Keywords
peptic ulcer - H. pylori - TNF-α - prostaglandins - vanoprazan
Introduction
Peptic ulcers, marked by the erosion of the gastrointestinal mucosa, represent a
significant clinical challenge in gastroenterology. The intricate interplay between
genetic, environmental, and microbial factors underscores the complexity of peptic
ulcer pathogenesis. Epidemiological studies have provided valuable insights into the
prevalence and incidence of peptic ulcers, shedding light on the burden of this
condition and its evolving trends over time [1]. Estimates suggest that approximately 5–10+% of individuals will
experience a peptic ulcer at some time in their lives. This statistic underscores
the substantial prevalence of this condition, making it a noteworthy concern in
gastroenterological practice. The annual incidence of peptic ulcers varies across
populations, ranging from 0.3 to 1.9 cases per thousand individuals [2]. This incidence rate highlights the ongoing
and considerable impact of peptic ulcers on healthcare systems worldwide. In recent
decades, epidemiological studies have observed a notable shift in the landscape of
peptic ulcer complications, particularly in developed countries. The overall
incidence of complications related to peptic ulcers has shown a decreasing trend,
indicating a positive trajectory in the management and prevention of severe outcomes
associated with this condition [3]. This
decline in incidence is attributed to several factors, including improved diagnostic
techniques, enhanced understanding of risk factors, and advancements in therapeutic
interventions [4]. While much progress has
occurred in understanding the etiology of peptic ulcers, their management remains
a
daunting task for healthcare professionals. This review aims to delve into the
current landscape of peptic ulcer management, emphasizing the challenges faced in
clinical practice and the imperative for exploring innovative therapeutic
approaches. Peptic ulcers, comprising gastric and duodenal ulcers, have long been
recognized as major contributors to gastrointestinal morbidity and healthcare
expenditures [5]. These abnormalities are
predominantly linked to Helicobacter pylori (H. pylori) infection, the
consumption of nonsteroidal anti-inflammatory drugs (NSAIDs), and less frequent
contributors like smoking and stress [6]. The
prevalence of peptic ulcers varies globally, with H. pylori infection being a
predominant factor in developing countries and NSAID use playing a significant role
in industrialized nations [7]. Consequently,
the burden of peptic ulcers is substantial, affecting millions of individuals
worldwide and necessitating a comprehensive understanding of their pathophysiology
and effective management strategies [8].
Despite advancements in medical science, peptic ulcer management poses persistent
challenges. The recurrence rates of peptic ulcers, especially in H.
pylori-infected individuals, remain a concern. Additionally, the rise of
antibiotic resistance poses a threat to the conventional treatment regimens
targeting H. pylori. Furthermore, NSAID-induced ulcers, a common scenario in
the aging population, present a management conundrum due to the limited options for
pain relief in patients requiring long-term NSAID therapy [9]. The multifactorial nature of peptic ulcers
demands a nuanced approach that goes beyond the conventional strategies,
necessitating the exploration of novel therapeutic interventions [10]. The limitations of current treatment
modalities underscore the need for novel therapeutic approaches in peptic ulcer
management. Traditional regimens, including proton pump inhibitors (PPIs) and
antibiotics, have been the mainstay of therapy for H. pylori-associated
ulcers [11]. However, the emergence of
antibiotic resistance and suboptimal patient compliance pose significant challenges
to the effectiveness of these regimens [12].
Additionally, the management of NSAID-induced ulcers relies on discontinuing or
reducing NSAID use, which may not be feasible in many clinical scenarios. Therefore,
there is a compelling need for innovative strategies that address the specific
challenges associated with each subtype of peptic ulcer [13].
This review seeks to offer a thorough examination of the present challenges in
managing peptic ulcers and delve into the most recent advancements in therapeutic
strategies. We will critically examine the existing literature on H. pylori
eradication strategies, assess the impact of antibiotic resistance on treatment
outcomes, and evaluate alternative approaches such as probiotics and phage therapy
[14]. Furthermore, we will delve into the
intricacies of NSAID-induced ulcers, analyzing the limitations of current management
strategies and highlighting emerging interventions, including mucosal protective
agents and targeted drug delivery systems [15]. The scope of this review encompasses a thorough examination of recent
research findings, clinical trials, and emerging trends in peptic ulcer management.
By synthesizing the existing knowledge, we aim to provide healthcare professionals,
researchers, and policymakers with a comprehensive understanding of the current
landscape and future directions in peptic ulcer therapeutics [16]. Our review will not only elucidate the
challenges faced in clinical practice but also shed light on promising avenues for
the development of novel and more effective therapeutic interventions.
Epidemiology, Causes, Types, and Pathophysiology of Peptic Ulcers
Epidemiology, Causes, Types, and Pathophysiology of Peptic Ulcers
Peptic ulcers (PUs) exhibit a multifaceted epidemiological profile influenced by a
combination of, environmental, genetic and lifestyle factors. Understanding the
prevalence and risk factors is pivotal for effective management and prevention
strategies [17]. The estimated prevalence of
peptic ulcers underscores their significance in global health, affecting
approximately 5–10+% of individuals during their lifetime. While this prevalence
indicates a substantial burden, it is crucial to note variations across populations
and regions. Epidemiological data reveal an annual incidence ranging from 0.3 to 1.9
cases per thousand individuals, emphasizing the continued impact of peptic ulcers
on
healthcare systems [18]. Several factors
contribute to the development of peptic ulcers as shown in [Fig. 1] and identifying these risk factors is
essential for targeted interventions. Notably, H. pylori infection stands out
as a major risk factor, implicated in a significant proportion of peptic ulcer
cases. Other contributors include the use of nonsteroidal anti-inflammatory drugs
(NSAIDs), smoking, advanced age, and a genetic predisposition [19].
Fig. 1 Ulcerogenic/aggressive factors.
The prevalence of H. pylori-associated ulcers is higher in developing
countries, while NSAID-induced ulcers are more prevalent in industrialized nations.
Understanding these variations is crucial for tailoring preventive measures to
specific populations [20]. Recent
epidemiological studies have indicated a decreasing trend in the incidence of
complications related to peptic ulcers, especially in developed countries [21]. This decline can be attributed to
successful H. pylori eradication strategies, improved diagnostics, and better
management of risk factors. However, ongoing efforts are essential to address
healthcare disparities and variations in risk factor prevalence globally [22].
Helicobacter Pylori-Associated PUD
Helicobacter Pylori-Associated PUD
Helicobacter pylorus, a gram-negative bacillus residing within gastric epithelial
cells, plays a pivotal role in PUD etiology. Accountable for 90+% of duodenal ulcers
and 70+% to 90+% of gastric ulcers, H. pylori infection is widespread among
individuals with lower socioeconomic status and is frequently acquired during
childhood [23].
NSAID-Associated PUD
Mechanism of Action
Nonsteroidal anti-inflammatory drugs (NSAIDs) stand as the second most common
cause of PUD after H. pylori infection. Prostaglandins, protective to the
gastric mucosa, are inhibited by NSAIDs through the suppression of the COX-1
enzyme. This inhibition results in decreased production of gastric mucus and
bicarbonate, alongside a reduction in mucosal blood flow, contributing to the
development of peptic ulcers [24].
Mechanisms
The bacterium employs various virulence factors to adhere to and inflame the
gastric mucosa, leading to hypochlorhydria or achlorhydria, ultimately resulting
in gastric ulceration. Key virulence factors include:
Urease
Breaks down urea into ammonia, neutralizing the acidic gastric
environment.
Toxins (CagA/VacA)
Associated with inflammation of stomach mucosa and damage to host tissue.
Flagella
Provides motility, aiding movement toward the gastric epithelium [25].
Medications
Beyond NSAIDs
Medications beyond NSAIDs, including bisphosphonates, corticosteroids,
potassium chloride, and fluorouracil, have been implicated in the etiology
of PUD. Smoking, though exhibiting a non-linear correlation, plays a role in
duodenal ulcers, while alcohol can irritate the gastric mucosa, inducing
acidity [26].
Rare Causes of PUD
Uncommon Yet Significant Contributors
Rare causes of PUD encompass various conditions, including [27]:
-
Zollinger–Ellison Syndrome (ZES): marked by hypersecretion of gastric
acid.
-
Malignancies: Gastric, lung cancer, and lymphomas may contribute to
PUD.
-
Stress: Acute illness burns, and head injuries can exacerbate ulcer
formation.
-
Viral Infections, Vascular Insufficiency, Radiation Therapy: Uncommon
factors with potential ulcerogenic effects.
-
Inflammatory Conditions: Crohn’s disease contributes to mucosal
damage.
-
Chemotherapy: An additional contributor to the multifactorial landscape
of PUD.
-
Systemic Conditions: Cystic fibrosis and hyperparathyroidism induce a
hyper secretory environment.
Pathophysiology
A comprehensive understanding of the pathophysiology of peptic ulcers is
paramount for developing targeted therapeutic approaches [28]. Peptic ulcer disease (PUD) manifests
as a result of a delicate equilibrium disruption between the protective and
destructive factors within the gastric mucosa. This intricate interplay involves
various risk factors, each contributing mechanistically to the development of
peptic ulcers as shown in [Fig. 2
]
(Pathophysiology of Peptic ulcer)
[29].
Fig. 2 Pathophysiology of peptic ulcer.
Imbalance in Gastric Mucosal Factors
Protective Factors
The gastric mucosa is endowed with protective mechanisms that guard against
ulcer formation. These include the production of mucus, bicarbonate
secretion, and a robust blood flow that facilitates mucosal repair [30].
Destructive Factors
Conversely, destructive factors, such as H. pylori infection, NSAID
use, a family history of PUD, emigration from developed nations, and
specific ethnic predispositions, can compromise the protective mechanisms,
leading to the initiation and progression of peptic ulcers [31].
Defects in the Mucosa and Muscularis Mucosa
Peptic ulcers are characterized by defects in the mucosal layer that extend to
the muscularis mucosa. This compromise in structural integrity exposes the inner
layers to the corrosive effects of gastric acidity [32].
H. pylori Infection
Mechanism of Colonization
H. pylori, a Gram-negative bacterium, are a pivotal player in PUD. It
colonizes the gastric mucosa, initiating an inflammatory response. The
bacterium's unique ability to evade the host's immune system
allows for persistent colonization [33].
Impact on Bicarbonate Secretion
H. pylori further disrupt the delicate balance by impairing the
secretion of bicarbonate, a key component in neutralizing gastric acid. This
impairment promotes increased acidity within the gastric environment,
creating an ideal milieu for the development and progression of peptic
ulcers [34].
Gastric Metaplasia
Prolonged H. pylori infection can induce gastric metaplasia, wherein
the normal gastric epithelium undergoes transformation into an
intestinal-like mucosa. This alteration not only contributes to mucosal
damage but also enhances the vulnerability of the gastric lining to acidic
insults [35].
NSAID-Induced Ulcers
Prostaglandin Inhibition
Nonsteroidal anti-inflammatory drugs (NSAIDs), widely utilized for their
anti-inflammatory properties, pose a significant risk for peptic ulcers.
NSAIDs inhibit prostaglandin synthesis, compromising the mucosal
barrier's protective effects [36].
Compromised Bicarbonate Secretion
Similar to H. pylori, NSAIDs compromise the ability of mucosal cells
to secrete bicarbonate. This dual impact exacerbates the susceptibility of
the mucosa to gastric acidity [37].
Genetic and Ethnic Factors
Hereditary Predisposition
A family history of PUD, especially in first-degree relatives, indicates a
genetic predisposition. Specific genetic variations influence an
individual's susceptibility to peptic ulcers [38].
Ethnic Disparities
Certain ethnic groups, including African American and Hispanic populations,
exhibit an increased vulnerability to PUD. The mechanistic underpinnings of
these disparities warrant further exploration [39].
Peptic ulcer disease (PUD) is a complex gastroenterological condition, and
recent advances in molecular research have provided unprecedented insights
into the intricate pathways that govern its development [39]. Peptic ulcer disease (PUD) unfolds
through intricate molecular mechanisms involving altered levels of specific
prostaglandins, cytokines, and interleukins, each playing a distinctive role
in the erosion of the gastric layer and the subsequent development of ulcers
[40].
Inflammatory Mediators in Ulcer Formation
Inflammation plays a central role in the initiation and progression of peptic
ulcers. Recent studies have highlighted the involvement of various inflammatory
mediators in orchestrating the cascade of events leading to mucosal damage [41].
Tumor Necrosis Factor-alpha (TNF-α)
TNF-α, a key proinflammatory cytokine, has emerged as a pivotal player in
ulcer development. It induces mucosal damage by promoting the secretion of
other inflammatory mediators, disrupting the balance between protective and
aggressive factors in the gastric mucosa [42].
Interleukins (ILs)
Specific interleukins, such as IL-1 and IL-6, have been implicated in the
modulation of mucosal inflammation. These cytokines contribute to the
breakdown of the mucosal barrier, creating an environment conducive to ulcer
formation [43].
Leukotrienes and Prostaglandins
The interplay between leukotrienes and prostaglandins is crucial in
regulating gastric mucosal integrity. Imbalances in their production,
influenced by inflammatory stimuli, contribute to the erosive effects on the
mucosa, paving the way for ulceration [44]. In the context of PUD, a key player is the dysregulation of
prostaglandins, particularly the decrease in prostaglandin E2 (PGE2).
Prostaglandins are critical for maintaining the integrity of the gastric
mucosa by promoting mucus and bicarbonate secretion, which act as protective
barriers against the corrosive effects of gastric acid [45]. Nonsteroidal anti-inflammatory
drugs (NSAIDs), commonly implicated in peptic ulcer development, inhibit the
synthesis of prostaglandins by blocking the cyclooxygenase (COX) enzyme,
particularly COX-1 [46]. This
inhibition results in decreased PGE2 production, leading to compromised
mucosal defense mechanisms and an increased susceptibility to mucosal injury
[47].
Cytokines and Their Role in Ulcerogenesis
TGF-β (Transforming Growth Factor-beta)
TGF-β, traditionally recognized for its role in tissue repair, exhibits a
dual role in ulcerogenesis. While it participates in mucosal healing,
dysregulation of TGF-β signaling can lead to fibrosis and scarring,
perpetuating the ulcerative process [48].
IL-10 (Interleukin-10)
IL-10, known for its anti-inflammatory properties, serves as a crucial
counterbalance to proinflammatory cytokines. Dysregulation of IL-10
expression can disrupt this balance, fostering an inflammatory
microenvironment that facilitates ulcer development [49].
Signaling Pathways
NF-κB (Nuclear Factor-kappa B)
NF-κB, a central player in inflammatory responses, is implicated in the
pathogenesis of peptic ulcers. Activation of NF-κB signaling pathways
contributes to the transcription of proinflammatory genes, perpetuating the
inflammatory milieu in the gastric mucosa [50].
MAPK (Mitogen-Activated Protein Kinase) Pathway
The MAPK pathway, comprising extracellular signal-regulated kinases (ERK),
c-Jun N-terminal kinases (JNK), and p38, is intricately involved in cellular
responses to stress and inflammation. Dysregulation of the MAPK pathway has
been linked to the erosion of the mucosal barrier, fostering conditions
conducive to ulcer formation [51].
Mechanisms of Erosion
The mechanisms by which these inflammatory mediators contribute to the erosion of
the gastric layer involve a complex interplay of events as shown in [Fig. 3] (Intricated mechanisms involved in
peptic ulcer erosion) [52]. The decreased
prostaglandin levels, especially PGE2, compromise the protective mucosal
barrier, allowing gastric acid to exert its corrosive effects on the underlying
tissue. TNF-α, IL-1, and IL-6 contribute to inflammation and disrupt the finely
tuned equilibrium between protective and aggressive factors in the gastric
mucosa [53]. TNF-α, in particular, is
known to induce apoptosis of gastric epithelial cells, further compromising the
mucosal barrier. In addition to their direct effects on the gastric mucosa,
these mediators also influence other crucial pathways. For instance, the
activation of NF-κB, a downstream target of TNF-α, promotes the transcription of
pro-inflammatory genes, sustaining the inflammatory environment [54]. The MAPK pathway, including ERK, JNK,
and p38, when dysregulated, contributes to the erosion of the mucosal barrier,
creating an environment conducive to ulcer formation [55].
Fig. 3 Intricated mechanisms involved in peptic ulcer erosion.
Diagnostic Approaches
Accurate diagnosis of peptic ulcer disease (PUD) is essential for guiding
appropriate therapeutic interventions and preventing complications [56]. The diagnostic landscape has evolved
significantly, incorporating a range of tools and techniques to identify and
classify peptic ulcers. This comprehensive overview details the latest
diagnostic approaches, emphasizing the importance of a thorough initial
assessment and subsequently delving into specific investigations [57].
Initial Investigations
Upper Gastrointestinal Endoscopy
Regarded as the primary and highly accurate diagnostic test for peptic ulcer
disease (PUD), upper gastrointestinal endoscopy demonstrates sensitivity and
specificity of up to 90+%. Specifically advised for individuals aged 50 and
above experiencing new-onset dyspeptic symptoms, this procedure enables the
direct observation of gastric and duodenal ulcers [58]. The American Society of
Gastrointestinal Endoscopy advocates for its application in patients who exhibit
upper abdominal pain or dyspeptic symptoms indicative of PUD, particularly in
the presence of alarm symptoms [59].
Helicobacter pylori Carbon-13 Urea Breath Test or Stool Antigen
Test
Rapid and reliable, these non-invasive tests assess the presence of H.
pylori infection, a significant contributor to PUD. The carbon-13 urea
breath test detects the radiolabeled carbon dioxide exhaled by the lungs in the
presence of urease produced by H. pylori. Stool antigen tests and
serologic testing are alternative methods to identify H. pylori infection
[60].
Full Blood Count (FBC)
A complete blood workup, including FBC, aids in identifying anaemia, a potential
consequence of bleeding associated with peptic ulcers. Additionally, liver
function tests, and levels of amylase and lipase contribute to a comprehensive
assessment [61].
Investigations to Consider
Fasting Serum Gastrin Level
When Zollinger-Ellison syndrome is suspected, measuring fasting serum gastrin
levels becomes crucial. Increased levels may indicate the presence of
gastrin-secreting tumors [62].
Urine NSAID Screen
Given the role of NSAIDs in peptic ulcer development, a urine screen for
nonsteroidal anti-inflammatory drugs (NSAIDs) can be considered, especially
in patients with a history of NSAID use [63].
Helicobacter pylori Testing
Serologic Testing, Urea Breath Test, and Stool Antigen Test
These tests aid in detecting H. pylori infection. These tests not only
diagnose the infection but also play a crucial role in confirming
eradication post-treatment [64].
Endoscopic Biopsy
Endoscopic biopsy, while not routinely recommended, becomes essential if
eradication treatment fails or if antibiotic resistance is suspected.
Biopsies from multiple sites increase sensitivity, with gastric ulcers
commonly found on the lesser curvature and duodenal ulcers in the first part
of the duodenum [65].
Imaging Studies
Barium Swallow and Abdominal CT Scan
In situations where upper gastrointestinal endoscopy is contraindicated, a
barium swallow may be indicated. Additionally, a contrast-enhanced abdominal
CT scan can provide insights into complications such as perforation and
gastric outlet obstruction [66].
Current Treatment Options
Current Treatment Options
Initial Management
Eradication of Helicobacter pylori (H. pylori)
Central to PUD management is the identification and eradication of H.
pylori infection. Successful eradication is associated with higher
healing rates, as demonstrated in a meta-analysis revealing significantly
elevated ulcer remission rates in patients free of H. pylori compared
to those with persistent infection. Treatment regimens for H. pylori
involve a multi-faceted approach, and the choice of therapy is paramount in
achieving lasting eradication [67].
Discontinuation of NSAIDs
NSAIDs and peptic ulcer development, discontinuation or avoidance of NSAIDs is a
crucial step in managing PUD. NSAIDs, including aspirin, elevate the risk of
peptic ulcer disease and are linked to increased complications, making their
cessation an integral component of initial management [68].
Addressing Rare or Unclear Causes
Unraveling the etiology of peptic ulcers is essential. Rare causes, such as
infections, Crohn's disease, or ischemia, require specific and targeted
interventions. Gastrointestinal bleeding, often linked to severe coronavirus
infections, emphasizes the need for a comprehensive evaluation to exclude rare
causes of PUD. The prevalence of PUD in this context underscores the importance
of addressing potential complications promptly [69].
Initial Antisecretory Therapy
Initial Antisecretory Therapy
Choice of Therapy – Proton Pump Inhibitors (PPIs)
Antisecretory therapy takes center stage in promoting ulcer healing. Proton pump
inhibitors (PPIs), exemplified by omeprazole, have emerged as the preferred
choice due to their superior efficacy compared to H2-receptor
antagonists (H2RAs). PPIs provide robust acid suppression, resulting
in easy controlling of symptoms and more rates of ulcer healing. Notably, PPIs
outperform H2RAs in healing NSAID-related ulcers, further solidifying
their role in the therapeutic arsenal [70].
Medical Treatment
Antisecretory Drugs and Other Interventions
Antisecretory drugs, primarily PPIs, stand as the cornerstone of medical
treatment for PUD. These drugs block acid production, offering symptomatic
relief and fostering the healing process. Management may incorporate calcium
supplements to mitigate the potential risk of bone fractures linked with
long-term PPI use. NSAID-induced PUD necessitates the discontinuation or dose
reduction of NSAIDs, and prostaglandin analogues like misoprostol may be
employed as prophylaxis [71].
H. pylori-Induced PUD Treatment
The first-line treatment for H. pylori-induced ulcer involves a triple
regimen composed of two antibiotics and a PPI. The selection of antibiotics
considers the presence of antibiotic resistance. If initial therapy fails, then
quadruple therapy with bismuth and alternative antibiotics is instituted [72].
Refractory Disease and Surgical Treatment
Surgical treatment becomes imperative in cases of refractory disease, where
patients remain unresponsive to medical interventions or are at high risk of
complications. Refractory peptic ulcers, those persisting despite 8–12 weeks of
PPI therapy, may be indicative of persistent H. pylori infection,
ongoing NSAID use, or significant comorbidities hindering ulcer healing.
Surgical options, such as vagotomy or partial gastrectomy, are considered for
such cases, ensuring a comprehensive approach to address the underlying causes
[73].
Advances and Challenges in Peptic Ulcer Treatment and Management
In the realm of treating Peptic Ulcer Disease (PUD), recent advances reflect a
shift towards more nuanced and personalized strategies. Traditional approaches
to Helicobacter pylori (H. pylori) eradication have evolved, with
tailored regimens acknowledging the variable landscape of antibiotic resistance
[74]. This move optimizes treatment
outcomes and seeks to mitigate the diminishing efficacy of conventional
therapies. A noteworthy breakthrough comes in the form of vonoprazan, a novel
acid suppressant. By competitively inhibiting gastric
H+/K+-ATPase, vonoprazan exhibits promise in
eradicating clarithromycin-resistant H. pylori strains. However, the
prolonged use of acid suppressants, whether traditional or novel, introduces
potential side-effects, including hypergastrinemia, pneumonia, bacterial
overgrowth, and C. difficile infection, necessitating careful consideration in
treatment planning [75].
In the preventive arena, ongoing research into a vaccine against H. pylori offers
hope for a ground-breaking development. While still in its developmental phase,
this vaccine holds potential as a primary prevention measure, aiming to reduce
the incidence of H. pylori infection and its associated complications
[76]. Moreover, the quest for novel
therapeutic avenues has led to the exploration of natural products, particularly
monoterpenes derived from medicinal plants. These compounds, with diverse
chemical structures, exhibit anti-ulcer, healing, and antimicrobial activities,
positioning them as promising alternatives for PUD management [77].
However, persistent challenges underscore the complexity of effectively managing
PUD. Antibiotic resistance in H. pylori, though showing a declining
trend, remains a significant hurdle. Resistance rates, particularly to
clarithromycin, impact the success rates of conventional antibiotic-based
therapies. Moreover, the side-effects associated with prolonged acid suppressant
use, including vonoprazan, necessitate vigilant monitoring and careful dosage
considerations [78]. As efforts are
directed towards developing new anti-H. pylori drugs and exploring
natural compounds, bridging gaps in translating these findings to clinical
applications remains a challenge. Further research is needed to understand the
mechanisms of action, optimal dosages, and potential interactions of
monoterpenes, positioning them as potential but yet-to-be-standardized
therapeutic agents. The landscape of PUD treatment is marked by a dichotomy of
promising advances and persistent challenges. Tailored eradication strategies,
novel acid suppressants, vaccine development, and the exploration of natural
compounds represent positive strides. However, the intricate web of challenges,
including antibiotic resistance, side-effects of acid suppressants, and the need
for innovative H. pylori management, necessitates ongoing research and a
comprehensive approach to enhance the precision and efficacy of PUD treatment
modalities [79].
Conclusion
In summarizing our dive into peptic ulcer management, some crucial points emerge.
Strategies targeting Helicobacter pylori, along with new acid suppressants
and the prospect of an H. pylori vaccine, mark significant progress. Natural
compounds like monoterpenes also show promise. Challenges, such as H. pylori
resistance and how to best use acid suppressants, remain. The conclusion here is a
call for ongoing research. Understanding new therapies, figuring out the right
doses, and decoding potential interactions are the tasks ahead. In essence, this
review points to the importance of ongoing research in peptic ulcer management. The
journey forward involves a steady pursuit of knowledge, delving deeper into the
details of treating peptic ulcers. As we stand at the brink of scientific progress,
the focus remains on the ongoing evolution of peptic ulcer management through
dedicated research.
