What can I eat for breakfast if I have H Pylori?/Helicobacter pylori (H. pylori) is a gram-negative spiral-shaped bacterium that affects up to 50% of the population worldwide, with a higher prevalence in developing countries.[rx][rx][rx] H. pylori are the most important cause for chronic or atrophic gastritis, peptic ulcer, gastric lymphoma, and gastric carcinoma; however, these complications are less often seen in children and adolescents compared to adults.[rx] H. pylori infection is usually acquired in early childhood and persists in the absence of treatment.[rx] A phase 3 clinical trial in children in China documented the efficacy and safety of an oral recombinant H. pylori vaccine, a future option to reduce the incidence of H. pylori infection.[rx]
Helicobacter pylori, previously known as Campylobacter pylori, is a Gram-negative, microaerophilic bacterium usually found in the stomach. It was identified in 1982 by Australian doctors Barry Marshall and Robin Warren, who found that it was present in a person with chronic gastritis and gastric ulcers, conditions not previously believed to have a microbial cause.[rx][rx][rx] It is also linked to the development of duodenal ulcers and stomach cancer.[rx] However, over 80% of individuals infected with the bacterium are asymptomatic, and it may play an important role in the natural stomach ecology.[rx]
Types of Helicobacter Pylori
The spiral morphology and flagellar motility then assist in penetration into the viscous mucus layer, where the more pH-neutral conditions allow the growth of the gastric Helicobacter species.
(i) Helicobacter felis.
- The spiral-shaped Helicobacter felis was first isolated from the stomach of a cat [rx] and was later also found in dogs. Subsequently designated H. felis [rx], it was probably also the Helicobacter species originally described by Bizzozero in 1893 [rx]. H. felis is one of the Helicobacterspecies with zoonotic potential [rx, rx].
- It has a helical morphology with typical periplasmic fibers, which can be used for microscopic identification. H. felis requires high humidity and can only poorly if at all, be cultured on standard growth media used for the culture of H. pylori [rx]. H. felis is highly motile; on agar plates, it does not really form colonies but rather grows as a lawn [rx].
(ii) Helicobacter mustelae.
- The ferret pathogen H. mustelae was isolated shortly after H. pylori and was originally classified as Campylobacter pylori subsp. Mustela [rx, rx, rx]. It was subsequently shown to have characteristics different from H. pylori [rx] and was later classified as H. mustelae [rx].
- H. mustelae is a relatively small rod, which has multiple polar and lateral sheathed flagella. Interestingly, H. mustelae is phylogenetically closer to the enterohepatic Helicobacter species [rx], based on its 16S rRNA gene sequence, urease sequences, and fatty acid profile [rx, rx], but to our knowledge, H. mustelae has not been implicated in enteric colonization in ferrets.
(iii) Helicobacter acinonychis.
- H. acinonychis, a pathogen of cheetahs and other big cats (formerly named Helicobacter Acinonyx [rx]), is currently the closest known relative to H. pylori [rx] and has been suggested to have diverged from its last common ancestor (H. pylori) only relatively recently[rx].
- The presence of H. deinonychus is associated with chronic gastritis and ulceration, a frequent cause of death of cheetahs in captivity [rx]. Furthermore, eradication treatment of H. deinonychus led to the resolution of gastric lesions in tigers [rx], similar to the effect of antibiotic treatment of H. pylori infection [rx].
- H. deinonychus is susceptible to antibiotic therapy, as used for H. pylori infection, and utilizes similar mechanisms for antimicrobial resistance [rx].
(iv) Helicobacter heilmannii.
- The diverse species H. heilmannii was originally designated Gastrospirillum hominis and is a Helicobacter species with a wide host range [rx, rx]. It has been isolated from several domestic and wild animals, including dogs, cats, and nonhuman primates, and is also observed in a small percentage of humans with gastritis [rx].
- In the latter, colonization may reflect a zoonosis, as there is an association between colonization with this bacterium and close contact with dogs and cats carrying the same bacterium [rx]. Its morphology resembles that of H. felis, but H. heilmannii lacks the periplasmic fibers.
Mechanism of Action of Helicobacter Pylori
The first line of defense against pathogenic bacteria is the acidity of the stomach and the gastric mucosa barrier. It was suggested that, by taking probiotics, this first line of defense could be stronger due to the production of antimicrobial substances competing with H. pylori for adhesion receptors, stimulating mucin production and stabilizing the gut mucosal barrier.
- Probiotics may inhibit H. pylori growth by secreting short-chain fatty acids and antibacterial substances. Short-chain fatty acids such as acetic, propionic, and lactic acids are produced during the carbohydrates metabolism by probiotics and as a consequence, a pH reduction is found. In 1989, Bhatia et al. [rx] were the first group to observe an antagonistic effect of a Lactobacillus strain against H. pylori-related to short-chain fatty acids. Also, the antimicrobial activity could be due to the inhibition of urease activity of H. pylori as has been shown in other publications [rx].
- Certain Lactobacillus species synthesize antimicrobial compounds related to the bacteriocin classes. Bacteriocins are proteinaceous toxins with potential anti-H. pylori activity. They are small and dialysable peptidic structures with antimicrobial activities. Antimicrobial activity of the bacteriocins varied among the H. pylori strains and also the type of bacteriocins produced by Lactobacillus sp. Some bacteriocins have shown a stronger antibacterial activity against H. pylori strains than others, although both were produced by Lactobacillus spp. [rx].
Competition for adhesion
- There are several possible mechanisms by which probiotic bacteria can inhibit the adhesion of H. pylori. The adhesion of H. pylori to epithelial cells is important in determining the outcome in H. pylori-associated diseases; the ability of the bacteria to establish physical contact with the gastric epithelium is affected by the influence of the epithelial mucosa, receptors associated with the adhesion of H. pylori to the epithelium, and immune cells [rx]. There are several possible mechanisms by which probiotic bacteria can inhibit the adhesion of H. pylori, mainly lactic acid and bacteriocins [rx].
- Mucosal surfaces have protective strategies to defend against noxious substances and pathogens found within the intestinal lumen. Some strategies, such as mucins, large complex glycoproteins that protect intestinal mucosal surfaces from microbial pathogens by limiting access of environmental matter to their epithelial cells [rx]. Several mucins have been identified.
- H. pylori is known to suppress MUCI and MUC5 gene expression in a human gastric cell line [rx]. It has been shown that in vitro studies with probiotics such as L. Plantarum and L. rhamnosus increase the expression of MUC2 and MUC3 genes and therefore extracellular secretion of mucin by colon cell cultures can inhibit the adherence of pathogenic bacteria. This ability of these strains restores the mucosal permeability of gastric mucosa and inhibits the adherence of pathogenic bacteria such as H. pylori.
- The inflammatory response to gastric H. pylori infection is characterized by the release of various inflammatory mediators such as chemokines and cytokines. Probiotics could modify the immunologic response by the modulation of anti-inflammatory cytokines secretion, which would result in a reduction of gastric activity and inflammation [rx].
Causes of Helicobacter Pylori
It is not clear exactly how Helicobacter pylori is passed from one person to another, and why only some people with the infection go on to develop ulcers.
- People who do have Helicobacter pylori almost always catch it in childhood, probably from other children. It usually stays in the stomach throughout their lifetime unless it is treated with specific antibiotics. Helicobacter pylori is actually becoming less common and nowadays it is unusual for children to catch it, even if someone else in the family has it. People living in the UK today who have Helicobacter pylori are unlikely to pass it on and do not need to take any special measures to avoid giving it to others.
- Most persons who are infected with H. pylori never suffer any symptoms related to the infection; however, H. pylori causes chronic active, chronic persistent, and atrophic gastritis in adults and children. Infection with H. pylori also causes duodenal and gastric ulcers. Infected persons have a 2- to 6-fold increased risk of developing gastric cancer and mucosal-associated-lymphoid-type (MALT) lymphoma compared with their uninfected counterparts. The role of H. pylori in non-ulcer dyspepsia remains unclear.
- H. pylori have developed an acid acclimation mechanism that promotes the adjustment of periplasmic pH in the harsh acidic environment of the stomach by regulating urease activity. The urease gene cluster is composed of seven genes, including catalytic subunits (ureA/B), an acid-gated urea channel (ureI), and accessory assembly proteins (ureE–H) [rx]. The metal cofactor nickel has to be inserted into the apoenzyme for heterodimer urease activity through the action of the four accessory proteins, among which UreE appears to be an important metallochaperone [rx].
- H. pylori-NAP belongs to the DNA-protecting proteins under starved conditions (Dps) family, which has significant structural similarities to the dodecameric ferritin family. NAP was first identified to stimulate high production of oxygen radicals from neutrophils, leading to damage of local tissues, and promote neutrophil adhesion to endothelial cells during H. pylori infection [rx].
The series of steps – the pathogenic mechanisms – which H. pylori go through when establishing themselves in the stomach are as follows
- Attachment – Often initially done with pili (hairlike structures found on the surface of a microorganism, such as a bacterium), other adhesins (surface antigens that bind receptors) may also contribute to an intimate attachment. The secretion system may transfer substances that become receptors, thus further contributing to the attachment process.
- Toxin production – Toxins increase the secretion of water and electrolytes (enterotoxins) and cause cell death by halting protein synthesis.
- Cell invasion – H. pylori activates the process of endocytosis (a process of cellular ingestion by which the plasma membrane folds inward to bring substances into the cell) and then destroys the host cell, thus creating tissue damage.
- Loss of microvilli/villi – The substances secreted into the host cell during the ‘Cell Invasion’ step cause the rearrangement of the actin filaments, resulting in a loss of the microvilli (tiny hairlike structures that project from the surface of certain epithelial layers of the body’s internal organs).
Symptoms of Helicobacter Pylori
When signs or symptoms do occur with H. pylori infection, they may include
- An ache or burning pain in your abdomen
- Abdominal pain that’s worse when your stomach is empty
- Sharp, sudden, persistent stomach pain
- Bloody or black stools
- Bloody vomit or vomit that looks like coffee grounds
- skin color change, mild diarrhea
- mild nausea
- loss of appetite
- Stool that is bloody, dark red, or black
- Trouble breathing
- Dizziness or fainting
- Feeling very tired for no reason
- Pale skin color
- Vomit that has blood or looks like coffee grounds
- Severe, sharp stomach pain
- Loss of appetite
- Frequent burping
- Unintentional weight loss
A number of other symptoms may be associated with H. pylori infection, including
- Excessive burping
- Feeling bloated
- Lack of appetite, or anorexia
- Unexplained weight loss
- Trouble swallowing
- Blood in the stool
The symptoms just mentioned could be signs of a serious problem, such as
- Perforation – when the ulcer burrows through the stomach or duodenal wall.
- Bleeding – when acid or the ulcer breaks a blood vessel.
- Obstruction – when the ulcer blocks the path of food trying to leave the stomach.
Diagnosis of Helicobacter Pylori
Diagnostic tests are indicated in patients:
- With active peptic ulcer disease (duodenal or gastric),
- With a history of peptic ulcer disease, who have not been previously treated,
- With low-grade gastric MALT lymphoma,
- Who have undergone endoscopic resection of early gastric cancer,
- With uninvestigated dyspepsia, younger than 55 years old (without alarm symptoms).
Available tests for the detection of Helicobacter pylori include
- antibody tests,
- urea breath tests,
- stool antigen tests,
- endoscopic biopsies.
Blood tests detect the presence of antibodies of Helicobacter pylori. However, blood antibodies can persist years after the complete eradication of the bacteria. They may be useful in diagnosing the infection, but they are not good for a determined successful eradication.
Invasive methods to detect H. pylori infection
- Histology – As the standard method to diagnose H. pylori infection, histological examination provides critical information related to the mucosa (e.g., presence and severity of inflammation, intestinal metaplasia, glandular atrophy, dysplasia, and neoplasia). Several studies have recommended that both antrum and corpus biopsies be collected[rx–rx]. The gold standard for gastric biopsy collection is the updated Sydney classification system, which indicates sampling from 5 biopsy sites.
- Culture –A recently obtained gastric biopsy specimen is the ideal specimen for culturing H. pylori because no notable amount of commensal bacterial flora is expected (except in patients with reduced gastric acid production, in whom an overabundance of commensal bacteria is possible). Procedures that are less invasive than biopsy collection include gastric juice sampling or the string test. Specimens from gastric juice samples or the string test can also be used for culture; however, the sensitivity is lower than when biopsy specimens are used[rx–rx].
- Polymerase chain reaction – PCR allows researchers and clinicians to identify H. pylori in small samples that have few bacteria present. It does not require any special processing supplies or transportation, and it can be performed on samples obtained by both invasive and noninvasive methods. Moreover, PCR can be performed faster than many other diagnostic methods, used to identify diverse bacterial genotypes, and employed in epidemiological studies. A considerable drawback of PCR is that it can detect DNA segments of the dead bacterium in the gastric mucosa of patients after treatment; consequently, it can produce false-positive results[rx,rx,rx].
- Rapid urease test – The RUT utilizes the ability of H. pylori to produce large quantities of urea as the basis for diagnosing infection. Biopsies obtained during endoscopy are placed in a medium containing urea and a pH indicator. If urease is present, the urea is broken down into carbon dioxide and ammonia, which increases the pH of the medium and causes a subsequent color change in the pH indicator. The RUT produces a result in a range of minutes up to 24 h, depending on the number of bacteria in the biopsy. The RUT is inexpensive, rapid, widely available, and highly specific.
- Serology – Several types of tests have been used to identify antibodies against H. pylori. The enzyme immunoassay (EIA) test has been the most prevalently used. Most commercial EIA tests are based on detecting IgG, with sensitivity and specificity values ranging from 60% to 100%. Critical factors important in evaluating the quality of serology tests for the detection of active H. pylori infection include the prevalence of infection, variations in geography, and characteristics of the study populations. Local validation of a serology test is necessary, and it is imperative to make adjustments to cut-off levels for specific populations. In general, tests containing complex antigen mixtures of various strains show the highest sensitivity[rx].
- Urea breath test – The UBT is based on the ability of H. pylori, if present in the gastric environment, to break down orally absorbed 13C- or 14C-labeled urea into CO2 and ammonia. 13CO2 or 14CO2 diffuses into the blood, is exhaled via the lungs, and can be measured in the exhaled air. The test is easy to perform and does not require endoscopy. 13C is a nonradioactive innocuous isotope, and it can be safely used in children and women of childbearing age. An isotope ratio mass spectrometer is generally used to measure 13C in breath samples; however, the machine is expensive[rx].
- Stool antigen test – The SAT uses an enzyme immunoassay to detect the presence of antigens against H. pylori in stool samples. It is a reliable method to diagnose an active infection and to confirm an effective treatment of infection. Stool samples may be stored for 24 h at room temperature or 72 h at 4 °C. Without refrigeration, the SAT suffers a significant reduction of sensitivity within 2 to 3 d[rx].
- Serologic testing for IgG antibodies – against H. pylori requires validation of the assay in children, since antibody levels differ in children and adults, probably because of the duration of infection and the differences in bacterial load[rx,rx,rx,rx]. In addition, commercially available serologic tests demonstrate lower accuracy compared with testing in a research setting[rx], with sometimes up 33% false positive and 25% false-negative results[rx,rx,rx]. Serology is more and more frequently reported to be unsatisfactory for screening for H. pylori infection in children[rx,rx]. Testing should not rely on office tests[rx]. After eradication, there is a slow decline in antibody titer. Many patients remain seropositive 1 year after eradication[rx]. At acquisition of the infection, there is a temporary rise in IgM[rx,rx,rx,rx,rx]. IgA is also reported to be a useful serologic screening tool[rx]. Immunoblot has become the reference method used to confirm doubtful results[rx]. Specific serologies for cytotoxic strains may be helpful in selecting patients for treatment[rx].
- Breath test – If you have a breath test, you’ll swallow a preparation containing urea. If H. pylori bacteria are present, they will release an enzyme that breaks down this combination and will release carbon dioxide, which a special device then detects.
- Endoscopy – If you have an endoscopy, your doctor will insert a long, thin instrument called an endoscope into your mouth and down into your stomach and duodenum. An attached camera will send back images on a monitor for your doctor to view. Any abnormal areas will be inspected. If necessary, special tools used with the endoscope will allow your doctor to take samples from these areas.
- Carbon-13 and C-14 breath tests – are based on the fact that urease from H. pylori will hydrolyze the ingested labeled urea into ammonia and labeled bicarbonate, which is exhaled as labeled carbon dioxide[rx]. Whether a test meal should be given, or whether the labeled urea should simply be given after a period of fasting, or whether the addition of citric acid would be beneficial is not clear[rx–rx]. A standardized and simplified C-13 breath test was recently described in children[rx]. The high sensitivity and specificity of the 13 C-breath test in the detection of H. pylori infection in children has been unequivocally demonstrated[rx,rx,rx]
|Diagnostic method||Sensitivity and specificitya||Typical application||Remarks|
|Histology||>95%||“Gold standard” in routine hospital diagnostics||Requires expert pathologist; also provides histological data on inflammation and atrophy|
|Culture biopsy||>95%||Alternative gold standard||Allows for testing of antimicrobial sensitivity; requires specific microbiological expertise|
|Rapid urease (CLO) test||>90%||Cost-effective and rapid test||Requires an additional test for confirmation of H. pylorii nfection|
|Urea breath test||>95%||Alternative gold standard||Very useful, reliable test to evaluate the success of eradication treatment of H. pylori; limited availability due to requirement of expensive equipment|
|Fecal antigen test||>90%||Not widely used yet||Simple test but may not be reliable for evaluation of the success of eradication treatment of H. pylori|
|Serology||80-90%||Mainly used for epidemiological studies||Insufficient reliability for routine screening; cannot prove ongoing infection due to immunological memory|
Treatment of Helicobacter Pylori
- Proton pump inhibitors (PPIs) – These drugs stop acid from being produced in the stomach. Drugs that reduce the amount of acid in your stomach by blocking the tiny pumps that produce it. They include dexlansoprazole, esomeprazole, lansoprazole, pantoprazole, or rabeprazole. Some examples of PPIs are omeprazole, esomeprazole, lansoprazole, and pantoprazole.
- Antibiotics – to kill the bacteria in your bodies, such as amoxicillin, clarithromycin, metronidazole, tetracycline, or tinidazole. You’ll most likely take at least two from this group.
- Histamine (H-2) blockers – These medications block a substance called histamine, which triggers acid production. Medicines that block the chemical histamine, which prompts your stomach to make more acid. These are cimetidine, famotidine, nizatidine, or ranitidine
- Bismuth subsalicylate – More commonly known as Pepto-Bismol, this drug works by coating the ulcer and protecting it from stomach acid.
First-line treatment in areas with low clarithromycin resistance
- The most frequently used strategy is triple therapy. This therapy is composed of a PPI (lansoprazole 30 mg/12 h, omeprazole 20 mg/12 h, pantoprazole 40 mg/12 h, rabeprazole 20 mg/12 h, or esomeprazole 40 mg/24 h), clarithromycin (500 mg/12 h), and amoxicillin (1 g/12 h), taken for 7 to 14 d.
- The duration of therapy is controversial, although a meta-analysis suggested that 14 d provides eradication rates 5% higher than those for 7 d. In cases of allergy to penicillin, metronidazole is an option to replace amoxicillin, as it is equally effective and considered equivalent[rx].
First-line treatment in areas with high clarithromycin resistance
- Quadruple therapy – In areas that have high resistance to clarithromycin, quadruple therapy can be used. This therapy includes a combination of a PPI, bismuth subsalicylate (525 mg, × 4 daily), and 2 antibiotics, metronidazole (250 mg × 4 daily) and tetracycline (500 mg, × 4 daily), for 10 to 14 d. This regimen is well tolerated, and patients tend to adhere to the schedule; however, this therapy is not available in all areas. It is recommended that doctors have other alternatives in mind, such as sequential therapy or quadruple therapy without bismuth[rx].
- Sequential therapy – Sequential therapy was proposed by a group of Italian researchers. It involves the combination of a PPI and amoxicillin (1 g, × 2 daily) for 5 d, followed by a PPI and tinidazole clarithromycin/metronidazole (500 mg, × 2 daily) for 5 d. Most studies have shown that sequential therapy and bismuth-based quadruple therapy have equivalent success in first-line therapy[rx]. Sequential therapy was evaluated in a pediatric population with iron deficiency[rx]. Children aged 12 to 15 years with an active H. pylori infection were evaluated for serum ferritin and then were randomized into 2 groups to receive either standard or sequential eradication therapy. Six weeks after completing the therapy, eradication was detected by the UBT, and serum ferritin levels were measured
- Concomitant therapy – Concomitant therapy is used instead of sequential therapy in areas where the resistance to clarithromycin is greater than 20% and bismuth-based quadruple therapy is not available. Concomitant therapy involves the simultaneous administration of 3 antibiotics (metronidazole, clarithromycin, and amoxicillin) and a PPI for 10 d. This therapy is effective and well-tolerated compared to conventional triple therapy[rx].
- Hybrid therapy – Hybrid therapy is a recently reported therapy that consists of 2 steps: (1) treatment with a PPI and amoxicillin (1 g/12 h) for 7 d, followed by (2) a PPI and 3 antibiotics, amoxicillin (1 g/12 h), metronidazole (500 mg/12 h), and clarithromycin (500 mg/12 h), for 7 d. In a study comparing hybrid and sequential therapies, the eradication rates were 89.5% and 76.7% (P = 0.001), respectively. Similar severe adverse effects were observed in patients in both treatment groups. Specifically, 2.4% of patients in the hybrid therapy group and 3.8% of patients in the sequential therapy group reported adverse effects[rx].
Second-line treatment in areas that have a low clarithromycin resistance
- Options available in areas with a low resistance to clarithromycin include bismuth-based quadruple therapy and therapies with a PPI and levofloxacin/amoxicillin[rx,rx]. However, levofloxacin use has been questioned, based on an increase in levofloxacin resistance[rx]. Therefore, susceptibility studies should be performed before starting therapy.
Second-line treatment in areas that have high clarithromycin resistance
- For the case in which bismuth-based quadruple therapy fails, a triple therapy containing a PPI, levofloxacin, and amoxicillin is recommended. Again, the increase in levofloxacin resistance should be taken into account[rx].
- After 2 failed treatments in areas that have either a low or high clarithromycin resistance, it is not advisable to prescribe further antibiotic treatments. Whenever possible, biopsy specimens should be obtained to culture and test for susceptibility[rx].
- Rescue or salvage therapies have obtained good results in these cases. One rescue therapy is the use of rifabutin (150 mg, × 2 daily), amoxicillin (1 g, × 2 daily), and ciprofloxacin (500 mg, × 2 daily) for 14 d. Although this therapy achieves an excellent response, severe adverse effects have been observed[rx].
- Other rescue therapies include a double dose of PPIs plus azithromycin (500 mg/d for 3 d), followed by a double dose of PPIs plus furazolidone (200 mg, × 3 daily) for 10 d in addition to a base therapy of furazolidone (200 mg, × 2 daily), bismuth substrate (120 mg, × 4 daily), and tetracycline (500 mg, × 4 daily) in combination with a PPI at the doses described. For this treatment, the rate of recurrence of H. pylori infection after a successful eradication has been estimated at 11.5%[rx].
Eradication of H. pylori in pregnancy
- If a patient is diagnosed with peptic ulcer during pregnancy or lactation, the condition should be managed only with acid suppression. Eradication of H. pylori should be completed after childbirth. Bismuth, quinolones, and tetracyclines are contraindicated in pregnancy, and metronidazole should be avoided[rx].
|Triple therapy||Duration: 7-14 d|
|PPI twice a day at a higher dose or esomeprazole 40 mg by mouth daily|
|Amoxicillin 1 g by mouth bid|
|Clarithromycin 500 mg by mouth twice daily|
|Quadruple therapy||Duration: 10-14 d|
|PPI twice a day at a higher dose or esomeprazole 40 mg by mouth daily|
|Tetracycline 500 mg by mouth four times daily|
|Bismuth 120 mg four times daily|
|Metronidazole 250 mg four times daily|
|Sequential therapy||Duration: 10 d|
|PPI twice a day at a higher dose or esomeprazole 40 mg by mouth daily|
|Amoxicillin 1 g by mouth bid|
|PPI twice a day at a higher dose or esomeprazole 40 mg by mouth daily|
|Clarithromycin 500 mg by mouth twice daily|
|Tinidazole 500 mg by mouth twice daily|
PPI: Proton pump inhibitor.
- The resistance of H. pylori to commonly used antibiotics is on the rise worldwide. Overall, H. pylori resistance to metronidazole is prevalent, while resistance to amoxicillin and tetracycline are low; however, the picture is far more complex at the regional level.
- For example, amoxicillin resistance is below 3% in America and Europe, but over 60% in Africa[rx]. Africa also has the highest rates of resistance to metronidazole (92.4%) and tetracycline (43.9%)[rx]. Metronidazole resistance is above 50% in much of the world but there are indications that metronidazole resistance may be dropping in northern Europe[rx].
Bismuth quadruple therapy
- This therapy contains two antibiotics, tetracycline, and metronidazole, plus bismuth and PPI for 14 days [rx]. This therapy is preferred as a first-line treatment option for areas with a high incidence of clarithromycin resistance and also as second-line therapy when first treatment with the classical triple therapy against H. pylori was failed [rx].
- This therapy works totally independent of clarithromycin, the most problematic antibiotic in terms of resistance. Related to metronidazole, the use of high doses and prolonged treatment duration allows minimizing the impact on metronidazole-resistant strains, providing high eradication rates even in areas with the high level of resistance to this antibiotic [rx].
- Sequential therapy uses the same antibiotics as standard triple therapy, but they are given them sequentially: 5 days with a PPI plus amoxicillin, followed by 5 days of PPI plus clarithromycin and amoxicillin [rx].
- Amoxicillin is administrated first, due to the fact that amoxicillin disrupts the bacterial cell walls to prevent the development of efflux channels transferring the rest of the antibiotics out of bacteria [rx].
Non-bismuth quadruple therapy
- It is another valid therapy in countries with high incidence to clarithromycin resistance. This therapy contains PPI [but without bismuth], clarithromycin, amoxicillin, and metronidazole for 10 days. The main disadvantage of this treatment is a large number of pills in comparison with other therapies [rx].
- This therapy is based on 7 days of therapy with PPI and amoxicillin, followed by 7 days quadruple therapy with a PPI, amoxicillin, clarithromycin, and metronidazole. There are not many data in the literature, comparing this therapy with others, the standard or sequential therapies, but the results do not indicate that hybrid therapy will be superior to sequential therapy
- Due to the increase of clarithromycin resistance, levofloxacin, a broad spectrum quinolone, is used for the H. pylori eradication in order to substitute clarithromycin in triple or sequential regimens.
- The eradication rate of therapies containing levofloxacin could be more than 90%, especially in areas where the local resistance to levofloxacin is low [less than 10%]. As for clarithromycin and metronidazole, an increase of levofloxacin resistance is being found, due to the fact that quinolones are often used for the treatment of urinary infections.
Use of probiotics in treating H. pylori infection
- It has been suggested that probiotics compete directly with H. pylori by interfering with H. pylori adherence or by producing antimicrobial molecules. The efficacy of Lactobacillus reuteri (L. reuteri) in H. pylori eradication therapy has been investigated. In this study, H. pylori infection was identified by gastric histopathology and 13C-UBT.
Other proposed regimes
A number of other eradication regimens have been proposed. In the Table below they are compared to with standard regimes.
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|Regimen||Duration, days||Drugs used||Notes|
|Triple therapy||7–14||PPI (standard dose) bid, amoxicillin 1 g bid, and clarithromycin 0.5 g bid||First-line therapy in areas with low clarithromycin resistance|
|Sequential therapy||10||1st 5 days: PPI (standard dose) bid and amoxicillin 1 g bid
2nd 5 days: metronidazole 0.5 g bid and clarithromycin 0.5 g bid
|Concomitant therapy||7–10||PPI (standard dose bid), amoxicillin 1 g bid, metronidazole 0.5 g bid, and clarithromycin 0.5 g bid||First-line therapy|
|Hybrid therapy||14||1st week: PPI (standard dose) and amoxicillin 1 g bid
2nd week: PPI (standard dose), amoxicillin 1 g, metronidazole 0.5 g and clarithromycin 0.5 g bid
|Bismuth-containing quadruple therapy||10–14||PPI (standard dose) bid, tetracycline 0.5 g qid, metronidazole 0.25 g qid and bismuthstandard dose qid||First-line or second-line therapy|
|Levofloxacin-based triple therapy||10||PPI (standard dose) bid, levofloxacin 0.5 g qid and amoxicillin 1 g bid||Second-line therapy if there is no fluoroquinolone resistance|
|Levofloxacin-based quadruple therapy||10||PPI (standard dose) bid, bismuth standard dose qid and two antibiotics selected by sensitivity tests||Third line therapy if there is no fluoroquinolone resistance|
|Culture-guided therapy||10||PPI (standard dose) bid, bismuth standard dose qid, levofloxacin 0.5 g qid and amoxicillin 1 g bid||Third line therapy|
|High-dose dual PPI therapy||14||PPI (high dose) qid and amoxicillin 0.5 g qid||Third line therapy|
|Rifabutin triple therapy||14||PPI (standard dose) bid, rifabutin 0.15 g bid and amoxicillin 1 g bid||Third line therapy|
Note: bid – twice daily, qid – four times a day
An ulcer can lead to serious complications if left untreated, including:
- Internal bleeding that can become life-threatening.
- A hole in the stomach that can lead to infection.
- Scar tissue that can block the stomach or intestine, preventing it from emptying food.
- severe stomach pain
- black or tarry stool
- stool with bright red blood
- vomit with bright red blood
- vomit that looks like coffee grounds
- feeling weak or short of breath
- feeling dizzy or faint
- chills or fever
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