Variable hematologic presentation of autoimmune gastritis: age-related progression from iron deficiency to cobalamin depletion
As many of you likely already know, H. pylori has reached the penultimate in scientific fame as winner of the 2005 Nobel Prize in Physiology or Medicine. Independently of that, the topic of infectious triggers to autoimmune disease has been popular for some time, too. This article ties these two topics together nicely.
This study examines three cohorts of patients with autoimmune gastritis: those with iron deficiency anemia (IDA), those with normocytic blood indices, and those with macrocytic anemia. They find that all groups have evidence for an autoimmune polyendocrine syndrome and for antibodies against intrinsic factor, suggesting a similar pathologic process occurring. The IDA group was largely younger with a high incidence of H. pylori seropositivity, while the macrocytic anemia group, all meeting the criteria for pernicious anemia, was older with a low incidence for H. pylori infection. The RBC indices additionally show positive correlation with increasing age. The authors suggest that these data suggest that the three cohorts may be different phases of the same disease process. If true, this would open new doors to understanding pernicious anemia, and possibly help devise earlier routes for intervention prior to full-blown disease development.
The authors admit that this study is simply correlative and suggest that a study be done to follow the IDA cohort over time to determine if they really develop PA as per the model proposed. I would ask that if their model is strictly true, why is the serologic incidence of antibodies against H. pylori so low in the PA group? Does anyone know whether IgG against H. pylori really disappears that reliably after eradication?

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