H. pylori Infection 101 & H. pylori Associated Diseases

H. pylori: Causes, Symptoms, Treatment

H. pylori Infection 101 & H. pylori Associated Diseases

Helicobacter pylori (H. pylori) is a type of bacteria. These germs can enter your body and live in your digestive tract. After many years, they can cause sores, called ulcers, in the lining of your stomach or the upper part of your small intestine. For some people, an infection can lead to stomach cancer.

Infection with H. pylori is common. About two-thirds of the world’s population has it in their bodies. For most people, it doesn’t cause ulcers or any other symptoms. If you do have problems, there are medicines that can kill the germs and help sores heal.

As more of the world gets access to clean water and sanitation, fewer people than before are getting the bacteria. With good health habits, you can protect yourself and your children from H. pylori.

For decades, doctors thought people got ulcers from stress, spicy foods, smoking, or other lifestyle habits. But when scientists discovered H. pylori in 1982, they found that the germs were the cause of most stomach ulcers.

After H. pylori enters your body, it attacks the lining of your stomach, which usually protects you from the acid your body uses to digest food. Once the bacteria have done enough damage, acid can get through the lining, which leads to ulcers. These may bleed, cause infections, or keep food from moving through your digestive tract.

You can get H. pylori from food, water, or utensils. It’s more common in countries or communities that lack clean water or good sewage systems. You can also pick up the bacteria through contact with the saliva or other body fluids of infected people.

Many people get H. pylori during childhood, but adults can get it, too. The germs live in the body for years before symptoms start, but most people who have it will never get ulcers. Doctors aren’t sure why only some people get ulcers after an infection.

If you have an ulcer, you may feel a dull or burning pain in your belly. It may come and go, but you’ll probably feel it most when your stomach is empty, such as between meals or in the middle of the night. It can last for a few minutes or for hours. You may feel better after you eat, drink milk, or take an antacid.

Other signs of an ulcer include:

Ulcers can bleed into your stomach or intestines, which can be dangerous to your health. Get medical help right away if you have any of these symptoms:

It’s not common, but H. pylori infection can cause stomach cancer. The disease has few symptoms at first, such as heartburn. Over time, you may notice:

  • Belly pain or swelling
  • Nausea
  • Not feeling hungry
  • Feeling full after you eat just a small amount
  • Vomiting
  • Weight loss for no reason

If you don’t have symptoms of an ulcer, your doctor probably won’t test you for H. pylori. But if you have them now or have in the past, it’s best to get tested. Medicines nonsteroidal anti-inflammatory drugs (NSAIDs) can also damage your stomach lining, so it’s important to find out what’s causing your symptoms so you can get the right treatment.

To start, your doctor will ask you about your medical history, your symptoms, and any medicines you take. Then she’ll give you a physical exam, including pressing on your belly to check for swelling, tenderness, or pain. You may also have:

  • Tests of your blood and stool, which can help find an infection
  • Urea breath test. You’ll drink a special liquid that has a substance called urea. Then you’ll breathe into a bag, which your doctor will send to a lab for testing. If you have H. pylori, the bacteria will change the urea in your body into carbon dioxide, and lab tests will show that your breath has higher than normal levels of the gas.

To look more closely at your ulcers, your doctor may use:

  • Upper gastrointestinal endoscopy. In a hospital, a doctor will use a tube with a small camera, called an endoscope, to look down your throat and into your stomach and the upper part of your small intestine. The procedure may also be used to collect a sample that will be examined for the presence of the bacteria. You may be asleep or awake during the procedure, but you’ll get medicine to make you more comfortable.
  • Upper GI tests. In a hospital, you’ll drink a liquid that has a substance called barium, and your doctor will give you an X-ray. The fluid coats your throat and stomach and makes them stand out clearly on the image.
  • Computed tomography (CT) scan. It’s a powerful X-ray that makes detailed pictures of the inside of your body.

If you have H. pylori, your doctor may also test you for stomach cancer. This includes:

  • Physical exam
  • Blood tests to check for anemia, when your body doesn’t have enough red blood cells. It could happen if you have a tumor that bleeds.
  • Fecal occult blood test, which checks your stool for blood that’s not visible to the naked eye
  • Endoscopy
  • Biopsy, when a doctor takes a small piece of tissue from your stomach to look for signs of cancer. Your doctor may do this during an endoscopy.
  • Tests that make detailed pictures of the insides of your body, such as a CT scan or magnetic resonance imaging (MRI)

If you have ulcers caused by H. pylori, you’ll need treatment to kill the germs, heal your stomach lining, and keep the sores from coming back. It usually takes 1 to 2 weeks of treatment to get better.

Your doctor will probably tell you to take a few different types of drugs. The options include:

  • Antibiotics to kill the bacteria in your body, such as amoxicillin, clarithromycin (Biaxin), metronidazole (Flagyl), tetracycline (Sumycin), or tinidazole (Tindamax). You’ll most ly take at least two from this group.
  • Drugs that reduce the amount of acid in your stomach by blocking the tiny pumps that produce it. They include dexlansoprazole (Dexilant), esomeprazole (Nexium), lansoprazole (Prevacid), omeprazole (Prilosec), pantoprazole (Protonix), or rabeprazole (Aciphex).
  • Bismuth subsalicylate, which may also help kill H. pylori along with your antibiotics
  • Medicines that block the chemical histamine, which prompts your stomach to make more acid. These are cimetidine (Tagamet), famotidine (Fluxid, Pepcid), nizatidine (Axid), or ranitidine (Zantac).

Your treatment could mean you’ll take 14 or more pills per day for a few weeks, which seems a lot of medicine. But it’s really important to take everything that your doctor prescribes and to follow her instructions.

If you don’t take antibiotics the right way, bacteria in your body can become resistant to them, which makes infections harder to treat.

If your medications bother you, talk to your doctor about your treatment options and how you can handle side effects.

About 1-2 weeks after you finish your treatment, your doctor may test your breath or stool again to make sure the infection is gone.

You can protect yourself from getting an H. pylori infection with the same steps you take to keep other germs at bay:

  • Wash your hands after you use the bathroom and before you prepare or eat food. Teach your children to do the same.
  • Avoid food or water that’s not clean.
  • Don’t eat anything that isn’t cooked thoroughly.
  • Avoid food served by people who haven’t washed their hands.

Though stress, spicy foods, alcohol, and smoking don’t cause ulcers, they can keep them from healing quickly or make your pain worse. Talk to your doctor about ways to manage your stress, improve your diet, and, if you smoke, how you can get help to quit.

Most ulcers caused by H. pylori will heal after a few weeks of treatment. If you’ve had one, you should avoid taking NSAIDs for pain, since these drugs can damage your stomach lining. If you need pain medicine, ask your doctor to recommend some.

You can find information about H. pylori infection and ulcers from the American College of Gastroenterology. For information on stomach cancer, as well as online and local support groups, visit the American Cancer Society.

SOURCES:

National Digestive Diseases Information Clearinghouse: “Peptic Ulcer Disease and H. Pylori.”

National Cancer Institute: “Helicobacter pylori and Cancer.”

KidsHealth: “Infections: Helicobacter Pylori.”

National Institute of Diabetes and Digestive and Kidney Diseases: “The Burden of Digestive Diseases: Peptic Ulcer Disease.”

American College of Gastroenterology: “Peptic Ulcer Disease.”

UpToDate. “Helicobacter pylori infection and treatment.”

American Cancer Society: “How is stomach cancer diagnosed?” “How is stomach cancer treated?” and “Signs and symptoms of stomach cancer.”

© 2018 WebMD, LLC. All rights reserved.

Source: https://www.webmd.com/digestive-disorders/h-pylori-helicobacter-pylori

Helicobacter Pylori Infection: Practice Essentials, Background, Pathophysiology

H. pylori Infection 101 & H. pylori Associated Diseases

  1. [Guideline] Sugano K, Tack J, Kuipers EJ, et al, for the faculty members of Kyoto Global Consensus Conference. Kyoto global consensus report on Helicobacter pylori gastritis. Gut. 2015 Sep. 64 (9):1353-67. [Medline].

  2. Mladenova I, Durazzo M. Transmission of Helicobacter pylori. Minerva Gastroenterol Dietol. 2018 Sep. 64 (3):251-4. [Medline].

  3. Horiki N, Omata F, Uemura M, et al. Annual change of primary resistance to clarithromycin among Helicobacter pylori isolates from 1996 through 2008 in Japan. Helicobacter. 2009 Oct. 14(5):86-90. [Medline].

  4. Fallone CA. Epidemiology of the antibiotic resistance of Helicobacter pylori in Canada. Can J Gastroenterol. 2000 Nov. 14(10):879-82. [Medline].

  5. Hage N, Renshaw JG, Winkler GS, Gellert P, Stolnik S, Falcone FH. Improved expression and purification of the Helicobacter pylori adhesin BabA through the incorporation of a hexa-lysine tag. Protein Expr Purif. 2015 Feb. 106:25-30. [Medline]. [Full Text].

  6. Tomb JF, White O, Kerlavage AR, et al. The complete genome sequence of the gastric pathogen Helicobacter pylori. Nature. 1997 Aug 7. 388(6642):539-47. [Medline].

  7. Lowenthal AC, Hill M, Sycuro LK, et al. Functional analysis of the Helicobacter pylori flagellar switch proteins. J Bacteriol. 2009 Dec. 191(23):7147-56. [Medline]. [Full Text].

  8. Giannakis M, Chen SL, Karam SM, et al. Helicobacter pylori evolution during progression from chronic atrophic gastritis to gastric cancer and its impact on gastric stem cells. Proc Natl Acad Sci U S A. 2008 Mar. 105(11):4358-63. [Medline].

  9. Lehours P. Actual diagnosis of Helicobacter pylori infection. Minerva Gastroenterol Dietol. 2018 Sep. 64 (3):267-79. [Medline].

  10. Pullen LC. Does H pylori eradication explain rising obesity? Medscape Medical News from WebMD. June 9, 2014. Available at http://www.medscape.com/viewarticle/826406. Accessed: June 19, 2014.

  11. Lender N, Talley NJ, Enck P, et al. Review article: associations between Helicobacter pylori and obesity – an ecological study. Aliment Pharmacol Ther. 2014 Jul. 40(1):24-31. [Medline].

  12. Koletzko L, Macke L, Schulz C, Malfertheiner P. Helicobacter pylori eradication in dyspepsia: New evidence for symptomatic benefit. Best Pract Res Clin Gastroenterol. 2019 Jun – Aug. 40-1:101637. [Medline].

  13. Luther J, Dave M, Higgins PD, Kao JY. Association between Helicobacter pylori infection and inflammatory bowel disease: a meta-analysis and systematic review of the literature. Inflamm Bowel Dis. 2010 Jun. 16(6):1077-84. [Medline].

  14. Jackson L, Britton J, Lewis SA, et al. A population-based epidemiologic study of Helicobacter pylori infection and its association with systemic inflammation. Helicobacter. 2009 Oct. 14(5):108-13. [Medline].

  15. Hsu PI, Wu DC, Chen WC, et al. Randomized controlled trial comparing 7-day triple, 10-day sequential, and 7-day concomitant therapies for Helicobacter pylori infection. Antimicrob Agents Chemother. 2014 Oct. 58(10):5936-42. [Medline].

  16. Pellicano R, Zagari RM, Zhang S, Saracco GM, Moss SF. Pharmacological considerations and step-by-step proposal for the treatment of Helicobacter pylori infection in the year 2018. Minerva Gastroenterol Dietol. 2018 Sep. 64 (3):310-21. [Medline].

  17. Greenberg ER, Anderson GL, Morgan DR, 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 Aug 6. 378(9790):507-14. [Medline].

  18. Liou JM, Lin JT, Chang CY, et al. Levofloxacin-based and clarithromycin-based triple therapies as first-line and second-line treatments for Helicobacter pylori infection: a randomised comparative trial with crossover design. Gut. 2010 May. 59(5):572-8. [Medline].

  19. Apostolopoulos P, Koumoutsos I, Ekmektzoglou K, et al. Concomitant versus sequential therapy for the treatment of Helicobacter pylori infection: a Greek randomized prospective study. Scand J Gastroenterol. 2016 Feb. 51(2):145-51. [Medline].

  20. Yoon H, Kim N, Lee BH, et al. Moxifloxacin-containing triple therapy as second-line treatment for Helicobacter pylori infection: effect of treatment duration and antibiotic resistance on the eradication rate. Helicobacter. 2009 Oct. 14(5):77-85. [Medline].

  21. Papastergiou V, Georgopoulos SD, Karatapanis S. Treatment of Helicobacter pylori infection: meeting the challenge of antimicrobial resistance. World J Gastroenterol. 2014 Aug 7. 20(29):9898-911. [Medline].

Source: https://emedicine.medscape.com/article/176938-overview

What is H. Pylori? Test & Treatment

H. pylori Infection 101 & H. pylori Associated Diseases

According to some estimates, more than half of the population is a host for Helicobacter pylori, which is most commonly acquired in childhood. Read on to find out when and how H. pylori infection is tested for and treated.

Infection

Helicobacter pylori (H. pylori) is a gram-negative, spiral-shaped pathogenic bacterium that colonizes the stomach [1].

This bacterium is the second most commonly studied pathogen (after E. coli) [2]. Marshall and Warren were awarded the 2005 Nobel Prize in Medicine for linking the presence of H. pylori to inflammation of the stomach (gastritis) and peptic ulcer disease [3].

How Do You Get It?

Infection with H. pylori is most often acquired in early childhood and persists for life [4].

A specific immune response, skewed toward Th1, is triggered during the infection [5].

In spite of the immune response, H. pylori is frequently not cleared from the body completely because the bacterium is equipped with an array of mechanisms that allow it to evade or inhibit host responses [5].

Prevalence

This bacterium is one of the most prevalent human pathogens, infecting more than 50% of the human population [4]. H. pylori is present in approximately 70 – 80% of the population in developing countries and 13% – 50% of the population in developed countries [2].

In recent years, there has been a decrease in the prevalence of H. pylori infection in developed countries. In the United States, less than 6% of the children are infected by H. pylori. A similar trend is becoming apparent in other parts of the developed world [6].

Research indicates that H. pylori has been around at least since human migration Africa about 60,000 years ago [7].

Overview

The H. pylori bacterium can be detected in most biological fluids. This includes saliva, breath, blood, feces, and urine, in addition to the bacterium’s primary site of residence in the stomach lining [8].

Urease is an enzyme produced by H. pylori which can be used to detect its presence [8]. Common assessments include gastric biopsies for rapid urease detection (rapid urease test (RUT)), the 13C-urea breath test (13C-UBT) or fecal antigen determination (fecal antigen test (FAT)) [8].

Breath Test

The noninvasive 13C-UBT and FAT are of comparable diagnostic accuracy with biopsy-based tests and are the methods of choice in the test-and-treat setting and for controlling the effect of eradication treatments [8].

How Effective Are Different Testing Methods?

Table: Different Methods of H. pylori Testing with Their Effectiveness (Sensitivity and Specificity) [9, 10]

TestSensitivitySpecificity
Urease (breath) test67%100%
Serology (blood) test for H. pylori antibodies84%60%
Stomach biopsy – histopathology (examining tissues under the microscope)83%100%
Stomach biopsy – H. pylori culture64%100%
Stool antigen test86-97% (depending on antigen tested)93-97%

Higher sensitivity (true positive rate) demonstrates that the test is better at detecting H. pylori in the true presence of H. pylori. Lower specificity (true negative rate) indicates that the test may show those without H. pylori as having H. pylori. This means that the stomach biopsy and blood test, for example, may not detect H. pylori in about 20% of people with H. pylori infections.

H. pylori serology test may detect antibodies against H. pylori either in individuals with active infections or even after infections have been eradicated. Therefore, the serology test is not a good test to follow up after H. pylori treatment [9].

Standard Eradication Treatment

Eradication of virulent H. pylori is necessary for people with the negative symptoms of infection, such as stomach ulcers. However, there are conflicting opinions whether asymptomatic H. pylori-positive children and adults should be treated, broadly because the antibiotic treatments themselves have strong side effects [11, 12].

The conventional treatment for H.

pylori, called the standard triple therapy, consists of a short course of two antibiotics (typically clarithromycin and amoxicillin) along with proton pump inhibitors (stomach acid-reducing drugs, e.

g.omeprazole or lansoprazole) [13, 14]. 14-day triple therapy was superior to the equivalent 7- or 10-day triple therapy [14].

Because H. pylori is adapted to an acidic environment, reducing stomach acid with a proton pump inhibitor inhibits H. pylori growth and is beneficial during the short-term standard triple therapy [15]. However, long-term treatment with PPI therapy can result in atrophy (wasting) of the stomach lining [15].

Standard treatment for H. pylori infection can alter healthy gut microbiota, leading to bloating, diarrhea, and nausea [13].

These side effects are estimated to affect over 50% of patients and are associated with decreased compliance and treatment failure [16]. Resistance to antibiotics or reinfection from remaining H.

pylori bacteria can also cause the failure of the treatment to clear H. pylori.

The effectiveness of the standard triple therapy ranges between 60% and 80% [16].

Compliance

Lack of observance to doctor’s prescriptions is the main cause of eradication failure [2, 17]. Treatment compliance lower than 80% decreases treatment success rates [14].

Cytochrome P450 2C19 (CYP2C19) Mutation

Another cause of eradication failure is a mutation in cytochrome P450 2C19 (CYP2C19). CYP2C19 is the principal enzyme involved in the metabolism of proton pump inhibitors (omeprazole or lansoprazole). When CYP2C19 works more effectively than usual, the drugs get degraded faster and have lower efficacy [18].

CYP2C19 SNPs affecting the effectiveness of proton pump inhibitors include rs4244285(A) and rs4986893(A) [19].

H. pylori Reservoir in the Mouth

Dental plaque can act as a reservoir of H. pylori, making proper oral hygiene maintenance essential to preventing reinfection [20].

Several studies suggest that untreated periodontal disease increases the risk of becoming reinfected after H. pylori eradication. Reducing the number of oral H. pylori using an antiseptic mouthwash and/or periodontal treatment is recommended to improve the eradication rate following antibiotic therapy [21].

For example, in one study, the treatment of an oral infection increased the success rate of H. pylori eradication from the stomach from 61% to 82% [22].

Antibiotic Resistance

Increased resistance to the antibiotic clarithromycin has accounted for a dramatic decline in the efficacy of standard triple therapies across the world [23]. Alternative antibiotic regimens have been shown to overcome clarithromycin resistance and are now preferred treatments achieving improved eradication rates (over 90%) [23].

Nutrient Availability

H. pylori infection impairs the absorption of iron andvitamin B12 [24].

Vitamin C concentration is 20% lower in H. pylori-infected subjects [24].

The concentration of β-carotene and vitamin E in the stomach is also decreased [24].

Some studies also reported a decrease in folate absorption in infected individuals [24].

Hormones that Regulate Appetite

Several studies show that infected subjects have lower levels ofghrelin and a higher concentration ofleptin.

Since leptin decreases appetite, and ghrelin stimulates the release of growth hormone, H. pylori infection could result in decreased growth, especially in children who are already at risk for malnutrition [24, 25].

In some studies of infected children, the eradication of H. pylori increased ghrelin levels and resulted in growth increases in both weight and height [26].

The research on the links between H. pylori and leptin are ghrelin levels are conflicting in some cases, however. The majority of studies found lower levels of circulating ghrelin in H. pylori-positive subjects in Asia and Europe but not in the United States.

Conflicting results were also obtained when the effect of H. pylori eradication on ghrelin levels was evaluated [25, 27]. In a study of infected veterans, ghrelin levels were nearly six-fold higher than pre-eradication, but leptin levels also increased significantly seven months following eradication [27].

Gut Microbiota

H. pylori alters the stomach bacterial community, increasing bacteria in the Proteobacteria, Spirochete, and Acidobacteria species and decreasing bacteria in the Actinobacteria, Bacteroidetes and Firmicutes species [13, 26].

H. pylori infection also alters the ratio of fecal Bifidobacterium/E. coli in children, but this can be improved by ingesting probiotics in the form of yogurt [26].

Source: https://selfhacked.com/blog/h-pylori-part-1/

Which extragastric diseases is Helicobacter pylori (H pylori) infection associated with?

H. pylori Infection 101 & H. pylori Associated Diseases

  1. [Guideline] Sugano K, Tack J, Kuipers EJ, et al, for the faculty members of Kyoto Global Consensus Conference. Kyoto global consensus report on Helicobacter pylori gastritis. Gut. 2015 Sep. 64 (9):1353-67. [Medline].

  2. Mladenova I, Durazzo M. Transmission of Helicobacter pylori. Minerva Gastroenterol Dietol. 2018 Sep. 64 (3):251-4. [Medline].

  3. Horiki N, Omata F, Uemura M, et al. Annual change of primary resistance to clarithromycin among Helicobacter pylori isolates from 1996 through 2008 in Japan. Helicobacter. 2009 Oct. 14(5):86-90. [Medline].

  4. Fallone CA. Epidemiology of the antibiotic resistance of Helicobacter pylori in Canada. Can J Gastroenterol. 2000 Nov. 14(10):879-82. [Medline].

  5. Hage N, Renshaw JG, Winkler GS, Gellert P, Stolnik S, Falcone FH. Improved expression and purification of the Helicobacter pylori adhesin BabA through the incorporation of a hexa-lysine tag. Protein Expr Purif. 2015 Feb. 106:25-30. [Medline]. [Full Text].

  6. Tomb JF, White O, Kerlavage AR, et al. The complete genome sequence of the gastric pathogen Helicobacter pylori. Nature. 1997 Aug 7. 388(6642):539-47. [Medline].

  7. Lowenthal AC, Hill M, Sycuro LK, et al. Functional analysis of the Helicobacter pylori flagellar switch proteins. J Bacteriol. 2009 Dec. 191(23):7147-56. [Medline]. [Full Text].

  8. Giannakis M, Chen SL, Karam SM, et al. Helicobacter pylori evolution during progression from chronic atrophic gastritis to gastric cancer and its impact on gastric stem cells. Proc Natl Acad Sci U S A. 2008 Mar. 105(11):4358-63. [Medline].

  9. Lehours P. Actual diagnosis of Helicobacter pylori infection. Minerva Gastroenterol Dietol. 2018 Sep. 64 (3):267-79. [Medline].

  10. Pullen LC. Does H pylori eradication explain rising obesity? Medscape Medical News from WebMD. June 9, 2014. Available at http://www.medscape.com/viewarticle/826406. Accessed: June 19, 2014.

  11. Lender N, Talley NJ, Enck P, et al. Review article: associations between Helicobacter pylori and obesity – an ecological study. Aliment Pharmacol Ther. 2014 Jul. 40(1):24-31. [Medline].

  12. Koletzko L, Macke L, Schulz C, Malfertheiner P. Helicobacter pylori eradication in dyspepsia: New evidence for symptomatic benefit. Best Pract Res Clin Gastroenterol. 2019 Jun – Aug. 40-1:101637. [Medline].

  13. Luther J, Dave M, Higgins PD, Kao JY. Association between Helicobacter pylori infection and inflammatory bowel disease: a meta-analysis and systematic review of the literature. Inflamm Bowel Dis. 2010 Jun. 16(6):1077-84. [Medline].

  14. Jackson L, Britton J, Lewis SA, et al. A population-based epidemiologic study of Helicobacter pylori infection and its association with systemic inflammation. Helicobacter. 2009 Oct. 14(5):108-13. [Medline].

  15. Hsu PI, Wu DC, Chen WC, et al. Randomized controlled trial comparing 7-day triple, 10-day sequential, and 7-day concomitant therapies for Helicobacter pylori infection. Antimicrob Agents Chemother. 2014 Oct. 58(10):5936-42. [Medline].

  16. Pellicano R, Zagari RM, Zhang S, Saracco GM, Moss SF. Pharmacological considerations and step-by-step proposal for the treatment of Helicobacter pylori infection in the year 2018. Minerva Gastroenterol Dietol. 2018 Sep. 64 (3):310-21. [Medline].

  17. Greenberg ER, Anderson GL, Morgan DR, 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 Aug 6. 378(9790):507-14. [Medline].

  18. Liou JM, Lin JT, Chang CY, et al. Levofloxacin-based and clarithromycin-based triple therapies as first-line and second-line treatments for Helicobacter pylori infection: a randomised comparative trial with crossover design. Gut. 2010 May. 59(5):572-8. [Medline].

  19. Apostolopoulos P, Koumoutsos I, Ekmektzoglou K, et al. Concomitant versus sequential therapy for the treatment of Helicobacter pylori infection: a Greek randomized prospective study. Scand J Gastroenterol. 2016 Feb. 51(2):145-51. [Medline].

  20. Yoon H, Kim N, Lee BH, et al. Moxifloxacin-containing triple therapy as second-line treatment for Helicobacter pylori infection: effect of treatment duration and antibiotic resistance on the eradication rate. Helicobacter. 2009 Oct. 14(5):77-85. [Medline].

  21. Papastergiou V, Georgopoulos SD, Karatapanis S. Treatment of Helicobacter pylori infection: meeting the challenge of antimicrobial resistance. World J Gastroenterol. 2014 Aug 7. 20(29):9898-911. [Medline].

Source: https://www.medscape.com/answers/176938-44702/which-extragastric-diseases-is-helicobacter-pylori-h-pylori-infection-associated-with

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