Non-Addisonian Megaloblastic Anemias

It is perhaps surprising that megaloblastic anemia does not occur more frequently after total gastrectomy (Witts, 1962). MacDonald et al. (1947) traced 46 patients who had lived for three years or more after total gastrectomy and who were not known to have received prophylactic liver therapy. Only 12 patients had anemia of a pernicious type. This had seldom developed within 2 years, and two patients survived 10 and 20 years, respectively, without anemia. Witts compares these periods with the time (2 to 38 months) taken for idiopathic pernicious anemia to relapse after cessation of liver therapy (Schwartz and Legere, 1944). He remarks that cessation of substitution therapy in established pernicious anemia thus produces a prompter and more constant effect on blood formation than does complete removal of the stomach. This is perhaps because substitution therapy in the patients with pernicious anemia had not been intensive enough to maintain normal concentrations of vitamin Bi2 in the liver and other tissues. 

One would expect these megaloblastic anemias to respond to vitamin Bi2, and this is normally the case. But in one patient megaloblastic anemia developing two years after total gastrectomy responded poorly to Bi2 and quickly to folic acid (Conway and Conway, 1951). 

Megaloblastic Anemias Associated with Intestinal Strictures, Blind 

Megaloblastic anemia may follow operations or diseases which lead to stenosis or blind loops in the small intestine, or anastomosis of the small with the large bowel. The essential feature in most cases is an area of stagnation in the small intestine. Experimental anemia in the rat (Watson et al., 1948) and a hypothesis are discussed on page 143. In the rat antibiotics were effective, and so was folic acid, but not vitamin B12. 

Some 60 cases from the literature have been reviewed by Cameron et al. (1949). This included most of the series previously reviewed by Barker and Hummel (1939). A few other cases have been encountered by Thompson and Ungley (to be published). The patients usually responded well to liver extract or to vitamin B12 by injection, although one had failed to respond to as much as 400 pg. of B12 daily by mouth (Fig. 8). Concentrations of B12 in the serum were low in five of seven cases listed by Mollin and Ross (1954). Subacute combined degeneration may occur even though the gastric juice contains free hydrochloric acid. 

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