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Epidemiology of Helicobacter pylori infection

Malaty, Hoda M.View Profile. Best Practice & Research21.2 (Apr 2007): 205-14.

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Helicobacter pylori infection is now recognised as a worldwide problem. It is the most common cause of chronic gastritis, and is strongly linked to peptic ulcer disease and gastric cancer. While the infection is usually acquired in childhood, there is typically a long period of latency with disease manifestations not appearing until adulthood. Gastric cancer does not usually manifest until old age. The infection has a high morbidity rate, but a low mortality rate and is curable with antibiotic therapy.

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Geographical distribution of the prevalence of Helicobacter pylori infection

The prevalence of H. pylori infection varies from country to country with large differences between developed and developing countries1-5 (Figure 1). The epidemiology of H. pylori infection in developing countries, such as India, Saudi Arabia or Vietnam, is characterised by a rapid rate of acquisition of the infection such that approximately 80% of the population is infected by the age of 20,1,2,6 because the disease is most often acquired in childhood7-11 or when young children are present in the household. In developing countries the prevalence of infection peaks in the 20 to 30year old age group. The prevalence of the infection varies between subpopulations within the same country, especially in relation to age. 12-17 In a study in Houston, Texas, of 485 asymptomatic individuals (50% Black and 50%f white) ages 15 to 80years of age showed that it increased at a rate of 1% per year.12 These results are similar to the patterns in developed countries such as the United Kingdom, Australia and France that also show an increasing prevalence with age.12 This increase in prevalence with age may be attributable either to new acquisition of infection among the population or the effect of different birth cohorts, each with a different rate of acquisition in childhood.

The prevalence of H. pylori is inversely related to socioeconomic status8,10,12,18,19 the major variable being the status during childhood, the period of highest risk. Attempts to understand the different rates of infection in defined groups have focused on differences in socioeconomic status defined by occupation, family income level, and living conditions. Each of these variables measures a different component of the socioeconomic complex. Within the United States, studies in a cohort of Blacks and White Hispanics examined the relationship between current and childhood socioeconomic status and the prevalence of H. pylori infection.7 There was an inverse correlation between low socioeconomic status during childhood, irrespective of the present social class. These results were confirmed in a study done in Korea.8 For populations in which the social class is more or less homogeneous, such as in China and Russia, the density of living conditions is the most significant risk factor.18,20 A study of the effect of childhood conditions in a sample of monozygotic and dizygotic twins, reared together or apart with differing in socioeconomic status, revealed that the strongest effects on the acquisition of H. pylori were the density of living and household income during childhood.21 Variation in acquisition of the infection among ethnic and racial groups appears to be primarily related to differential exposure (e.g., cultural background, social, dietary and environmental factors)7,12,22 and not to (or less) differences in genetic predisposition.23

Changing prevalence of Helicobacter pylori infection

In the US infection is low among white and economically advantaged Americans. However, minority populations have a higher frequency of infection: US data indicate that black children aged 5 to 9years have an overall infection frequency of 30%. Around the world, infection among children ranges from

approximately 35% in Russia to 20% in China and Poland, 12% in Korea and America to <10% in France, Belgium and Finland. 2,8,18,20,24-26 Despite high rates of infection in certain pockets of the globe, the frequency of H. pylori infection is declining worldwide. For instance, in one study conducted in Matsumoto, Japan, the rate of infection declined by up to 20% between 1986 and 1994 among individuals aged 9 to 70years of age.27

A recent study from Russia examined the effect of recent improvement in standards of living on the prevalence of H. pylori in Russian children by conducting 2 cross-sectional studies among children in St. Petersburg. The first study was undertaken in 1995 and the second a decade later. H. pylori status was evaluated using the same ELISA method for anti-H. pylori IgG (HM-CAP). The research found that the initial overall prevalence of H. pylori infection was 44% and decreased to 13% ten years later. In both studies, the prevalence increased with age. In 1995 the prevalence was 30% among children younger than 5years. A decade later the prevalence in the same age group is 2%, p =0.001. The authors concluded that improvements in the standard of living in Russia have resulted in a marked reduction in H. pylori transmission. Different rates of acquisition H. pylori form the basis for the differences in prevalence of infection between and among populations. The changes in Russia are a dramatic example of how sensitive H. pylori acquisition is to improvement in standards of living.28

This finding regarding socioeconomic status during childhood holds true for all subgroups in the United States. For instance, in a pediatric study conducted in Arkansas, children coming from a family with an income of <$5000 had up to a 60% rate of infection between the ages of 11 and 20years, whereas those with a family income of >$25,000 had only a 15% rate of infection. 29 This phenomenon has also been observed in other countries. In recently developed countries, such as Korea although approximately 80% of individuals >20years of age are infected (reflecting the fact that Korea only became a developed country within the past 20years), the prevalence of infection in young children is inversely related to the socioeconomic class of their family. Those aged 10 to 19years who are in a high socioeconomic class had a 20% frequency of H. pylori infection, while those of the same age who are in a low socioeconomic class have a 60% frequency.8

A study from Kazakhistan was conducted among unrelated asymptomatic individuals between the ages 10 and 60years and examined various aspects of the local household environment and access to water.30 The study reported that transmission of H. pylori is largely opportunistic and can be water borne. If the rate of H. pylori transmission is to be reduced it will require an improvement in overall sanitation including waste disposal, clean water, safe food as well as in household hygienic practices. A cross sectional study conducted in children residing in industrial and rural areas in Italy reported that the seroprevalence of H. pylori infection was significantly higher in children residing in rural areas compared to those in industrial areas.31 The study also found that in rural areas, children having dogs were at

greatest risk for H. pylori acquisition but this effect was not observed among children from the industrial areas.

Routes of transmission

H. pylori is a true 'opportunistic bacterium' that will use any method available for gaining access to the human stomach. Gastro-oral (e.g., exposure to vomit) and fecal-oral routes are believed to be the primary means of transmission. The bacterium can also be transmitted through exposure to contaminated food or water. 32-33 The majority of the data support the notion that transmission is mainly within families. H. pylori status was determined in 41 families with 'family' being defined as a husband and wife living together with biological children.34 Prior to disclosure of the results of H. pylori testing, one of the parents was randomly selected as the index case. The results revealed that if the index case, whether it was the mother or father, was positive, the children and spouse in that family were also likely to test positive for H. pylori (Figure 2). If the index case was negative, then the children and spouse were likely to negative as well. In this study in the US, there was no difference whether the index case was the father or the mother. In contrast, in countries where the father has little contact with the children, infection appears almost always to be linked to the mother. Thus, close contact and the level of household sanitation appear to be the most important variables. These finding support the concept that the most likely sources of transmission are person-to-person and/or exposure to a common source of infection. H. pylori from two Hispanic families living in Houston were examined for relatedness based of the genotypes using the cagA, vacA and iceA genes. H. pylori isolates from the children and their mothers had the same genotype and were different from those associated with children's fathers or brothers-in-law.24 The high rate of transmission to spouses also suggests that genetic factors are less critical than living conditions for transmission of the bacterium.

Relationship between Helicobacter pylori infection and associated diseases

Helicobacter pylori infection causes chronic gastritis, peptic ulcer disease, primary gastric B-cell lymphoma and (indirectly) gastric adenocarcinoma.35-40 All patients with infection develop gastric damage.41 Approximately 17% of infected patients develop peptic ulcer, and one quarter of such patients experience an ulcer complication.37 Numerous trials have shown that ulcer relapse is prevented following cure of the infection.42 Histologic and serologic studies have also shown that the infection preceded the ulcer and H. pylori infection is now accepted as one of the two major causes of peptic ulcers (the other being use of non-steroidal anti-inflammatory drugs).43 In a Veterans Affairs population in Houston with 100 consecutive duodenal ulcer and 154 gastric ulcer patients, 99% with duodenal ulcer were positive for H. pylori ; 30% of whom were found to be using non-steroidal anti-

inflammatory drugs (NSAIDs).43 In contrast, 92% of patients with gastric ulcers were infected with the bacterium and 58% of the patients were also taking NSAIDs. Eight percent with gastric ulcer were taking NSAIDs alone, and were not infected.43 What is the cause of non-H. pylori and non-NSAID ulcers? One of the above papers evaluated the presence of NSAID use by measuring serum salicylate levels. This approach was only useful for aspirin. More sophisticated approaches looking for evidence of COX-1 inhibition have shown that NSAID use is much more common than expected in these patients 44 and probably accounts for a sizable proportion of cases. Additional possibilities include other infections (herpes simplex), other drugs such as alendronate45 as well as misdiagnosis by the endoscopist. Peptic ulcer disease is a chronic relapsing disorder with typical morphologic and endoscopic appearances. One important reason for the observed differences in the ulcer prevalence and ulcer recurrence rates in clinical trials is the interpretation of the findings by the endoscopists, who we believe are the weakest link in this chain. 37 The areas for future investigation include identifying the uncommon causes of ulcerative lesions in the upper gastrointestinal tract as well as their natural history.

The exact prevalence of H. pylori infection in gastric cancer patients remains difficult to estimate because infection can be lost from individuals before cancer or its precursor conditions arise. Yamaji et al46 analysed 10,234 consecutive Japanese by serum anti-H. pylori antibody (IgG ELISA), confirming the relationship between serum positivity and gastric cancer and pointed out that, particularly in the elderly, the weak response of H. pylori antibody carried a high risk for gastric cancer. A Swedish population-based case-control study using CagA immunoblot (and not IgG ELISA) showed the CagA immunoblot to be a more sensitive marker of past infection, and reported that the estimated proportion of non-cardia adenocarcinoma in the general Swedish population attributable to H. pylori is 71% for both histologic subtypes, ranking with the association between smoking and lung cancer.47 Another study using ELISA combined 12 previous studies from USA, Europe and Asia, where 1228 gastric cancer cases were considered. They found that 5.9 is the best estimate of the relative risk of non-cardia associated with H. pylori infection and that the organism does not increase the risk of cardia cancer.48

Atrophic gastritis and intestinal metaplasia are well established precursor lesions of intestinal-type of gastric cancer. Asaka et al reported the results of a multicenter study undertaken to evaluate the relationship between H. pylori infection, atrophic gastritis and intestinal metaplasia in Japan.49 Atrophic gastritis increased from 9.4% in individuals below 20years of age to >70% in those aged 60 or older and was strongly associated with H. pylori infection. The overall prevalence of atrophic gastritis in H. pylori infection was 82.9% compared with 9.8% in uninfected subjects (OR=44.8). Intestinal metaplasia was present in 43.1% of H. pylori positive persons compared with 6.2% among the uninfected (OR=11.5). The authors concluded that atrophic gastritis and intestinal metaplasia were strongly associated with H. pylori . The data suggest that the risk of development of early gastric cancer will continue to remain high in Japan.49

Changes in the environment and human behavior that influence the prevalence of Helicobacter pylori infection

It is now apparent that the decrease in age-adjusted prevalence of H. pylori infection in industrialised countries is related both to improved living conditions during childhood and to loss of infection. Although H. pylori infection is usually a chronic and life-long infection, spontaneous elimination of the infection was reported as early as 1992 using serologic tests50 and was confirmed using breath tests51 and by histology52 from both developed and underdeveloped countries. These observations have subsequently been confirmed in a number of populations.9,27,53,54 A longitudinal study that examined Black and White children, living in the same community and attending the same schools, over a 12-year period provided additional insights into the change in pattern of infection.9 They found that the rates of acquisition and disappearance of H. pylori infection were identical for the total population. However, there were differences between the two races. More Black children remained infected (or more likely became reinfected) during the observation period compared to White children (in whom the infection was lost in 50% during the observation period). The study suggested that the higher rate of acquisition and the lower rate of loss of infection among Black children might be due to differences in access to health care facilities or to more intense exposure for whatever reason. The high rate of loss of H. pylori infection among White children was not related to H. pylori 'eradication therapy' as it had not yet been discovered. The greater loss than acquisition of H. pylori infection in the White children is consistent with the continuing decrease in the rate of the infection in the white population in the United States.9

A cohort study conducted on Japanese children and adults from a typical mountain village evaluated the seroepidemiology of H. pylori over a 9year-period and also compared the results with the age-specific seroprevalence from two independent cross-sectional surveys conducted in the same population during same period.27 The cohort study found the rate of disappearance to be greater than the rate of acquisition and these results were confirmed in the two cross-sectional studies. Of particular interest was the observation that there was a decrease in prevalence in every age group (Figure 3). The fall in prevalence during the observation period did not reflect changes in the rate of acquisition of H. pylori in childhood but rather the higher rate of loss of the infection. The continuing change in the epidemiology of H. pylori infection complicates our understanding of the actual prevalence of H. pylori. The higher rate of loss of infection compared to acquisition may be related to changes in standards of living in successive generation or to changes in medical practice leading to the greater use of antimicrobials for other common infections.

It is impossible entirely to separate environmental factors from genetic influences. An early twin study on Swedish population suggested that there was a genetic component for acquiring H. pylori infection23 and a follow-up study on the same twins population has questioned if there are genetic influences for peptic ulcer disease in common with genetic influences for H. pylori infection.55 Comparisons of MZ and

DZ cross-twin and cross-trait correlations in that study demonstrated that despite the similarity in heritability for the two traits (peptic ulcer disease and H. pylori infection), the genetic influences for liability to peptic ulcer disease are independent of such genetic effects for acquiring H. pylori infection.55 It is feasible that the relationship between H. pylori and peptic ulcer disease could be mediated by familial environmental factors, (i.e. environmental experiences or situations that are shared by family members). Examples of familial environmental factors that may mediate the association between H. pylori and peptic ulcer disease are diet, smoking, or drug consumption (e.g., alcohol, caffeine, NSAID consumption).

The prevalence of infection-induced ulcer is falling in the Western World

During the past three decades, the occurrence of peptic ulcer disease has declined remarkably in the United States, Europe, Australia, and Japan.56-58 The risk of peptic ulcer was highest among those born at the beginning of the century and has decreased in all subsequent generations.59,60 The rapid change in the pattern of peptic ulcer in successive generations, (i.e., a birth cohort phenomenon) is more likely due to changes in environmental factors than changes in the genes of the affected patients.59 Another possibility is that there may have been a change in the prevalence of particularly virulent H. pylori (e.g., cagA positive). Serologic studies have shown that the prevalence of these putative virulence factors has not changed in any population. This can be interpreted as either we have not examined the critical factors involved or that this is not the correct explanation. The later appears most likely.

In the past there was interest in genetic factors that might play an important role in the etiology of peptic ulcer disease.61,62 However, the pattern of inheritance was not simple Mendelian and it was suggested that the genetic basis was multifactorial. Initially, the strongest evidence of a genetic influence on peptic ulcer came from studies showing an increased risk of duodenal ulcer in individuals with hyperpepsinogenemia. 63,64 This evidence disappeared when it has became evident that elevated serum pepsinogen I was also a feature of H. pylori infection.65,66 The reason that family members of patients with peptic ulcer are at increased risk can be explained by the fact that they are at increased risk of infection (clustering effect of infection in families), that they are more likely to have a similar strain, or they shared a common environment. The marked geographical variation in the incidence rates of peptic ulcer in different parts of the world along with the rapid rate of change in incidence provides strong evidence that environmental factors are the most important features that modulate the development of an ulcer. 67

Summary

Worldwide, rates of H. pylori infection are declining, yet the infection remains a destructive, transmissible, infectious disease with serious health consequences. Although it may appear to be asymptomatic, in reality it is a latent infection that is quietly and purposely destroying the stomach.

The infection is curable with antibiotic therapy, although residual damage may remain (atrophy with dysplasia) and a poor outcome (e.g., gastric cancer) may still result. Treatment of H. pylori infection with antibiotic therapy reduces the risk of a poor outcome, but may not eliminate it.

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Word count: 4785

© 2006 Elsevier Ltd

Indexing (details)

Cite

MeSH African Americans -- statistics & numerical data, Comorbidity, European Continental Ancestry Group -- statistics & numerical data, Gastritis -- microbiology, Helicobacter Infections -- ethnology, Helicobacter Infections -- transmission, Humans, Prevalence, Social Class, Stomach Neoplasms -- microbiology, Stomach Ulcer -- epidemiology, Stomach Ulcer -- microbiology, Helicobacter Infections -- epidemiology (major), Helicobacter pylori (major)

Identifier / keyword Helicobacter pylori, epidemiology

Title Epidemiology of Helicobacter pylori infection

Author Malaty, Hoda M.

Publication title Best Practice & Research

Volume 21

Issue 2

Pages 205-14

Publication year 2007

Publication date Apr 2007

Year 2007

Publisher Elsevier Limited

Place of publication Kidlington

Country of publication United States

Publication subject MEDICAL SCIENCES--GASTROENTEROLOGY

CODEN BPRCB6

Source type Scholarly Journals

Language of publication English

Document type EDB, Journal Article

DOI

http://dx.doi.org/10.1016/j.bpg.2006.10.005

Accession number 17382273

ProQuest document ID 1132053612

Document URL http://search.proquest.com/docview/1132053612?accountid=8083

Copyright © 2006 Elsevier Ltd

Last updated 2013-02-09

Database ProQuest Central

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