FOLATE deficiency, a common occurrence in patients with inflammatory bowel disease,1 , 2 has been ascribed in part to the therapeutic use of sulfasalazine.1 In vitro, this drug is an inhibitor of the intestinal transport of folic acid (pteroylmonoglutamate or PteGlu)1 and of several folate enzymes in the liver.3 However, a clear relation between the use of sulfasalazine (salicylazosulfapyridine) and the development of folate malabsorption and deficiency has not been shown. Previous descriptions of folate deficiency in patients with inflammatory bowel disease failed to distinguish between sulfasalazine users and nonusers.1 , 2 Inhibition of folate absorption by sulfasalazine is presumed to be a cause . . .
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Halsted et al. (1981) studied this question.
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