- Email: [email protected]
Influence of necropsy on clinical practice
indeed assist homosexuals in the USA their campaigns for the inclusion of homosexuality in equal opportunity laws. We find it troubling that some scientists such as Hamer and LeVay decline to consider the possible impact of their research in societies outside the USA.’I The present debate ignores the fact that discrimination against homosexual people is not based on rationality. The accepted premises of homophobic policies and indeed homophobic feelings and behaviour cannot be falsified or eliminated by empirical data.5 Indeed, the only reasonable use of the results of genetics research into the causes of homosexuality is to develop screening devices, and to use these to establish whether a fetus is likely to be a homosexual
homosexuality might advance
to
person.
Homosexual people had reason to consider as insulting research that tries to show a biological causation for homosexuality. The real question is: is there ethically anything wrong with a choice that would result in homosexual people? We believe not.’ We think that the quest into what determines sexual orientation should not take place in societies that are deeply homophobic. Hamer’s suggestion that his results should not be used against homosexual people seems strange in today’s society. We cannot see that his findings could be used in any other way at present. A US National Institute for Sexual Health, should it ever come to be, would do well to support research into the causes of homophobia and possible ways to reduce its disastrous impact on homosexual people, instead of sponsoring fanciful and potentially socially dangerous research into the genetics of sexual orientation.
Figure: Correlation of annual necropsy rate primary disease diagnosis coincidence
with the lack of
correlation with non-coincidence of the primary disease diagnosis for the period examined is shown in the figure. The slight differences in the necropsy rate over the years correlated with the tendency for a decline in noncoincidence, but the period of observation does not allow a definitive conclusion. On the other hand, during the same period, some advanced technologies were adopted in our diagnostic units.
*Ljubomir S Kovachev, Evlogi
E
Marinov, Petrana A Christova
Departments of *General Surgery, Pathology, and Public Health, Higher Medical Institute, 5800 Pleven, Bulgaria
Little
arrows
Udo Schüklenk, *Michael Ristow
SiR-Waldron (Dec 2, p 1475)’ describes
Monash
attribute their chronic ill health to acute exposure to environmental chemicals, although they have no abnormal signs, and their biochemical and haematological profiles are normal. He finds himself unable to support their belief, though unable to refute it-the classic toxicologist’s dilemma.2 He suspects somatoform disorder as the underlying problem, and notes that the patients should be protected against unscrupulous physicians and charlatans. With the latter warning we must all agree. Patients of exactly this type present frequently to allergists; their problems attract some publicity and have earned the dubious epithet of "total allergy syndrome" from the news media. Although this term irks us immunologists immensely, there is no doubt that the numbers of these patients are increasing, and that their suffering is real. A subset of those who satisfy the criteria for chronic fatigue syndrome (CFS) also attribute the onset of their illness to an acute chemical exposure, and in this group I agree with Mane that "the illness may be triggered by one factor and promoted by another". This belief of the patients is not to be ridiculed; there are known biochemical pathways to explain the association, and normal biochemical and haematological indices merely tell us that we are looking in the wrong place for enlightenment. Most of us protect ourselves against xenobiotics through the cytochrome P450 oxidase enzyme systems of the liver and other organs, but the P450 system is itself susceptible to damage from carbon monoxide, hydrogen cyanide, and other common hazards.’ Once damaged, it is easy to see how further chemical exposures, at milder doses, could keep the system perpetually off balance, leading to a long-term sensitivity state in which the original chemical plus many other ambient chemicals would no longer be tolerated. A similar progression is seen in post-teargas asthma, which can remain troublesome years after the initial gassing and, in its later stages, can be provoked by exertion, cold air, tobacco fumes, and car exhaust fumes.’
University, Centre for Human Bioethics, Clayton, Australia; and *University Hospital Bergmannsheil Bochum, PO Box 100250, 44702 Bochum, Germany
1 Editorial. Inquiring into sex. Lancet 1995; 346: 1309. 2 Lautmann R ed. Homosexualität—Handbuch der Theorie—and Forschungsgeschichte. Frankfurt: Campus, 1993. 3 Schüklenk U, Ristow M. Sollte Forschung nach den Ursachen der Homosexualität stattfinden? Ethik Med 1995; 7: 71-86. 4 Billings P. Genetic discrimination and behavioural genetics: the analysis of sexual orientation. In: Fujiki N, Macer DRJ, eds. Intractable neurological disorders, human genome, research and society. Proceedings of the third international bioethics seminar in Fukui, Nov 19-21, 1993. Christchurch, Tsukuba: Eubios Ethics
Institute, 1994: 37. 5 Schuklenk U, Ristow M. The ethics of research into the
causes
of
homosexuality. J Homosex (in press).
Influence of necropsy
on
clinical practice
discrepancies between clinical diagnosis and findings influenced by necropsy rates? We did a retrospective analysis of the necropsy and clinical records for 256 of 289 (88-5%) patients who died at the department of general surgery, 1989-94. Their mean age was 60 (27-89) years. Of these, 189 patients (65%) were admitted as emergencies, and necropsy was not done on 24 (12%). 15 (5%) patients were admitted in a terminal phase of their disease. During the first 24 h after admission, 38 (13%) patients succumbed; 114 (40%) patients died in intensive SiR-Are
necropsy
care.
In 256 necropsies, clinical diagnosis was correct in 233 for the primary disease; for other major diseases correct diagnosis was made in 148 (58%). Complications of primary disease were correctly diagnosed in 192 (66%). Agreement of necropsy findings with clinical diagnoses was found in ten of 16 patients who died a sudden unexpected death (62-5%). The influence of annual necropsy rate in
(91%)
patients
who
267
homosexuality might advance
to
person.
Homosexual people had reason to consider as insulting research that tries to show a biological causation for homosexuality. The real question is: is there ethically anything wrong with a choice that would result in homosexual people? We believe not.’ We think that the quest into what determines sexual orientation should not take place in societies that are deeply homophobic. Hamer’s suggestion that his results should not be used against homosexual people seems strange in today’s society. We cannot see that his findings could be used in any other way at present. A US National Institute for Sexual Health, should it ever come to be, would do well to support research into the causes of homophobia and possible ways to reduce its disastrous impact on homosexual people, instead of sponsoring fanciful and potentially socially dangerous research into the genetics of sexual orientation.
Figure: Correlation of annual necropsy rate primary disease diagnosis coincidence
with the lack of
correlation with non-coincidence of the primary disease diagnosis for the period examined is shown in the figure. The slight differences in the necropsy rate over the years correlated with the tendency for a decline in noncoincidence, but the period of observation does not allow a definitive conclusion. On the other hand, during the same period, some advanced technologies were adopted in our diagnostic units.
*Ljubomir S Kovachev, Evlogi
E
Marinov, Petrana A Christova
Departments of *General Surgery, Pathology, and Public Health, Higher Medical Institute, 5800 Pleven, Bulgaria
Little
arrows
Udo Schüklenk, *Michael Ristow
SiR-Waldron (Dec 2, p 1475)’ describes
Monash
attribute their chronic ill health to acute exposure to environmental chemicals, although they have no abnormal signs, and their biochemical and haematological profiles are normal. He finds himself unable to support their belief, though unable to refute it-the classic toxicologist’s dilemma.2 He suspects somatoform disorder as the underlying problem, and notes that the patients should be protected against unscrupulous physicians and charlatans. With the latter warning we must all agree. Patients of exactly this type present frequently to allergists; their problems attract some publicity and have earned the dubious epithet of "total allergy syndrome" from the news media. Although this term irks us immunologists immensely, there is no doubt that the numbers of these patients are increasing, and that their suffering is real. A subset of those who satisfy the criteria for chronic fatigue syndrome (CFS) also attribute the onset of their illness to an acute chemical exposure, and in this group I agree with Mane that "the illness may be triggered by one factor and promoted by another". This belief of the patients is not to be ridiculed; there are known biochemical pathways to explain the association, and normal biochemical and haematological indices merely tell us that we are looking in the wrong place for enlightenment. Most of us protect ourselves against xenobiotics through the cytochrome P450 oxidase enzyme systems of the liver and other organs, but the P450 system is itself susceptible to damage from carbon monoxide, hydrogen cyanide, and other common hazards.’ Once damaged, it is easy to see how further chemical exposures, at milder doses, could keep the system perpetually off balance, leading to a long-term sensitivity state in which the original chemical plus many other ambient chemicals would no longer be tolerated. A similar progression is seen in post-teargas asthma, which can remain troublesome years after the initial gassing and, in its later stages, can be provoked by exertion, cold air, tobacco fumes, and car exhaust fumes.’
University, Centre for Human Bioethics, Clayton, Australia; and *University Hospital Bergmannsheil Bochum, PO Box 100250, 44702 Bochum, Germany
1 Editorial. Inquiring into sex. Lancet 1995; 346: 1309. 2 Lautmann R ed. Homosexualität—Handbuch der Theorie—and Forschungsgeschichte. Frankfurt: Campus, 1993. 3 Schüklenk U, Ristow M. Sollte Forschung nach den Ursachen der Homosexualität stattfinden? Ethik Med 1995; 7: 71-86. 4 Billings P. Genetic discrimination and behavioural genetics: the analysis of sexual orientation. In: Fujiki N, Macer DRJ, eds. Intractable neurological disorders, human genome, research and society. Proceedings of the third international bioethics seminar in Fukui, Nov 19-21, 1993. Christchurch, Tsukuba: Eubios Ethics
Institute, 1994: 37. 5 Schuklenk U, Ristow M. The ethics of research into the
causes
of
homosexuality. J Homosex (in press).
Influence of necropsy
on
clinical practice
discrepancies between clinical diagnosis and findings influenced by necropsy rates? We did a retrospective analysis of the necropsy and clinical records for 256 of 289 (88-5%) patients who died at the department of general surgery, 1989-94. Their mean age was 60 (27-89) years. Of these, 189 patients (65%) were admitted as emergencies, and necropsy was not done on 24 (12%). 15 (5%) patients were admitted in a terminal phase of their disease. During the first 24 h after admission, 38 (13%) patients succumbed; 114 (40%) patients died in intensive SiR-Are
necropsy
care.
In 256 necropsies, clinical diagnosis was correct in 233 for the primary disease; for other major diseases correct diagnosis was made in 148 (58%). Complications of primary disease were correctly diagnosed in 192 (66%). Agreement of necropsy findings with clinical diagnoses was found in ten of 16 patients who died a sudden unexpected death (62-5%). The influence of annual necropsy rate in
(91%)
patients
who
267