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Abstract

Peptic ulcer disease (PUD) is a common acid-related gastrointestinal disorder characterized by mucosal damage in the stomach or duodenum. Its major etiological factors include Helicobacter pylori infection and non-steroidal anti-inflammatory drug (NSAID) use, along with lifestyle, genetic, and hypersecretory conditions. The present review provides a comprehensive overview of PUD, including its epidemiology, pathophysiology, clinical features, diagnostic approaches, and conventional allopathic management strategies such as proton pump inhibitors, H? receptor antagonists, cytoprotective agents, and H. pylori eradication regimens. In addition, it highlights the role of herbal medicines traditionally used in Ayurveda and other systems, supported by phytochemical and pharmacological evidence. The review also compares allopathic and herbal therapies, discusses current research trends such as nanotechnology and polyherbal formulations, and addresses limitations of herbal therapy. Overall, PUD management requires an integrated understanding of both evidence-based medicine and complementary approaches for improved therapeutic outcomes.

Keywords

Peptic ulcer disease; Helicobacter pylori; NSAIDs; Proton pump inhibitors; Herbal medicine

Introduction

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Peptic ulcer disease is an acid-induced lesion of the gastrointestinal tract, most commonly occurring in the stomach or proximal duodenum, and is characterized by mucosal disruption that extends beyond the muscularis mucosa into the submucosa or even deeper layers such as the muscularis propria. [1] The global prevalence is estimated to be around 5–10%, although recent epidemiological data indicate a decline in incidence, hospital admissions, and mortality. This reduction is largely attributed to improved hygiene practices and the widespread use of effective therapies, particularly those targeting Helicobacter pylori infection. [2, 3] Traditionally, peptic ulcer formation was thought to result primarily from increased gastric acid secretion combined with dietary factors and stress; however, current understanding emphasizes a multifactorial pathogenesis involving an imbalance between aggressive factors and mucosal defense mechanisms.

The major risk factors for peptic ulcer disease include Helicobacter pylori infection, non-steroidal anti-inflammatory drug (NSAID) use, alcohol consumption, smoking, and conditions such as Zollinger–Ellison syndrome. [4] Among these, H. pylori infection and NSAID use are the most significant contributors to both gastric and duodenal ulcers. However, only a minority of individuals exposed to these risk factors develop ulcers, highlighting the role of genetic and individual susceptibility, including cytokine gene polymorphisms such as interleukin-1β (IL1B). [5] The risk of complications increases significantly with NSAID and aspirin use, especially when combined with anticoagulants, corticosteroids, or selective serotonin reuptake inhibitors, which further elevate the risk of upper gastrointestinal bleeding. [6] Interestingly, a proportion of cases—termed idiopathic peptic ulcers—occur in the absence of H. pylori infection, NSAID use, or aspirin exposure. These cases, which account for about one-fifth of patients, may be associated with mechanisms such as psychological stress, ischemia, drug-induced injury, radiotherapy, infections, eosinophilic infiltration, surgical alterations like gastric bypass, or metabolic disturbances, although their exact pathogenesis remains incompletely understood. [7, 8]

  1. Epidemiology

Peptic ulcer disease (PUD) is a common global gastrointestinal disorder, with a lifetime risk of developing the condition estimated to be approximately 5% to 10%. It represents a significant public health concern due to its association with morbidity, complications, and healthcare utilization worldwide. However, in recent decades, there has been a noticeable decline in the incidence of PUD across many regions. This reduction is largely attributed to improved sanitation and hygiene practices, widespread eradication of Helicobacter pylori infection, and more cautious and rational use of non-steroidal anti-inflammatory drugs (NSAIDs), which are major contributing factors to ulcer formation. [5] Epidemiological patterns also show variation in ulcer types and demographic distribution. Duodenal ulcers are significantly more common than gastric ulcers, occurring approximately four times more frequently. In addition, duodenal ulcers show a higher prevalence in males compared to females, whereas gastric ulcers tend to have a more balanced gender distribution. [7]

  1. Etiology

Peptic ulcer disease (PUD) has various causes; however, Helicobacter pylori-associated PUD and NSAID-associated PUD account for the majority of the disease etiology.[1]

Table 1: Cause of Peptic ulcer [6, 7]

Category

Cause

Mechanism/Details

Common Causes

Helicobacter pylori infection

Gram-negative bacillus colonizing gastric epithelium; responsible for ~90% of duodenal ulcers and 70–90% of gastric ulcers. Causes mucosal inflammation and damage.

 

NSAIDs

Inhibit COX-1 enzyme, reducing prostaglandin synthesis, mucus production, bicarbonate secretion, and mucosal blood flow.

 

Medications

Includes corticosteroids, bisphosphonates, potassium chloride, and fluorouracil.

Lifestyle Factors

Smoking

Increases risk of duodenal ulcers and impairs ulcer healing.

 

Alcohol

Irritates  gastric  mucosa  and  increases  gastric  acid secretion.

Rare Causes

Zollinger–Ellison Syndrome

Gastrin-secreting tumor causing excessive gastric acid production.

 

Malignancy

Gastric cancer, lung cancer, and lymphomas may present with ulceration.

 

Stress-related ulcers

Associated with severe illness, burns, head injury, trauma, or intensive care admission.

 

Viral infections

Certain viral infections can damage gastric mucosa, particularly in immunocompromised patients.

 

Vascular insufficiency

Reduced blood supply to the gastric mucosa leading to ischemic injury.

 

Radiation therapy

Causes direct mucosal injury and ulcer formation.

 

Crohn Disease

Chronic inflammatory bowel disease that may involve the upper gastrointestinal tract.

 

Chemotherapy

Cytotoxic agents damage rapidly dividing gastrointestinal mucosal cells.

Table 2: Virulence Factors of Helicobacter pylori [8-9]

Virulence Factor

Function

Urease

Converts urea into ammonia, neutralizing gastric acid and allowing bacterial survival.

CagA/VacA Toxins

Cause gastric mucosal inflammation, epithelial damage, and ulcer formation.

Flagella

Provide motility, enabling movement through gastric mucus toward epithelial cells.

Table 3: Hypersecretory Conditions Associated with PUD [10-12]

Condition

Mechanism

Zollinger–Ellison Syndrome

Gastrinoma causes excessive gastrin secretion and acid hypersecretion.

Systemic Mastocytosis

Increased histamine release stimulates gastric acid secretion.

Cystic Fibrosis

Associated with altered gastrointestinal secretions and increased ulcer risk.

Hyperparathyroidism

Hypercalcemia stimulates gastrin release, increasing acid production.

Antral G-cell Hyperplasia

Increased gastrin-producing cells lead to excessive gastric acid secretion.

Table 4: Comparison of Major Causes of Peptic Ulcer Disease [13-15]

Cause

Frequency

Primary Mechanism

H. pylori infection

Most common

Mucosal inflammation and epithelial damage

NSAID use

Second most common

Reduced prostaglandin-mediated mucosal protection

Hypersecretory states

Rare

Excess gastric acid secretion

Medications

Less common

Direct mucosal injury or impaired protection

Stress-related illness

Rare

Ischemia and impaired mucosal defense

Malignancy

Rare

Tumor-associated ulceration
  1. Pathophysiology

The peptic ulcer disease (PUD) mechanism results from an imbalance between gastric mucosal protective and destructive factors.

Table 5: Risk factors predisposing to the development of PUD [16-21]

Risk Factor

How It Increases Risk of Peptic Ulcer Disease (PUD)

Helicobacter pylori infection

H. pylori colonizes the gastric mucosa and causes chronic inflammation (gastritis). It damages epithelial cells, decreases bicarbonate secretion, disrupts the mucus barrier, and may increase gastric acid secretion through increased gastrin release. These effects weaken mucosal defenses and promote ulcer formation, especially duodenal ulcers.

NSAID Use

NSAIDs inhibit cyclooxygenase (COX) enzymes, reducing prostaglandin synthesis. Prostaglandins normally stimulate mucus and bicarbonate secretion, maintain mucosal blood flow, and promote epithelial repair. Their loss makes the mucosa vulnerable to acid injury. NSAIDs may also directly damage the gastric epithelium.

First-Degree Relative with PUD

Individuals with a parent, sibling, or child who has PUD have a higher risk due to genetic susceptibility, inherited patterns of gastric acid secretion, increased likelihood of H. pylori infection within families, and shared environmental factors.

Emigrant from a Developing Nation

People who immigrate from regions with high H. pylori prevalence often acquire the infection during childhood because of crowded living conditions, poor sanitation, or limited access to clean water. Since H. pylori infection can persist for life, the risk of PUD remains elevated even after migration.

African American/ Hispanic Ethnicity

These populations have historically shown a higher prevalence of

H. pylori infection and may experience socioeconomic and healthcare-access factors associated with increased ulcer risk. The association is primarily related to environmental and epidemiologic factors rather than ethnicity itself.
  1. Symptoms

The symptoms of peptic ulcer disease (PUD) typically include epigastric pain, dyspepsia, nausea, vomiting, bloating, belching, early satiety, and loss of appetite. In complicated cases, patients may present with weight loss, hematemesis, melena, or signs of anemia due to gastrointestinal bleeding.

Table 6: Symptoms [22]

Symptom

Description

Epigastric pain (most common)

Burning, gnawing, or aching pain in the upper central abdomen (epigastrium).

Pain related to meals

Pattern depends on ulcer location (gastric vs. duodenal ulcer).

Nocturnal pain

Pain may wake the patient from sleep, especially with duodenal ulcers.

Bloating

Sensation of abdominal fullness or distension.

Belching

Frequent burping due to dyspepsia.

Nausea

Feeling of sickness in the stomach; may occur with or without vomiting.

Vomiting

Occurs in some patients, particularly if gastric outlet obstruction develops.

Early satiety

Feeling full after eating a small amount of food.

Loss of appetite

More common with gastric ulcers because eating may worsen pain.

Weight loss

Often seen in gastric ulcers due to reduced food intake.

Weight gain

May occur in duodenal ulcers because eating relieves pain, leading to increased food intake.

 

  1. Diagnosis of Peptic Ulcer Disease

Diagnosis of peptic ulcer disease involves a combination of clinical evaluation, endoscopic assessment, laboratory investigations, and detection of Helicobacter pylori infection. The process begins with a detailed history focusing on epigastric pain, relation to meals, NSAID use, and associated alarm symptoms such as weight loss, vomiting, gastrointestinal bleeding, or anemia.

Table 7. Diagnosis of Peptic Ulcer Disease (PUD) [23-24]

Diagnostic Method

Purpose

Key Findings/ Advantages

Clinical Assessment

Initial evaluation of suspected PUD

Identifies symptoms, risk factors, and possible complications.

Upper Gastrointestinal Endoscopy (EGD)

Gold standard test for diagnosis

Direct visualization of ulcers, allows biopsy, assesses bleeding, and helps exclude malignancy.

H. pylori Testing

Detects H. pylori infection, a major cause of PUD

Can be performed using invasive or non-invasive methods.

Laboratory Investigations

Evaluates complications and associated conditions

Detects anemia, bleeding, and other abnormalities.
  1. Allopathic Treatment

Allopathic treatment of peptic ulcer disease primarily focuses on reducing gastric acid secretion, eradicating underlying causes, and promoting mucosal healing. Conventional antiulcer therapy includes proton pump inhibitors, H2 receptor antagonists, antacids, potassium-competitive acid blockers, and cytoprotective agents. These drugs act by either suppressing acid production, neutralizing existing acid, or enhancing mucosal defense mechanisms. In cases associated with Helicobacter pylori infection, combination antibiotic regimens are used along with acid-suppressing agents to achieve eradication and prevent recurrence. Treatment selection depends on the severity of symptoms, underlying etiology, and presence of complications. [25] Overall, allopathic therapy remains the cornerstone of evidence-based peptic ulcer management.

Table 8. Mechanisms of action and adverse effects of the most commonly used antiulcer treatment options. [26-30]

Drug Class

Examples

Mechanism of Action

Common Adverse Effects

Proton Pump Inhibitors (PPIs)

Omeprazole, Lansoprazole, Rabeprazole, Esomeprazole, Pantoprazole

Irreversibly inhibit the gastric H?/K?-ATPase (proton pump) in parietal cells, producing profound suppression of gastric acid secretion.

Headache, abdominal pain, diarrhea, nausea, vomiting, constipation, flatulence, vitamin B12 deficiency, osteoporosis/fracture risk (long-term use)

H? Receptor Blockers

Cimetidine, Famotidine, Nizatidine, Ranitidine

Block histamine H? receptors on gastric parietal cells, reducing acid secretion.

Headache, dizziness, anxiety, depression, thrombocytopenia, rare cardiovascular effects

Antacids

Aluminum hydroxide, Magnesium hydroxide

Neutralize gastric acid and increase gastric pH (>4), reducing pepsin activity. Magnesium salts also retain water osmotically.

Nausea, vomiting, hypophosphatemia, chalky taste, constipation (Al), diarrhea (Mg), abdominal cramps, electrolyte imbalance

Potassium-Competitive Acid Blocker (P-CAB)

Vonoprazan

Reversibly inhibits H?/K?-ATPase by competing with potassium at the final step of acid secretion.

Nasopharyngitis, diarrhea, constipation, upper respiratory tract inflammation, eczema, back pain, contusion

Cytoprotective Agents

Misoprostol, Sucralfate

Protect the gastric mucosa. Misoprostol increases mucus and bicarbonate secretion and improves blood flow. Sucralfate forms a protective barrier over ulcer sites.

Diarrhea, abdominal pain, headache, constipation

Table 9. Helicobacter pylori Eradication Treatment Regimens [31-34]

Treatment Line

Regimen

Duration

Eradication Rate

First-Line Therapy

Standard Triple Therapy: PPI + Clarithromycin + Amoxicillin (or Metronidazole if penicillin allergy)

7–14 days

70–85%

Second-Line Therapy

Bismuth Quadruple Therapy: PPI + Bismuth + Tetracycline + Metronidazole

14 days

77–93%

Second-Line Therapy

Non-Bismuth Concomitant Therapy: PPI + Clarithromycin + Amoxicillin + Metronidazole

14 days

75–90%

Second-Line Therapy

Levofloxacin Triple Therapy: PPI + Amoxicillin + Levofloxacin

14 days

74–81%

Salvage (Rescue) Therapy

Rifabutin-Based Triple Therapy: PPI + Rifabutin + Amoxicillin

10 days

66–70%

8. Herbal Treatment of Ulcers

Herbal medicines have been widely utilized for centuries in traditional medical systems such as Ayurveda, Traditional Chinese Medicine (TCM), and Unani for the management of gastrointestinal disorders, including peptic ulcer disease. Their continued use is largely attributed to their broad pharmacological activities, perceived safety profile, affordability, and strong cultural and community acceptance. [35] Unlike many synthetic drugs, medicinal plants often contain a complex mixture of bioactive compounds that act synergistically to produce therapeutic effects such as acid suppression, mucosal protection, antioxidant activity, and enhancement of gastric defense mechanisms. In recent years, advances in pharmacognosy, phytochemistry, and experimental pharmacology have validated the anti-ulcer potential of several herbal agents, supporting their traditional use with scientific evidence.

A wide range of medicinal plants has demonstrated significant efficacy in both the prevention and treatment of peptic ulcers. These plants contain diverse phytoconstituents such as flavonoids, tannins, alkaloids, saponins, and terpenoids, which contribute to their gastroprotective effects by inhibiting gastric acid secretion, enhancing mucus and bicarbonate production, and reducing oxidative stress and inflammation in the gastric mucosa. Experimental studies, including in vitro assays and in vivo animal models, as well as limited clinical trials, have shown promising results for many herbal formulations. [36, 37] This chapter aims to present a comprehensive review of important anti-ulcer medicinal plants, their active phytoconstituents, and the scientific evidence supporting their therapeutic role in peptic ulcer management, highlighting their potential as complementary or alternative approaches in modern gastroenterology.

Table 10: List of medicinal plants possess anti-ulcer activity [38-45]

Sr. No.

Common Name

Biological Source

Major Phytoconstituents

Mechanism of Antiulcer Action

1

Aloe Vera

Leaf gel of Aloe vera

Aloin, Aloe-emodin, Polysaccharides, Acemannan

Increases mucus secretion, antioxidant activity, promotes ulcer healing and tissue regeneration

2

Licorice

Roots of Glycyrrhiza glabra

Glycyrrhizin, Liquiritin, Flavonoids

Enhances mucus production, cytoprotective effect, inhibits gastric acid secretion

3

Turmeric

Rhizomes of Curcuma longa

Curcumin, Demethoxycurcumin, Volatile oils

Antioxidant, anti-inflammatory, inhibits gastric mucosal damage

4

Neem

Leaves and bark of Azadirachta indica

Nimbidin, Nimbin, Azadirachtin, Flavonoids

Reduces acid secretion, enhances mucosal defense, antioxidant activity

5

Indian Gooseberry (Amla)

Fruits of Phyllanthus emblica

Vitamin C, Gallic acid, Ellagic acid, Tannins

Antioxidant activity, increases mucosal protection, accelerates healing

6

Holy Basil (Tulsi)

Leaves of Ocimum sanctum

Eugenol, Ursolic acid, Rosmarinic acid

Reduces gastric acid secretion, antioxidant and anti-inflammatory effects

7

Bael

Fruits of Aegle marmelos

Marmelosin, Tannins, Coumarins

Cytoprotective action, reduces gastric acidity, enhances mucus production

8

Drumstick

Leaves of Moringa oleifera

Quercetin, Kaempferol, Vitamins, Alkaloids

Antioxidant activity, mucosal protection, inhibition of ulcer formation

9

Guava

Leaves of Psidium guajava

Quercetin, Tannins, Flavonoids

Anti-secretory, antioxidant, gastroprotective effects

10

Pomegranate

Peel and fruits of Punica granatum

Ellagitannins, Punicalagin, Flavonoids

Antioxidant activity, strengthens gastric mucosa, reduces ulcer index

11

Ginger

Rhizomes of Zingiber officinale

Gingerols, Shogaols, Zingerone

Anti-inflammatory, antioxidant, inhibits gastric acid secretion

12

Ashwagandha

Roots of Withania somnifera

Withanolides, Alkaloids, Sitoindosides

Stress-induced ulcer protection, antioxidant activity

13

Garlic

Bulbs of Allium sativum

Allicin, Sulfur compounds, Flavonoids

Antioxidant activity, anti-H. pylori activity, mucosal protection

14

Cabbage

Leaves of Brassica oleracea

Vitamin U (S-methylmethionine), Glucosinolates

Accelerates ulcer healing and promotes mucosal regeneration

15

Banana

Fruits of Musa paradisiaca

Leucocyanidin, Flavonoids, Pectin

Enhances mucus secretion, strengthens mucosal barrier, cytoprotection

Table 11: Comparison of Allopathic and Herbal Therapies [46]

Feature

Allopathic Treatment

Herbal Treatment

Scientific evidence

Extensive

Variable

Speed of healing

Rapid

Usually slower

H. pylori eradication

Effective

Limited evidence

Standardization

High (fixed doses, regulated formulations)

Often variable (depends on plant source, preparation, and dose)

Side effects

Well characterized and monitored

May be underreported or less well documented

Cost

Moderate to high

Often lower

Clinical guidelines

Established and evidence-based

Limited standardized clinical guidelines

9. Current Research Trends in Peptic Ulcer Disease

Current research in peptic ulcer disease is increasingly focused on developing safer and more effective therapeutic strategies beyond conventional acid-suppressing drugs. One major area of interest is the use of herbal formulations in combination with proton pump inhibitors (PPIs) to enhance ulcer healing and reduce side effects. Researchers are also exploring plant-derived compounds with anti-Helicobacter pylori activity, aiming to develop natural alternatives or adjuncts to antibiotic therapy, especially in the context of rising antibiotic resistance. Another promising field is nanotechnology-based drug delivery systems, which improve targeted delivery of anti-ulcer agents, enhance drug stability, and increase therapeutic efficacy at the gastric mucosal level. In addition, there is growing interest in polyherbal gastroprotective formulations, where multiple medicinal plants are combined to achieve synergistic effects such as acid reduction, mucosal protection, and anti-inflammatory activity. Finally, antioxidant-based mucosal healing strategies are being studied extensively, focusing on reducing oxidative stress in gastric tissues to promote faster and more complete ulcer healing. [47, 48]

10. Limitations of Herbal Therapy

Herbal therapy in peptic ulcer disease has several important limitations that restrict its use as a standalone treatment. One major concern is the lack of standardization, as herbal products often vary widely in preparation, dosage, and potency. This leads to inconsistent concentrations of active constituents, making therapeutic effects unpredictable. Additionally, there is a scarcity of large-scale, well-designed clinical trials, which limits strong scientific validation of their efficacy and safety. Herbal remedies may also pose risks of herb–drug interactions, especially when used alongside conventional medications such as proton pump inhibitors, antibiotics, or NSAIDs. Furthermore, quality control issues remain significant, including contamination, adulteration, and variability in manufacturing practices. Because of these limitations, herbal therapies are best used as complementary approaches rather than replacements for evidence-based treatments, particularly in clinically significant cases such as peptic ulcers associated with Helicobacter pylori infection or NSAID use. [49-52]

CONCLUSION

Peptic ulcer disease remains a significant gastrointestinal disorder despite a global decline in incidence due to improved hygiene, reduced H. pylori prevalence, and rational NSAID use. Allopathic therapy, including acid-suppressive agents and antibiotic-based eradication regimens, remains the cornerstone of effective and evidence-based management. However, increasing interest in herbal medicines highlights their potential as complementary therapies due to their gastroprotective, antioxidant, and anti-inflammatory properties. Although many medicinal plants show promising antiulcer activity, limitations such as lack of standardization, variable efficacy, and insufficient clinical trials restrict their standalone use. Future research focusing on integrated approaches, novel drug delivery systems, and validated herbal formulations may enhance treatment outcomes and provide safer, more effective management strategies for peptic ulcer disease.

REFERENCES

  1. Narayanan M, Reddy KM, Marsicano E. Peptic ulcer disease and Helicobacter pylori infection. Mo Med. 2018;115(3):219-224.
  2. Lanas Á, Carrera-Lasfuentes P, Arguedas Y, et al. Risk of upper and lower gastrointestinal bleeding in patients taking nonsteroidal anti-inflammatory drugs, antiplatelet agents, or anticoagulants. Clin Gastroenterol Hepatol. 2015;13(5):906-912.e2.
  3. Huang JQ, Sridhar S, Hunt RH. Role of Helicobacter pylori infection and non-steroidal anti-inflammatory drugs in peptic-ulcer disease: a meta-analysis. Lancet. 2002;359(9300):14-22.
  4. Snowden FM. Emerging and reemerging diseases: a historical perspective. Immunol Rev. 2008;225(1):9-26.
  5. Lanas A, Chan FKL. Peptic ulcer disease. Lancet. 2017;390(10094):613-624.
  6. Kandarkar PS, Devkar BG. A review on herbal potential for treatment of peptic ulcer. Int J Creat Res Thoughts. 2023;11:012.
  7. Sung JJY, Kuipers EJ, El-Serag HB. Systematic review: global incidence and prevalence of peptic ulcer disease. Aliment Pharmacol Ther. 2009;29(9):938-946.
  8. ASGE Standards of Practice Committee, Banerjee S, Cash BD, et al. The role of endoscopy in the management of patients with peptic ulcer disease. Gastrointest Endosc. 2010;71(4):663-668.
  9. Malfertheiner P, Megraud F, O’Morain CA, et al. Management of Helicobacter pylori infection—the Maastricht V/Florence Consensus Report. Gut. 2017;66(1):6-30.
  10. Strand DS, Kim D, Peura DA. 25 years of proton pump inhibitors: a comprehensive review. Gut Liver. 2017;11(1):27-37.
  11. Sachdeva AK, Zaren HA, Sigel B. Surgical treatment of peptic ulcer disease. Med Clin North Am. 1991;75(4):999-1012.
  12. Chatila AT, Bilal M, Guturu P. Evaluation and management of acute pancreatitis. World J Clin Cases. 2019;7(9):1006-1020.
  13. Gomes CA, et al. Acute calculous cholecystitis: review of current best practices. World J Gastrointest Surg. 2017;9(5):118-126.
  14. Gnanapandithan K, Feuerstadt P. Mesenteric ischemia. Curr Gastroenterol Rep. 2020;22(4):17.
  15. Young PJ, et al. PEPTIC study protocol. Crit Care Resusc. 2018;20(3):182-189.
  16. Ayoub F, et al. PPI therapy for ulcer rebleeding prevention. Gastroenterol Res. 2018;11(3):200-206.
  17. Sonnenberg A. Historic changes of Helicobacter pylori-associated diseases. Aliment Pharmacol Ther. 2013;38:329-342.
  18. Søreide K, et al. Perforated peptic ulcer. Lancet. 2015;386:1288-1298.
  19. Zhang BB, et al. VacA genotypes and duodenal ulcer risk. Mol Biol Rep. 2014;41:7241-7254.
  20. Datta De D, Roychoudhury S. Host genetic factors in H. pylori disease. World J Gastroenterol. 2015;21:2883-2895.
  21. Lanas Á, et al. NSAIDs and GI bleeding risk. Clin Gastroenterol Hepatol. 2015;13:906-912.e2.
  22. Masclee GM, et al. Risk of upper GI bleeding from drug combinations. Gastroenterology. 2014;147:784-792.
  23. Huang JQ, et al. NSAIDs and peptic ulcer disease meta-analysis. Lancet. 2002;359:14-22.
  24. Charpignon C, et al. Idiopathic peptic ulcer disease. Aliment Pharmacol Ther. 2013;38:946-954.
  25. Levenstein S, et al. Stress and peptic ulcer risk. Clin Gastroenterol Hepatol. 2015;13:498-506.e1.
  26. McColl KEL. NSAID-negative, H. pylori-negative ulcer. Gastroenterol Clin North Am. 2009;38:353-361.
  27. Siddique O, et al. Helicobacter pylori infection update. Am J Med. 2018;131:473-479.
  28. Hooi JKY, et al. Global prevalence of Helicobacter pylori. Gastroenterology. 2017;153:420-429.
  29. Zaki M, et al. H. pylori effects on gastric secretion. Am J Physiol Gastrointest Liver Physiol. 2013;304:G715-G722.
  30. El-Omar EM, et al. Gastric acid hyposecretion in H. pylori infection. Gastroenterology. 1997;113:15-24.
  31. Moss SF, et al. Somatostatin changes in duodenal ulcer disease. Lancet. 1992;340:930-932.
  32. Bhala N, et al. NSAIDs and GI effects meta-analysis. Lancet. 2013;382:769-779.
  33. Mofleh IA. Spices and herbal xenobiotics. World J Gastroenterol. 2010;16:2710-2719.
  34. Alqasoumi S, et al. Gastroprotective effects of liquorice. Saudi Pharm J. 2011;19:125-132.
  35. Rachana D, et al. Antiulcer activity of turmeric. Indian J Pharmacol. 2007;39:231-235.
  36. Park MY, et al. Aloe vera and gastric ulcer healing. J Ethnopharmacol. 2009;123:34-40.
  37. Goel RK, et al. Ocimum sanctum antiulcer effect. Indian J Exp Biol. 1991;29:701-704.
  38. Shukla A, et al. Centella asiatica and gastric ulcer. Indian J Pharmacol. 1999;31:235-241.
  39. Morgan AG, et al. Deglycyrrhizinated liquorice in ulcers. BMJ. 1982;284:182-183.
  40. Chandran B, Goel A. Curcumin in peptic ulcers. J Clin Gastroenterol. 2012;46:e18-e22.
  41. Panahi Y, et al. Aloe vera clinical trial. Phytother Res. 2015;29:255-261.
  42. Dey A, et al. Polyherbal formulation in ulcer. J Ayurveda Integr Med. 2014;5:24-30.
  43. Naser B, et al. Herbal therapy meta-analysis. Forsch Komplementmed. 2006;13:282-287.
  44. Borrelli F, Izzo AA. Plant-based antiulcer remedies. Phytother Res. 2000;14:581-591.
  45. Ammon HP. Boswellic acids review. Planta Med. 2006;72:1100-1116.
  46. Sairam K, et al. Ocimum sanctum gastric defense. Indian J Exp Biol. 2001;39:137-142.
  47. Cañizares P, et al. Garlic extract and H. pylori. J Antimicrob Chemother. 2004;54:613-614.
  48. Sidhu GS, et al. Curcumin and wound healing. Wound Repair Regen. 1998;6:167-177.
  49. Rege NN, et al. Ayurvedic formulation in ulcers. Indian J Pharmacol. 1999;31:426-431.
  50. Ekor M. Herbal medicine safety issues. Front Pharmacol. 2014;4:177.
  51. Heinrich M, et al. Ethnopharmacology and drug discovery. Drug Discov Today. 2020;25:948-954.
  52. Patwardhan B, et al. Integrative medicine approaches. EPMA J. 2015;6:14.

Reference

  1. Narayanan M, Reddy KM, Marsicano E. Peptic ulcer disease and Helicobacter pylori infection. Mo Med. 2018;115(3):219-224.
  2. Lanas Á, Carrera-Lasfuentes P, Arguedas Y, et al. Risk of upper and lower gastrointestinal bleeding in patients taking nonsteroidal anti-inflammatory drugs, antiplatelet agents, or anticoagulants. Clin Gastroenterol Hepatol. 2015;13(5):906-912.e2.
  3. Huang JQ, Sridhar S, Hunt RH. Role of Helicobacter pylori infection and non-steroidal anti-inflammatory drugs in peptic-ulcer disease: a meta-analysis. Lancet. 2002;359(9300):14-22.
  4. Snowden FM. Emerging and reemerging diseases: a historical perspective. Immunol Rev. 2008;225(1):9-26.
  5. Lanas A, Chan FKL. Peptic ulcer disease. Lancet. 2017;390(10094):613-624.
  6. Kandarkar PS, Devkar BG. A review on herbal potential for treatment of peptic ulcer. Int J Creat Res Thoughts. 2023;11:012.
  7. Sung JJY, Kuipers EJ, El-Serag HB. Systematic review: global incidence and prevalence of peptic ulcer disease. Aliment Pharmacol Ther. 2009;29(9):938-946.
  8. ASGE Standards of Practice Committee, Banerjee S, Cash BD, et al. The role of endoscopy in the management of patients with peptic ulcer disease. Gastrointest Endosc. 2010;71(4):663-668.
  9. Malfertheiner P, Megraud F, O’Morain CA, et al. Management of Helicobacter pylori infection—the Maastricht V/Florence Consensus Report. Gut. 2017;66(1):6-30.
  10. Strand DS, Kim D, Peura DA. 25 years of proton pump inhibitors: a comprehensive review. Gut Liver. 2017;11(1):27-37.
  11. Sachdeva AK, Zaren HA, Sigel B. Surgical treatment of peptic ulcer disease. Med Clin North Am. 1991;75(4):999-1012.
  12. Chatila AT, Bilal M, Guturu P. Evaluation and management of acute pancreatitis. World J Clin Cases. 2019;7(9):1006-1020.
  13. Gomes CA, et al. Acute calculous cholecystitis: review of current best practices. World J Gastrointest Surg. 2017;9(5):118-126.
  14. Gnanapandithan K, Feuerstadt P. Mesenteric ischemia. Curr Gastroenterol Rep. 2020;22(4):17.
  15. Young PJ, et al. PEPTIC study protocol. Crit Care Resusc. 2018;20(3):182-189.
  16. Ayoub F, et al. PPI therapy for ulcer rebleeding prevention. Gastroenterol Res. 2018;11(3):200-206.
  17. Sonnenberg A. Historic changes of Helicobacter pylori-associated diseases. Aliment Pharmacol Ther. 2013;38:329-342.
  18. Søreide K, et al. Perforated peptic ulcer. Lancet. 2015;386:1288-1298.
  19. Zhang BB, et al. VacA genotypes and duodenal ulcer risk. Mol Biol Rep. 2014;41:7241-7254.
  20. Datta De D, Roychoudhury S. Host genetic factors in H. pylori disease. World J Gastroenterol. 2015;21:2883-2895.
  21. Lanas Á, et al. NSAIDs and GI bleeding risk. Clin Gastroenterol Hepatol. 2015;13:906-912.e2.
  22. Masclee GM, et al. Risk of upper GI bleeding from drug combinations. Gastroenterology. 2014;147:784-792.
  23. Huang JQ, et al. NSAIDs and peptic ulcer disease meta-analysis. Lancet. 2002;359:14-22.
  24. Charpignon C, et al. Idiopathic peptic ulcer disease. Aliment Pharmacol Ther. 2013;38:946-954.
  25. Levenstein S, et al. Stress and peptic ulcer risk. Clin Gastroenterol Hepatol. 2015;13:498-506.e1.
  26. McColl KEL. NSAID-negative, H. pylori-negative ulcer. Gastroenterol Clin North Am. 2009;38:353-361.
  27. Siddique O, et al. Helicobacter pylori infection update. Am J Med. 2018;131:473-479.
  28. Hooi JKY, et al. Global prevalence of Helicobacter pylori. Gastroenterology. 2017;153:420-429.
  29. Zaki M, et al. H. pylori effects on gastric secretion. Am J Physiol Gastrointest Liver Physiol. 2013;304:G715-G722.
  30. El-Omar EM, et al. Gastric acid hyposecretion in H. pylori infection. Gastroenterology. 1997;113:15-24.
  31. Moss SF, et al. Somatostatin changes in duodenal ulcer disease. Lancet. 1992;340:930-932.
  32. Bhala N, et al. NSAIDs and GI effects meta-analysis. Lancet. 2013;382:769-779.
  33. Mofleh IA. Spices and herbal xenobiotics. World J Gastroenterol. 2010;16:2710-2719.
  34. Alqasoumi S, et al. Gastroprotective effects of liquorice. Saudi Pharm J. 2011;19:125-132.
  35. Rachana D, et al. Antiulcer activity of turmeric. Indian J Pharmacol. 2007;39:231-235.
  36. Park MY, et al. Aloe vera and gastric ulcer healing. J Ethnopharmacol. 2009;123:34-40.
  37. Goel RK, et al. Ocimum sanctum antiulcer effect. Indian J Exp Biol. 1991;29:701-704.
  38. Shukla A, et al. Centella asiatica and gastric ulcer. Indian J Pharmacol. 1999;31:235-241.
  39. Morgan AG, et al. Deglycyrrhizinated liquorice in ulcers. BMJ. 1982;284:182-183.
  40. Chandran B, Goel A. Curcumin in peptic ulcers. J Clin Gastroenterol. 2012;46:e18-e22.
  41. Panahi Y, et al. Aloe vera clinical trial. Phytother Res. 2015;29:255-261.
  42. Dey A, et al. Polyherbal formulation in ulcer. J Ayurveda Integr Med. 2014;5:24-30.
  43. Naser B, et al. Herbal therapy meta-analysis. Forsch Komplementmed. 2006;13:282-287.
  44. Borrelli F, Izzo AA. Plant-based antiulcer remedies. Phytother Res. 2000;14:581-591.
  45. Ammon HP. Boswellic acids review. Planta Med. 2006;72:1100-1116.
  46. Sairam K, et al. Ocimum sanctum gastric defense. Indian J Exp Biol. 2001;39:137-142.
  47. Cañizares P, et al. Garlic extract and H. pylori. J Antimicrob Chemother. 2004;54:613-614.
  48. Sidhu GS, et al. Curcumin and wound healing. Wound Repair Regen. 1998;6:167-177.
  49. Rege NN, et al. Ayurvedic formulation in ulcers. Indian J Pharmacol. 1999;31:426-431.
  50. Ekor M. Herbal medicine safety issues. Front Pharmacol. 2014;4:177.
  51. Heinrich M, et al. Ethnopharmacology and drug discovery. Drug Discov Today. 2020;25:948-954.
  52. Patwardhan B, et al. Integrative medicine approaches. EPMA J. 2015;6:14.

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Pradeep Singh Patel
Corresponding author

Shambhunath Institute of Pharmacy, Jhalwa, Prayagraj, Uttar Pradesh, India

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Arvind Kumar Srivastva
Co-author

Department of pharmaceutical chemistry, Shambhunath Institute of Pharmacy, Jhalwa, Prayagraj, Uttar Pradesh, India

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Shailesh Pathak
Co-author

Department of Pharmacy, Shambhunath Institute of Pharmacy, Jhalwa, Prayagraj, Uttar Pradesh, India

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Chandan Chaurasiya
Co-author

Shambhunath Institute of Pharmacy, Jhalwa, Prayagraj, Uttar Pradesh, India

Pradeep Singh Patel, Arvind Kumar Srivastva, Shailesh Pathak, Chandan Chaurasiya, Peptic Ulcer Disease: A Comprehensive Review of Pathophysiology and Allopathic vs Herbal Treatment Strategies, Int. J. of Pharm. Sci., 2026, Vol 4, Issue 8, 3996-4005. https://doi.org/10.5281/zenodo.22086714

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