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Clinical Trial Summary

Iron-deficiency anemia (IDA) represents a global public health problem which has a significant impact on human health and social and economic development. Inadequate iron intake, chronic blood loss and impaired iron absorption are among the causes of IDA There are an association between H. pylori infection and IDA, but the biological explanation for H. pylori infection causing iron-deficiency anemia remains unknown. Initially, sideropenic anemia was considered to be caused by occult blood loss due to chronic superficial active gastritis caused by H. pylori, but subsequent studies did not confirm this theory . H. pylori infection can cause disorders in iron assimilation and increased iron requirements. Hypoacidity caused by pangastritis and a low level of ascorbic acid in the stomach of patients infected with H. pylori may affect the absorption of iron in the duodenum . In addition, levels of lactoferrin gastric mucosa (an iron-binding protein) are high in patients infected with iron-deficient H. pylori, showing a possible role between increased lactoferrin sequestration and iron utilization by the body . H. pylori also competes with the host for available food grade iron. H. pylori has several iron acquisition systems, which can capture iron available in the microenvironment of the stomach lumen . Moreover, there are studies that indicate that an iron-deficiency anemia which does not respond to iron therapy can be resolved by eradicating H. pylori from the stomach . ABO blood group seem to be looked into as risks for H. pylori related stomach malignancy, nevertheless, there are actually inconsistent scientific studies because of numerous confounding outcomes. Blood group antigens have the receptor properties for toxins, parasitic organisms and bacteria, exactly where this bacteria could assist in annexation or intrusion and avert multitude approval components .


Clinical Trial Description

Iron-deficiency anemia (IDA) represents a global public health problem which has a significant impact on human health and social and economic development. Inadequate iron intake, chronic blood loss and impaired iron absorption are among the causes of IDA There are an association between H. pylori infection and IDA, but the biological explanation for H. pylori infection causing iron-deficiency anemia remains unknown. Initially, sideropenic anemia was considered to be caused by occult blood loss due to chronic superficial active gastritis caused by H. pylori, but subsequent studies did not confirm this theory . H. pylori infection can cause disorders in iron assimilation and increased iron requirements. Hypoacidity caused by pangastritis and a low level of ascorbic acid in the stomach of patients infected with H. pylori may affect the absorption of iron in the duodenum . In addition, levels of lactoferrin gastric mucosa (an iron-binding protein) are high in patients infected with iron-deficient H. pylori, showing a possible role between increased lactoferrin sequestration and iron utilization by the body . H. pylori also competes with the host for available food grade iron. H. pylori has several iron acquisition systems, which can capture iron available in the microenvironment of the stomach lumen . Moreover, there are studies that indicate that an iron-deficiency anemia which does not respond to iron therapy can be resolved by eradicating H. pylori from the stomach . ABO blood group seem to be looked into as risks for H. pylori related stomach malignancy, nevertheless, there are actually inconsistent scientific studies because of numerous confounding outcomes. Blood group antigens have the receptor properties for toxins, parasitic organisms and bacteria, exactly where this bacteria could assist in annexation or intrusion and avert multitude approval components . ;


Study Design


Related Conditions & MeSH terms


NCT number NCT05841433
Study type Observational
Source Assiut University
Contact Aliaa AB shehab, Bachelor's
Phone 01064480804
Email aliaashehab812@gmail.com
Status Not yet recruiting
Phase
Start date June 1, 2023
Completion date October 30, 2025