441 her Alzheimer’s disease she talks about the value to her of support groups "... for us to have someone with whom we can relate, someone walking the same bridge we are walking". Research undertaken by Keady2 from the University of Wales in Bangor with a cohort of patients from the Bristol memory disorders clinic confirms that "... sufferers viewed the provision of memory groups/clubs as an essential part of their ability to adapt positively to the changes they were going through." In a follow-up study that I am conducting I have also become aware of the importance to the person with dementia of being able to share their emotions and fears with someone who empathises. The focus of emotional support in dementia care has for many years centred on the carer, and it should now widen to include also the person with dementia. In the same issue of The Lancet Dean comments (p 1497) that "... a more open approach [to telling people that they have dementia] will require more emotional support and counselling." Dementia spans many disciplines. It is essential that we take a wider perspective of the care offered to the person with dementia than merely that of the medical model. Jane Gilliard School for Policy Studies (Centre for Health and Social Care) and *Department of Care of the Elderly, University of Bristol, Blackberry Hill Hospital, Bristol BS16 2EW, UK 1 McGowin DF. Living in the labyrinth. Cambridge: Mainsail Press, 1993. 2 Keady J, Nolan M, Gilliard J. Listen to the voices of experience. J Dementia Care 1995; May/June: 15-17. Amyloidosis in Alzheimer’s disease SIR—Buée and others (July 1, p 59) provide partial supporting evidence for our work (April 15, p 956) but miss our overall point. We provided aminoacid sequence data showing that a fragment of apolipoprotein E (apo E) copurified with amyloid )3 (A&bgr;) from senile plaques in a patient with Alzheimer’s disease (AD). Furthermore, we showed that this fragment of apo E can, in vitro, form amyloid-like fibrils that are Congo-red positive. Buee et al have provided evidence confirming that apo E and A&bgr; are complexed, at least in some cases of AD, with a dot-blot technique. Another group have also found apo E and A&bgr; complexed in all cases tested, irrespective of apo E isotype.’ Buee and colleagues suggest that apo E is a risk factor only in a subgroup of AD patients. It has always been our hypothesis that the apo E4 allele acts to accelerate a process that can occur in its absence.2 The point of our observations that an apo E fragment can form amyloid-like fibrils in vitro is that AD can be viewed as both an A(3 and apo E amyloidosis. Critical to amyloid formation is the conversion of a protein from its normal conformation into a predominantly &bgr;-pleated structure. The initiation or further promotion of this fibrillogenesis may be by apo E, possibly other amyloid associated proteins such as apo Al or proteoglycans, and A&bgr; peptides in an amyloid conformer state A&bgr;ac).3 We have proposed that some proteins, such as apo E or A&bgr;, when misfolded, can propagate this misfolding to identical units, either autocatalytically or to other proteins that are induced to fold into the same abnormal conformation.4 Hence in AD there are several different factors that can drive amyloid fibril formation. *Thomas Wisniewski, Bias Frangiorie Department of Pathology, NYU Medical Center, New York, NY 10016, USA 1 Naslund J, Tjernberg LO, Wernstedt C, et al. Characterization of stable complexes involving apolipoprotein E and amyloid-peptide in Alzheimer’s disease brain. Neuron (in press). 2 Wisniewski T, Castaño EM, Golabek A, Vogel T, Frangione B. Acceleration of Alzheimer’s fibril formation by apolipoprotein E in vitro. Am J Pathol 1994; 145: 1030-35. 3 Soto C, Frangione B. Two conformational states of amyloid-peptide: Implications for the pathogenesis of Alzheimer’s disease. Neurosci Lett 1995; 186: 115-18. 4 Wisniewski T, Golabek A, Kida E, Wisniewski K, Frangione B. Conformational mimicry in Alzheimer’s disease: role of apolipoproteins in amyloidogenesis. Am J Pathol (in press). Treatment of acute myeloid leukaemia in pregnancy SIR—Acute myeloid leukaemia (AML) during pregnancy is fortunately a rare event, but one that presents difficulties for mother and fetus. We describe such a case in whom the use of granulocyte colony-stimulating factor (G-CSF) resulted in significant clinical and haematological improvement allowing time for the fetus to mature sufficiently so that a safe delivery could be achieved. A 27-year-old woman presented with severe bone pain during the 26th week of pregnancy. Full blood count revealed: haemoglobin 8-4 g/dL, white-cell count 8.2×109/L with 14% neutrophils and 35% blast cells, and platelets 72×109/L. Bone marrow examination showed 95% replacement by malignant blast cells which were positive for myeloperoxidase and CD13 by flow cytometry, thus confirming a diagnosis of AML (MO subtype). Cytogenetic analysis of the marrow revealed an abnormal clone with karyotype 47 XX, t(6;8), t(7;12), +21. As she was otherwise well we decided to delay specific chemotherapy so that the pregnancy could proceed for as long as possible. A Hickman line was inserted and 1 week later she developed fever in association with a positive blood culture (Staphylococcus epidermidis). By this stage she had become neutropenic (0.72X 109/L). She was treated with antibiotics and filgrastim (G-CSF) in an attempt to control the infection and allow further time for fetal maturation. A 12-day course of filgrastim resulted in the disappearance of blast cells from the peripheral blood and normalisation of the neutrophil count (from 0.7×109/L to a maximum of 7.2×109/L) and platelet count (from 54×109/L to 280X 109/L). Repeat marrow examination disclosed a reduction in blast cell infiltrate from 95% to 55% and a significant improvement in the degree of granulocytic maturation. A caesarean section was done at 32 weeks’ gestation and a healthy baby boy was delivered. Because of satisfactory blood counts, we planned to allow an extended period for wound healing and maternal bonding to occur. However, 4 weeks after delivery blast cells again appeared in the blood and the neutrophil and platelet counts declined. A second course of filgrastim failed to improve the situation again and chemotherapy with idarubicin, cytarabine, and etoposide was instituted. Complete remission was achieved after the first course and, after two more courses of chemotherapy, total body irradiation, and high-dose cytarabine, was followed by peripheral blood stem cell rescue. The patient and her baby remain well with no evidence of leukaemia 5 months after the transplant procedure. There are perhaps only 100 reported cases of spontaneous complete remissions of AML and most of these occur after blood transfusions or during severe bacterial infections.’ It is postulated that viable lymphocytes or natural-killer cells present in whole blood or white cell preparations may possess anti-leukaemic properties, whereas during severe infections a range of cytokines are generated, such as tumour necrosis factor and y-interferon, which may have direct or indirect anti-leukaemic activity. Haemopoietic growth factors are increasingly used in myeloid malignancies in an