95 FAILURE OF PREVENTIVE MEDICINE?
SIR,-Since the objective of "preventive medicine" is
prove the health of the general public and not to secure legislation, I do not understand why Dr Muir Gray (Dec. 24/31, p. 1338) cites a dearth of legislation as evidence of failure. Even on this basis, however, his case is a poor one. There has been a mass of recent legislation seeking to improve the health of the public. The fact that measures have been introduced piecemeal is irrelevant. The old Public Health Acts to which he refers were consolidating Acts which tidied up a great deal of legislation which had been introduced in much the same way as today’s. Parliament is now so hard pressed that it has little time for such consolidating Acts. Nevertheless, it has passed legislation such as the Abortion Act, Health and Safety at Work Act, Toxic Waste Disposal Act, and Prevention of Pollution Act, all of which contribute to the promotion of health of the public. In the long term, actions such as the promotion of family-planning services and the cleaning up of the environment may prove more important for the survival of our species than dissuading the young from enjoying the pleasures of food and fornication, cigarettes and cognac. If Dr Gray is seeking only to prove that linguistic differences are an important factor in the failure of the health educational programmes devised by members of social classes 1 and 2 to influence members of social classes 4 and 5, he has a case which few would dispute. But then he would surely have chosen a more suitable title. It is as important for community medicine as it is for clinical medicine to define proper objectives. Only when you know what your target is can you assess whether you are heading towards it. When we seek to reduce dependency, handicap, and pain, we are on firm ground. All would agree that these are sound objectives. The assumption that promotion of longevity is desirable or widely desired is as unwarranted as is the assumption that an earlier death from coronary thrombosis or carcinoma of bronchus will involve more pain and disability than the later alternatives. We are mortal and must die sooner or later. Many young people, having seen old people endure years of arthritic pain, poverty, squalor, and social isolation, may actively choose to enjoy a short life rather than endure a long one. We cannot measure pain, misery, or happiness, and so cannot study them scientifically to show whether the bargain offered is a good one or
I suspect that differences in outlook and
objectives are as important as linguistic differences in determining responses to health education. I do not know whether the proper objectives of community medicine should give precedence to the long-term survival needs of our species or to the shorter-term aims of minimising dependency, handicap, and suffering. I am sure, however, that unless we start pursuing more appropriate objectives than "longevity" and "prevention of (specified) disease", we will be doing a disservice both to our discipline and to mankind. Today many people appreciate that, in a world facing problems of overpopulation and resource depletion, it is quality of life not quantity which we need. In this they are ahead of the medical establishment, who would indeed be well advised to do a little more fundamental thinking. Scunthorpe Health District, Scunthorpe DN15 8DT.
J. S. ROBERTSON
the ferrous form. Ha’m iron derived from foods of animal origin may be converted to haemin (Fe+++) which can be directly absorbed by the mucosal cell. Medicinal iron, however, is always in the ferrous form (usually as the sulphate, gluconate or fumarate salt) and is readily absorbed without the need for endogenous gastric acid or exogenous ascorbic acid, a common but unnecessary ingredient in many commercial preparations of oral iron. Queens Hospital Center, Jamaica, N.Y. 11432, U.S.A. and Health Sciences Center, S.U.N.Y
COMMON FAMILIAL COMPONENT IN LUNG CANCER AND CHRONIC OBSTRUCTIVE PULMONARY DISEASE
SIR,-On behalf of the Johns Hopkins Pulmonary Epidemiology Group I thank Dr Orie and his colleagues’ for drawing our attention to their significant observations,2 which we regret having missed in our literature search, and Dr Lynch and his colleagues3 who recorded their pedigree study confirming "a common thread" in lung cancer and chronic obstructive pulmonary disease (C.O.P.D.). Despite differences in design and data source, the family-history data from these two investigations are not only compatible with, but also support our finding of a common familial component in lung cancer and C.O.P.D.4 Although the Groningen and Omaha studies are retrospective, Lynch’s observation3 of an association between the frequency of C.O.P.D. and increasing genetic relationship ("co-ancestry") to lung-cancer probands in twelve lung-cancer pedigrees and the Dutch workers’ findings2 that 89% of cancer patients had a positive personal history of chronic non-specific lung disease (C.N.S.L.D.) and 77% had a positive family history of C.N.S.L.D. compared with 33-35% of neighbourhood controls are consistent with our pulmonary-function tests of firstdegree relatives of cases (lung cancer and C.O.P.D.) and controls. While the many reports of coexistence of lung cancer and chronic lung disease in the same individual (e.g., lung cancer and bullous diseases and bronchogenic carcinoma and emphysema,6 especially centrilobular7) had been suggestive, inability to distinguish their sequence of onset precluded inferences as to cause and effect. Now, however, we have evidence for the increased occurrence of pulmonary dysfunction in the family members of lung-cancer cases.2-4 Further studies by the Johns Hopkins group (unpublished)-including analysis of our findings with other adjustments (e.g., socioeconomic status) in addition to the ones already used; with single ascertainment per family to avoid unequal contribution by any one kindred; and by considering relatives separately by type of family relationship--confirm the previously reported excess of aberrancy in forced expiration in relatives of lung cancer and c.o.P.D. cases.
These pulmonary-function data on family members and controls permit the conclusion not only that there is "a very strong positive correlation between C.N.S.L.D. and squamous cell lung cancer" and that C.N.S.L.D. is likely "prerequisite for the development of the carcinoma"2 but also that airflow limitation as determined by simple spirometry may be an essential element in the process. Thus, our model postulating a common familial component shared by lung cancer and C.O.P.D. with the ultimate clinical manifestations dependent upon one or more cofactors4 is sup-
CIMETIDINE AND IRON ABSORPTION
SiR,-Dr Esposito’ suggests that cimetidine reduction of acid secretion may interfere with the absorption of medicinal ferrous sulphate. This seems unlikely in view of the fact that gastric acidity reduces dietary iron from the ferric to
R. Lancet, 1977, ii, 1132.
1. Orie, N. G. M., Sluiter, H. J., van der Wal, A. M. Lancet, 1977, ii, 1138. 2. van der Wal, A. M., Huizinga, E., Orie, N. G. M., Sluiter, H. J., de Vries, K. Scand. J. res. Dis. 1966, 46, 161. 3. Lynch, H. T., Guirgis, H. A., Harris, R. F. Lancet, 1977, ii, 815. 4. Cohen, B. H., and others ibid. p. 523. 5. Stoloff, I. L., Kanofsky, P., Magilner, L. Archs envir. Hlth, 1971, 22, 163. 6. Bedrossian, C. W. M. Cancer Bull. 1972, 24, 102. 7. Anderson, A. E., Jr., Foraker, A. G. Cancer, 1974, 33, 1017
ported by retrospective data of other investigators and our own cross-sectional and retrospective data. To determine whether the relationship of pulmonary dysfunction to lung cancer is
MARKER CHROMOSOME IN MULTIPLE MYELOMA AND PLASMA CELL LEUKAMIA
the temporal sequence of development must be examined. In a longitudinal, follow-up study we are trying to clarify the role of pulmonary impairment, the common familial component(s), and the cofactors, along with the natural history of C.O.P.D. and lung cancer. We hope that others will undertake similar studies. Only through such efforts can these complex interrelationships be understood and intervention and prevention procedures for both C.O.P.D. and lung cancer be made more rational.
Department of Epidemiology, Johns Hopkins University School of Hygiene and Public Health, Baltimore, Maryland 21205 U.S.A.
*24 h culture without phytohsemaggtutinin. no. 14 chromosomes
t7 metaphases showed that both 14q+ markers.
BERNICE H. COHEN
support the proposal of McCaw et al.12 that genes on chromosome 14 are involved in the regulation of lymphoid cell
findings MARKER CHROMOSOMES IN MULTIPLE MYELOMA AND PLASMA-CELL LEUKÆMIA
SIR,-Various types of chromosomal abnormalities have been detected in the malignant cells of patients with lymphoproliferative disorders—e.g., Burkitt’s lymphoma,1-3 Hodgkin’s
disease,4and malignant lymphomas.s
An abnormal chromosome 14 with extra bands at the end of the long arm (14q+) has been observed very frequently. There are only two previous reports6·’ of this 14q+ marker in multiple myeloma (two patients) and plasma-cell leukaemia (1 patient). We have found a 14q+ marker chromosome in bone-marrow cells of three myeloma patients and in the peripheral blood leucocytes of one patient with plasma-cell leuksEmia, out of a total of twenty-two patients with myelomatosis. The chromosomes were analysed by quinacrine fluorescence.8 Patients 1 and 2 had IgG-kappa type myelomas and patient 3 an IgA-lambda type. All three patients had high concentrations of serum-paraproteins (7-92, 6.24, and 6-80 g/dl, respectively) when bone-marrow aspirates were taken for chromosome examination. Patient 4 had plasma-cell leukaemia with an IgA-kappa-type paraprotein level of 1.32 g/dl (about 5 times higher than normal). The cytogenetic data for these four patients (see table) showed that they all had a hyperdiploid clone in which the 14q+ marker had a high frequency. In the diploid cells both no. 14 chromosomes were normal. In some cells from patient 4, both no. 14 chromosomes were replaced by 14q+ markers. Patient 2 had trisomy 13 and trisomy 15, whereas patient 1 had trisomy 15 as well as the 14q+ markers. There were no changes in the total number of chromosomes in the D group of patients 3 and 4. The origin of the extra band at the end of the 14q+ markers could not be determined because of the complex nature of the chromosomal rearrangements.’ However, a translocation between chromosomes no. 11 and 14 (t[ll;14] [q23;q32]) was detected in patient 4. The clinical details and the complete chromosomal analysis for these patients will be reported elsewhere. The 14q+ chromosome is consistently present in various types of lymphoid cell malignancies but not in the myeloproliferative disorders. The assumption that 14q+ is a common cytogenetic marker in lymphoid disorders is supported by the high proportion of myeloma patients with a large acrocentric marker chromosome found by conventional methods.9-11 Our Manolov, G., Manolova, Y. Nature, 1972, 237, 33. Zech, L., Haglund, U., Nilsson, K., Klein G. Int. J. Cancer, 1976, 17, 47. McCaw, B., K., Epstein, A. L., Kaplan, H. S., Hecht, F. ibid. 1977, 19, 482. Fukuhara, S., Shirakawa, S., Uchino, H. Nature, 1976, 259, 210. Fleischman, E. W., Prigogina, E. L. Hum. Genet., 1977, 35, 269. Wurster-Hill, D. H., McIntyre, O. R., Cornwell III, G. G., Maurer, L. H. Lancet, 1973, ii, 1031. 7. Philip, P. Hereditas, 1975, 80, 155. 8. Rowley, J. D. Blood, 1976, 48, 1. 9. Tassoni, E. M., Durant, J. R., Becker, S., Kravitz, B. Cancer Res. 1967, 27, 1. 2. 3. 4. 5. 6.
806. 10. Itani, S.,
Hoshino, T., Kawasaki, S., Nakayama, S. Acta hæm. Jap. 1970, 33, 54. 11. Dartnall, J. A., Mundy, G. R., Baikie, A. G. Blood, 1973, 42, 229.
proliferation. We thank Dr John Hopper for patient’s samples. W.L. was a postdoctoral trainee supported by National Research Service Award T32, USPHS GM 7190. Franklin McLean Memorial Research and Department of Medicine,
WEITZE LIANG JANET D. ROWLEY
University of Chicago, Chicago, Illinois 60637, U.S.A.
DUPLICATION OF PART OF CHROMOSOME NO. 1 IN MYELOPROLIFERATIVE DISEASES seen a patient with myelofibrosis transforminto acute ing myeloblastic leukaemia who had a duplication of the distal part of the long arm of chromosome no. 1 in bonemarrow cells.’ Fifteen patients with blood disorders who had either trisomy 1 or duplication of part of this chromosome in bone-marrow and/or abnormal blood-cells have- previously been described.2-9 In these patients, although the duplicated
of duplicated part of chromosome and/or abnormal blood-cells.
1 in bone-marrow
Only q23-25 (shadowed) is duplicated in all patients. part of chromosome
1 was of variable length, there was of the chromosome, q23-25 (see figure), only portion that was duplicated in all. The diagnosis in seven patients was polycythaemia vera, three had myelofibrosis either initially or one
B. K., Hecht, F., Harnden, D. Sci. U.S.A. 1975, 72, 2071.
G., Teplitz, R. L. Proc.
Gahrton, G., Friberg, K., Lindsten, J., Zech, L. Hereditas (in the press). Nowell, P., Jensen, J., Gardner, F., Scott, M., Chaganti, R. S. K., German, J. Cancer, 1976, 38, 1873. 3. Oshimura, M., Hayata, I., Surabhi, K., Sandberg, A. ibid. p. 748. 4. Rowley, J. D. ibid. 1975, 36, 1148. 5. Rowley, J. D. Proc. natn. Acad. Sci. U.S.A. 1975, 72, 152. 6. Warburton, D., Bluming, A. Blood, 1973, 42, 799. 7. Westin, J., Wahlström, J., Swolin, B. Scand. J. Hæmat. 1976, 17, 183. 8. Wurster-Hill, D., and others. Sem. Hemat. 1976, 13, 13. 9. Yamada, K., Furusawa, S. Blood, 1976, 47, 679.