This report describes a 26 year old woman, of Pakistani origin, who presented five months postpartum with severe megaloblastic anaemia as a result of nutritional folate deficiency. This case was unusual in that a small number of myeloblasts were present in the peripheral blood at presentation, and this circulating population temporarily increased in size when folate replacement was begun. We also highlight the need to recognise the non-linear relation between haematocrit and red blood cell folate concentration when the haematocrit is very low (< 0.15) and emphasise the importance of the clinical history.T he 20th century saw important and fundamental advances in our understanding of the pathogenesis and treatment of the megaloblastic anaemias. In 1926, Minot and Murphy 1 discovered that pernicious anaemia, a previously fatal disease, could be treated by the ingestion of liver. Vitamin B12, which is the vitamin responsible, was subsequently isolated in 1948.2 3 Folic acid, originally called Wills's factor, was discovered in 1931 when Dr Lucy Wills, 4 studying nutritional anaemias in India, observed that the macrocytic anaemia of pregnancy was more common in poorer women and was corrected by dietary supplements of yeast or yeast extract (Marmite). Seventy years later, megaloblastic anaemia still holds surprises.
CASE REPORT Presenting featuresA 26 year old woman, originally from Pakistan and living in the UK for two years, presented feeling extremely weak and tired. At the time of presentation she was five months postpartum and continuing to breast feed her healthy son. She was a vegetarian but ate very little. Her main food source was chapattis, which she ate with no accompaniments, and very small amounts of fruit. The patient had been taking ferrous sulfate (200 mg daily) for 10 months because normochromic normocytic anaemia had been noted during pregnancy. No haematinic assays were performed at this time. There was no other relevant past medical history. Physical examination revealed no abnormalities except a tachycardia and extreme pallor.Investigations included a full blood count, which revealed: haemoglobin (Hb), 28 g/litre; mean cell volume (MCV), 100 fl; no reticulocytes present; white blood cell count (WBC), 1.4 × 10 9 /litre (neutrophils, 0.3 × 0 9 /litre), and platelets 16 × 10 9 /litre. Blood film examination showed gross anisopoikilocytosis, tear drop poikilocytes, and basophilic stippling of erythrocytes. A small population of myeloblasts was identified in the peripheral blood (fig 1A-C). In addition, circulating megaloblasts were easily found (fig 1D), although there was no neutrophil hypersegmentation. The bone marrow aspirate was hypercellular. Erythropoiesis was greatly expanded, left shifted, and megaloblastic. Granulopoiesis was also hyperplastic and giant metamyelocytes were present. There was no excess of myeloblasts. The bone marrow trephine specimen was hypercellular at 95% with loss of fat spaces. The hyperplastic, left shifted erythroid series was again prominent. Occasional giant metamye...