Your browser does not fully support modern features. Please upgrade for a smoother experience.
Submitted Successfully!
Thank you for your contribution! You can also upload a video entry or images related to this topic. For video creation, please contact our Academic Video Service.
Version Summary Created by Modification Content Size Created at Operation
1 Elyse M. Cornett -- 3288 2022-12-16 19:46:24 |
2 Reference format revised. Lindsay Dong Meta information modification 3288 2022-12-19 06:43:23 |

Video Upload Options

We provide professional Academic Video Service to translate complex research into visually appealing presentations. Would you like to try it?
No, upload directly Yes
Cite
If you have any further questions, please contact Encyclopedia Editorial Office.
Roberts, L.T.;  Issa, P.P.;  Sinnathamby, E.S.;  Granier, M.;  Mayeux, H.;  Eubanks, T.N.;  Malone, K.;  Ahmadzadeh, S.;  Cornett, E.M.;  Shekoohi, S.; et al. Treatment Options of Helicobacter pylori. Encyclopedia. Available online: https://encyclopedia.pub/entry/38910 (accessed on 27 March 2026).
Roberts LT,  Issa PP,  Sinnathamby ES,  Granier M,  Mayeux H,  Eubanks TN, et al. Treatment Options of Helicobacter pylori. Encyclopedia. Available at: https://encyclopedia.pub/entry/38910. Accessed March 27, 2026.
Roberts, Logan T., Peter P. Issa, Evan S. Sinnathamby, Mallory Granier, Holly Mayeux, Treniece N. Eubanks, Kevin Malone, Shahab Ahmadzadeh, Elyse M. Cornett, Sahar Shekoohi, et al. "Treatment Options of Helicobacter pylori" Encyclopedia, https://encyclopedia.pub/entry/38910 (accessed March 27, 2026).
Roberts, L.T.,  Issa, P.P.,  Sinnathamby, E.S.,  Granier, M.,  Mayeux, H.,  Eubanks, T.N.,  Malone, K.,  Ahmadzadeh, S.,  Cornett, E.M.,  Shekoohi, S., & Kaye, A.D. (2022, December 16). Treatment Options of Helicobacter pylori. In Encyclopedia. https://encyclopedia.pub/entry/38910
Roberts, Logan T., et al. "Treatment Options of Helicobacter pylori." Encyclopedia. Web. 16 December, 2022.
Treatment Options of Helicobacter pylori
Edit
This entry is adapted from the peer-reviewed paper 10.3390/life12122038

Helicobacter pylori is among the most common infections worldwide, and it can lead to burdensome sequela for the patient and the healthcare system, without appropriate treatment. Due to constantly fluctuating resistance rates, regimens must be constantly assessed to ensure effectiveness. 

treatment options Helicobacter pylori

1. Introduction

The gram-negative, spiral-shaped bacterium Helicobacter pylori is a widespread and prevalent opportunistic pathogen most commonly associated with gastritis, peptic ulcers, and various other gastrointestinal ailments [1]. There is robust evidence that H. pylori is acquired during childhood in most people, and is significantly determined by geography and quality of life [2]. Since the primary means of H. pylori infection are by oral–oral and fecal–oral transmission, risk factors include contaminated food or water supplies, contact with domestic animals, smoking, alcohol consumption, ill contacts, closely packed living situations, poor sanitation, poor hygiene, and most importantly, low socioeconomic status [3].
H. pylori were discovered as spiral bacteria in the stomach of dogs by Giulio Bizzozero in 1892. Since they are Campylobacter-like spiral bacteria, Barry Marshall and Robin Warren dubbed them Campylobacter pyloridis in 1983. Goodwin et al. designated them Helicobacter pylori in 1989 because of their helical form, and prevalence in the pyloric area of the stomach. H. pylori are a 0.5–1 m wide, 2–4 m long, S-shaped, short helical, Gram-negative bacteria that infect more than half of the world’s population [4].
H. pylori are a short helical, S-shaped, Gram-negative bacteria measuring 0.5–1 m in width and 2–4 m in length. They are particularly prevalent in the pyloric area of the stomach, where they cause persistent gastric infection. It is believed that more than half of the world’s population is infected with these bacteria. The specific modes of transmission and infection with H. pylori are yet unknown, but the feces-to-mouth and mouth-to-mouth pathways via water or food consumption are believed to be quite common [4].

2. Etiology, Epidemiology, Pathophysiology

H. pylori can be transmitted by the fecal–oral, gastric–oral, oral–oral, and sexual pathways. Lower socioeconomic status is a significant risk factor for a higher infection prevalence [5]. The prevalence of H. pylori varies across the globe, with a 5% prevalence in children younger than ten years old in the United States. It is more prevalent in the Hispanic and African American populations than the White population [5].
In H. pylori infection, four key factors contribute to the development of clinical illnesses such as gastritis and ulcer. First, the urease activity of H. pylori serves a crucial function in neutralizing the stomach’s acidic environment. Second, the H. pylori bacterium moves toward the host gastric epithelial cells via flagella-mediated motility. The subsequent interaction between bacterial adhesins and host cell receptors results in effective colonization and sustained infection. In addition, H. pylori produce numerous effector proteins/toxins, such as cytotoxin-associated gene A (Cag A) and vacuolating cytotoxin A (VacA), that cause host tissue damage. H. pylori gastritis is characterized by both acute and chronic inflammation due to the stimulation of eosinophils, neutrophils, mast cells, and dendritic cells. Additionally, the gastric epithelial layer secretes chemokines to trigger innate immunity and activates neutrophils, which further damage the host tissue, resulting in the establishment of gastritis and ulcer [5].

3. Antibiotics Overview

3.1. Clarithromycin

Clarithromycin is a broad-spectrum antimicrobial (macrolide class) known for covering atypical organisms. Clarithromycin is one of the five approved macrolides in the United States. It is well-known for its use against H. pylori as it remains a staple therapeutic in the triple therapy regimen. Similarly to others in the macrolide class, clarithromycin is a bacteriostatic antibiotic that reversibly binds the large 50S subunit of bacterial ribosomes at the 23S ribosomal RNA (rRNA) to inhibit protein synthesis [6][7].
Though widely considered the most effective antimicrobial agent for treating and eradicating H. pylori, the use of clarithromycin is not without significant side effects [8][9]. Adverse events associated with using clarithromycin are cited as high as 86%, most of which are gastrointestinal or taste-related [10]. The most common adverse event is taste perversion, reported with a frequency of 58% in a randomized, double-blind trial. Gastrointestinal side effects, including nausea, vomiting, diarrhea, and abdominal discomfort, are also especially common [11]. Such adverse events tend to present more commonly in children [12]. As a known cytochrome P450 (CYP) 3A4 enzyme inhibitor, clarithromycin can influence the pharmacokinetics of other drugs, and consequently induce hepatotoxicity.

3.2. Amoxicillin

Amoxicillin is an oral aminopenicillin within the beta-lactam class of antibiotics. Amoxicillin has garnered favorability because, in addition to gram-positive coverage typical of natural penicillins, it also has utility against gram-negative pathogens, including Haemophilus, Neisseria, Proteus, and E. coli [13]. Furthermore, the use of beta-lactamase inhibitors (e.g., clavulanate) can increase amoxicillin’s effectiveness against resistant gram-negative and methicillin-susceptible Staphylococcus aureus (MSSA) [14][15]. Commonly used to treat infections of the respiratory tract, urinary system, and ear, amoxicillin is also frequently used to treat H. pylori as it is one of the medications in the triple therapy regimen [16][17]. Beta-lactams bind penicillin-binding proteins, inhibiting transpeptidation, and consequently inducing autolytic destruction of the bacterial cell wall [18].

3.3. Bismuth Subsalicylate

Bismuth subsalicylate is an antacid, antidiarrheal, anti-inflammatory, and bactericidal agent which is widely known as the active ingredient in Pepto-Bismol [19][20]. Bismuth subsalicylate is fragmented in the stomach into salicylate and bismuth, which is minimally absorbed to act as a bactericidal agent. In the alimentary canal, bismuth reduces inflammation, minimizes fluid excretion, and prevents bacterial adhesion [20][21][22]. Bismuth subsalicylate is generally well tolerated, although common side effects include diarrhea, nausea, bitter taste, and dark stools [23]. Rarely, patients may present with a blackened tongue, mood changes, or neurotoxicity [24][25]. Contraindications for bismuth subsalicylate use include patients with gastrointestinal ulcers, bleeding problems, black stools before administration, or already consuming medications high in salicylate (such as anticoagulants, methotrexate, etc.)

3.4. Metronidazole

Metronidazole is a narrow-spectrum synthetic antimicrobial of the nitroimidazole class. The reduction of metronidazole, following its entry into the bacterium, is thought to produce an intermediate responsible for cytotoxic and antimicrobial effects [26][27]. Though side effects are uncommon, metronidazole may cause vomiting, nausea, diarrhea, and abdominal pain. Patients taking metronidazole in oral form also complain of a metallic taste. More serious and rarer adverse events include numbness, peripheral neuropathy, and seizures [28]. Significantly, alcohol can interact with metronidazole in a disulfiram-like reaction that typically presents with flushing, cramping, vomiting, tachycardia, and palpitations [29][30].

3.5. Tetracycline/Doxycycline

Since the 1950s, tetracycline is a broad-spectrum bacteriostatic agent that inhibits protein synthesis by binding to the 30S subunit, and effectively limiting hydrogen bond formation between amino acids [31][32]. In addition to its function as an antibacterial agent, tetracycline has antiparasitic activity, inhibiting the growth of Plasmodium falciparum, Giardia lamblia, and Trichomonas vaginalis [33]. Tetracycline has long been reported to interfere with bone mineralization and calcification; consequently, its use is contraindicated in patients under the age of 8 years [33]. Importantly, the risk of maternal hepatotoxicity renders tetracycline a potential teratogen, and its use should be avoided in pregnant and breastfeeding women [34].

3.6. Levofloxacin

Levofloxacin is a broad-spectrum antibiotic of the fluoroquinolone class. Known for its concentration-dependent bactericidal activity, high-dose, short-course levofloxacin has become an attractive therapy that maximizes the chance of regimen course completion, while minimizing the risk for resistance development [35]. Levofloxacin acts on gram-positive and gram-negative bacteria by inhibiting DNA replication, specifically DNA gyrase and topoisomerase, and is accordingly considered a bactericidal [36]. From a safety perspective, it is important to note that levofloxacin and the fluoroquinolone class possess a black box warning label for their association with tendinopathy and tendon rupture, central nervous system effects, and peripheral neuropathy [37]. Mild and common side effects of levofloxacin use include gastrointestinal symptoms, diarrhea, abdominal pain, and central nervous system-related disturbances such as dizziness, headache, and insomnia [38][39]. Other potential complications include psychiatric disturbances, such as agitation, disorientation, suicide ideation, QT prolongation, drug absorption interactions, hyper- and hypoglycemia, and photosensitivity.

4. Acid Suppressants Overview

4.1. Proton Pump Inhibitors (PPIs)

Proton pump inhibitors (PPIs) are a class of medications that effectively reduce gastric acid production by irreversibly inhibiting the luminal H+/K+ ATPase of parietal cells within the stomach [40]. Accordingly, PPIs commonly treat gastroesophageal reflux disease, and peptic ulcer disease. They are also vital in H. pylori eradication as they are commonly included in triple therapy regimens [41][42]. Considering H. pylori’s preference for an acidic environment, raising gastric mucosal pH with PPIs can hinder bacterial growth, and allow gastric ulcer recovery. PPIs are also thought to allow antibiotics to concentrate in the stomach, further strengthening the efficacy of the triple therapy regime [43]. Though typically well-tolerated, PPIs can cause abdominal discomfort, dizziness, and nausea [44][45]. In addition, PPI use is commonly associated with an increased risk of enteric infections [45]. Considering drug metabolism, lower doses are generally recommended for patients with hepatic disease [46].

4.2. Vonoprazan

Vonoprazan belongs to a new class of acid-suppressant medications known as K-competitive acid blockers. K-competitive acid blockers, also called acid pump antagonists, exert their effect by minimizing potassium availability in the lumen, reducing K+/H+ ATPase cotransport, and consequently decreasing gastric acid production [47][48]. Unlike PPIs, vonoprazan binds reversibly, and has a longer half-life [49][50]. Importantly, vonoprazan was FDA-approved in 2022 to be used in triple therapy regimens to treat H. pylori [51][52].

5. First-Line Therapies

5.1. Bismuth Quadruple Therapy

The bismuth quadruple therapy (BQT) is the recommended first-line initial treatment option when areas are exhibiting high levels (>15%) of clarithromycin resistance, and low-level dual clarithromycin and metronidazole resistance (<15%) [53]. It is also the recommended first-line therapy in patients with recent macrolide exposure, or who are allergic to penicillin [54]. The BQT includes bismuth subsalicylate, metronidazole, tetracycline, and a PPI [54]. It consists of 300 to 524 mg of bismuth subsalicylate four times daily, 500 mg of metronidazole 3 to 4 times daily or 250 mg 4 times daily, and 500 mg of tetracycline hydrochloride four times daily with a standard-dose PPI [55].

5.2. Clarithromycin Triple Therapy

Clarithromycin triple therapy consists of a standard dose of PPI, clarithromycin 500 mg, and amoxicillin 1 g, all taken twice a day, or metronidazole 500 mg three times daily [54].

5.3. Concomitant Therapy

The so-called “Concomitant Therapy” consists of a standard dose of PPI, clarithromycin 500 mg, and amoxicillin 1 g with the addition of metronidazole 500 mg or tinidazole 500 mg, all taken twice a day [54]. It should be considered in patients intolerant of bismuth. Concomitant therapy over 14 days yields the highest cure rates [56].

5.4. Sequential Therapy

Clarithromycin-based sequential therapy consists of a standard dose of PPI plus amoxicillin 1 g twice daily for five days [54]. This is followed by a PPI, clarithromycin 500 mg, and either metronidazole or tinidazole at a dose of 500 mg twice daily for an additional five days. While it is comparable to clarithromycin-based triple therapy, its complexity detracts from its viability as a first-line agent. Sequential therapy has been shown to have an eradication rate of 84.3% [54]. It has not been shown to have superior outcomes to either a 14-day clarithromycin-based triple therapy or a 10–14-day bismuth quadruple therapy. Tolerability and compliance are similar to the clarithromycin-based triple therapy [57]. Due to the complexity of sequential therapy, and the lack of evidence of superiority compared to 14-day clarithromycin triple therapy, clarithromycin-containing sequential therapy has not been endorsed by guidelines in North America as a first-line treatment [58].

5.5. Hybrid Therapy

Hybrid therapy is a combined sequential and concomitant therapy. It consists of a standard dose of PPI plus Amoxicillin 1 g taken twice a day for seven days, followed by PPI, Amoxicillin, Clarithromycin 500 mg, and either metronidazole or tinidazole 500 mg taken twice a day for an additional seven days [54]. While there are a lack of data supporting hybrid therapy’s effectiveness in North America, it has been shown to have high cure rates in international studies.

6. Common Substitutions and Cautions

6.1. Penicillin Allergy

Amoxicillin is used in many first-line therapies to treat an H. pylori infection [59]. Several therapies do not contain amoxicillin, such as the bismuth quadruple therapy. The clarithromycin-based triple therapy can also be used if metronidazole is substituted for penicillin.

6.2. Alternatives to Clarithromycin

Clarithromycin-based triple therapy may be a first-line therapy to treat H. pylori with low regional levels of resistance. This therapy is not recommended when clarithromycin resistance rates are >15–20% [60]. Other therapies such as the bismuth quadruple or sequential therapies are suggested [61]. Levofloxacin-based therapies are also used as an alternative to clarithromycin. Levofloxacin has been shown to potentially have an eradication rate of >90%, especially where there is low resistance to levofloxacin [62]. The resistance to quinolones is rising; however, levofloxacin is discouraged as a first-line treatment [63].

6.3. Metronidazole and Alcohol Use

Metronidazole is contraindicated in patients who recently consumed alcohol or products that contain propylene glycol. Patients should avoid consuming alcohol until three days after metronidazole-containing therapy. There have been reports of a disulfiram reaction occurring in patients consuming alcohol while being administered metronidazole. Typically, disulfiram reactions present with flushing, nausea, vomiting, tachycardia, and palpitations [64][65].

6.4. Tetracyclines and Pregnancy

Tetracycline is contraindicated in pregnant women due to a risk of hepatotoxicity in the mother, and permanent discoloration of the teeth in the fetus [66]. There is also a risk of impaired fetal bone growth development [66]. For this reason, bismuth quadruple therapy is not advised in pregnant patients. Other first-line therapies, such as standard triple therapy, are recommended in their place.

6.5. Follow Up Eradication Confirmation

It is recommended that patients receive post-treatment eradication testing at least four weeks after the completion of antibiotic therapy [67]. PPIs should be withheld for at least one to two weeks before testing to avoid false negatives [68].

7. Second-Line Agents for Treatment Failure

7.1. Suggested Approach

With increasing H. pylori strain diversity, many first-line treatments can be ineffective at eradication. Patients require a second-line salvage therapy regimen to be administered when a refractory infection occurs or when there is a persistent positive non-serological test occurring up to four weeks after the first-line treatments are administered. When choosing a second-line therapy, patient allergies, first-line therapies previously used, local geographic resistance rates, and sensitivities should be considered. Due to low global resistance rates to amoxicillin, this antibiotic may be reused in second-line therapy regimens even if it was initially used in first-line treatment. Other previously used regimens should be avoided. Suppose there is a failure of first-line therapy in a penicillin-allergic patient. In that case, it is advised that the patient receives allergy testing to identify if they have a true penicillin allergy [54].

7.2. Bismuth Quadruple Therapy

Bismuth quadruple therapy (BQT), discussed in “initial antibiotic selection,” may be used for 14 days as a second-line regimen in treatment if previously unused as the first-line option [54]. Many alternative forms of bismuth-containing therapies are quadruple therapy variations of levofloxacin- and rifabutin-based triple therapy regimens.

7.3. Levofloxacin-Based Therapy

Levofloxacin-based triple therapy, consisting of levofloxacin, amoxicillin, and a proton pump inhibitor, is typically administered over 10 to 14 days as a second-line regimen. The dosages of each component are administered as follows: 500 mg of levofloxacin daily, 750 mg of amoxicillin three times daily, and a standard dose of a proton pump inhibitor twice daily. Levofloxacin-based therapy regimens are not indicated as second-line treatments in regions of the world with resistance rates greater than 15%, unless the strain has known sensitivity to the drug. This is due to levofloxacin experiencing increasing rates of primary and secondary resistance. Primary resistance rates ranging from 11 to 30% have been documented from data from over 50,000 patients across 45 countries, and those rates rise to 19–30% when considering secondary resistance after unsuccessful H. pylori treatment [69].
Levofloxacin-based quadruple therapies exist in addition to their triple therapy counterparts. Four popular regimens exist that all center around levofloxacin, with three of them containing bismuth as a core component.
LOAD therapy, containing levofloxacin, omeprazole, nitazoxanide, and doxycycline, is a novel treatment regimen for H. pylori eradication. Therapy lasts 7–10 days compared to the traditional 14 days of the standard triple therapy, with dosages consisting of 250 mg of levofloxacin once daily, 40 mg of omeprazole twice daily, 500 mg of nitazoxanide twice daily, and 100 mg of doxycycline once daily.

7.4. High-Dose Dual Therapy

High-dose dual therapy, consisting of a proton pump inhibitor and 750 mg of amoxicillin given four times a day or 1 g three times daily over 14 days, is a superior regimen to standard rescue therapies in H. pylori infections. In one study, infections were eradicated in 95.3% of patients given the high-dose dual therapy regimen [70]. This can be particularly useful in patients with dual clarithromycin and levofloxacin-resistant strains.

7.5. Rifabutin Triple Therapy

Rifabutin triple therapy, a regimen consisting of 750 mg of amoxicillin three times daily, a proton pump inhibitor twice daily, and 300 mg of rifabutin given once daily over 14 days, has been shown to exhibit eradication rates of 83.8% versus 57.7% found in amoxicillin and proton pump inhibitor administered alone [71]. The significant difference in efficacy is most likely attributable to the increased prevalence of amoxicillin resistance in H. pylori strains, similar to the differences in the efficacy of other previously mentioned regimens.

7.6. Clarithromycin-Based therapy

In clarithromycin-based therapy containing a proton pump inhibitor, bismuth, and tetracycline, eradication rates in non-resistant strains of H. pylori have been shown to be greater than 95% successful [72]. Clarithromycin should be considered when macrolide resistance is not a concern, and the local resistance rates are less than 15%. While clarithromycin is still considered for use in rescue therapy following unsuccessful H. pylori eradication, the high prevalence of resistance in H. pylori strains to the antimicrobial often indicates the use of other drug classes in treatment [69].

7.7. Factors Associated with Treatment Failure

While many factors are associated with the failure of H. pylori eradication, the main contributors are patient noncompliance and increased antimicrobial resistance, especially to quinolones and macrolides. This resistance has also been shown to be both primary and secondary in various H. pylori strains throughout different regions of the world [69]. When considering that many antimicrobials function at a higher pH than stomach acid allows, inadequate acid suppression during treatment is also a major source of failure to eradicate infections. This possible point of failure focuses on the cytochrome P450 gene CYP2C19. This gene is responsible for the majority of the metabolism of early-generation proton pump inhibitors. It has been shown to have many polymorphisms affecting an individual’s drug clearance rate. Those with polymorphisms that increase metabolism have been associated with higher rates of eradication failure, despite exposure to susceptible antibiotics [69].

7.8. Probiotics

Probiotics, live microorganisms that can be administered as therapy, may have a future role in eradicating H. pylori by alleviating antibiotics’ side effects. The most commonly used probiotic organisms include Lactobacillus and Bifidobacterium, two Gram (+) organisms. Posed benefits to the host include promoting gut maturation/integrity, pathogen antagonism, and immune system modulation. A primary characteristic of these bacteria is their ability to anaerobically digest saccharides to produce lactic acid, a cellular product that inhibits H. pylori. Their beneficial effects come from nonimmunological mechanisms such as strengthening the mucosal barrier of the GI tract, as well as secretion of antimicrobial substances such as short-chain fatty acids. They also exhibit beneficial effects through immunological mechanisms, such as releasing anti-inflammatory cytokine secretion that reduces inflammation, and gastric acid production [72][73][74]. Several studies show the beneficial effects of probiotics when combating H. pylori. The indications for use are a supplement to first-line therapies that may help alleviate some treatment-related side effects [62].

8. Conclusions

It has been proven that receiving treatment to eradicate H. pylori infections is more beneficial than not, due to the long-term complications associated with non-treatment, such as gastritis, gastric ulcerations, and malignancies. However, choosing the appropriate treatment regimen is immensely dynamic, due to high resistant rates, prescription costs, side effects, and patient non-adherence. Due to high clarithromycin resistance rates, bismuth quadruple therapy can often be the most appropriate initial antibiotic selected for eradication. If resistance is not a local problem, clarithromycin triple therapy is still a viable first-line option due to its inexpensiveness, and well-established effectiveness. Combination capsules circumvent patient adherence concerns but should only be considered contingent upon patient affordability. If side effects create a barrier to adherence, probiotics should be considered as an addition to a regimen to ease the side effect burden. When deciding between other second-line regimens, it is important to make a patient-specific selection based on allergies, effectiveness, affordability, side effects, and ease of administration. As current regimens encounter fluctuations in resistance patterns, repurposed medications such as rifabutin may pose substantial benefits in eradicating infections in treatment-failure patients.

References

  1. Guevara, B.; Cogdill, A.G. Helicobacter pylori: A Review of Current Diagnostic and Management Strategies. Dig. Dis. Sci. 2020, 65, 1917–1931.
  2. Hooi, J.K.Y.; Lai, W.Y.; Ng, W.K.; Suen, M.M.Y.; Underwood, F.E.; Tanyingoh, D.; Malfertheiner, P.; Graham, D.Y.; Wong, V.W.S.; Wu, J.C.Y.; et al. Global Prevalence of Helicobacter pylori Infection: Systematic Review and Meta-Analysis. Gastroenterology 2017, 153, 420–429.
  3. Kotilea, K.; Bontems, P.; Touati, E. Epidemiology, Diagnosis and Risk Factors of Helicobacter pylori Infection. In Helicobacter pylori in Human Diseases: Advances in Microbiology, Infectious Diseases and Public Health Volume 11; Kamiya, S., Backert, S., Eds.; Advances in Experimental Medicine and Biology; Springer International Publishing: Cham, Switzerland, 2019; pp. 17–33. ISBN 978-3-030-21916-1.
  4. Öztekin, M.; Yılmaz, B.; Ağagündüz, D.; Capasso, R. Overview of Helicobacter pylori Infection: Clinical Features, Treatment, and Nutritional Aspects. Diseases 2021, 9, 66.
  5. Parikh, N.S.; Ahlawat, R. Helicobacter pylori; StatPearls Publishing: Tampa, FL, USA, 2022.
  6. Zuckerman, J.M.; Qamar, F.; Bono, B.R. Review of Macrolides (Azithromycin, Clarithromycin), Ketolids (Telithromycin) and Glycylcyclines (Tigecycline). Med. Clin. N. Am. 2011, 95, 761–791, viii.
  7. Sturgill, M.G.; Rapp, R.P. Clarithromycin: Review of a New Macrolide Antibiotic with Improved Microbiologic Spectrum and Favorable Pharmacokinetic and Adverse Effect Profiles. Ann. Pharmacother. 1992, 26, 1099–1108.
  8. Khademi, F.; Faghri, J.; Moghim, S.; Esfahani, B.N.; Fazeli, H.; Poursina, F.; Adibi, P.; Madhi, M.; Safaei, H.G. The Study of Mutation in 23S RRNA Resistance Gene of Helicobacter pylori to Clarithromycin in Patients with Gastrointestinal Disorders in Isfahan—Iran. Adv. Biomed. Res 2014, 3, 98.
  9. Yakoob, J.; Jafri, W.; Abbas, Z.; Abid, S.; Naz, S.; Khan, R.; Khalid, A. Risk Factors Associated with Helicobacter pylori Infection Treatment Failure in a High Prevalence Area. Epidemiol. Infect 2011, 139, 581–590.
  10. Peterson, W.L.; Graham, D.Y.; Marshall, B.; Blaser, M.J.; Genta, R.M.; Klein, P.D.; Stratton, C.W.; Drnec, J.; Prokocimer, P.; Siepman, N. Clarithromycin as Monotherapy for Eradication of Helicobacter pylori: A Randomized, Double-Blind Trial. Am. J. Gastroenterol 1993, 88, 1860–1864.
  11. Wood, M.J. The Tolerance and Toxicity of Clarithromycin. J. Hosp. Infect 1991, 19 (Suppl. A), 39–46.
  12. Gribble, M.J.; Chow, A.W. Erythromycin. Med. Clin. N. Am. 1982, 66, 79–89.
  13. Geddes, A.M.; Klugman, K.P.; Rolinson, G.N. Introduction: Historical Perspective and Development of Amoxicillin/Clavulanate. Int. J. Antimicrob. Agents 2007, 30 (Suppl. S2), S109–S112.
  14. Aronoff, S.C.; Jacobs, M.R.; Johenning, S.; Yamabe, S. Comparative Activities of the Beta-Lactamase Inhibitors YTR 830, Sodium Clavulanate, and Sulbactam Combined with Amoxicillin or Ampicillin. Antimicrob. Agents Chemother. 1984, 26, 580–582.
  15. Carcione, D.; Siracusa, C.; Sulejmani, A.; Leoni, V.; Intra, J. Old and New Beta-Lactamase Inhibitors: Molecular Structure, Mechanism of Action, and Clinical Use. Antibiotics 2021, 10, 995.
  16. Salvo, F.; De Sarro, A.; Caputi, A.P.; Polimeni, G. Amoxicillin and Amoxicillin plus Clavulanate: A Safety Review. Expert. Opin. Drug. Saf. 2009, 8, 111–118.
  17. Amoxicillin: A Broad Spectrum Antibiotic. Available online: https://www.researchgate.net/publication/304704877_Amoxicillin_A_Broad_Spectrum_Antibiotic (accessed on 22 November 2022).
  18. Bernatová, S.; Samek, O.; Pilát, Z.; Serý, M.; Ježek, J.; Jákl, P.; Siler, M.; Krzyžánek, V.; Zemánek, P.; Holá, V.; et al. Following the Mechanisms of Bacteriostatic versus Bactericidal Action Using Raman Spectroscopy. Molecules 2013, 18, 13188–13199.
  19. Madisch, A.; Morgner, A.; Stolte, M.; Miehlke, S. Investigational Treatment Options in Microscopic Colitis. Expert. Opin. Investig. Drugs 2008, 17, 1829–1837.
  20. Bierer, D.W. Bismuth Subsalicylate: History, Chemistry, and Safety. Rev. Infect. Dis 1990, 12 (Suppl. S1), S3–S8.
  21. Pitz, A.M.; Park, G.W.; Lee, D.; Boissy, Y.L.; Vinjé, J. Antimicrobial Activity of Bismuth Subsalicylate on Clostridium Difficile, Escherichia Coli O157:H7, Norovirus, and Other Common Enteric Pathogens. Gut Microbes 2015, 6, 93–100.
  22. Sheele, J.; Cartowski, J.; Dart, A.; Poddar, A.; Gupta, S.; Stashko, E.; Ravi, B.S.; Nelson, C.; Gupta, A. Saccharomyces Boulardii and Bismuth Subsalicylate as Low-Cost Interventions to Reduce the Duration and Severity of Cholera. Pathog. Glob. Health 2015, 109, 275–282.
  23. Vilaichone, R.; Prapitpaiboon, H.; Gamnarai, P.; Namtanee, J.; Wongcha-um, A.; Chaithongrat, S.; Mahachai, V. Seven-Day Bismuth-Based Quadruple Therapy as an Initial Treatment for Helicobacter pylori Infection in a High Metronidazole Resistant Area. Asian Pac. J. Cancer Prev. 2015, 16, 6089–6092.
  24. Sainsbury, S.J. Fatal Salicylate Toxicity from Bismuth Subsalicylate. West. J. Med. 1991, 155, 637–639.
  25. Borbinha, C.; Serrazina, F.; Salavisa, M.; Viana-Baptista, M. Bismuth Encephalopathy—A Rare Complication of Long-Standing Use of Bismuth Subsalicylate. BMC Neurol. 2019, 19, 212.
  26. Freeman, C.D.; Klutman, N.E.; Lamp, K.C. Metronidazole. A Therapeutic Review and Update. Drugs 1997, 54, 679–708.
  27. Müller, M. Mode of Action of Metronidazole on Anaerobic Bacteria and Protozoa. Surgery 1983, 93, 165–171.
  28. Hernández Ceruelos, A.; Romero-Quezada, L.C.; Ruvalcaba Ledezma, J.C.; López Contreras, L. Therapeutic Uses of Metronidazole and Its Side Effects: An Update. Eur. Rev. Med. Pharmacol. Sci. 2019, 23, 397–401.
  29. Kurian, M.; Ganapathy, D.; Jain, A.R. Recent Advances of Metronidazole-A Review. Drug Invent. Today 2018, 10, 3536–3541.
  30. Mergenhagen, K.A.; Wattengel, B.A.; Skelly, M.K.; Clark, C.M.; Russo, T.A. Fact versus Fiction: A Review of the Evidence behind Alcohol and Antibiotic Interactions. Antimicrob. Agents Chemother. 2020, 64, e02167-19.
  31. Roberts, M.C. Tetracycline Resistance Determinants: Mechanisms of Action, Regulation of Expression, Genetic Mobility, and Distribution. FEMS Microbiol. Rev. 1996, 19, 1–24.
  32. Katiyar, S.K.; Edlind, T.D. Enhanced Antiparasitic Activity of Lipophilic Tetracyclines: Role of Uptake. Antimicrob. Agents Chemother. 1991, 35, 2198–2202.
  33. Speer, B.S.; Shoemaker, N.B.; Salyers, A.A. Bacterial Resistance to Tetracycline: Mechanisms, Transfer, and Clinical Significance. Clin. Microbiol. Rev. 1992, 5, 387–399.
  34. Chopra, I.; Roberts, M. Tetracycline Antibiotics: Mode of Action, Applications, Molecular Biology, and Epidemiology of Bacterial Resistance. Microbiol. Mol. Biol. Rev. 2001, 65, 232–260.
  35. Anderson, V.R.; Perry, C.M. Levofloxacin. Drugs 2008, 68, 535–565.
  36. Hooper, D.C. Mode of Action of Fluoroquinolones. Drugs 1999, 58 (Suppl. S2), 6–10.
  37. Tanne, J.H. FDA Adds “Black Box” Warning Label to Fluoroquinolone Antibiotics. BMJ 2008, 337, 135.
  38. Erden, B.F.; Ulak, G.; Yildiz, F.; Utkan, T.; Ozdemirci, S.; Gacar, N. Antidepressant, Anxiogenic, and Antinociceptive Properties of Levofloxacin in Rats and Mice. Pharmacol. Biochem. Behav. 2001, 68, 435–441.
  39. Croom, K.F.; Goa, K.L. Levofloxacin: A Review of Its Use in the Treatment of Bacterial Infections in the United States. Drugs 2003, 63, 2769–2802.
  40. Sachs, G.; Shin, J.M.; Howden, C.W. Review Article: The Clinical Pharmacology of Proton Pump Inhibitors. Aliment Pharmacol. Ther. 2006, 23 (Suppl. S2), 2–8.
  41. Richter, J.E. Gastrooesophageal Reflux Disease. Best Pract. Res. Clin. Gastroenterol. 2007, 21, 609–631.
  42. Sachs, G.; Shin, J.M.; Briving, C.; Wallmark, B.; Hersey, S. The Pharmacology of the Gastric Acid Pump: The H+,K+ ATPase. Annu. Rev. Pharmacol. Toxicol. 1995, 35, 277–305.
  43. Chiba, T.; Malfertheiner, P.; Satoh, H. Proton Pump Inhibitors: A Balanced View; Karger Book: Basel, Switzerland, 2013.
  44. Yibirin, M.; De Oliveira, D.; Valera, R.; Plitt, A.E.; Lutgen, S. Adverse Effects Associated with Proton Pump Inhibitor Use. Cureus 2021, 13, e12759.
  45. Abraham, N.S. Proton Pump Inhibitors: Potential Adverse Effects. Curr. Opin. Gastroenterol. 2012, 28, 615–620.
  46. Ahmed, A.; Clarke, J.O. Proton Pump Inhibitors (PPI). In StatPearls; StatPearls Publishing: Treasure Island, FL, USA, 2022.
  47. Graham, D.Y.; Dore, M.P. Update on the Use of Vonoprazan: A Competitive Acid Blocker. Gastroenterology 2018, 154, 462–466.
  48. Shin, J.M.; Sachs, G. Long Lasting Inhibitors of the Gastric H,K-ATPase. Expert Rev. Clin. Pharmacol. 2009, 2, 461.
  49. Echizen, H. The First-in-Class Potassium-Competitive Acid Blocker, Vonoprazan Fumarate: Pharmacokinetic and Pharmacodynamic Considerations. Clin. Pharmacokinet. 2016, 55, 409–418.
  50. Fock, K.M.; Ang, T.L.; Bee, L.C.; Lee, E.J.D. Proton Pump Inhibitors. Clin. Pharmacokinet. 2008, 47, 1–6.
  51. Vonoprazan, a Novel Potassium-Competitive Acid Blocker, as a Component of First-Line and Second-Line Triple Therapy for Helicobacter pylori Eradication: A Phase III, Randomised, Double-Blind Study | Gut. Available online: https://gut.bmj.com/content/65/9/1439 (accessed on 22 November 2022).
  52. Garnock-Jones, K.P. Vonoprazan: First Global Approval. Drugs 2015, 75, 439–443.
  53. Kim, S.J.; Chung, J.-W.; Woo, H.S.; Kim, S.Y.; Kim, J.H.; Kim, Y.J.; Kim, K.O.; Kwon, K.A.; Park, D.K. Two-Week Bismuth-Containing Quadruple Therapy and Concomitant Therapy Are Effective First-Line Treatments for Helicobacter pylori Eradication: A Prospective Open-Label Randomized Trial. World J. Gastroenterol. 2019, 25, 6790–6798.
  54. Chey, W.D.; Leontiadis, G.I.; Howden, C.W.; Moss, S.F. ACG Clinical Guideline: Treatment of Helicobacter pylori Infection. Am. J. Gastroenterol. 2017, 112, 212–239.
  55. Mégraud, F. The Challenge of Helicobacter pylori Resistance to Antibiotics: The Comeback of Bismuth-Based Quadruple Therapy. Therap. Adv. Gastroenterol. 2012, 5, 103–109.
  56. Greenberg, E.R.; Anderson, G.L.; Morgan, D.R.; Torres, J.; Chey, W.D.; Bravo, L.E.; Dominguez, R.L.; Ferreccio, C.; Herrero, R.; Lazcano-Ponce, E.C.; et al. 14-Day Triple, 5-Day Concomitant, and 10-Day Sequential Therapies for Helicobacter pylori Infection in Seven Latin American Sites: A Randomised Trial. Lancet 2011, 378, 507–514.
  57. Comparative Effectiveness and Tolerance of Treatments for Helicobacter pylori: Systematic Review and Network Meta-Analysis | The BMJ. Available online: https://www.bmj.com/content/351/bmj.h4052 (accessed on 22 November 2022).
  58. Fallone, C.A.; Chiba, N.; van Zanten, S.V.; Fischbach, L.; Gisbert, J.P.; Hunt, R.H.; Jones, N.L.; Render, C.; Leontiadis, G.I.; Moayyedi, P.; et al. The Toronto Consensus for the Treatment of Helicobacter pylori Infection in Adults. Gastroenterology 2016, 151, 51–69.e14.
  59. Savoldi, A.; Carrara, E.; Graham, D.Y.; Conti, M.; Tacconelli, E. Prevalence of Antibiotic Resistance in Helicobacter pylori: A Systematic Review and Meta-Analysis in World Health Organization Regions. Gastroenterology 2018, 155, 1372–1382.e17.
  60. Kim, S.Y.; Choi, D.J.; Chung, J.-W. Antibiotic Treatment for Helicobacter pylori: Is the End Coming? World J. Gastrointest. Pharmacol. Ther. 2015, 6, 183–198.
  61. Renewed Interest in the Management of Helicobacter pylori Infection. Supplements and Featured Publications. 2021. Available online: https://www.ajmc.com/view/renewed-interest-in-the-management-of-helicobacter-pylori-infection (accessed on 11 August 2022).
  62. Goderska, K.; Agudo Pena, S.; Alarcon, T. Helicobacter pylori Treatment: Antibiotics or Probiotics. Appl. Microbiol. Biotechnol. 2018, 102, 1–7.
  63. Gisbert, J.P.; Romano, M.; Gravina, A.G.; Solís-Muñoz, P.; Bermejo, F.; Molina-Infante, J.; Castro-Fernández, M.; Ortuño, J.; Lucendo, A.J.; Herranz, M.; et al. Helicobacter pylori Second-Line Rescue Therapy with Levofloxacin- and Bismuth-Containing Quadruple Therapy, after Failure of Standard Triple or Non-Bismuth Quadruple Treatments. Aliment Pharmacol. Ther. 2015, 41, 768–775.
  64. Finegold, S.M. Metronidazole. Ann. Intern. Med. 1980, 93, 585–587.
  65. Williams, C.S.; Woodcock, K.R. Do Ethanol and Metronidazole Interact to Produce a Disulfiram-like Reaction? Ann. Pharmacother. 2000, 34, 255–257.
  66. Shutter, M.C.; Akhondi, H. Tetracycline. In StatPearls; StatPearls Publishing: Treasure Island, FL, USA, 2022.
  67. Graham, D.Y. Transitioning of Helicobacter pylori Therapy from Trial and Error to Antimicrobial Stewardship. Antibiotics 2020, 9, 671.
  68. Saleem, N.; Howden, C.W. Update on the Management of Helicobacter pylori Infection. Curr. Treat. Options Gastroenterol. 2020, 18, 476–487.
  69. Shah, S.C.; Iyer, P.G.; Moss, S.F. AGA Clinical Practice Update on the Management of Refractory Helicobacter pylori Infection: Expert Review. Gastroenterology 2021, 160, 1831–1841.
  70. Yang, J.-C.; Lin, C.-J.; Wang, H.-L.; Chen, J.-D.; Kao, J.Y.; Shun, C.-T.; Lu, C.-W.; Lin, B.-R.; Shieh, M.-J.; Chang, M.-C.; et al. High-Dose Dual Therapy Is Superior to Standard First-Line or Rescue Therapy for Helicobacter pylori Infection. Clin. Gastroenterol. Hepatol. 2015, 13, 895–905.e5.
  71. Saracino, I.M.; Pavoni, M.; Zullo, A.; Fiorini, G.; Saccomanno, L.; Lazzarotto, T.; Antonelli, G.; Cavallo, R.; Borghi, C.; Vaira, D. Rifabutin-Based Triple Therapy Or Bismuth-Based Quadruple Regimen As Rescue Therapies For Helicobacter pylori Infection. Eur. J. Intern. Med. 2020, 81, 50–53.
  72. Papastergiou, V.; Georgopoulos, S.D.; Karatapanis, S. Treatment of Helicobacter pylori Infection: Meeting the Challenge of Antimicrobial Resistance. World J. Gastroenterol. 2014, 20, 9898–9911.
  73. Pantuzza, L.L.; Ceccato, M.D.G.B.; Silveira, M.R.; Junqueira, L.M.R.; Reis, A.M.M. Association between Medication Regimen Complexity and Pharmacotherapy Adherence: A Systematic Review. Eur. J. Clin. Pharmacol. 2017, 73, 1475–1489.
  74. Bhatia, S.J.; Kochar, N.; Abraham, P.; Nair, N.G.; Mehta, A.P. Lactobacillus Acidophilus Inhibits Growth of Campylobacter Pylori in Vitro. J. Clin. Microbiol. 1989, 27, 2328–2330.
More
© Text is available under the terms and conditions of the Creative Commons Attribution (CC BY) license; additional terms may apply. By using this site, you agree to the Terms and Conditions and Privacy Policy.
Upload a video for this entry
Information
Subjects: Pharmacology & Pharmacy
Contributors MDPI registered users' name will be linked to their SciProfiles pages. To register with us, please refer to https://encyclopedia.pub/register :
Logan T. Roberts
, Peter P. Issa , Evan S. Sinnathamby ,
Mallory Granier
,
Holly Mayeux
,
Treniece N. Eubanks
,
Kevin Malone
,
Shahab Ahmadzadeh
, Elyse M. Cornett , Sahar Shekoohi , Alan D. Kaye
View Times: 1.3K
Revisions: 2 times (View History)
Update Date: 21 Dec 2022
Table of Contents
    Notice
    You are not a member of the advisory board for this topic. If you want to update advisory board member profile, please contact office@encyclopedia.pub.
    OK
    Confirm
    Only members of the Encyclopedia advisory board for this topic are allowed to note entries. Would you like to become an advisory board member of the Encyclopedia?
    Yes
    No
    ${ textCharacter }/${ maxCharacter }
    Submit
    Cancel
    There is no comment~
    ${ textCharacter }/${ maxCharacter }
    Submit
    Cancel
    ${ selectedItem.replyTextCharacter }/${ selectedItem.replyMaxCharacter }
    Submit
    Cancel
    Confirm
    Are you sure to Delete?
    Yes No
    Academic Video Service
    Feedback