Causes of "natural" sudden death Why the government ... - Europe PMC

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2 Health and Safety Commission. Ef'cis on health of exposure to asbestos. London: HMSO. 1985. Causes of "natural" sudden death. SIR,-The important paperĀ ...
the relative risks of passive smoking as distinct from total attributable risk. Though total attributable risk mav guide overall policy, it is, in our experience, relative risk that is the most useful way of discussing and explaining risks at work. Later Dr Delamothe compares the relative risks of asbestos and passive smoking in just this way. He confuses, however, the relatively high historic risks of working with asbestos with the very low risks of occupying a building containing asbestos in its structure. It is exposure to asbestos from occupying a building, not working with asbestos, that was estimated to be 50-100 times less risky than passive smoking in the review prepared by Doll and Peto for the Health and Safety Commission.' I agree that there is a risk and that action is needed, but the risk needs careful statement and the action must be practicable. J T CARTER Health and Safetv Executive, London 'W2 4TF I Delamothe T. Passive guidelines on smoking. Br Med 7 1988; 297:1565. (17 December.) 2 Health and Safety Commission. E f'cis on health of exposure to asbestos. London: HMSO. 1985.

Causes of "natural" sudden death SIR,-The important paper by Dr Anthony C Thomas and others' on causes of "natural" sudden death rightly emphasises the preponderance of cor(onary heart disease. Among the 24 cases of norA-ischaemic heart disease there were no cases of sarcoid heart disease. Perhaps this is due to the comparatively small sample and geographical variation. Sarcoid is not a rare cause of sudden death.2" Of the first 300 cases of sarcoid heart disease we have collected in the United Kingdom, 49 presented as sudden death and were first diagnosed at a coroner's postmortem examination. In an additional 28 known cases death was sudden, making a total of 77 sudden deaths. Among those presenting in this way there was an emphasis on young men and there were 17 men below the age of 45 and 12 below the age of 35 years. Twenty eight cases were in East Anglia. My experience of coroners' postmortem examinations is similar to that of the authors, and indeed the true diagnosis in several cases was obtained only by my reluctance to accept the first verdict and my insistence on seeing the pathological material myself. Many pathologists' preoccupation with coronary artery disease as a cause of sudden death not infrequently leads to the illogical verdict of "ischaemic heart disease with normal coronary arteries" and a failure to look further. Reviews of sudden death4' make no reference to sarcoidosis. The postmortem diagnosis will often need a scrupulous examination, but if sarcoid heart disease is not even considered it is unlikely that it will be uncovered. I would simply make the plea that in any review of causes of sudden death it should be mentioned-albeit to report a negative. HUGH A FLEMING

Cambridge CB2 2AS I Thomas AC, Knapman PA, Krikler DM, Davies M1. Community study of the causes of "natural" sudden death.

BrMedj 1988;297:1453-5. (3 December.) 2 Fleming HA, Bailey SM. Sarcoid heart disease-report of 197 UK cases with necropsy confirmation in 62. J R Coll Physicians Lond 1981;15:245-53. 3 Fleming HA. Death from sarcoid heart disease, United Kingdom series 1971-1986, 300 cases with 138 deaths. In: Grassi C, et al, eds. Sarcoidosts and other granulomasous disorders. Amsterdam: Excerpta Medica, 1988:19-33. 4 World Health Organisation. Sudden cardiac death. WHO Tech Rep Ser 1985;No 726. 5 Kannel WB, Schatzkim A. Sudden death: lessons from subsets in population studies. 7Am Coll Cardsol 1985;5:1418-9B.

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6 MicCabe WC, Morganroth J. Sudden death revisited. CardiovascularMedtctne 1985;10:10-4. 7 Campbell RWF. Sudden death. Current Opinion in Cardiology 1987;2:13-8. 8 Buxton AE. Sudden cardiac death. Ann Intern Med 1986;104: 716-7.

Why the government will not abolish the Medical Practices Committee SIR,-Recent parliamentary concern at the condition of some doctors' premises and criticism of the Medical Practices Committee in the national press are linked.' For all citizens to have reasonably equal access to doctors it is necessary for doctors to be equally distributed between attractive and less attractive areas. To achieve this the state had two options: (a) compulsory direction of doctors or (b) inducement payments in the least attractive areas. Instead the Medical Practices Committee was created and the profession was given the power to decide where new entrants to general practice could become NHS principals. Since all doctors had the same contract with the state, they could all be paid roughly similar sums without regard to local conditions or individual professional skills. Unfortunately in some areas both the cost of living and consequently practice expenses were much higher than elsewhere. The inevitable crisis came in 1965, leading to the direct reimbursement of the largest expense items as a means of resolving the problem of high expenses, but the cost of living was ignored. This led to demands for a London weighting, later inner city, allowance. All three of these are inducement payments by another name. The unresolved problems of 1965 are surfacing again. If the profession stopped directing our young colleagues (through the Medical Practices Committee) on behalf of the state then the state would have no alternative but to make some areas more attractive than others financially. London weighting, etc, would then cease to be a cause of conflict at the conference of local medical committees and would become the responsibility of government. Members of the Medical Practices Committee are senior principals elected and selected by other principals, but those whom they control are only aspirant principals and so have no voice in their appointment -hardly a democratic arrangement. The Medical Practices Committee's continued existence is assured because (a) it directs labour, normally impossible in a democracy in peacetime, and (b) it saves the government a lot of money. So the state will continue to give legitimacy to what elsewhere would be an unlawful restrictive practice. DAVID PARSONS London SE4 1XF I Beecham L. From the GMSC. Br Med J 1989;298:54. (7 Januarv.)

Pet birds as a risk -factor for lung cancer SIR,-Drs Peter A Holst and others' suggest that keeping birds is an independent risk factor for lung cancer. Their assumption is made on the basis of 49 patients included in the study. They propose that inhalation of avian antigens causes macrophage dysfunction and a consequential decrease in both humoral and cellular immunity. Two of the references given to support this hypothesis2" do not make the claims ascribed to them by the authors. McSharry et al described a decreased peripheral (rather than a local) humoral response

to pigeon antigens in exposed subjects who smoked. Daniele et al mentioned extrinsic allergic alveolitis (hypersensitivity pneumonitis) and its effect on the cellular and soluble constituents of bronchoalveolar lavage fluid, without claiming any immunosuppressive effect. Drs Holst and others do not mention whether any patients had bird breeder's lung, the numbers and species of birds kept, or, indeed, the methods of husbandry used. Our own work suggests that there is no such impairment of either cellular or humoral immune responses in pigeon breeders with or without symptoms (S P Reynolds et al, seventh European congress on diseases of the chest, Dublin, 1988).4 Indeed, our more recent data indicate the reverse to be true-that is, values of bronchoalveolar lavage interleukin-1, interleukin-2 fibronectin, and immunoglobulins (specific and non-specific) are raised in the lung of both patients with the disease and some symptomless patients. The finding of greatly increased numbers of activated effector cells in the bronchoalveolar lavage fluid of bird breeders with symptoms (S P Reynolds et al, seventh European congress on diseases of the chest, Dublin, 1988)6 is not in keeping with the concept that such people are in some way

immunocompromised. K P JONES

J H EDWARDS Department of Microbiology, University of Wales College of Medicine, Cardiff CF4 4XN S P REYNOLDS B H DAVIES

Asthma and Allergy Unit, Sully Hospital, Penarth, South Glamorgan I Holst PA, Kromhout D, Brand R. Pet birds as an isdependent risk factor for lung cancer. Br Med J 1988;297:1319-21. (19 November.) 2 McSharry C, Banham SW, Boyd G. Effect of cigarette smoking on the antibody response to inhaled antigens and the prevalence of extrinsic allergic alveolitis among pigeon breeders. Clin Allergy 1985;15:487-94. 3 Daniele RP, Elias JA, Epstein PE, Rossman MD. Bronchoalveolar lavages: role in the pathogenesis and management bf interstitial lung disease. Ann Intern Med 1985;102:93-108. 4 Reynolds SP, Jones ED, Jones KP, Edwards JH, Davies BH. A study into the effects of direct and indirect challenge on bronchoalveolar lavage fluid findings in pigeon breeder's disease. In: Grassi C, RizzatoG, Pozzi E, eds. XI world congress on sarcoidosis and other granulomatous disorders, Milan, 6-11 September 1987. Amsterdam: Elsevier Science Publishers, 1988:675-9. (Excerpta Medica international congress series No 756.) 5 Reynolds SP, Jones KP, Davies BH. The value of soluble immune proteins in the assessment of interstitial pulmonary disease. Thorax 1988;43:239-40. 6 Costabel U, Bross KJ, Ruhle KH, Lohr GW, Matthys H. Ia-like antigens on T-cells and their subpopulations in pulmonary sarcoidosis and in hypersensitivity penumonitis. Am Rev RespirDis 1985;131:337-42.

That condor moment? SIR,-The recent observation by Dr Hoist and his colleagues' that keeping pet birds may increase the risk of developing lung cancer is clearly important. It may now be germane to investigate whether this factor shows the same kind of synergy with tobacco smoking that can be shown for asbestos exposure. We suggest that someone should investigate those populations of rural Iceland, the Faroes, and the outer isles of Scotland whose members were once in the habit of alleviating the harsh conditions of the northern winter by smoking young gannets. E W BENBOW R W STODDART D M A MANN

Department of Pathology, University of Manchester, Manchester M 13 9PT 1 Holst PA, Kromhout D, Brand R. Pet birds as an independent risk 'factor for lung cancer. Br Med J 1988;297:1319-21. (19 November.)

BMJ VOLUME 298

14 JANUARY 1989