Helicobacter and Ulcers Helicobacter and UlcersHistoryTests Duodenal ulcerHelicobacter pyloriElectron micrograph over Helicobacter organisms How is Helicobacter infection caught and transmitted? The bacteria can only exist in the human stomach (full name - Helicobacter pylori) The bacteria is not found in animals. The bacteria can not survive in the environment. Helicobacter is an infection that is acquired in early childhood (before the age of 5 years). Infection as an adult is rare. The known risk factors for getting the infection in childhood relate to lower socio-economic living conditions (ie. lack of hot running water in the home, overcrowding in the home) Childhood living conditions have dramatically changed in New Zealand over the last 50-60 years consequently “catching” Helicobacter in childhood has become much less common. Helicobacter infection is gradually becoming less common in our community. This is happening "independent" of any effect of antibiotic treatment. Recent studies in NZ show that about 5% of European children become infected with Helicobacter by the age of 20 years. In contrast, almost half of Pacific Island children (living in NZ) are infected by a similar age. It is still unclear how the bacteria is spread but it appears to require close contact between children. It is more likely to spread from one child to another in larger families in more crowded living conditions. Current Treatment Guidelines The recommended treatment is a combination of 3 medications - omeprazole, amoxicillin and clarithromycin. The use of clarithromycin was the major breakthrough in treatment combinations. Treatment became shorter (7-day duration) and more effective (success rates approx 90%). The main reason for treatment failure is now antibiotic resistance. This is mainly for clarithromycin. Resistance rates are around 15%. Because of increased antibiotic resistance it is now recommended that the initial treatment is for 2 weeks. What if the initial treatment fails? Resistance to clarithromycin is very common after failed treatment with omeprazole, clarithromycin and amoxicillin. This means that repeating the same treatment has a very low chance of success (perhaps 10% chance of success). Second-line treatment is difficult. De-Nol two tabs twice daily (now given as GastroDenol), omeprazole 20mg twice daily, tetracycline 500mg four times per day, metronidazole 400mg three times per day is useful. This is probably better taken for 10-14 days but this is "tough" treatment There is a high chance of nausea, diarrhoea and sometimes vomiting. Access to tetracycline requires a special authority High doses of omeprazole with Amoxil is another option. Levofloxacin is a useful drug (in combination with other drugs) but is expensive and not available in NZ. These options need to be discussed with a gastroenterologist If a second attempt at treatment fails. The merits of further attempts at eradication needs to be carefully considered. Often it is more appropriate to have no further antibiotic treatment. This depends on the underlying problem. If a peptic ulcer it is worth trying again. If the infection was found on routine testing then perhaps no treatment is appropriate. Who should have antibiotic treatment? Answer: probably everybody with proven infection. People with peptic ulcer disease (duodenal and gastric ulcers) definitely need to have treatment. They also need to have a follow-up test to check that eradication has been successful (see tests). If the issue is indigestion symptoms but a normal gastroscopy apart from evidence of Helicobacter infection; There is some conflicting information. Any benefit of treatment is likely to be modest. Treatment is more likely to be successful (in relieving symptoms) if the problem is upper abdominal discomfort particularly if improved by meals. If the main symptom is heartburn then there is unlikely to be any gain from eradication treatment. If the issue is indigestion symptoms and a positive Helicobacter test but no gastroscopy has been performed to date - the answer is different. Antibiotic treatment for Helicobacter can be given. This approach is called “test and treat”. There has been a lot of work in this area but it is a more "muddling approach" to a problem. There is no definite diagnosis. Some people will respond well but if there are continuing symptoms then a gastroscopy is required. Helicobacter and acid reflux (heartburn) Helicobacter infection is not the cause of acid reflux - heartburn. Some reports have suggested that acid reflux may actually be worse after treatment for Helicobacter. This issue is still being debated. There is no doubt that reflux is becoming more common in our community. This change has happened at the time when the rate Helicobacter infection is decreasing. In my view these observations are not “cause and effect”. It is worthwhile taking eradication treatment for Helicobacter if long-term treatment of stomach acid with a PPI is required. This may help maintain a healthy lining on the stomach wall. Helicobacter and gastric cancer (stomach cancer) Large population studies have consistently shown a 2 to 3-fold increased risk of gastric cancer with Helicobacter infection. There are good reasons to think that the risk is even greater than this – perhaps a 5-6 fold risk. Gastric cancer is more common in Maori and Pacific Island populations partly due to high rates of Helicobacter infection. It is estimated that 50% of the gastric cancer risk is due to Helicobacter infection. Eradication of this infection is likely to reduce the risk of getting gastric cancer. At this time there is no public policy of preventing gastric cancer by treating large numbers of people. There are several large studies that show a reduction in the risk of gastric cancer after successful treatment of the bacteria It is very sensible to check for Helicobacter if there is a family history of stomach cancer. Helicobacter and the risk of ulcers with anti-inflammatory drugs Helicobacter infection increases the risk of having an ulcer in people taking anti-inflammatory drugs about 3-fold. The risk of bleeding into the stomach with anti-inflammatory drugs is also greater in people with Helicobacter infection. Testing then treating for Helicobacter pylori infection prior to starting anti-inflammatory drugs (NSAIDs) is a proven strategy but has not become a common practice. History of peptic ulcers In 1983 Dr Marshall (a microbiology trainee working in Perth) reported that he had grown a bacterium from the stomach. Previously it was believed that nothing could grow in the "acidic" environment of the stomach. This discovery started a revolution in thinking about diseases of the stomach. The initial name for the bacteria was Campylobacter. The new full name is Helicobacter Pylori. Helicobacter was found to be the cause of most peptic ulcers (ulcers of the stomach and duodenum). Antibiotic treatment was the new, "radical" and amazing treatment for "ulcers". Previous treatments had involved reducing stomach acid. It soon became apparent that the Helicobacter infection was difficult to eradicate. Antibiotics that were effective in the test-tube did not work when given alone. It was realized that combinations of antibiotics would be required. After a few years “triple therapy” became the established treatment. This early “triple therapy” had only modest success rates. It was poorly tolerated because of side-effects. A large number of tablets needed to be taken over 2 weeks Prior to the discovery of Helicobacter surgery of the stomach was a frequent treatment. This is never performed now. People who have had a operation for peptic ulcer in the past may have some persisting problems (indigestion, diarrhoea, poor absorption of some nutrients). Treatment with long-term medication (to reduce gastric acid) was a common treatment before the discovery of antibiotic treatment for Helicobacter. Treatment for acid may still be required in the long-term but is because of another problem. The standard treatment for peptic ulcers is now antibiotic treatment for Helicobacter as outlined below. There are some interesting historical observations about Helicobacter and stomach ulcers over the last 150 years. There is good evidence that Helicobacter has infected human stomachs for thousands of years. Duodenal ulcers appear to be relatively recent consequence of Helicobacter infection, perhaps only over the last 150 years. The incidence of duodenal ulcers started to increase around 1900 and then peaked in the 1950’s. Since then there has been a gradual decline in the incidence of duodenal ulcers. In New Zealand, endoscopists practicing in areas with a predominantly European middle class population now rarely observe duodenal ulcers. The reasons for this remarkable change in pattern of disease are speculative. The increase in ulcer disease up to 1950 may be due to increasing amounts of acid in the stomach. Perhaps due to improved nutrition. High acid conditions in the stomach are required to form peptic ulcers. The decrease in ulcer disease over the last 50 years relates to higher living standards. Gradual decrease in Helicobacter infection. This is because of less person to person transmission of the bacteria during childhood. Tests for Helicobacter that do not involve gastroscopy and biopsy - What can they tell us? Types of tests. Blood tests (serology) measure the antibody to Helicobacter and not the actual presence of infection. There are false positives and false negative results.The test will be incorrect about 20% of the time. Urea breath test.This involves two breath samples 30 mins apart. The test is very accurate but is more expensive. There is limited use of this test in NZ now Faecal antigen test is a good test but does involve the "hassle" of obtaining a faeces sample. All these tests hope to detect the presence or absence of infection but cannot give the diagnosis for the indigestion. When treating a positive test with antibiotics (without knowledge of underlying diagnosis), Many people will have ongoing symptoms. A gastroscopy may still be required. Some of apparent response is not due to the antibiotics. Symptoms that were going to resolve anyway (placebo effect). What if the test is negative? The diagnosis of the indigestion symptoms is unlikely to be an ulcer (unless you are taking aspirin or anti-inflammatory drugs). The most likely the diagnosis is gastro-oesophageal reflux (heartburn). Or maybe there will be no clear diagnosis (termed "functional dyspepsia”). Gastroscopy is very helpful, even if normal, for reassurance and planning sensible treatment. Symptoms cannot be used as a means of determining success of antibiotic treatment. Serology tests (blood test) cannot be used for follow-up. The most useful tests after eradication treatment has been given are the urea breath test and the faecal antigen test. The success rate of treatment (for getting rid of the bacteria) has been about 90%. However with increasing rates of antibiotic resistance this may be reducing to 80%. A follow-up faecal antigen test must be performed at least 8 weeks after finishing treatment and omeprazole or similar drugs need to be discontinued for 2 weeks before the test. It is important to have an accurate follow-up test is there has been a diagnosis of peptic ulcer, particularly if there has been bleeding from the ulcer.