Rome gastroduodenal update; low-dose and standard-dose PPIs perform similarly.[2][10][11] An ineffective PPI should be stopped at 8 weeks.

Stopping a PPI

Double-dose PPI (standard dose twice daily, or a double-strength dose once daily) has not been studied in any RCT and is not FDA-approved, which reinforces the recommendation against dose escalation. When stopping, either tapering or abrupt discontinuation is acceptable. Patients should be warned that rebound acid hypersecretion may cause transient upper GI symptoms after withdrawal of prolonged therapy. This should not be misread as treatment failure or as proof of an ongoing indication. As-needed H2RAs, antacids, or on-demand PPI are reasonable bridging strategies; approximately half of patients who discontinue remain off continuous PPI at 6 months, three-quarters of them using an H2RA or antacid. Severe symptoms persisting beyond 2 months after discontinuation suggest either a continuing indication or a non–acid-mediated cause. Observational associations between long-term PPI use and fracture, chronic kidney disease and pneumonia have not been reproduced in randomized comparisons with placebo, so fear of these associations should not drive discontinuation where an indication exists.[12]

H2-receptor antagonists. H2RAs (e.g., famotidine) were effective versus placebo, but trial quality is lower and contamination with GERD is likely. Most guidelines still place PPIs first; the NICE guidelines propose both options. Note that in uninvestigated dyspepsia, the head-to-head data favour PPIs.[2][7][13][14] The 2025 Italian consensus reached no consensus on routine use of H2RAs, antacids, alginates, or mucosal protectants.[11]

Step 3: Central Neuromodulators

In functional dyspepsia, ACG/CAG places TCAs before prokinetics on the basis of superior evidence for TCAs in this indication. In uninvestigated dyspepsia in patients under 60, the same guideline explicitly states that the panel found no preference in the order in which prokinetic or TCA therapy is prescribed, and grades the recommendation low quality because no antidepressant trials exist in undiagnosed dyspepsia and TCAs are unlikely to affect peptic ulcer disease or GERD.[1]

Guideline disagreement on sequencing

The British Society of Gastroenterology 2022 guideline sequences therapy as acid suppression (PPI or H2RA), then a prokinetic, then central neuromodulators (TCAs), with referral for psychological therapy if medical therapy fails — placing prokinetics before neuromodulators, the reverse of ACG/CAG in FD.[15]

Tricyclic antidepressants

ACG/CAG recommended conditional use of TCAs on account of TCA adverse events (constipation, dry mouth, urinary retention, somnolence) and because a significant proportion of patients prefer not to take an antidepressant.[1] In the Functional Dyspepsia Treatment Trial, amitriptyline 50 mg nightly achieved adequate relief in 53% versus 40% with placebo, with the effect concentrated in epigastric pain. Benefit was independent of change in depression or anxiety scores, which is a useful counselling point for patients resistant to taking an "antidepressant."[1][16]

  • Amitriptyline or imipramine 10–25 mg nightly, titrated to 50 mg nightly.
  • Nortriptyline 10–75 mg nightly has better anticholinergic tolerability, but was of no benefit versus placebo in a randomized trial of 61 patients with FD.[7]
  • Adverse effects (dry mouth, drowsiness, constipation, urinary retention) are significantly more common than with placebo and prompt discontinuation; cumulative anticholinergic burden is a particular concern in older adults.[2][7]
  • Baseline electrocardiogram is prudent in older adults and in patients with cardiac risk factors or QT-prolonging co-medication.
  • Contraindications and cautions for TCAs: recent myocardial infarction, known arrhythmia or baseline QT prolongation, concurrent monoamine oxidase inhibitor, narrow-angle glaucoma, and clinically significant urinary retention. Additive QT risk with domperidone and other QT-prolonging agents must be checked before co-prescription.[1][17]
  • Allow 8–12 weeks before judging response.

Mirtazapine

It can be given 15 mg nightly. It is best suited to patients with prominent nausea and clinically significant weight loss; its H1 and 5-HT3 antagonism makes it the one agent in which weight gain is a therapeutic goal.[11] In the pivotal 8-week placebo-controlled trial of 34 patients with FD and >10% body-weight loss (without depression or anxiety), mirtazapine showed no benefit on overall FD symptoms, but did improve early satiation, nutrient tolerance, weight recovery, quality of life, and gastrointestinal-specific anxiety.[2][7] A subsequent 120-patient randomized trial of mirtazapine 15 mg nightly added to conventional therapy reported improvement in postprandial fullness, early satiation, nausea, quality of life, and weight.[18] Doses above 15 mg have not been studied in FD.

SSRIs and SNRIs

SSRIs are not effective and are not recommended for FD as such. Venlafaxine is ineffective and duloxetine was inferior to nortriptyline at 3 months.[1][16]

Step 4: Prokinetics

ACG/CAG gives a conditional recommendation for patients failing PPI, eradication, and TCA therapy.[1] The 2025 Italian consensus recommends against prokinetics as first-line and advises a short course preferentially in PDS-subtype patients.[11]

Availability caveat. None of the prokinetics eligible for the ACG/CAG review is available in the United States or Canada; availability elsewhere varies (acotiamide is licensed in Japan and India, itopride is unavailable in the UK and USA, and domperidone is available in Europe but not the USA). There are no clinical trials of metoclopramide in FD.[1][7]

Agent Mechanism Typical dose Availability and evidence status
Acotiamide Cholinesterase inhibitor; M1/M2 antagonist; enhances accommodation and emptying 100 mg three times daily Licensed for FD in Japan and India; most effective in PDS. A Japanese phase 3 trial confirmed efficacy of 100 mg three times daily in PDS for postprandial fullness, upper abdominal bloating, and early satiation, and a European 52-week open-label trial reported moderate or strong symptom improvement in 70.2% of patients[2][7][19][20][8]
Itopride D2 antagonist and cholinesterase inhibitor 50 mg three times daily Not available in the US or UK; benefit reported in PDS–EPS overlap; may improve quality of life[2][7][19]
Domperidone Peripheral D2 antagonist 10 mg three times daily Available in Europe; in the US obtainable only through an FDA expanded-access programme. Contraindicated in patients with a cardiac history; QT prolongation risk, with additive risk if co-prescribed with a TCA[1][13][21]
Mosapride 5-HT4 agonist Per licensed preparation Approved for FD and GERD in some Asian and South American countries; not available in the US or Europe[20]
Metoclopramide D2 antagonist; 5-HT4 agonist 10 mg up to four times daily (max 40–60 mg/day per indication) Available in the US but no FD trials; used off-label. FDA gives a boxed warning for tardive dyskinesia; it is contraindicated with any history of tardive dyskinesia. Avoid total treatment duration >12 weeks; use the lowest effective dose with periodic reassessment, and reduce the dose in older adults (higher tardive dyskinesia risk) and in renal or hepatic impairment[22][23]
Tegaserod 5-HT4 partial agonist — Some benefit in women with FD. Withdrawn from the US market in March 2007 after pooled trial data showed excess cardiovascular ischemic events, then re-approved in 2019 with a restricted label (women <65 years, no history of myocardial infarction, stroke, TIA, or angina, ≤1 additional cardiovascular risk factor), then commercially discontinued in 2022 for business reasons. Not currently marketed in the US[24][25]
Cisapride 5-HT4 agonist — Withdrawn worldwide (QT prolongation, torsades de pointes); drove most of the historical pooled benefit and caused excess adverse events[19]

Fundic Relaxants (5-HT1A Agonists)

  • Tandospirone 10 mg three times daily improves overall dyspeptic symptom severity, postprandial fullness, early satiation, and upper abdominal bloating, and increases gastric accommodation while delaying liquid emptying; evidence is predominantly Japanese.[2][7]
  • Buspirone 10 mg three times daily reduced bloating and postprandial fullness in a 17-patient crossover trial, but a 2025 systematic review and meta-analysis found no significant improvement in FD symptoms versus placebo, with no effect on postprandial fullness or nausea; only bloating severity improved. The multicentre placebo-controlled BESST trial in gastroparesis symptoms was likewise negative for early satiety and postprandial fullness. Tolerability is good and there is no dependence potential, and the Rome 2026 update still suggests buspirone may be used when early satiety, fullness and nausea predominate.[7][26][27][28]
  • Overall quality is low, and 5-HT1A agonists ranked poorly for symptom improvement in the network meta-analysis.[7][13]

Diet, Lifestyle, and Medication Review

  • Evidence for dietary intervention is low. Reasonable advice: frequent small meals, reduced fat content, and avoidance of identified individual triggers.[2]
  • The 2025 Italian consensus reached no consensus on any specific dietary regimen and explicitly discouraged exclusion diets, while endorsing general healthy lifestyle advice.[11]
  • Discontinue, dose-reduce, or substitute NSAIDs, aspirin, bisphosphonates, oral potassium and iron, and opioids where feasible.

Psychological Therapy

ACG/CAG suggests psychological therapy for FD not responding to drug therapy.[1] The 2025 Italian consensus recommends cognitive behavioral therapy (CBT) for patients not responding to medical therapy.[11] CBT and gut-directed hypnotherapy have shown large effect sizes in meta-analysis, but all RCTs are at high risk of bias given unblindable interventions, and availability is limited.[7]

Complementary and Alternative Medicine

ACG/CAG does not recommend routine use of complementary and alternative medicine.[1] The 2025 Italian consensus acknowledged perceived usefulness but found the evidence insufficient owing to poor methodology.[11] Antacids, sucralfate, and bismuth monotherapy lack evidence for symptom improvement in FD.[7]

Herbal preparations are the most frequently studied complementary agents in FD, and the evidence is not uniformly weak. In a Cochrane review of 41 trials, peppermint plus caraway oil probably produces a large improvement in global dyspepsia symptoms at 4 weeks, increases the improvement rate, and probably improves quality of life, with no clear excess of adverse events. Curcuma longa probably produces moderate improvement. STW-5 (Iberogast) may improve symptoms but the evidence is very uncertain. The Rome gastroduodenal update additionally lists Rikkunshito, ZhiZhu KuangZhong and Biling Weitong granules as superior to placebo.[29][20][2]

Rikkunshito, a Japanese KAMPO preparation with ghrelin-signalling and prokinetic effects, is marketed in Japan for FD. A meta-analysis of 52 RCTs reported a higher total clinical efficacy rate than Western medicine, with greater improvement in gastric emptying and lower recurrence at 6 months, though most comparators were active rather than placebo. The placebo-controlled Japanese DREAM study reported overall treatment efficacy improvement in 29.5% versus 21.1%, with benefit concentrated in PDS symptoms.[30][8][2]

Stepwise Treatment Algorithm

Template:Family tree/summary= Stepwise medical therapy for uninvestigated and functional dyspepsia
 
 
Dyspepsia, no indication for endoscopy
 
 
 
 
 
 
 
 
 
 
 
 
Step 1: Non-invasive H. pylori test
Eradicate if positive (14-day optimized bismuth quadruple)
Confirm cure ≥4 weeks later
 
 
 
 
 
 
 
 
 
 
 
 
Step 2: Standard-dose PPI once daily, 4–8 weeks
Do not escalate dose; stop if ineffective
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
EPS-predominant:
Step 3 TCA (amitriptyline 10–25 mg nightly, titrate to 50 mg)
 
PDS-predominant:
Mirtazapine 15 mg nightly if early satiation, nausea or weight loss
Short prokinetic course
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Refractory: reassess diagnosis, stop failed agents,
refer for CBT or gut-directed hypnotherapy
 
 

Pregnancy

Pregnancy is not addressed by the major FD guidelines, and the standard algorithm translates poorly to this population.

Endoscopy and test-and-treat. The low diagnostic yield of endoscopy and its procedural risks shift the balance against it. For eradication therapy in pregnancy, see Helicobacter pylori infection medical therapy.[21]

Acid suppression. H2RAs (cimetidine, famotidine) are the most commonly used antireflux agents in pregnancy. PPIs may be considered if lifestyle measures and antacids fail; a meta-analysis of 26 studies found no significant association between maternal PPI use and abortion, stillbirth, neonatal death, preterm birth or low birth weight, although one study reported a non-significant increase in congenital malformations.[21][31]

Prokinetics. The FDA letter categories (A–X) were retired in 2015 and replaced by the Pregnancy and Lactation Labeling Rule. The metoclopramide label states that published cohort studies, national registry studies and meta-analyses do not report an increased risk of adverse pregnancy-related outcomes. A Danish register cohort of 28,486 first-trimester–exposed pregnancies found no association with major congenital malformations, spontaneous abortion or stillbirth. Metoclopramide crosses the placenta and may cause extrapyramidal signs and methemoglobinemia in the neonate when given during delivery; monitor the neonate accordingly. Domperidone should not be used off-label in pregnancy because of cardiac safety concerns.[22][32][33][34]

Neuromodulators. TCAs have been associated with a possible increase in preterm delivery and perinatal complications with third-trimester use; they are best reserved for severe, refractory symptoms, with therapy individualised per ACOG guidance on antidepressants in pregnancy. SSRIs and SNRIs are ineffective in FD and therefore carry no favourable risk–benefit balance here.[34][21]

Preferred earlier steps. Because the pharmacological options are constrained, moving the "later steps" of the algorithm earlier is reasonable: peppermint oil, ginger (250 mg four times daily) and pyridoxine (10–25 mg every 8 hours) where nausea predominates, together with brain–gut behavioural therapy, hypnotherapy or acupuncture. Ginger accelerates gastric emptying relative to placebo but did not improve symptoms after acute administration in FD, and long-term data are lacking; it is offered here for nausea rather than for dyspeptic symptoms as such.[21][35][8]

Refractory Disease

  • Reassess the diagnosis before further drug escalation; revisit gastroparesis, celiac disease, medication effects, and ongoing opioid use.
  • Stop failed agents before adding new ones. Four-drug regimens with cumulative anticholinergic burden are a common and avoidable harm in older adults.
  • Refer for CBT or gut-directed hypnotherapy when pharmacotherapy fails.[1][11]
  • In Rome IV FD patients concurrently consuming opioids, opioid cessation should be actively encouraged; combined opioid cessation and neuromodulator therapy has been associated with an NNT of 5.7 for clinically meaningful improvement.[36]

Common Pitfalls

  • Doubling the PPI dose in non-responders — never studied in an RCT, not FDA-approved, and contrary to current consensus.[11][12]
  • Misreading rebound acid hypersecretion after PPI withdrawal as treatment failure, and reinstating indefinite therapy.[12]
  • Prescribing metoclopramide for FD on an assumption of class efficacy; there are no FD trials and there is a tardive dyskinesia boxed warning with a ≤12-week limit.[1][22]
  • Applying domperidone's cardiac contraindication to metoclopramide; the metoclopramide boxed warning concerns tardive dyskinesia, not cardiac disease.[22]
  • Failing to confirm eradication and then attributing persistent symptoms to FD when the infection was never cleared — benefit is nearly three-fold greater when eradication succeeds (NNT 4.5).[5]
  • Adding agents without stopping failed ones.
  • Interpreting the prokinetic Cochrane NNTB of 7 at face value; heterogeneity was 91% with demonstrable publication bias.[19]
  • Reflexively labelling refractory symptoms as functional without revisiting organic and medication-related causes.

References

  1. ↑ 1.00 1.01 1.02 1.03 1.04 1.05 1.06 1.07 1.08 1.09 1.10 1.11 1.12 1.13 1.14 Moayyedi PM, Lacy BE, Andrews CN, Enns RA, Howden CW, Vakil N (2017). "ACG and CAG Clinical Guideline: Management of Dyspepsia". Am J Gastroenterol. 112 (7): 988–1013. doi:10.1038/ajg.2017.154. PMID 28631728.
  2. ↑ 2.00 2.01 2.02 2.03 2.04 2.05 2.06 2.07 2.08 2.09 2.10 2.11 2.12 2.13 2.14 Törnblom H, Carbone F, Hasler WL, et al (2026). "Gastroduodenal Disorders". Gastroenterology. 170 (6): 1240–1260. doi:10.1053/j.gastro.2026.01.038. PMID 41713705 Check |pmid= value (help).
  3. ↑ Camilleri M, BouSaba J (2023). "Potential Value of Biomarker-Based Approaches for Evaluation and Management of Costly Functional Gastrointestinal Diseases". Clin Gastroenterol Hepatol. 21 (10): 2462–2472. doi:10.1016/j.cgh.2023.04.030. PMID 37164114 Check |pmid= value (help).
  4. ↑ 4.0 4.1 4.2 Chey WD, Howden CW, Moss SF, Morgan DR, Greer KB, Grover S, Shah SC (2024). "ACG Clinical Guideline: Treatment of Helicobacter pylori Infection". Am J Gastroenterol. 119 (9): 1730–1753. doi:10.14309/ajg.0000000000002968. PMID 39231499 Check |pmid= value (help).
  5. ↑ 5.0 5.1 5.2 Ford AC, Tsipotis E, Yuan Y, Leontiadis GI, Moayyedi P (2022). "Efficacy of Helicobacter pylori eradication therapy for functional dyspepsia: updated systematic review and meta-analysis". Gut. 71 (10): 1967–1975. doi:10.1136/gutjnl-2021-326583. PMID 35022266 Check |pmid= value (help).
  6. ↑ Feld L, Cifu AS (2018). "Management of Dyspepsia". JAMA.
  7. ↑ 7.00 7.01 7.02 7.03 7.04 7.05 7.06 7.07 7.08 7.09 7.10 7.11 7.12 7.13 Ford AC, Mahadeva S, Carbone MF, Lacy BE, Talley NJ (2020). "Functional dyspepsia". Lancet. 396 (10263): 1689–1702. doi:10.1016/S0140-6736(20)30469-4. PMID 33049222 Check |pmid= value (help).
  8. ↑ 8.0 8.1 8.2 8.3 Masuy I, Van Oudenhove L, Tack J (2019). Aliment Pharmacol Ther. Missing or empty |title= (help)
  9. ↑ Food and Drug Administration. Orange Book: Approved Drug Products with Therapeutic Equivalence Evaluations. Voquezna (vonoprazan). 2024.
  10. ↑ Pinto-Sanchez MI, Yuan Y, Hassan A, Bercik P, Moayyedi P (2017). "Proton pump inhibitors for functional dyspepsia". Cochrane Database Syst Rev. 11: CD011194. doi:10.1002/14651858.CD011194.pub3. PMID 29161458.
  11. ↑ 11.0 11.1 11.2 11.3 11.4 11.5 11.6 11.7 11.8 Sarnelli G, Pesce M, Barbara G, et al (2025). "Italian guidelines for the diagnosis and treatment of functional dyspepsia — joint consensus from SIGE, SINGEM, AIGO, SIED and SIMG". Dig Liver Dis. PMID 40628573 Check |pmid= value (help).
  12. ↑ 12.0 12.1 12.2 "AGA Clinical Practice Update on De-Prescribing of Proton Pump Inhibitors: Expert Review". Gastroenterology. 2022.
  13. ↑ 13.0 13.1 13.2 Ford AC, Moayyedi P, Black CJ, et al (2021). "Systematic review and network meta-analysis: efficacy of drugs for functional dyspepsia". Aliment Pharmacol Ther.
  14. ↑ Mason JM, et al (2005). Aliment Pharmacol Ther. Missing or empty |title= (help)
  15. ↑ Black CJ, Paine PA, Agrawal A, Aziz I, Eugenicos MP, Houghton LA, Hungin P, Overshott R, Vasant DH, Rudd S, Winning RC, Corsetti M, Ford AC (2022). "British Society of Gastroenterology guidelines on the management of functional dyspepsia". Gut. 71 (9): 1697–1723. doi:10.1136/gutjnl-2022-327737. PMID 35798375 Check |pmid= value (help).
  16. ↑ 16.0 16.1 Pasricha PJ, Talley NJ (2026). "Functional Dyspepsia". N Engl J Med. 394 (2): 166–176. doi:10.1056/NEJMcp2501860.
  17. ↑ Food and Drug Administration. Prescribing information, amitriptyline hydrochloride tablets. DailyMed.
  18. ↑ Cao L, Li G, Cao J, Li F, Han W (2025). "Randomized clinical trial: the effects of mirtazapine in functional dyspepsia patients". Therap Adv Gastroenterol. 18: 17562848241311129. doi:10.1177/17562848241311129. PMID 39758962 Check |pmid= value (help).
  19. ↑ 19.0 19.1 19.2 19.3 Pittayanon R, Yuan Y, Bollegala NP, et al (2018). "Prokinetics for functional dyspepsia". Cochrane Database Syst Rev.
  20. ↑ 20.0 20.1 20.2 Camilleri M, Sarnelli G, Andresen V, et al (2026). "Pharmacological, Pharmacokinetic, and Pharmacogenomic Aspects of Disorders of Gut-Brain Interaction". Gastroenterology. 170 (6): 1152–1170. doi:10.1053/j.gastro.2026.02.010. PMID 42031437 Check |pmid= value (help).
  21. ↑ 21.0 21.1 21.2 21.3 21.4 Liu BD, et al (2023). "Functional dyspepsia and pregnancy". Aliment Pharmacol Ther.
  22. ↑ 22.0 22.1 22.2 22.3 Food and Drug Administration. Prescribing information, metoclopramide tablets (Boxed Warning; section 8.1). DailyMed.
  23. ↑ Camilleri M, Kuo B, Nguyen L, et al (2022). "ACG Clinical Guideline: Gastroparesis". Am J Gastroenterol. 117 (8): 1197–1220. doi:10.14309/ajg.0000000000001874.
  24. ↑ Sayuk GS, Tack J (2022). "Tegaserod: What's Old Is New Again". Clin Gastroenterol Hepatol. 20 (10): 2175–2184.e19. doi:10.1016/j.cgh.2022.01.024. PMID 35123085 Check |pmid= value (help).
  25. ↑ Chang L, Sultan S, Lembo A, et al (2022). "AGA Clinical Practice Guideline on the Pharmacological Management of Irritable Bowel Syndrome With Constipation". Gastroenterology. 163 (1): 118–136. doi:10.1053/j.gastro.2022.04.016.
  26. ↑ Mohamedali Z, Amarasinghe G, Hopkins C, Moulton CD (2025). "Effect of buspirone on upper gastrointestinal disorders of gut-brain interaction: a systematic review and meta-analysis". J Neurogastroenterol Motil. PMID 39779200 Check |pmid= value (help). Vancouver style error: initials (help)
  27. ↑ Parkman HP, Yates KP, Sarosiek I, et al (2023). "Buspirone for early satiety and symptoms of gastroparesis: a multi-centre, randomised, placebo-controlled, double-masked trial (BESST)". Aliment Pharmacol Ther.
  28. ↑ Elsenbruch S, Ballou S, Keefer L, et al (2026). "Biopsychosocial Aspects of Adult and Pediatric Disorders of Gut-Brain Interaction". Gastroenterology. 170 (6).
  29. ↑ Báez G, Vargas C, Arancibia M, Papuzinski C, Franco JV (2023). "Non-Chinese herbal medicines for functional dyspepsia". Cochrane Database Syst Rev. doi:10.1002/14651858.CD013323.pub2.
  30. ↑ Ko SJ, et al (2021). J Gastroenterol Hepatol. 36: 64–74. Missing or empty |title= (help)
  31. ↑ AGA Clinical Practice Update (2024). "AGA Clinical Practice Update on Pregnancy-Related Gastrointestinal and Liver Disease". Gastroenterology.
  32. ↑ Sun L, Xi Y, Wen X, Zou W (2021). "Use of metoclopramide in the first trimester and risk of major congenital malformations". PLoS One. PMID 34543335 Check |pmid= value (help).
  33. ↑ Pasternak B, Svanström H, Mølgaard-Nielsen D, Melbye M, Hviid A (2013). "Metoclopramide in pregnancy and risk of major congenital malformations and fetal death". JAMA. 310 (15): 1601–1611.
  34. ↑ 34.0 34.1 Dude C, Jamieson DJ (2021). "Assessment of the safety of common medications used during pregnancy". JAMA.
  35. ↑ Geisman T, Sayuk GS (2023). Aliment Pharmacol Ther. Missing or empty |title= (help)
  36. ↑ Nikaki K, Sawyer L, Akande F, Vasant DH (2021). "Clinical Characteristics and Outcomes of Patients With Rome IV Functional Dyspepsia Who Consume Opioids: A Real-World Study". Neurogastroenterol Motil. 33 (12): e14215. doi:10.1111/nmo.14215. PMID 33929099 Check |pmid= value (help).

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