Epidemiological data about peptic ulcer disease (PUD) are scanty and often related to series investigated by X-rays. Endoscopic data appeared after 1980 and showed a three-fold increase of cases of PUD over earlier findings.5 A review of more than 1000 cases stated that the expected number of new PUD cases in a large children's hospital was evaluated as 3.5 per year.6 Others found that the incidence of PUD was 4.4/10 000 children with a frequency of 3-6% in children who had undergone gastroscopy.7
However, there is now evidence that the incidence of PUD is decreasing in adults as well as in children. The progressive decrease of PUD is probably related to modifications in the epidemiology of H. pylori infection. The slow but continuous improve ment of socioeconomic conditions, the diffuse use of antibiotics, and the decrease of the so-called ulcerogenic strains of H. pylori might reasonably explain this phenomenon.
H. pylori infection is one of the most diffuse infections in the world. There are areas at high risk of infection (in developing countries, such as those in the African or South American continents) and areas at low risk (such as Europe and North America).8 In high-risk countries, the rate of infection is very high in the first 2 years of life, and older children and adults are almost totally infected. In a study on a cohort of 248 Gambian children aged 3-45 months, the prevalence of positive breath tests (a specific and non-invasive test to detect H. pylori infection, see below) rose from 19% at 3 months of age to 84% by the age of 30 months. Reversion to a negative breath test, in association with declining specific antibody levels, occurred in 20% of children, suggesting that in the first years of life children may acquire and clear the infection before ultimately being infected with a persistent strain.9
In developed countries, transverse serological studies have demonstrated that the rate of infection increases slowly and regularly by 10% with each decade of life.8 In Italy, a recent epidemiolog-ical study showed that 11% of subjects from 6 to 18 years were infected,10 while the prevalence rate in people of 50-60 years was 50-60%. Longitudinal studies demonstrated that this increase of infected subjects with aging was related to an effective decrease of infection in the youngest cohorts, rather than to an increase of new cases with aging.11 This phenomenon is explained by the fact that each generation or cohort has a distinct and possibly unique environmental risk of exposure to the infection (cohort effect), linked to specific risk factors. These risk factors are well known and are socioeconomic, so that the cohort effect is considered to be the consequence of the improvement of socioeconomic conditions in the most recent decades. In Japan, a country that has had an impressive and fast economic development after the Second World War, epidemiological studies demonstrated a high prevalence rate of H. pylori infection in subjects born before the war, and a dramatic decrease in those born after the war and the industrial revolution.12
When the improvement of socioeconomic conditions was slow, but constant, as in the Netherlands, the decrease of the infection rate in childhood was continuous.13
The relationship between socioeconomic status and H. pylori infection has been emphasized by studies in subjects belonging to the same city or community, but with different socioeconomic conditions. Using family income as a measure of the socioeconomic class, the rate of acquisition of H. pylori in those children with family income less than $5000/year was twice that of those with incomes greater than $75 000/year in a study from Arkansas.14 Absence of a fixed hot-water supply and domestic crowding in childhood were powerful independent risk factors for current infection with H. pylori. Among current living conditions, only the number of children living in the house hold was independently associated with H. pylori infection.15 Different studies showed that the age of infection is in the first years of life.16-18
In a cohort of 224 children followed up retrospectively for 21 years by stored serum samples, the crude incidence rate per year was 1.4% for the whole cohort, ranging from 2.1% at 4-5 years and 1.5% at age 7-9 years to 0.3% at 21-23 years. The median age for seroconversion was 7.5 years. Nine of the 58 seropositive children cleared the infection during follow-up. The rate of seroreversion per year was 1.1%; it was highest among children at age 4-5 years (2.2% vs 0.2% at ages 18-19).16 The finding that children infected before 5 years of age could eradicate the infection spontaneously, as well as be re-infected more easily than older children, has been confirmed by others.14,17 A study of follow-up of 52 children successfully treated for H. pylori demonstrated that 11.5% of children who had eradicated the bacterium suffered reinfection, with the majority under 5 years of age. Only 4.3% of children older than 5 years were re-infected, even those living with H. pylori-positive parent in 81% of cases. The age of <5 years was the major risk factor for re-infection.17 In adults, the infection rate is approximately 0.3-0.5% per year and infection is rarely eradicated spontaneously, as demonstrated by longitudinal studies on stored samples.19,20
In addition to socioeconomic factors, genetic factors could play a role in the acquisition of the infection. A sibling study showed that the sero-prevalence rate was similar in genetically identical twins living under different socioeconomic circumstances.21 It should be acknowledged, however, that ethnic, genetic and socioeconomic factors are often intertwined and their various contributions are difficult to assess.
An important issue in the study of an infectious disease is its route of transmission. The absence of an animal reservoir, the demonstration of intra-familial clustering,22 as well as clustering of the infection among institutionalized children23 suggests that person-to-person transmission is the most probable route. Approximately 90% of parents and 70% of siblings of H. pylori-positive children showed seropositivity for H. pylori.22 In institutionalized children, including those living in a monastery, an inverse relationship between seroprevalence and age was demonstrated, with the increased rate of infection correlating with the age of entry more than the length of stay in the community.23 Both vertical transmission (from mother to child as well as from father to child), and horizontal transmission from sibling to sibling, have been demonstrated.24
H. pylori has been isolated from saliva and dental plaque,25 as well as from vomitus,26 suggesting that the most diffuse routes of transmission between siblings or children in communities could be the oro-oral or gastro-oral. Epidemics of vomiting could easily diffuse the infection.
In developing countries, H. pylori has been identified in water27 and in feces28 by studies using the polymerase chain reaction (PCR). Clusters of infection independent of income, but strictly related to water source, have been demonstrated; the infection rate was 12-fold higher in children from high-income families using community wells rather than municipal water in a study in Peru.27 The fecal-oral route of transmission typical of waterborn diseases is quite possible, particularly in conditions where there is a lack of a municipal water supply.
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