953

do so again. Their figures suggest the opposite conclusion. Their best estimate is that 0-8% of all deaths in the Netherlands (1030 in 1990) are caused by life-terminating acts without explicit and persistent request-ie, without the strict criteria for euthanasia being fulfilled, and often without the patient having previously expressed a wish for euthanasia. Euthanasia practised according to the strict criteria accounted for 1-8% of all deaths (2318 in 1990), suggesting that almost one-third of all euthanasia deaths in the Netherlands do not meet strict criteria. This is strong evidence that in practice the criteria are already being informally extended, precisely as predicted by the slippery slope argument, and in a way that leaves the doctors involved open to a charge of murder. In addition, van der Maas et al report that 14% (roughly 935 patients in 1990) of those whose requests for euthanasia were declined had a psychiatric illness. They do not say how or by whom this diagnosis was made, but since psychiatrists were excluded from the study, presumably general practitioners and physicians were responsible. It is well established that psychiatric disorder in the physically ill is common,l and that it is underdiagnosed in general practice2 and in hospital. The possibility therefore arises that at least some of the requests for euthanasia that were subsequently acted upon, arose as symptoms of treatable but undiagnosed psychiatric illness, particularly depression, rather than as rational reactions to serious physical disease. to

University Department of Psychiatry, Royal Edinburgh Hospital,

Edinburgh EH10 5HF, UK 1 2

S. G. POTTS

Derogatis LR, Morrow GR, Fetting J, et al. The prevalence of psychiatric disorder among cancer patients. JAMA 1983; 242: 1504-08. Johnstone A, Goldberg D. Psychiatric screening m general practice. Lancet 1976, i: 605-08.

3.

Maguire GP, Julier DL, Hawton KE, Bancroft JHJ. Psychiatric morbidity referral on two general medical wards. Br Med J 1974; i: 268-70.

and

asthma due to domestic

of

Allergic

use

insulating polyurethane foam SiR,—Hypersensidvity to isocyanates is responsible for most industrial occupational asthma.l,2 But as far as we are aware, there have been no other reports of bronchospasm after domestic use of commercial polyurethane foam for insulating homes. 8 years ago a 38-year-old man had bronchospasm after burning polyurethane packs. After changing jobs, respiratory symptoms disappeared. His most recent complaint was an immediate asthmatic reaction while insulating a window at home with a ployurethane foam; this was followed 24 h later by facial swelling with rash and pruritus while drilling the dry foam. Four months after this acute clinical manifestation, laboratory results showed blood eosinophilia (714 cells/pl) and high levels of specific IgE against isocyanates (6 U for toluene diisocyanate [TD I] and methylenediphenyl diisocyanate [MDI], normal range < 2). Skin-prick tests with common inhaled allergens were negative, but patch tests with the foam and MDIwere strongly positive after 24 h. Patch tests with other isocyanates were negative. The search for non-specific bronchial hyperreactivity was positive for 600 ug of carbachol. A bronchial provocation test, in a 6 m3 cabin with inhalation of 5, then 15, ppb TDI during 20 min remained negative. A realistic test with isolating foam containing 9% free MDI was strikingly positive: after 5 min the patient had severe bronchospasm with a 53% fall in FEVl (forced expiratory volume in 1 s). After subcutaneous terbutaline, FEValmost returned to the initial value. Fifteen months later, specific IgE against isocyanates had increased to 14 and 22-9 U for TDI and MDI, respectively. The patient admitted having slight breathlessness two or three times when painting cars with isocyanate-containing paints. During the realistic test we did not detect any isocyanate release with the spectrophotometric method used (’MDA 7100’); this discrepancy could be explained by particulate rather than gaseous isocyanate release, which could result in underestimates of isocyanate levels.3 This case of immediate bronchial hyperreactivity to an MDIcontaining foam with IgE and cell-mediated sensitisation to the same isocyanate shows the potential danger of domestic use of such polyurethane foams;4 this is especially true for patients with previous occupational or accidental sensitisation to isocyanates.

Specific warning labels should inform potential users. Pneumologie Service, Hopitaux Universitaires de Strasbourg, Hôpital Civil, BP 426, 67091 Strasbourg, France

A. DIETEMANN-MOLARD M. C. KOPFERSCHMITT-KUBLER P. D. MEYER R. TOMB

G. PAULI

1. O’Brien IM, Newmann-Taylor AJ, Burge PS, Hames MG, Fawcett IV, Pepys J. TDI induced asthma inhalation challenge. Tests and bronchial reactivity studies. Clin Allergy 1979; 9: 7-15. 2. Musk AW, Peters JM, Wegman DH. Isocyanates and respiratory disease: current status. Am J Industr Med 1988; 13: 331-49. 3. Brenner KS. Bestimmung von Isocyanaten am Arbeitsplatz: Stand de Technik. Polyurethane world congress, 1987. Proc SPI/FSK 1987: 156-61 4. Peters JM, Murphy RLH. Hazards to health: do it yourself polyurethane foam. Am Rev Respir Dis 1971, 104: 432-33

Cross-contamination and "confirmed" positive anti-HIV results SiR,—The very high sensitivity of the current generation of anti-HIV-1/2 assays can occasionally present difficulty. Specimens for a seroepidemiological study were set aside in the wells of microtitre plates and stored at -30°C before testing for anti-HIV. When they were thawed and tested some of the reactive specimens were observed to be clustered. The rest were scattered singly among the many unreactive specimens in the plates. When the clustered reactive specimens were tested by western blot (WB) some had positive patterns with strongly staining bands and others had positive patterns with weakly staining bands. However, the pattern of the bands on the strongly and weakly stained positive WB of specimens within each cluster were not materially different. To investigate the two sorts of WB-positive specimens further we made ten-fold dilutions in anti-HIV-negative human serum of 16 specimens that stained strongly and 16 that stained weakly, and tested them in the screening assay. The specimens were also tested by IgG antibody capture ELISA (GACELISA) HIV 1/2. In this

anti-HIV-specific immunoglobulin gives a signal proportional to the total immunoglobulin concentration in the specimen. GACELISA is therefore less susceptible than other assays to the effect of contamination of a negative specimen by a small volume of anti-HIV-positive serum. We found (table) that although almost all the anti-HIV reactions detected on screening had been at or near the maximum measurable optical density (OD) and the titres were typically 105 or more in the strongly WB reactive sera, the weakly WB reactive sera only had titres of neat (undiluted) to 10 - 2. Similarly, in the capture assay, the strongly WB reactive sera, with one exception, gave a maximum assay

ANTI-HIV EIA REACTIONS AND TITRES OF WB-POSITIVE SPECIMENS WITH STRONG AND WITH WEAK BANDS

*’Wellcozyme’ HIV 1 +2 maximum OD/cut-off ratio was 9 0 tHlghest log,o dilution at which specimen gave positive reaction in Wellcozyme 1+2

tWellcozyme GACELISA HIV1+2 maximum OD/cut-off ratio was 8 3

HIV

Allergic asthma due to domestic use of insulating polyurethane foam.

953 do so again. Their figures suggest the opposite conclusion. Their best estimate is that 0-8% of all deaths in the Netherlands (1030 in 1990) are...
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