489 reduced mortality when the incidence of infectious events remain unaltered. The answer may lie in the way incident events are detected and a minimum impact of mild infectious episodes on survival. For example, most studies do not begin to approach the sample size needed to detect differences in incidence of common childhood infections (May 23, p 1302) and Dr Arthur et al (Feb 8, p 361) show that in Ghana the incidence of infectious episodes was unchanged but the severity of disease was greater among placebo recipients. The same was true of the hospital-based measles trials in which all cases began with measles but those treated with vitamin A subsequently had fewer and less severe status

mav

complications.9 I agree with

Gopalan that

there

are

"no miracle

drugs, magic

bullets, and short-cuts in the war against poverty and undemutrition". But we now have more evidence that improving vitamin A status of deficient populations will substantially reduce childhood mortality than we’ve had before embarking on almost any other major public health initiative. A child dies needlessly from vitamin A deficiency every minute, while we await the eradication of

poverty.lO Johns Hopkins School of Hygiene and Public Health, Baltimore, Maryland 21205, USA

Bellagio Brief. Vitamin A deficiency and childhood mortality. New York: Helen Keller International, 1992: 1-8. 2. Sommer A, Tarwotjo I, Djunaedi E, et al, and the Aceh Study Group. Impact of vitamin A supplementation on childhood mortality: a randomized, controlled community trial. Lancet 1986; i: 169-73. 3. Rahmathullah L, Underwood BA, Thulasiraj RD, et al. Reduced mortality among children m Southern India receiving a small weekly dose of vitamin A. N Engl J Med 1990; 323: 929-35. 4. West KP Jr, Pokhrel RP, Katz J, et al. Efficacy of vitamin A in reducing preschool child mortality. a randomized, double-masked community trial in Nepal. Lancet 1991; 338: 67-71. 5. Muhilal, Permeisih D, Idjiradinata Y, Muherdiyantiningsih, Karyadi D. Vitamin A-fortified monosodium glutamate and health, growth, and survival of children. Nutr 1988; 48: 1271-76. Am Clin J 6. Vijayaraghavan K, Radhaiah G, Prakasam BS, Sarma SVR, Reddy V. Effect of massive dose of vitamin A on morbidity and mortality in Indian children. Lancet 1990; 336: 1342-45. 7. Daulaire NMP, Starbuck ES, Houston RM, Church MS, Stukel TA, Pandy MR. Childhood mortality after a high dose of vitamin A in a high risk population. BMJ 1992; 304: 207-10. 8. Sommer A, Tarwotjo I, Hussaini G, Susanto D. Increased mortality in children with mild vitamin A deficiency. Lancet 1983; ii: 585-88. 9. Coutsoudis A, Broughton M, Coovadia HM. Vitamin A supplementation reduces measles morbidity in young African children: a randomized, placebo-controlled, double-blind trial. Am J Clin Nutr 1991; 54: 890-95. 10. Humphrey JH, West JP Jr, Sommer A. Vitamin A deficiency and attributable mortality among under-5-year-olds. Bull WHO 1992; 70: 225-32.

Soft tissue sarcoma, aplastic anaemia, and

pesticides

SIR,-Mrs Brahams (Aug 8, p 363) makes some statements, which if reported correctly, are highly controversial. The expert witness based the case for association between malignant fibrous histiocytic sarcoma and exposure to pesticides on several factors: malignant fibrous histiocytic sarcoma is the rarest subgroup of soft tissue sarcomas, the site is abdominal, and the age was 44. The suggestion that these features are unusual is not in keeping with

experience.’ Malignant fibrous histiocytic sarcoma is the commonest individual type of soft tissue sarcoma, and the abdomen as a site and an age group in the 40s are by no means rare. In a current series of 38 consecutive cases seen in this department, 16 were malignant fibrous histiocytic sarcoma, and 4 were in the abdominal wall. The mean age for the whole group was 50 (range 21-80). Although this disease is more common in older age groups, 44 is by no means exceptional. While not wishing to comment on the specific question of a link between the tumour and pesticide exposure in this case, three of the reasons given would hardly seem to be valid.

more recent

University Department of Surgery, University of Wales College of Medicine, Heath Park, Cardiff CF4 4XN, UK

on

maternity

SIR,—The response of the Royal College of Obstetricians and Gynaecologists (RCOG) to the House of Commons Select Committee report on Maternity Services (July 25, p 233) is disappointing, but not surprising. This Select Committee report contains recommendations based on evidence given by professionals, pressure groups, and clients. Their implementation would mean a great advance in maternity services in the UK. I would comment on some points in the RCOG document. It is certain, as the RCOG states, that for some women, the application of technology is the only means by which they can achieve safe childbirth or a healthy baby. However, the use of technology in all pregnant women is not justified. Several studies have shown that the use of continuous electronic fetal heart rate monitoring in labour increases the frequency of instrumental and surgical delivery without improving perinatal mortality rates;1-3 and epidural analgesia is strongly associated with chronic backache.’ As the select committee states, "intervention in childbirth should be avoided unless there are clear medical indications to the

contrary...". ALFRED SOMMER

1

exposure to

Midwife’s view of reports services

L. E. HUGHES M. I. AHAMED

1 Lawrence W Jr, Donegan WL, Natarajan N, Mettlin C, Beart R, Winchester D. Adult soft tissue sarcomas. a pattern of care survey with the American College of Surgeons. Ann Surg 1987; 205: 349-59.

The RCOG does not seem to agree with the recommendation that women at low risk should be cared for by midwives in the community and referred to the obstetrician at their discretion. However, this system has proved very successful in the Netherlands: perinatal mortality rate in Wormerveer among women who had been cared for only by midwives in the community, and who delivered at home, was 1-3 per 1000 (1969-83);5 by comparison, perinatal mortality in England and Wales in 1990 was 8-1per 1000. The Wormerveer study showed a perinatal mortality rate of 51 7per 1000 among women who had been referred to an obstetrician during pregnancy. From this the RCOG concludes that such a high rate renders the system unacceptable, because there is "either insufficient flexibility or the interface between the two systems is inadequate to deal with them appropriately". Despite this high perinatal mortality the Dutch system seems to be too successful to be dismissed on these grounds. Efforts should be focused on improving communication channels and referral pathways between midwives, general practitioners, and hospital staff, to obtain a system that allows for fast and efficient referral. All pregnant women, independent of their risk category, should indeed have access to an obstetrician. The RCOG seems also to be very concerned about giving women the chance to make their own decisions. However, a system that consists of a predetermined number of hospital antenatal clinic visits and screening procedures does not allow women to make decisions. Care in the community could be a better way to offer women choice. Information about possible forms of care during pregnancy, screening tests available, and place of delivery does not need to be offered by a consultant. Midwives have been trained to, and are capable of, offering this information in an unbiased way. Only in this way will women have the opportunity to make decisions, and consumer choice will be increased. The RCOG states that it cannot promote any systematic move away from hospital delivery, because the element of uncertainty remains, despite good assessment of risk. The College does not seem to accept evidence from other countries showing that perinatal mortality rates are lower than in the UK, despite a very high percentage of home deliveries. The RCOG also states that the loss of babies in women transferred during labour is high. Yet, the Wormerveer study shows that the perinatal mortality rate for women delivered at hospital after referral during labour is 1 1 per 1000.5 I was surprised to note that the RCOG includes only obstetricians in "specialised staff’. May I remind the College that midwives are the specialists in normal pregnancy and labour: "... midwives are at least entitled to ... diagnose pregnancies and monitor normal pregnancies, to carry out examinations necessary for the monitoring of the development of normal pregnancies ... to care for and assist the mother during labour and to monitor the condition of the fetus in utero ... to recognise the warning signs of abnormality... which necessitate referral to a doctor ...".6

490

Evidence from research and mortality and morbidity rates suggests clearly that community-based care and non-intervention management of childbirth in low-risk women is the safest form of care. Moreover, women regard these as the most acceptable forms of care, according to the select committee report. Developing community-based care would "... help engender the belief that pregnancy for most women is a normal event... provide the ability for obstetricians to concentrate on abnormal pregnancies and give continuity of care, which may improve pregnancy outcomes". (Rider ACE, during a lecture at Surrey University, May, 1992). Professionals involved in childbirth should start thinking of what is best for women and their babies, and stop trying to retain control over a process which, after all, belongs only to those affected by

it-pregnant women. Obstetric

Hospital, University College Hospital,

MARIA-JOSE CONTI

London WC1 E 2AU, UK

IM, Parsons RJ, Lawrence GF, Arora SS. An assessment of continuous fetal heart rate monitoring in labour. Am J Obstet Gynecol 1978; 131: 526-32. 2. Wood C, Rain P, Oats J, Farrel E, Beischer N, Anderson I. A controlled trial of fetal heart rate monitoring in a low risk obstetric population. Am J Obstet Gynecol 1981; 141: 527-34. 3. MacDonald D, Grant A, Sheridan-Pereira M, Boylan P, Chalmers I. The Dublin randomized controlled trial of intrapartum fetal heart rate monitoring. Am J Obstet Gynecol 1985; 152: 524-39. 4. MacArthur C, Lewis M, Knox EG. Health after childbirth. London: HM Stationery 1. Kelso

Office, 1991. 5. Van Allen D, Eskes M, Treffers PE.

Midwifery in the Netherlands: the Wormerveer study; selection, mode of delivery, perinatal mortality and infant morbidity. Br J Obstet Gynaecol 1989; 96: 656-62. 6. European Community. Midwives Directive 80/155/EEC article 4.

Vincristine for thrombotic

thrombocytopenic

purpura

SIR,- Thrombotic thrombocytopenic purpura (TTP) is and characterised by consumption thrombocytopenia, fragmentation haemolytic anaemia, renal impairment, neurological deficit, and pyrexia, although not every patient has all these features. Treatment with fresh frozen plasma (FFP) has reduced the mortality from 80% to less than 20%,1-3 but such therapy is not always successful, may be difficult to administer in patients with renal failure, and carries the risk of transmitting viral infections. We report a 52-year-old man with TTP refractory to intensive FFP therapy (at least 4daily for 18 days). After 18 days vincristine was administered: 5 days later the platelet count improved, but fell after a further 6 days. A further bolus of vincristine led to a second response, again at 5 days and followed by clinical improvement. The patient received weekly maintenance vincristine for 3 weeks and rare

remains well 2 years later.4 This reproducible result encouraged us to introduce vincristine for other patients with TTP, and we have now treated 5 patients aged 20-72. All had severe TTP with platelets under 50 x 109/1 (range 4-46), haemoglobin under 12 g/dl (5-5-11-7), and

neurological dysfunction (3 encephalopathy, 1 hemiplegia, 1 seizure); 3 patients required renal dialysis for at least 10 days and 3 had fever. Vincristineinduced disease remission in every patient, all of whom

are

well

at

least 6 months later with

no

residual

neurological or renal impairment. Each patient responded with a rise in platelet count at around 5 days after treatment (figure). Vincristine has been little used for the treatment of TTP; indeed in two reports, only 2 out of 210 patients received this drug.2,3 Anecdotal reports of vincristine’s efficacy’-6 have been treated sceptically because the drug has usually been used with FFP or other therapies. 1-3 Although FFP had been given to 3 of our 5 patients, such treatment had failed in the index case and only small quantities were given to the other 2 cases. Steroids had been given to our index patient and 1 other, but in both for less than 5 days. Therefore neither FFP nor steroids had an important role in achieving remission of TTP in at least 3 of our patients. In contrast, the consistent time from the start of vincristine to the rise in platelet count is compelling evidence that this drug was effective. Furthermore, the fact that improvement in the platelet count predicted clinical improvement in every case confirms the belief that abnormal platelet aggregation is central to the pathophysiology of TTP.

Vincristine therapy for TTP (six treatments in 5 patients):

Drug administered

on

day 0.

First-line treatment for TTP is FFP, preferably by plasmapheresis,2 but we propose that vincristine should also be given at the time of diagnosis. We start with a 2 mg bolus followed by two further injections on alternate days, with assessment of any benefit after 5 days. If the platelet count responds, we continue

vincristine 1 mg every week for

at

least 3 weeks and monitor the

platelet count for evidence of relapse. Vincristine therapy for TTP should be assessed against historical controls, rather than denying patients entered into prospective studies the benefit of this treatment.

Departments of Haematology and Medicine, Royal Shrewsbury Hospital, Shrewsbury SY3 8QR, UK

N. T. J. O’CONNOR M. J. O’SHEA L. F. HILL

Kennedy SS, Zacharski LR, Beck JR. Thrombotic thrombocytopenic purpura. analysis of 48 unselected cases. Semin Thromb Hemost 1980; 6: 341-49. 2. Rock GA, Shumak KH, Buskard NA, et al. Comparison of plasma exchange with plasma infusion in the treatment of thrombotic thrombocytopenic purpura N Engl J Med 1991; 325: 393-97. 3. Bell WR, Brame HG, Ness PM, Kiekler TS. Improved survival in thrombotic thrombocytopenic purpura: hemolytic uraemic syndrome. N Engl J Med 1991; 1

325: 398-403.

4. O’Connor NTJ, Bruce-Jones P, Hill LF. Vincristine therapy for thrombotic thrombocytopenic purpura. Am J Hematol 1992; 39: 234-36. 5. Gutterman LA, Stevenson TD. Treatment of thrombotic thrombocytopenic purpura with vincristine. JAMA 1982; 247: 1433-36. 6. Welborn JL, Emrick P, Acevedo M. Rapid improvement of thrombotic thrombocytopenic purpura with vincristine and plasmapheresis. Am J Hematol

1990; 35: 18-21.

Screening

for

cystic fibrosis carriers

SIR,-A July 25 editorial on carrier screening for cystic fibrosis (CF) compares two strategies-one preconceptional and based in primary care and one aimed at women attending the antenatal clinic. The difficulties that studies of both these strategies have revealed cause you to caution against nationwide adoption of such screening. We agree: neither approach has the merit of cascade screening, starting off with individuals with CF. Carrier screening for any recessive genetic disease requires an adequate level of background knowledge in the population who are offered screening and of self-motivation in wishing to be screened. Cascade testing, starting with individuals with a family history and their spouses, then offering to test the relatives of all those who are positive, allows one to reach a knowledgeable group at increased risk and who are interested in being tested. We have found cascade testing very popular and successful

Midwife's view of reports on maternity services.

489 reduced mortality when the incidence of infectious events remain unaltered. The answer may lie in the way incident events are detected and a minim...
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