usually exhibit ring forms in the secondary or hereditary types.From the initial marrow sample the diagnosis of primary sideroblastic anaemia was suggested by the presence of numerous ring-sideroblasts at all stages of erythrocyte maturation. At first the megaloblastic changes were attributed to folate deficiency, in association with primary sideroblastic anaemia. This opinion was revised at an early stage, however, in view of the Schilling test, serum B12, and antibody results, which were characteristic of pernicious anaemia. The persistence of sideroblastic change in the marrow despite folate therapy and a response to vitamin B12 suggested a concurrent primary sideroblastic anaemia.The case illustrates the importance of investigating all cases of macrocytic anaemia by iron staining of the marrow together with estimation of the serum B12 and folate levels. The possibility that megaloblastosis and sideroblastosis may be due to separate conditions, as in this case, should be considered particularly when associated with a sub-optimal response to adequate B12 replacement therepy.
AcknowledgmentsWe wish to thank Dr Eric Jackson for advice and permission to publish details of the case, also Professor M. S. Losowsky and Roger Hall for their helpful criticism. Thanks also to Marion Stainthorpe and Mrs Brenda Day for secretarial assistance.