EXPERIMENTAL SIDEROBLASTIC ANAEMIA.

Abstract

There is increasing evidence that some defect of pyridoxine metabolism is implicated in human sideroblastic anaemia. Some cases of sideroblastic anaemia respond to treatment with pyridoxine although large doses may be necessary. Pyridoxine is known to be a necessary co‐enzyme in the early stages of haem synthesis (Schulman and Richert, 1957; Kikuchi, Kumar, Talmage and Shemin, 1958) and haemoglobin synthesis is impaired in sideroblastic anaemia where hypochromasia exists in the presence of abundant iron stores. Several species of animals develop a hypochromic anaemia when deprived of pyridoxine (Fouts, Helmer and Lepkovsky, 1940; Wintrobe, Follis, Miller, Stein, Alcayaga, Humphreys, Suksta and Cartwright, 1943; Hegsted and Rao, 1945; Kornberg, Tabor and Sebrell, 1945; Luckey, Briggs, Elvehjem and Hart, 1945; Poppen, Greenberg and Rinehart, 1952; Gershoff, Faragalla, Nelson and Andrus, 1959; Mirone and Jackson, 1959; Harriss, 1963; Shen, Wong and Oguro, 1964) but it is not clear from these reports whether the animals showed ‘ring’ sideroblasts and other features characteristic of human sideroblastic anaemia. In order to investigate more fully the relationship between sideroblastic anaemia and pyridoxine metabolism, we have attempted to reproduce in experimental animals a condition similar to the anaemia seen in man.Pyridoxine deficiency was produced in animals by feeding a diet deficient in pyridoxine or by giving drugs known to interfere with pyridoxine metabolism. The use of antituberculous drugs was suggested by the observation of Verwilghen, Lahaye, van Orshoven and Reybrouck (1963) that sideroblastic anaemia occurred in tuberculous patients treated with isoniazid, cycloserine, pyrazinamide and p‐aminosalicylic acid (PAS).