This cross-sectional population-based serosurvey demonstrates a high rate of past or current infection with
H. pylori in the Alaska Native population during the 1980s. The age when infection is acquired appears to be quite young, in that up to 40% of children were seropositive by the age of 4 years and almost 70% were seropositive by the age of 10 years. The cross-sectional prevalence of
H. pylori infection in Alaska Natives is similar to that observed in populations in developing countries. Previous seroepidemiological studies in developing countries have shown infection rates among children to be quite high, approaching 70 to 90% among children under age 10 years in some countries (
6,
8). However, marked differences in the seroprevalence of
H. pylori have been observed between various ethnic groups living in developed countries (
8,
12,
21). Graham et al. (
8) found a significantly higher seroprevalence of
H. pylori among Hispanics and African Americans than among non-Hispanic whites. Conversely, the rate of acquisition in persons over 20 years of age was similar in all three groups. This suggests that the risk of acquisition is greater in childhood or early adolescence for Hispanics and African Americans and may be related not to ethnic background but to the lower socioeconomic conditions experienced by these groups during childhood. This concept may explain the lower rates of infection found in Alaska Native children living in Anchorage than in Alaska Native children living in rural regions of the state. However, this observation did not hold true for Alaska Native children living in urban Fairbanks, where rates of infection were similar to those for Alaska Native children living in rural regions of Alaska.
The finding of persistently high rates of iron deficiency in persons <20 years of age and women of childbearing age in our study cohort is compatible with the rates found in earlier studies performed in Alaska (
2,
3,
5,
13,
17–
19,
20). These high rates of iron deficiency are in contrast to declining rates of iron deficiency among all age groups of the general U.S. population (
4). While menstrual blood loss can be considered a contributing factor for iron deficiency in women of childbearing age, factors for iron deficiency among those Alaska Natives <20 years of age may include inadequate intake of dietary iron or foods that enhance iron absorption (
5). In general, however, the typical Alaska Native subsistence diet (e.g., fish and marine and land mammals) is high in dietary bioavailable iron (
15).
The association of low serum ferritin levels, a marker of iron deficiency, with the presence of
H. pylori-specific IgG supports the earlier endoscopic findings of
H. pylori-associated gastritis as a cause of elevated stool heme levels (
22). This association appeared to be particularly strongest for those Alaska Natives <20 years of age, regardless of whether the analysis either included or excluded sera with indeterminate results. We have since found a similar association between both anemia and iron deficiency and
H. pylori seropositivity among young children residing in one rural Alaska village (
5). Our findings are also supported by another large serosurvey for
H. pylori in adults in Denmark in which serum ferritin levels were found to be significantly lower in adult men and postmenopausal women who were
H. pylori IgG positive than in noninfected persons (
14). A smaller study in Australia also showed that serum ferritin levels were significantly lower in women who were
H. pylori IgG positive than in women who were
H. pylori negative (
16). While blood loss associated with gastritis or bleeding duodenal or gastric ulcers may play an important role in the development of iron deficiency in Alaska Natives, other factors related to
H. pylori infection may also contribute. These include the sequestering of iron by the host in response to
H. pylori-related chronic gastric inflammation (
1) and the binding of iron by
H. pylori outer membrane iron binding proteins (
9,
23). Both of these mechanisms would act in the host to reduce the iron normally available for storage and utilization. Approximately one-quarter of iron-deficient persons had no serologic evidence of infection by
H. pylori, suggesting that other factors may be responsible for the observed iron deficiency in this population. These factors may include low levels of intake of iron or substances that enhance iron adsorption (i.e., vitamin C), high levels of intake of iron-inhibiting substances (i.e., tannins), or chronic infection by infectious agents other than
H. pylori.
In summary, the statewide serosurvey described here found a high prevalence of H. pylori-specific IgG among Alaska Natives. The rate of seropositivity increased with increasing age, in that 78% of the study cohort was positive by age 14 years. There were marked regional differences, with high rates of seropositivity occurring in the northern, western, and central regions of Alaska. However, an explanation for this regional variation remains to be determined. Overall, low serum ferritin levels were found in 20% of males and 36% of females, underscoring the persistence of iron deficiency anemia within this population. An association between low serum ferritin levels and the presence of H. pylori-specific IgG was found, particularly among persons less than 20 years of age, providing further support for a possible role of H. pylori in the etiology of the iron deficiency anemia observed among Alaska Natives.
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