Megaloblastic Anaemia Due to Anticonvulsants

SiR,-With reference to the several cases of megaloblastic anaemia due to anticonvulsants published in the British literature in recent years, we would like to report briefly on a case of ours, the first in the Italian literature and possibly the first discovered on the Continent. A 33-year-old farmer with a history of a severe anaemia of one and a half years' duration, resistant to liver and iron therapy and repeated blood transfusions, was found on admission to our hospital to have such severe anaemia as to require transfusion by the admitting physician. Next day the patient, who had high fever (38°-39° C.), showed the following blood picture: Hb, 25% ; R.B.C., 1,670,000; W.B.C., 2,200; haematocrit 13. There were numerous hyperchromic megalocytes and plurisegmented neutrophils. The bone marrow presented megaloblasts in nests, with all the forms of maturation represented. Gastric content was free from HCI, which, however, was demonstrable after histamine. After treatment with vitamin B12 the patient had a very modest and temporary reticulocyte increase (up to 4.5 % for a few days) without effect on the anaemia and the fever. A total of 1,750 ml. of blood was administered within 15 days with very little improvement (Hb 34%). Folic acid administration, 15 mg. intramuscularly every second day, provoked a prompt and marked reticulocyt crisis (up to 34% at the sixth day) with remission of fever and anaemia. When the patient was discharged his blood picture was as follows: Hb, 76% ; R.B.C., 3,500,000; W.B.C., 7,500. Folic acid was then continued by mouth. Four months later the patient had Hb, 98%; R.B.C., 4,640,000; W.B.C., 5,600. This patient, an epileptic, had been treated with phenobarbitone, and for five years since 1950 with primidone. This case closely corresponds to those published in the British literature.-We are, etc.,