1476
libraries select what they need instead of receiving donations that may not be relevant to their needs. The demand is very great from requesting libraries and the supply is diminishing from donor libraries. We therefore encourage to seriously consider becoming a member of this The WHO library is also a member of the Exchange, and we find it gratifying that duplicates of our books and periodicals are immediately requested by libraries as soon as the lists are sent out. The Exchange facilitates a constant circulation of information in the health sciences before it has a chance to become outdated.
librarians
exchange.
Office of Library and Health Literature Services, World Health Organization, 1211 Geneva 27, Switzerland
YVONNE GRANDBOIS
ACE inhibitors and LDL-apheresis with dextran sulphate adsorption SIR,-Treatment of patients with severe hypercholesterolaemia extracorporeal removal of low-density lipoproteins (LDLapheresis) with dextran sulphate columns is well tolerated, with
according to our experience in almost 800 treatments in 21 patients in the LDL-apheresis atherosclerosis regression study (LAARS). Professor Olbricht and colleagues (Oct 10, p 908) describe an anaphylactoid reaction in 2 patients during the first treatment with this type of LDL-apheresis, characterised by flushing, dyspnoea, low blood pressure, and bradycardia, which they attribute to the concomitant use of an angiotensin-converting enzyme (ACE) inhibitor. They postulate that this reaction is due to a decreased bradykinin catabolism caused by the drug, together with an increased bradykinin production due to stimulation of blood cells by the negatively charged dextran sulphate. We report a patient who had been treated without adverse events for over 1 year, in whom an atypical reaction during apheresis was noted after treatment with an ACE inhibitor was instituted. The patient was a 44-year-old man with severe primary hypercholesterolaemia (9-1 mmol/1) who had had two myocardial infarctions at age 35 and 42 years. Drug treatment included simvastatin, metoprolol tartrate, and aspirin. From April, 1991, he received biweekly LDL-apheresis, which was uneventful for more than 30 treatments up to July, 1992. Captopril was then added to the regimen for mild congestive heart failure. While he was on 6-25 mg and 12-5 mg twice daily, no adverse events took place during apheresis. After a dose increase to 25 mg twice daily, he had nausea, slight drop in blood pressure, and bradycardia, which resolved spontaneously in the supine position; thereafter the procedure was completed without problems. During the next treatment, while on the same dose of captopril, he had nausea, pounding headache, and flushing of head and neck, without symptoms of dyspnoea, stridor, urticaria, blood pressure drop, or bradycardia. These symptoms started the moment that plasma from the cholesterol-binding column was returned to the patient, and subsided within minutes after the procedure was stopped. Bacterial cultures were all negative. Since the previous 30 treatments had been without adverse effects, it was decided to rechallenge the patient, during which an identical reaction was seen. Clemastine or corticosteroids intravenously had no effect, but symptoms subsided within a few minutes when treatment was stopped. Once it was recognised that this reaction could be related to the use of an ACE inhibitor, captopril was withdrawn 24 h before treatment. No adverse reactions were noted in the two following treatments. These findings indicate that: the (bradykinin-mediated) anaphylactoid reaction to LDL-apheresis with dextran sulphate during the use of captopril can be highly non-specific and does not respond to conventional treatment; that it is dose-dependent; and that, once diagnosed, it can be avoided by withdrawing captopril 24 h before treatment-but this last probably does not apply to ACE inhibitors with longer half-lives, such as enalapril. Department of Medicine, Division of General Internal Medicine, University Hospital Nijmegen, Nijmegen, Netherlands
6500 HB
A. A. KROON M. J. T. M. MOL A. F. H. STALENHOEF
Occupational exposure to glutaraldehyde in tropical climates SIR,-The safety and biocidal efficacy of glutaraldehyde’ has led its endorsement by CDC and WHO2,3 as a substitute to formaldehyde in high-level disinfection and cold-sterilisation. In less developed countries, where the supply of sterile disposables and autoclaves are inadequate, the use of glutaraldehyde to control cross-infection in clinical settings that provide invasive services seems reasonable. Since safety considerations with glutaraldehyde largely relate to its volatility, stringent precautions in handling are relevant in warm tropical climates (average ambient temperatures up to 39°C), especially when ventilation may be inadequate. These to
factors increase the risk of vapourised glutaraldehyde exceeding the recommended threshold of 0-2 parts per million.4 Unfortunately, appreciation of these considerations appear to have eluded manufacturers and users. In an outpatient clinic in Nairobi (average annual temperature 23 [SD 4] °C, cetrimide and chlorhexidine were substituted by glutaraldehyde for instrument decontamination and housekeeping about 18 months ago. The glutaraldehyde was left in an open vessel (surface area about 600 cm2 all day in each location of about 11 4m3; ventilation was through 1 44 m2 windows, which remained open for about 10 h daily during a 5-day week. Our concern that there are probably excessive glutaraldehyde fumes prompted us to study individuals who regularly worked in these environments. DETAILS OF AFFECTED RESPONDENTS
Some respondents reported symptoms that mimicked those caused by formaldehyde fumes (table).5-7 We believe that these were adverse reactions to glutaraldehyde fumes. Except in case 2, these adverse reactions probably corresponded to development of hypersensitivity to glutaraldehyde. In addition, in contrast to the familiar smell of formaldehyde,7the smell of glutaraldehyde did not prompt the taking of precautions. As with formaldehyde,* hypersensitisation to glutaraldehyde may not be a function of concentration, especially among those with hypersensitivity to multiple allergens. In this regard, the use of 2% glutaraldehyde in housekeeping in intensive care units, where patients are already likely to have respiratory distress, is of concern. In the manufacturer’s cautions for brands available in Kenya (Cidex, Sporocidin) there is no mention of the volatile nature of
libraries select what they need instead of receiving donations that may not be relevant to their needs. The demand is very great from requesting libraries and the supply is diminishing from donor libraries. We therefore encourage to seriously consider becoming a member of this The WHO library is also a member of the Exchange, and we find it gratifying that duplicates of our books and periodicals are immediately requested by libraries as soon as the lists are sent out. The Exchange facilitates a constant circulation of information in the health sciences before it has a chance to become outdated.
librarians
exchange.
Office of Library and Health Literature Services, World Health Organization, 1211 Geneva 27, Switzerland
YVONNE GRANDBOIS
ACE inhibitors and LDL-apheresis with dextran sulphate adsorption SIR,-Treatment of patients with severe hypercholesterolaemia extracorporeal removal of low-density lipoproteins (LDLapheresis) with dextran sulphate columns is well tolerated, with
according to our experience in almost 800 treatments in 21 patients in the LDL-apheresis atherosclerosis regression study (LAARS). Professor Olbricht and colleagues (Oct 10, p 908) describe an anaphylactoid reaction in 2 patients during the first treatment with this type of LDL-apheresis, characterised by flushing, dyspnoea, low blood pressure, and bradycardia, which they attribute to the concomitant use of an angiotensin-converting enzyme (ACE) inhibitor. They postulate that this reaction is due to a decreased bradykinin catabolism caused by the drug, together with an increased bradykinin production due to stimulation of blood cells by the negatively charged dextran sulphate. We report a patient who had been treated without adverse events for over 1 year, in whom an atypical reaction during apheresis was noted after treatment with an ACE inhibitor was instituted. The patient was a 44-year-old man with severe primary hypercholesterolaemia (9-1 mmol/1) who had had two myocardial infarctions at age 35 and 42 years. Drug treatment included simvastatin, metoprolol tartrate, and aspirin. From April, 1991, he received biweekly LDL-apheresis, which was uneventful for more than 30 treatments up to July, 1992. Captopril was then added to the regimen for mild congestive heart failure. While he was on 6-25 mg and 12-5 mg twice daily, no adverse events took place during apheresis. After a dose increase to 25 mg twice daily, he had nausea, slight drop in blood pressure, and bradycardia, which resolved spontaneously in the supine position; thereafter the procedure was completed without problems. During the next treatment, while on the same dose of captopril, he had nausea, pounding headache, and flushing of head and neck, without symptoms of dyspnoea, stridor, urticaria, blood pressure drop, or bradycardia. These symptoms started the moment that plasma from the cholesterol-binding column was returned to the patient, and subsided within minutes after the procedure was stopped. Bacterial cultures were all negative. Since the previous 30 treatments had been without adverse effects, it was decided to rechallenge the patient, during which an identical reaction was seen. Clemastine or corticosteroids intravenously had no effect, but symptoms subsided within a few minutes when treatment was stopped. Once it was recognised that this reaction could be related to the use of an ACE inhibitor, captopril was withdrawn 24 h before treatment. No adverse reactions were noted in the two following treatments. These findings indicate that: the (bradykinin-mediated) anaphylactoid reaction to LDL-apheresis with dextran sulphate during the use of captopril can be highly non-specific and does not respond to conventional treatment; that it is dose-dependent; and that, once diagnosed, it can be avoided by withdrawing captopril 24 h before treatment-but this last probably does not apply to ACE inhibitors with longer half-lives, such as enalapril. Department of Medicine, Division of General Internal Medicine, University Hospital Nijmegen, Nijmegen, Netherlands
6500 HB
A. A. KROON M. J. T. M. MOL A. F. H. STALENHOEF
Occupational exposure to glutaraldehyde in tropical climates SIR,-The safety and biocidal efficacy of glutaraldehyde’ has led its endorsement by CDC and WHO2,3 as a substitute to formaldehyde in high-level disinfection and cold-sterilisation. In less developed countries, where the supply of sterile disposables and autoclaves are inadequate, the use of glutaraldehyde to control cross-infection in clinical settings that provide invasive services seems reasonable. Since safety considerations with glutaraldehyde largely relate to its volatility, stringent precautions in handling are relevant in warm tropical climates (average ambient temperatures up to 39°C), especially when ventilation may be inadequate. These to
factors increase the risk of vapourised glutaraldehyde exceeding the recommended threshold of 0-2 parts per million.4 Unfortunately, appreciation of these considerations appear to have eluded manufacturers and users. In an outpatient clinic in Nairobi (average annual temperature 23 [SD 4] °C, cetrimide and chlorhexidine were substituted by glutaraldehyde for instrument decontamination and housekeeping about 18 months ago. The glutaraldehyde was left in an open vessel (surface area about 600 cm2 all day in each location of about 11 4m3; ventilation was through 1 44 m2 windows, which remained open for about 10 h daily during a 5-day week. Our concern that there are probably excessive glutaraldehyde fumes prompted us to study individuals who regularly worked in these environments. DETAILS OF AFFECTED RESPONDENTS
Some respondents reported symptoms that mimicked those caused by formaldehyde fumes (table).5-7 We believe that these were adverse reactions to glutaraldehyde fumes. Except in case 2, these adverse reactions probably corresponded to development of hypersensitivity to glutaraldehyde. In addition, in contrast to the familiar smell of formaldehyde,7the smell of glutaraldehyde did not prompt the taking of precautions. As with formaldehyde,* hypersensitisation to glutaraldehyde may not be a function of concentration, especially among those with hypersensitivity to multiple allergens. In this regard, the use of 2% glutaraldehyde in housekeeping in intensive care units, where patients are already likely to have respiratory distress, is of concern. In the manufacturer’s cautions for brands available in Kenya (Cidex, Sporocidin) there is no mention of the volatile nature of
