This really interesting research was recently posted by Diogenes on TUK forum:
"Hashimoto’s thyroiditis (HT) is the most frequent autoimmune disease, and it has been reported to be associated with gastric disorders in 10–40% of patients while about 40% of patients with autoimmune gastritis also present HT. Some intriguing similarities have been described about the pathogenic mechanism of these two disorders, involving a complex interaction among genetic, embryological, immunologic, and environmental factors. CAG is characterized by a partial or total disappearance of parietal cells implying the impairment of both hydrochloric acid and intrinsic factor production. The clinical outcome of this gastric damage is the occurrence of a hypochlorhydric-dependent iron-deficiency anemia, followed by pernicious anemia concomitant with the progression to a severe gastric atrophy. Malabsorption of levothyroxine may occur as well. We have briefly summarized in this minireview the most recent achievements on this peculiar association of diseases that, in the last years, have been increasingly diagnosed."
"(3). e natural history of HT is the progressive reduction of thyroid function till overt hypothyroidism (24) with a rate of progression of 2–4% per year (23), while that of gastric atrophy features the progressive reduction, till disappearance, of parietal cells, leading to reduced or absent acid production (3, 22). These alterations interfere with absorption of essential nutrients leading, at first to iron-deficiency anemia, followed by PA"
"iron Deficiency and PA"
"Chronic atrophic gastritis is clinically silent in most cases and only a small percentage of patients may complain about dyspeptic symptoms. A well-described clinical feature of thyrogastric syndrome is represented by the presence of an iron-deficiency and/or a PA. In fact, it has been demonstrated that an iron-deficient anemia, refractory to oral iron therapy, in patients with HT, may be due to chronic atrophic gastritis (13). clinical signs of this disease appear after several years of its onset, when the progressive reduction to disappearance of the parietal cells leads to atrophy of the gastric mucosa, impairing the absorption of iron, vitamin B12 (cobalamin), folate, and other nutrients (22)."
"n the initial phase of the atrophic gastritis, the damage of parietal cells can lead to iron deficient microcytic anaemia as the only clinical sign (38). When the gastric atrophy becomes severe and/or the IFA is no longer produced, even the absorption of cobalamin becomes compromised. "