Gastropathic sideropenia

Abstract

There has been an increasing awareness recently of subtle, non-bleeding gastrointestinal conditions that may result in abnormal iron absorption leading to iron-deficiency anaemia (IDA) in the absence of gastrointestinal symptoms. Thus, the importance of coeliac disease as a possible cause of IDA refractory to oral iron treatment, without other manifestations of malabsorption syndrome, is increasingly being recognized. In addition, Helicobacter pylori has been implicated in several recent studies as a cause of IDA refractory to oral iron treatment, and the anaemia responds favourably to H. pylori eradication. Likewise, achlorhydric gastric atrophy or atrophic body gastritis (ABG), a condition associated with chronic idiopathic iron deficiency, has been shown to be responsible for refractory IDA in over 20% of patients with no evidence of gastrointestinal blood loss. It has also been suggested that H. pylori gastritis may represent an early phase of ABG in which infection may trigger an autoimmune process directed against gastric parietal cells by means of antigenic mimicry. In this review we examine in a critical manner the role of H. pylori gastritis in the causation of IDA, the role of ABG in the pathogenesis of iron malabsorption, the evidence supporting a possible cause-and-effect relationship between H. pylori gastritis and ABG, and the implications of these findings for the diagnostic work-up and management of IDA.

Refractory Iron-deficiency Anemia and Autoimmune Atrophic Gastritis in Pediatric Age Group

“…Two other pathologies were more recently recognized: Helicobacter pylori infection (Hp) and autoimmune atrophic gastritis (AAG). [1][2][3][4][5][6] In this context, Hershko proposed an algorithm for IDA diagnostic work-up. In pediatric patients, oral iron therapy can be introduced without an exhaustive diagnostic approach.…”

Extragastric diseases associated with Helicobacter pylori infection

“…However, many of the studies lack strong design features and statistical power and pay insufficient attention to potential confounding factors or the temporal ambiguity inherent in linking chronic infection and chronic nutritional deficit. Overall, the evidence shows a positive association, and plausible mechanisms by which the bacterium could cause, perpetuate, or worsen IDA have been proposed [22,23], but support for a causal relationship is not strong. Indeed, there is inadequate evidence to rule out the possibility that IDA renders one more susceptible to persistent H. pylori infection rather than the latter causing the former, although confounding by mutual risk factors is another plausible, and perhaps more likely, explanation of the observed association in the absence of a causal link.…”

“…Although the updated guidelines cited previously recommend that anti-H. pylori therapy be considered in infected patients with unexplained IDA and a recent review finds that a growing body of evidence links H. pylori to IDA in both children and adults [22], another review contends that this evidence consists primarily of case reports, observational studies, and small uncontrolled trials that lack methodologic rigor [23].…”

The gold standard improves: a better assay for HSCs

“…2 The NOD/SCID strain was initially derived from the SCID mouse by Shultz and colleagues at Jackson Laboratories. 3 In comparison to SCID mice, which do not make mature T and B cells, NOD/SCID mice have an excellent capacity for engraftment with human cells due to additional defects in natural killer (NK) cell and macrophage function, and circulating complement. 3 NOD/SCID-␤ 2 -microglobulin-null (NOD/SCID-␤ 2 m Ϫ/Ϫ ) mice have a more absolute immunodeficiency than the NOD/ SCID strain, and have virtually no NK cell function.…”