Comparison of acid outputs (mMol/h between infected and non-infected children along with effect of anti-
At least half the world's population are infected by
In this chapter, we will review and update the consequence of
2. Consequences of initial
H. pylori infection in children
There are not enough studies on the natural history of gastric infections in childhood years. In older children and adolescents, and adults it appears that
Some studies reported pan-gastritis involving both body and antrum in children infected with
H. pylori infection and gastric acid perturbation
Acid secretion by the gastric parietal cell is regulated by paracrine, endocrine, and neural pathways. The physiological stimuli for acid secretion include histamine, acetylcholine, and gastrin, each of which binds to receptors located on the basolateral plasma membranes of the cells. The antral region of stomach contains G cells which release hormone gastrin. When meal is ingested, the protein component stimulates G cell to release Gastrin, which travels through the bloodstream to parietal cells in the body region (fundus) to secret acid . Gastrin directly does not stimulate parietal cells but stimulates the adjacent enterochromafin-like cell (ECL cells) to release histamine, which in turn stimulates the parietal cells. Stimulation of acid secretion typically involves an activation of a cAMP-dependent protein kinase cascade that triggers the translocation and insertion of the proton pump enzyme, H,K-ATPase, into the apical plasma membrane parietal cells . As the acid accumulates and overcome the buffering effects of the food, the fall in intragastric pH inhibits further release of gastrin and thus prevents secretion of excessive amount of acids (negative feedback control).
H. pylori infection and increased acid output (hyperchlorhydria)
H. pylori infection and low acid output (hypochlorhydria)
In subjects with atrophic gastritis or body predominant gastritis, there also is increased gastrin release, but that is not accompanied with increased acid secretion. In such subjects, acid secretion is reduced or completely absent (achlorhydria) [36, 37]. The low acid secretion, despite increased gastrin levels, indicates markedly impaired ability of oxyntic mucosa to secret acid in response to gastrin. Following eradication of
3. Role of
H. pylori infection in gastric acid perturbation in children
There are only a few pediatric case reports on gastric acid secretion in
|Basal Acid Output (BAO)||0.23 ± 0.30||0.06||0.62 ±0.9||NS||0.65 ± 0.65|
|Stimulated Acid Output||2.04 ±1.4||0.001||3.4 ±2.5||NS||3.3 ±2.1|
4. Potential mechanisms of
H. pylori-induced hypochlorhydria
An alternative explanation for the impaired acid secretory function is infection-induced inflammation of the oxyntic mucosa, since the severity of inflammation of the body mucosa is more marked in subjects with
The molecular mechanisms underlying
4.1. Potential consequences of
H. pylori induced hypochlorhydria
H. pylori infection and iron deficiency anemia
5.1. Iron deficiency and iron deficiency anemia
Iron deficiency (ID) and iron deficiency anemia (IDA) are major public health problems, especially in children and women of childbearing age in developing countries , and is considered one of the ten leading global risks factors in terms of its attributable disease burden . It has been estimated that globally approximately 1.6 billion people, representing 25% of the total population are anemic . ID is considered to account for 50% of identified anemia, and 800,000 deaths worldwide can be attributed to IDA. Deficiency of this trace element has adverse implications on health at all stages of life. When iron deficiency occurs during critical windows of brain development, the resultant cognitive deficits may be irreversible and unresponsive to subsequent improvements in the iron status . In adults, ID and IDA can adversely impact physical work capacity and work productivity - variables that may have a detrimental impact on their economic potential .
H. pylori and iron deficiency anemia
Several reports have demonstrated an association between
In Bangladesh, a randomized controlled community based study was conducted to determine whether or not
The results of the study indicated that iron status, as reevaluated on day-90, improved in all groups. However, the improvement was significantly higher among 3 groups receiving iron (anti-
H. pylori and iron absorption
Non-heme iron absorption requires an acidic milieu. Non-water-soluble iron compounds, e.g. ferrous and ferric pyrophosphate are often used in the fortification programs because they cause no unacceptable organoleptic changes in the fortified food. However, these compounds need gastric acid for their solubilization and absorption. Therefore, if gastric acid output is compromised as a consequence of
|1P value for iron absorption from ferrous fumarate compared with that from ferrous sulfate within each group.|
5.3.1. Mechanism of IDA
The interaction between
H. pylori and vitamin C
Ascorbic acid is the reduced form of the vitamin, which can act as a potent antioxidant for neutralizing nitrite-derived mutagens protecting against gastric carcinogenesis . Vitamin C is first absorbed and then is actively secreted, mainly in the antral mucosa, from plasma into gastric juice. Once there, it is able to react with nitrosating agents preventing N-nitroso compounds formation; however, vitamin C in the stomach interacts with iron improving its absorption. In children
In developing countries, low intake of vitamin C-enriched food is associated with higher prevalence of
The combination of micronutrient deficiency and more frequent enteric infections consequent to
I gratefully acknowledge Dr. Mohammed Abdus Salam, Director, Research & Clinial Administration and Strategy, icddr,b for his review and valuable comments.
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