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than 3 g/dl but were haemodynamically stable (5 had iron deficiency anaemia, 1 had malaria, and in the remaining 2 the cause of anaemia was undetermined); these 2 had signs of mild respiratory distress, 1 with malaria and the other with a chest infection and malaria. None of these died. In addition we gave blood to 6 children who did fulfil these criteria: 5 (15-6%) with falciparum hyperparasitaemia (> 10%) in have documented of a in which we Hb, anticipation precipitous drop in such patients, and 1 with an Hb of 3-5 g/dl who was in a poor clinical condition. Thus, on an intention-to-treat basis (including the immediate deaths), we would have transfused 36% of children with an Hb less than 5-1 g/dl and we found a mortality of 6%. We emphasise the importance of clinical signs and not haemoglobin values in decisions about criteria for blood transfusion. Although the recommendation to transfuse children with an Hb of less than 5 ’0 g/dl if there is respiratory distress and less than 3-0 g/dl if there is not, is a reasonable starting point, it would have still led us to transfuse a considerable number of children (especially older children with iron deficiency anaemia) who were easily managed conservatively. A further consideration in decisions about which, if any, level of haemoglobin should form part of the criteria of transfusion is that Lackritz and colleagues’ findings are based on capillary Hb values, which in our experience can be up to 1 ’4 g/dl lower than in venous samples; most African hospitals (when they have accurate means of measurement) use venous samples. Furthermore, some situations such as malaria hyperparasitaemia are not covered by these criteria. The most important message from their timely paper is surely that we must define transfusion guidelines based on simple clinical criteria that can be used under a wide range of conditions by all health care personnel, whatever their

clinical experience. C. NEWTON K. MARSH N. PESHU I. MWANGI

This analysis would be followed by reassessment, further analysis, and action. One of the strategies chosen might be monitoring of growth, but only if it is culturally acceptable, is likely to be well done by trained and motivated workers who have adequate time and resources, and the mothers and communities are able to participate. You outline reasons why growth monitoring as commonly practised has not been successful and suggest that "the separate contribution of growth monitoring to the effectiveness of child health programmes" had not been documented. It is true that very little well-designed research to evaluate this monitoring has been conducted. One of the presentations in Nyeri did address this issue. The study was conducted in rural south India, and in the context of

of interventions, including primary health care, showed no added benefit resulting from the use of growth charts, even though growth was monitored well.’’There is a need for further studies of this type in other cultural settings and also for operations research, as you suggest. a set

Division of Nutritional Sciences,

SABU GEORGE MICHAEL LATHAM NANCY GEREIN JENNY CERVINSKAS

Savage Hall, Cornell University, Ithaca, NY 14853, USA, CIDA, Hull, Canada, and IDRC, Ottawa, Canada

monitoring: intermediate technology or expensive luxury? Lancet 1985, ii: 1337-38. 2. Grant JP. The state of the world’s children. London: Oxford, 1985 3. Rohde JE. Editorial Ind J Paed 1990; 55: S1-S2. 4 Anon. Growth promotion, not growth monitoring. Lancet 1992; 339: 1409. 5. George SM, Latham MC, Abel R. Effectiveness of growth monitoring in Indian villages. FASEB J 1992; 6: 1498. 6 George SM, Latham MC, Abel R. Successful growth monitoring in south Indian villages. In: Proceedings of the Nyeri Colloquium on Growth Promotion for Child Development" Ottawa: IDRC (in press). 1 Editorial. Growth

C. R. J.

Kilifi Research Unit. Kenya Medical Research Institute. PO Box 426, Kilifi, Kenya

The practice of SIR,-In your July

growth monitoring

18 editorial

(p 149) you cite the opinion ot

the

international colloquium held in Nyeri, Kenya, in participants May, 1992. We were the organisers of that colloquium on growth promotion for child development. We agree that the question raised by the title of a 1985 Lancet editorial-"Growth monitoring: intermediate technology or expensive luxury?"-is still relevant.’1 We are pleased that you raise important questions on the current practice of growth monitoring. Our concern, however, is that you tend to equivocate, and you cite UNICEF documents that are now outdated. The Nyeri colloquium was preceded by a UNICEF workshop on monitoring of growth held in Nairobi in May, 1992, which considered the findings of the eight country evaluations on the practice of such monitoring and reached consensus on how to promote the growth of children. At these meetings, it was emphasised that growth monitoring should not be advocated as a global strategy-but nutrition-oriented measures for growth promotion should be. Poorly implemented programmes have sometimes been used as an alibi for not implementing better nutrition strategies. The workshop also recommended that growth monitoring should no longer be promoted as an "entry point" to improve the functioning of health systems. Monitoring of growth has a long history of enthusiastic promotion,2 and sometimes also of strong advocacy3 and bloated rhetoric. The Nyeri colloquium was convened because we recognised there was little scientific proof for the effectiveness of this monitoring. The available evidence was reviewed. The main outcome of the meeting has been included in the Nyeri declaration on growth promotion for child developmentwhich suggests that growth promotion programmes should, almost always, include assessment based on information from the mother, the community, and the health workers. Furthermore, dependent on local conditions and availability of resources, possible strategies were suggested. The declaration emphasised that the information from these assessments should lead to an analysis of the factors influencing growth and this in turn should lead to advice and action. at an

Possible genomic imprinting in familial adenomatous polyposis SiR,-In the report by Ms Cottrell and colleagues (Sept 12, p 626), we note that of the 21 familial adenomatous polyposis (FAP) patients in the three illustrated pedigrees, 11inherited the gene from the father, 6 from the mother, and the parental origin of 4 could not be ascertained. These data are in line with trends seen in our polyposis registry. Among a total of 294 ascertained FAP patients, 127 (43%, 63 male, 64 female) inherited the APC gene from the father, 115 (39%, 56 male, 59 female) from the mother (p 0-09, x2-test), and 52 (8, also evenly divided) were first cases. As a measure of intensity of phenotypic expression, we examined inheritance of FAP in those who also had desmoid disease. Of 37 such patients, 23 (62%, 11 male, 12 female) inherited the APC gene from the father and 14 (38%,4 male, 10 female) from the mother (p=0-25). We are now collaborating with another polyposis registry to enlarge the sample size of patients with this rare disease. The small differences we showed are compatible with the frequency of genomic imprinting in Huntington’s chorea and myotonic dystrophy.’1 =

Department of Surgery, New York Hospital Cornell Medical Center, New York 10021, USA

CATHERINE C. COSTELLO JEROME J. DECOSSE

1. Hall HG. Genomic imprinting review and relevance to human diseases

Am JHum

Genet 1990, 46: 857-73

Pre-pregnancy clinics for diabetic women SIR,-Dr uregory ana rroiessor i attersau (Sept iz, p 656 review many of the logical and scientific arguments for prepregnancy care of diabetic women, noting that reduction in congenital malformations is only one of at least six aims of such care. However, they base their decision not to institute a pre-pregnancy clinic on their view that the overall congenital malformation rate is no different in centres with or without such clinics. For many reasons, including differences in populations, methods of defining abnormalities, and, especially, methods of ascertainment, it is difficult to compare congenital abnormality rates from different centres. If a junior doctor in Edinburgh had looked out the notes of all diabetic women whose pregnancies had continued beyond 24

Possible genomic imprinting in familial adenomatous polyposis.

918 than 3 g/dl but were haemodynamically stable (5 had iron deficiency anaemia, 1 had malaria, and in the remaining 2 the cause of anaemia was undet...
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