Refractory irondeficiency and H pylori infection

There are a number of potential biological explanations for iron deficiency observed in H. pylori infection apart from bleeding secondary to peptic ulcer disease. Currently, there is no evidence to support that chronic gastritis secondary to H. pylori results in occult blood loss. However, H. pylori infection in some settings might give rise to hypochlorhydria, low ascorbic acid levels, and increased lactoferrin (a host iron-binding protein) sequestration by the organisms. Also, H. pylori possesses multiple iron acquisition systems in its genome, which makes it an avid competitor for iron uptake with the host in the gastric microenvironment [46].

There are a number of case reports as well as case control studies, and recently a population study, supporting the role of H. pylori infection as a potential cause of otherwise unexplained refractory iron deficiency [47-49]. H. pylori infections, especially those with atrophic gastritis, are more likely to have unexplained refractory iron-deficiency anemia compared to the age- and sex-matched controls without iron deficiency [50]. Baysoy et al. [51] describe a group of children undergoing investigation for upper gastrointestinal symptoms and found that those with H. pylori were more likely to have lower iron stores compared those without infection. However, eradication of H. pylori has not consistently increased hemoglobin levels

Table 1. Purported extragastric manifestations of H. pylori infection

Manifestations

Cardiovascular

Neurological

Autoimmune

Atherosclerotic heart disease, stroke Parkinson disease, migraine

Autoimmune thrombocytopenia purpura, Reynaud's phenomenon, Sjögren's syndrome, diabetes mellitus

Chronic urticaria, angioedema, rosacea, alopecia areata

Refractory iron deficiency, halitosis, hyperemesis gravidarum, anorexia, glaucoma, oral ulcers, urethritis

Dermatological Others in control studies. One study confirmed an increase in hemoglobin level in Korean female athletes [52], whereas a large control household randomized open-label trial involving 290 Alaskan children with iron deficiency and H. pylori infection in a population that has a high prevalence of this infection, failed to show that H. pylori eradication improved isolated iron deficiency or mild anemia up to 14 months after treatment initiation. The limitation is that this study was not designed to detect small effects, with only 2 patients had hemoglobin less than 100 g/L [53]. Further randomized control trials in different populations, with age groups with varying degree of anemia are still needed to confirm the association between H. pylori and refractory iron deficiency. Despite this, the Canadian consensus conference on H. pylori still recommends, in the absence of other causes of iron deficiency, H. pylori should be tested for and treated [33].

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