1026 All ten convalescent sera had specific antibody to KHFV with titres equal to or greater than 1:4096 with the antigens in rat and Apodemus lung and A-549 cells, which are consistent only with specific infection by a virus serologically identical to KHFV. Acute-phase sera from two patients in their first week of disease gave titres of 1:128 and 1:256; in both patients titres rose to 1:8192 by the fourth week of convalescence. The single acute-phase serum on the eleventh patient had an antibody titre of 1:256. These findings-a 32-fold rise in specific antibody titres in paired sera from two patients and the unusually high titres in the ten convalescent sera-are diagnostic of Korean hsemorrhagic fever. of Central Nervous
Laboratory N.I.N.C.D.S.,
System Studies,
National Institutes of Health, Bethesda, Maryland 20205, U.S.A. Virus Research Institute, Hupeh Medical College,
P. W. LEE
C. J. GIBBS, JR D. C. GAJDUSEK
Wu-Chang, Hupeh, People’s Republic of China Virology Laboratory, VA Medical Center,
C. M. HSIANG
West Haven, Connecticut
G. D. HSIUNG
understand why femorosaphenous arteriochosen for vascular access for the eight patients on regular dialysis described by Dr Nordling and his colleagues (April 5, p. 765). However, they do not explain why they gave anticoagulants. Anticoagulation of arteriovenous fistulse is rarely practised in dialysis patients, especially in the presence of high-pressure large-vessel nstulae. It is not surprising that hsematomas were recorded in four patients, and we wonder if the two fatal bleeding episodes could have been related to inadequate hxmostasis following anticoagulation. Use of femorosaphenous and like arteriovenous fistulas should be a rare event. After shunt surgery these patients should be regularly assessed with a view to re-establishment of arteriovenous Sstulae in the forearm or antecubital fossa. Junior doctors and nurses should be trained to preserve the forearm veins in the non-dominant arm, and this drill should start whilst the renal failure patient is being nursed in intensive care or in medical, surgical, and nephrology units.
SIR,-We
can
fistulas
Sefton General
Liverpool L15
were
Hospital, 2HE
RASHEED AHMAD BERYL LARGE
were interested to read, in that letter by Dr Nordand colleagues, of two cases of fatal bleeding following the creation of arteriovenous fistula;, and would like to report a similar case. A 34-year-old female with chronic renal failure due to analgesic nephrocalcinosis underwent five operations for establishment of an arteriovenous fistula at the wrist between January, 1975, and January, 1976. In March, 1976, a subcutaneous arteriovenous graft was established in the left thigh using a bovine carotid ’Artegraft’ (Johnson & Johnson). The graft was arranged in a straight configuration from the left common femoral artery to the left popliteal vein. She started on haemodialysis 2 weeks later. 6 months following the placement of the graft she presented with congestive cardiac failure and a pericardial effusion. Her cardiac output was 5-1Vmin/m2, and flow studies of the graft gave a value of 2.21/min. The flow through the graft was reduced to between 300 and 400 ml/min by partial ligation of the graft; she improved clinically and was discharged to haemodialysis at home. In January, 1977, she bled massively from the graft after haemodialysis. Her husband unsuccessfully attempted to con-
SIR,-We
ling
to
abnormalities. In a review to be published in the British Journal of Surgery, P. J. Guillou, S. H. Leveson, and R. C. Kester examined the nature and incidence of complications in over 86 arteriovenous grafts of both biological and synthetic types; we have now abandoned biological grafts for hsemodialysis because of the severe problems. The choice of graft would seem to lie between reinforced expanded PTFE (’Gore-Tex’) or a ’Dac-
ron’ velour graft (’Microvel’, ’Vasculour II’). Department of Surgery, St James’s University Hospital, Leeds LS9 7TF
K. R. WEDGWOOD R. C. KESTER
MATERNAL DIET AND PROLACTIN
VASCULAR ACCESS IN HÆMODIALYSIS venous
hsemorrhage with a tourniquet and she died en route hospital. Necropsy revealed a 3 mm perforation in the graft, probably at a cannulation site, there being no other vascular trol the
p. 623) throw inthe mechanisms through which poor maternal nutrition may affect the duration of lactational amenorrhoea. Demographic and epidemiological studies in developing countries have consistently shown an inverse association between indices of maternal nutrition and the length of lactational amenorrhoea.1-4 It was generally thought that the mechanism(s) were behavioural rather than physiological. It was assumed that poorly nourished women had less access to supplementary food for their infants and therefore breast fed more frequently and intensely than well nourished women did. The higher frequency and intensity of suckling was thought to stimulate prolactin release, leading to a more profound suppression of ovarian function.2 However, the observations of Lunn et al. suggest that, although prolactin levels changed strikingly from season to season or after maternal dietary supplementation, there was no concomitant alteration in the frequency of breastfeeding. This would indicate a physiological mechanism. However, one should not exaggerate the effects of maternal nutrition on lactational amenorrhoea and certainly one would not, as suggested by Lunn et al., expect a significant increase in fertility as a result of maternal nutritional programmes since the effects on post-partum sterility are likely to be small. For instance a longitudinal study in Bangladesh’ showed that the average duration of amenorrhoea in poorly nourished women with a body weight less than 38.5 kg was 17.9 months as compared with 16-8 months in well nourished women who weighed more than 42.4 kg. Another Bangladesh study,2 which used weight for height as an index of nutrition, found that the median duration of amenorrhoea was 21.2 months in the lowest nutritional group and 20.2months in women with the highest nutritional status. Similarly,’ in Guatemala,’ undernourished women with a mean weight of 43.7 kg had amenorrhoea for 14.8months, whereas better nourished with a mean weight of 55-6 kg experienced women amenorrhaea for an average of 13.22 months. Nutritional differentials probably only account for 1-1.5 months of additional amenorrhoea in these populations, and this is only a small fraction of the total birth interval, which
SiR,-Dr Lunn and colleagues (March 22,
teresting
1.
new
light
on
Chowdhury AKMA. Effect of maternal nutrition on fertility in rural Bangladesh. In: Mosley WH, ed. Nutrition and human reproduction. New York:
Plenum Press, 1978: 401-09. 2. Huffman SL, Chowdhury AKMA, Chakraborty J, Mosley WH. Nutrition and post-partum amenorrhœa in rural Bangladesh. Popul Stud 1978; 32: 251-60. 3. Bongaarts J, Delgado H. Effects of nutritional status on fertility in rural Guatemala. In: Menken J, Leridon H, eds. Natural fertility. Liège: Ordina Editions, 1979: 107-33. 4. Chavez A, Martinez C. Nutrition and development of infants from poor rural areas. III: Maternal nutrition and its consequences on fertility. Nutr Rep Int 1973; 7: 1-8.