Incidence of Gastric Parietal Cell Antibody in Families of Patients with Iron Deficiency Anaemia

Abstract

There is an association of pernicious anaemia with iron deficiency anaemia (Faber and Gram, 1924). There is also a high incidence (85 per cent) of gastric parietal cell antibody in the sera of patients with pernicious anaemia (Taylor, Roitt, Doniach, Couchman and Shapland, 1962) and a less marked, but significantly increased incidence (33 per cent) in patients with iron deficiency anaemia who have a histamine fast achlorhydria (Dagg, Goldberg, Anderson, Beck and Gray, 1964). Pernicious anaemia has a familial incidence (Askey, 1940; Callender and Denborough, 1957) and there is also an increased frequency of achlorhydria in relatives of patients with pernicious anaemia (Askey, 1940; Neel, 1947). In addition te Velde, Abels, Anders, Arends, Hoedemaeker and Nieweg (1964) have found the gastric parietal cell antibody in 20 per cent of relatives of patients with pernicious anaemia, compared with 6 per cent in a control series. Because of the association of iron deficiency anaemia with pernicious anaemia and the increased incidence of histamine fast achlorhydria and parietal cell antibody in both diseases, the occurrence of the antibody has been assessed in the families of patients with iron deficiency anaemia, histamine fast achlorhydria and gastric parietal cell antibody. In a group of 22 patients with iron deficiency anaemia, histamine fast achlorhydria and gastric parietal cell antibody, Dagg, Goldberg, Gibbs and Anderson (1966) found that seven had a 58Co vitamin B12 absorption test (Schilling, 1953) characteristic of pernicious anaemia, and six of these had reduced serum vitamin B12 levels; that is these patients had latent pernicious anaemia. In 10 of the 22 patients the serum vitamin B12 levels and the Schilling test were normal, and in the remaining five patients the serum vitamin B12 was low but the Schilling test was normal. Since it appeared possible that the familial incidence of gastric parietal cell antibody would be higher in relatives of the patients with latent pernicious anaemia than in relatives of those without latent pernicious anaemia, 11 families from these 22 patients were investigated, six of which had propositi with latent pernicious anaemia and five of which had propositi without latent pernicious anaemia (Table I). The relatives of the remaining 11 patients were unwilling to co‐operate in these investigations.

Gastric secretory response to iron therapy.

“…Although they are very common in frank and latent pernicious anaemia (Wright et al, 1966) there is no proof that these antibodies cause gastritis, and it is possible that they are produced as a reaction to mucosal damage, the result of iron deficiency (Markson and Moore, 1962;Moulton, 1964) or of other factors (Edwards and Coghill, 1966). MacFadyen, Goldberg, Dagg, and Anderson (1965) found a significant history of bleeding only among those iron-deficient patients with both achlorhydria and antibodies who did not have relatives with antibodies. The equally low incidence of parietal-cell antibodies in patients who had had partial gastrectomy for duodenal ulcer and in others with gastric carcinoma has also suggested that antibodies may be a reaction to gastritis, but that few patients are able to produce them (Kravetz, van Noorden, and Spiro, 1967).…”

Detection of latent pernicious anaemia in iron-deficiency anaemia.

“…This observation has been pursued by investigating the incidence of gastric antibody in 76 relatives of six of the patients with latent pernicious anaemia and in 72 relatives of five of the patients without latent pernicious anaemia. Ten of the 76 relatives of the latent-pernicious-anaemia propositi possessed the gastric antibody in their serum, but only two of the 72 relatives of propositi without latent pernicious anaemia possessed the gastric antibody, a difference which is statistically significant (P<0.05) (McFadyen et al, 1966). Te Velde et al (1964) found the gastric antibody in 20% of a large group of relatives of patients with pernicious anaemia compared with 6 % in a control series.…”

The Effect of Iron Stores on Gastric Acid Secretion by Rats

“…Existing observations suggest that iron deficiency and its consequent anaemia may result in pathological changes in gastric mucosa including gastritis and gastric atrophy which in turn may lead to reduced secretion of gastric acid (Davidson and Markson, 1955; Badenoch, Evans and Richards, 1957) but Valberg, Taylor, Witts and Richards (1961) were unable to find any significant pathological change in gastric mucous membranes of iron deficient rats. The most striking reduction in gastric acid has been observed in those patients described as having idiopathic microcytic hypochromic anaemia with circulating antibodies to parietal cells (Shearman, Delamore and Gardner, 1966; Dagg, Goldberg, Anderson, Beck and Gray, 1964;MacFadyen, Goldberg, Dagg and Anderson, 1965). Patients with iron deficiency anaemia due to blood loss and without circulating antibodies to parietal cells have shown lesser degrees of hypochlorhydria (Shearman et al, 1966;Dagg et al, 1964).…”