Megaloblastic Anaemia during Primidone Therapy

B A R B I T U R A T E S have been widely used for many years in the treatment ofepilepsy but megaloblastic anaemia attributable to them has only once been recorded (Hobson et at., 1956). Since the structurally related phenytoin and primidone have been used as anticonvulsants either alone or in combination with barbiturates, megaloblastic anaemia has become an increasingly recognised complication of this type of therapy. Kidd and Mollin (1957) refer to twenty-four cases in the literature and describe two of their own. Further cases are reported by Barker (1957), by Volterra and Romualdi (1957) and recently by Hawkins and Meynell (1958). The mechanism by which megaloblastosis is induced by such drugs is unknown, but reported observations support the belief that in some way deficiency of vitamin BIP or folic acid may develop. Serum vitamin B,, assays were carried out in ten of the previously recorded cases (Badenoch, 1954; Rhind & Varadi, 1954; Girdwood, 1956; Geydell, 1957; Kidd & Mollin, 1957; and Hawkins & Meynell, 1958). Only the two cases reported by Kidd and Mollin (1957) showed subnormal values and even so their Case 1 failed to react to vitamin B,, but responded completely to folic acid, their Case 2 being diagnosed post mortem. Patients who have responded satisfactorily to vitamin B,, therapy but in whom the serum level of this substance was normal or was not assayed include one of Badenoch's cases (1954), Case 1 of Ryan and Forshaw (1955), Case 1 of Geydell (1957), Case 2 of Newman and Sumner (1957), Cases 1 , 3, 4, 5 and 6 of Hawkins and Meynell (1958) and those mentioned briefly by Richards (1956). We present details of this patient as she appears unique in that she had a very low serum vitamin BIZ level before treatment and responded clinically and haematologically to this substance.