ing to make secular or cross cultural comparisons between large epidemiological datasets for children. The rapidly developing epidemic of adult obesity in most.
BMI (kg/m2)
Editorials
36 34
99.6
32 98
30 28
91
26
75
24
50
22
25
20
9
18
2 0.4
16 14 12 10 8 -1 0
2
4
6
8
10
12
14
16
18
20
22
Age (years)
Body mass index centiles for boys (those for girls are very similar)
ing to make secular or cross cultural comparisons between large epidemiological datasets for children. The rapidly developing epidemic of adult obesity in most affluent nations, and the consequent need to be able to monitor changing levels of fatness in children, gives urgency to the debate. This prompted the World Health Organisation International Obesity Task Force (IOTF) to work with the European Childhood Obesity Group (ECOG) to formulate a solution. The group, under the chairmanship of Professor Bill Dietz from Boston, is still considering its recommendations.5 At first sight the problem seems readily soluble. We simply need to choose a reference population and define some appropriate centile cut offs. However, this raises several problems. First is the inevitable political tussle about which population might best be used as the reference. In this respect the United States, whose National Center for Health Statistics’ growth curves have dominated paediatrics for many years, is surely out of the running since it leads the world in obesity. The possibility of generating a globally pooled database has been examined.
This reveals that the morphometric differences in the timing of height and weight growth among some populations (especially among Asiatics and South Americans) generate very different patterns of body mass index which could create serious anomalies in classification of obesity at certain ages. Aggregated centiles which exclude some of the atypical growth curves will shortly be published. Second, and most importantly for epidemiologists, is the problem of monitoring change over time. If growth curves are regularly updated to account for secular changes in nutrition then 10% of the population will always be above the 90th centile. To overcome this it is necessary to identify a reference dataset collected at a specified time. Ideally this would be several decades ago, before the serious emergence of obesity, but this is not essential. The Child Growth Foundation charts could be used to make both retrospective and prospective comparisons of secular change pegged to the British 1990 measurements. Alternatively the forthcoming IOTF charts could be chosen, but whatever the choice it is important to establish a reference fixed in time. Third is the problem of identifying health based cut offs for categorising obesity and underweight. In adults these are based, albeit crudely, on known risk ratios for different levels of body mass index. No such data exist for children. A possible solution to this dilemma has been suggested by the IOTF/ECOG working group.5 It involves identifying the centiles corresponding to the adult cut offs of 20, 25, and 30 kg/m2 and extrapolating back to childhood. The validity of this approach is currently being explored in a variety of datasets from around the world. The solution to these issues is by no means trivial, and the IOTF/ECOG recommendations are awaited with interest. Andrew M Prentice Head of energy metabolism MRC Dunn Clinical Nutrition Centre, Cambridge CB2 2DH
1
2
3 4 5
International Obesity Task Force. Obesity: preventing and managing the global epidemic. Report of WHO consultation on obesity, Geneva, 3-5 June 1998. Geneva: WHO, 1998. Child Growth Foundation. BMI charts. UK cross-sectional reference data: 1990/1. Available from Child Growth Foundation, 2 Mayfield Avenue, London W4 1PW. Cole TJ, Freeman JV, Preece MA. Body mass index reference curves for the UK, 1990. Arch Dis Child 1995;73:25-9. Cole TJ, Green PJ. Smoothing reference centile curves: the LMS method and penalized likelihood. Stat Med 1992;11:1305-19. Dietz WH, Robinson TN. Use of the body mass index (BMI) as a measure of overweight in children and adolescents. J Pediatr 1998;132:191-3.
Prophylactic mastectomy: deliverance or delusion? We don’t know, so we need to start registering all cases now
T
o prophesy the future we no longer need to examine the entrails of sacrificial animals. Mutant genes predisposing affected individuals to life threatening conditions such as vascular disease and malignancy have been identified. Although the multifactorial and environmental wild cards remain, the genetic card deck is gradually being laid face up on the table. But without effective interventions, knowledge of genetic risk may serve only to fuel anxiety and encourage the adoption of denial behaviour. 1402
Germ line genetic mutations are responsible for only 5-10% of cases of breast cancer, but worried individuals form a disproportionately large part of the clinical workload. Almost half the cases of familial breast cancer and 75% of those with both ovarian and mammary malignancy are due to BRCA1 mutations, located on chromosome 17q21.1 The 185delAG mutation is present in 1% of Ashkenazi Jewish women and in 21% of those developing breast cancer before the age of 40.2 The other major breast cancer susceptibility gene is BMJ VOLUME 317
BMJ 1998;317:1402–3
21 NOVEMBER 1998
www.bmj.com
Editorials BRCA2, located on chromosome 13q12-q13, encoding a 3418 aminoacid protein of, at present, unknown function.3 The lifetime risk of cancer in women carrying a BRCA1 pathogenic mutation, previously estimated at 90%,4 5 has been revised down to 56%.6 Breast surgeons will nevertheless be faced with an increasing number of well informed young women with pathological mutations. These consultations are as difficult for the doctor as for the patient since no proved preventive approaches exist. Though options such as tamoxifen will probably reduce the incidence, none will obliterate the risk.7 Intensive surveillance is an option but without proof of benefit. Many women will want to resort to the more desperate measure of bilateral prophylactic mastectomy, believing that this will save their lives.8 For some this may prove to be a vain hope. Prophylactic mastectomy was performed on a large number of women in the United States for a range of ill defined indications. The Subcutaneous Mastectomy Data Evaluation Center collected information from 1500 treated women with varying indications for surgery and reported that 6% had unsuspected ductal carcinoma in situ or invasive disease.9 Hartmann et al carried out a retrospective cohort analysis of 950 women who underwent prophylactic mastectomy at the Mayo Clinic in 1980-93.10 The Gail model predicted 76 cancers during the mean 17 years of follow up whereas the actual number was 7. The original “high risk group” was not well characterised so that the risk of breast cancer may have been overestimated. In the absence of any evidence of benefit, it is now assumed that this same operation will be the answer to the genetically endangered maiden’s prayer. In the Sprague-Dawley rat/DMBA model system removal of ostensibly 100% of the mammary tissue had no effect on subsequent development of neoplasms.11 Breast cancers evolved in all animals, possibly because of the difficulty in removing all subcutaneous mammary tissue. While it could be argued that the diffuse nature of rat breasts makes this a poor model, such problems may also occur in humans with sanctuaries from surgery located in the inferior aspect and the axillary tail. Unless action is taken, another 10 years will see us in the same state of ignorance. While a randomised trial could compare subcutaneous and total mastectomy, in reality the current prejudices of both patients and doctors would probably inhibit accrual. Only a legally binding system of registering all women who have undergone any kind of prophylactic mastectomy
could help determine the relative efficacy of the procedure in high risk individuals. At present no mechanism exists since these individuals do not have cancer and therefore are not reported to cancer registries and only some will have undergone counselling and testing in specialist cancer genetics units.12 Moreover, the present patchy nature of the links between NHS clinical genetics and breast surgery units, with inequalities of service provision and waiting lists, means that many women are driven into the private sector. Breast and plastic surgeons may not be depended on to report their cases as, even under optimal circumstances, they are likely to misremember. Pathologists, who have shown their ability to report cancer cases to registries accurately, constitute a more reliable source. Were all cases of prophylactic mastectomy to be reported to a central registry linked to cancer registries, individuals subsequently diagnosed with breast cancer could be identified. The price of inactivity will be high. Prophylactic mastectomy will be otherwise a lottery like procedure in which there will be no winners. Ian S Fentiman Professor of surgical oncology Guy’s Hospital, London SE1 9RT
1
Miki Y, Swensen J, Shattuck-Eidens D, Futreal PA, Harshan K, Tavtigian S, et al. A strong candidate for the breast and ovarian cancer susceptibility gene BRCA1. Science 1994;266:66-71. 2 Fitzgerald MG, MacDonald DJ, Krainer M, Hoover E, O’Neil E, Unsal H, et al. Germ-line BRCA1 mutations in Jewish and non-Jewish women with early onset breast cancer. N Engl J Med 1996;334:143-9. 3 Wooster R, Bignell G, Lancaster G, Swift S, Seal S, Mangion J, et al. Identification of the breast cancer gene BRCA2. Nature 1995;378:789-91. 4 Ford D, Easton DF, Bishop DT, Narod SA, Goldgar DE and the Breast Cancer Linkage Consortium. Risks of cancer in BRCA1 mutation carriers. Lancet 1994;343:692-5. 5 Porter DE, Cohen BB, Wallace MR, Smythe E, Chetty U, Dixon JM, et al. Breast cancer incidence, penetrance and survival in probable carriers of BRCA1 gene mutation in families linked to BRCA1 on chromosome 17q12-21. Br J Surg 1994;81:1512-5. 6 Struewing JP, Hartge P, Wacholder S, Baker SM, Berlin M, McAdams M, et al. The risk of cancer associated with specific mutations of BRCA1 and BRCA2 among Ashkenazi Jews. N Engl J Med 1997;336:1401-8. 7 Powles TJ, Hardy JR, Ashley SE, Farrington GM, Cosgrove D, Davey JB, et al. A pilot study to evaluate the acute toxicity and feasibility of tamoxifen for prevention of breast cancer. Br J Cancer 1989;60:126-33. 8 Holzgreve W, Beller FK, Niedner W, Niehaus H. Bilateral subcutaneous mastectomy as a prophylactic operation to prevent breast cancer. Breast Dis 1989;2:27-33. 9 Pennisi VR. Subcutaneous mastectomy data: a final statistical analysis of 1500 patients. Aesth Plast Surg 1989;8:15-21. 10 Hartmann L, Jenkins R, Schaid D, Yang P. Prophylactic mastectomy (PM): preliminary retrospective cohort analysis. Proc Am Assoc Cancer Res 1997;38:1123. 11 Wong JH, Jackson CF, Swanson JS, Palmquist MA, Oyama AA, Miller SG, et al. Analysis of the risk reduction of prophylactic partial mastectomy in Sprague-Dawley rats with 7,12-dimethylbenzanthracene-induced breast cancer. Surgery 1986;99:67-71. 12 Genetics and cancer services. Report of a working party for the chief medical officer. London: Department of Health,1996.
The “professional cleansing” of nurses The systematic downgrading of nurses damages patient care Personal view p 1463
BMJ 1998;317:1403–4
BMJ VOLUME 317
A
ll readers of this editorial will be looked after by a nurse at some time in their lives. For the vast majority the experience will be a pleasant and rewarding one—unlike that outlined by Hamon (p 1463).1 My initial response to her personal view was a series of depressing questions. Why would nurses who have received a rigorous and systematic education 21 NOVEMBER 1998
www.bmj.com
be party to such poor quality of care? How could professionals, trained to give high quality of care, allow standards to slide so far? How could nurses go home each evening and be content with what they have done and seen in the name of modern health care? I cannot defend the poor practices reported, but there are explanations. 1403
