908
geographically, but by size. A higher uptake rate was achieved in the two smaller institutions (120 and 128 tests per 1000 units of accommodation) than in the larger two (35 and 33 per 1000). For five establishments (including Saughton, previously publishedl) medical officers have provided data for earlier years (table). Again the patterns have varied with time. Significant variation in test uptake by Saughton inmates has been associated with two interventions—namely, the initiation in 1988 of an AIDS education programme and the anonymous surveillance study with linked risk factor questionnaire done in August, 1991.5 In Perth, test requests rose steeply from 8 per 1000 admissions in 1987 to 15 in 1988-91, whereas in the women’s prison uptake was 66 per 1000 admissions in the first two years (12% positive) but only 15 per 1000 after that (2% positive). Glenochil Prison and Young Offenders’ Institution and Greenock Prison underwent a change of function during 1986-91, and there were sharp increases in admissions associated with
a
fall-off in HIV
test
requests.
Comparing the uptake of confidential named HIV tests in Scottish prisons has highlighted the possible influence of HIV seroprevalence amongst drug users in the communities served by local prisons on inmates’ uptake of testing. We encourage other services to publish statistics for inter-prison comparison of uptake of confidential named HIV testing and, for local prisons, to relate uptake of HIV seroprevalence among drug users in the local communities.
S. M. GORE
Scottish Office,
J. BASSON
Edinburgh
Immunology Unit, A. G. BIRD
University of Edinburgh Communicable Diseases (Scotland) Unit,
D.
Glasgow
J. GOLDBERG
SM, Jolliffe DW, Bird AG. Prisoners’ uptake of confidential, named HIV testing. Lancet 1992; 339: 1491-92. 2. Centers for Disease Control. Publicly funded HIV counselling and testing: United States 1990. MMWR 1991; 40: 666-75. 3. Centers for Disease Control. HIV prevention in the US correctional system 1991. MMWR 1992; 41: 389-97. 4. Goldberg DJ, Emslie JA, Smyth W, Reid D. A system for surveillance of voluntary HIV testing; results of the first 2 years, 1989-1990. AIDS 1992, 6: 495-500. 5. Bird AG, Gore SM, Jolliffe DW, Burns SM. Anonymous HIV surveillance in Saughton Prison, Edinburgh AIDS 1992; 6: 725-33. 1. Gore
anaphylactoid reactions during venom immunotherapy
ACE inhibitors and
StR,—Severe allergic reactions to hymenoptera stings are usually to hypersensitivity to hymenoptera venom, and require specific immunotherapy.’ Since systemic reactions could occur during immunotherapy protocols, (3-blockers are contraindicated in patients treated with venom desensitisation and should be replaced for systemic hypertension by alternative drugs such as angiotensinconverting enzyme (ACE) inhibitors. ACE inhibitors, however, can related
induce
cough, angio-oedema, and anaphylactoid reactions in high-flux membrane dialysis,2 which may be related to allergic mechanisms.’ We report two cases of enalapril-induced anaphylactoid reactions during venom immunotherapy. Patient 1--(M/52, history of life-threatening reactions after wasp stings, immediate hypersentitivity to yellow jacket wasp venom). When admitted for immunotherapy, the patient had been treated for hypertension with enalapril (20 mg daily) for 2 years. started without Desensitisation was discontinuing the antihypertensive treatment. A few minutes after the first administration of pure venom solution, the patient had generalised pruritus with a severe fall in blood pressure. He received intravenous dextran and recovered quickly. Enalapril was stopped achieved without further adverse effect. maintained with 100 jig wasp venom then Immunotherapy every month, provided that enalapril had been stopped 24 h before the venom injection. On the third month of desensitisation, the patient had a severe anaphylactoid reaction 30 min after injection, and needed oxygen, dextran infusion, and 05 mg subcutaneous and desensitisation
was
was
undergoing venom immunotherapy. Department of Respiratory Diseases, Allergy Unit, Haut- Lévêque Hospital,
MRC Biostatistics Unit, Institute of Public Health, University Forvie Site, Cambridge CB2 2SR, UK
HIV
adrenaline. He had forgotten to stop enalapril the day before. No reactions were observed after enalapril was consistently discontinued before venom administration. Patient 2-(M/34, treated with p-blockers for hypertension, generalised reaction to wasp venom). Immunotherapy was proposed after (3-blockers had been changed to enalapril. Desensitisation was started but an anaphylactoid reaction occurred after the second injection of pure venom solution. The ACE inhibitor was discontinued and replaced by calcium antagonists so that venom immunotherapy could be achieved. Since nifedipine was not well tolerated enalapril was reintroduced a few months later, but subsequent venom administration induced an anaphylactoid reaction. Enalapril was stopped again and desensitisation could be maintained without advise effect. A common mechanism of ACE inhibitor anaphylactoid reaction is thought to be a decrease in the breakdown of bradykinin, which is a potent vasodilator: During immunotherapy with venom, serum histamine increased up to the third hour after venom administration.s Since histamine induces vasodilatation, an increase in its serum concentration combined with an alteration of the kinin/killikrein system could elicit anaphylactoid reactions. Therefore, ACE inhibitors should be used with caution in allergic patients treated with desensitisation, and avoided in those more
33604 Pessac, France, and Respirology Service, Centre Hospitalier De Libourne
MANUEL TUNON-DE-LARA PASCALE VILLANUEVA MICHEL MARCOS ANDRÉ TAYTARD
J.
1. Hunt KJ, Valentine MD, Sobotka AK, Benton AW, Amodio FJ, Lichtenstein LM. A controlled trial of immunotherapy m insect hypersensitivity. N Eugl J Med 1978;
299: 157-61 L, Waer M, Vanrenterghem Y, Michielsen P Angiotensin-convertingenzyme inhibitors and anaphylactoid reactions to high-flux membrane dialysis. Lancet 1990; 336: 1360-62. 3. O’Hollaren MT, Porter GA Angiotensin converting enzyme inhibitors and the allergist Ann Allergy 1990; 64: 503-06. 4. Wood SM, Mann RD, Rawlins MD. Anglo-oedema and urticaria associated with angiotensin converting enzyme inhibitors. BMJ 1987, 294: 91-92. 5. Philip-Joet F, Anfosso-Capra, Reynaud-Gaubert, Arnaud A. Efficacité et tolérance d’accoutumance au venin d’hyménoptères en 3 heures 30 Rev Fr Allergol 1990; 30: 221-24. 2. Verresen
Anaphylactoid reactions, LDL apheresis with dextran sulphate, and ACE inhibitors SiR,—Treatment of patients with severe hypercholesterolaemia by low-density lipoprotein (LDL) apheresis with dextran sulphate adsorption is widely used in Europe and Japan. After plasma separation by a polysulphone filter, LDL-cholesterol is adsorbed to low-molecular-weight dextran sulphate covalently bound to cellulose. We did 556 treatments in 14 patients. During the initial 5 min of their first treatments, patients 10 and 12 had flushing, dyspnoea, blood pressure below 60/30 mm Hg, and bradycardia
(42-46/min). An immediate stop of treatment and administration of large fluid volumes restored the vital indices. Further LDL apheresis by other methods was uneventful in patient 12, but was accompanied by slight hypotension in patient 10. Anaphylactoid reactions induced by dextran or by ethylene oxide (ETO), the sterilant of the system, were excluded by the absence of significant dextran and ETO antibody titres. Both patients received angiotensin-converting enzyme (ACE) inhibitors (enalapril 10 mg or captopril 25 mg). The other 12 patients were not on ACE inhibitors, and their 554 treatments with dextran sulphate adsorption were without serious side-effects.’1 Because of its strong negative charges dextran sulphate is a potent activator of the contact activation system, including Hageman factor (HF), high-molecular-weight kininogen, prekallikrein, and coagulation factor XI. As a result, kallikrein generates bradykinin from high-molecular-weight kininogenLDL apheresis with dextran sulphate is associated with increased bradykinin generation.3 Bradykinin is rapidly inactivated by kinases I and II. Kinase II and ACE are identical, and bradykinin catabolism is decreased by ACE inhibitors,.-’ Diminished generation and
geographically, but by size. A higher uptake rate was achieved in the two smaller institutions (120 and 128 tests per 1000 units of accommodation) than in the larger two (35 and 33 per 1000). For five establishments (including Saughton, previously publishedl) medical officers have provided data for earlier years (table). Again the patterns have varied with time. Significant variation in test uptake by Saughton inmates has been associated with two interventions—namely, the initiation in 1988 of an AIDS education programme and the anonymous surveillance study with linked risk factor questionnaire done in August, 1991.5 In Perth, test requests rose steeply from 8 per 1000 admissions in 1987 to 15 in 1988-91, whereas in the women’s prison uptake was 66 per 1000 admissions in the first two years (12% positive) but only 15 per 1000 after that (2% positive). Glenochil Prison and Young Offenders’ Institution and Greenock Prison underwent a change of function during 1986-91, and there were sharp increases in admissions associated with
a
fall-off in HIV
test
requests.
Comparing the uptake of confidential named HIV tests in Scottish prisons has highlighted the possible influence of HIV seroprevalence amongst drug users in the communities served by local prisons on inmates’ uptake of testing. We encourage other services to publish statistics for inter-prison comparison of uptake of confidential named HIV testing and, for local prisons, to relate uptake of HIV seroprevalence among drug users in the local communities.
S. M. GORE
Scottish Office,
J. BASSON
Edinburgh
Immunology Unit, A. G. BIRD
University of Edinburgh Communicable Diseases (Scotland) Unit,
D.
Glasgow
J. GOLDBERG
SM, Jolliffe DW, Bird AG. Prisoners’ uptake of confidential, named HIV testing. Lancet 1992; 339: 1491-92. 2. Centers for Disease Control. Publicly funded HIV counselling and testing: United States 1990. MMWR 1991; 40: 666-75. 3. Centers for Disease Control. HIV prevention in the US correctional system 1991. MMWR 1992; 41: 389-97. 4. Goldberg DJ, Emslie JA, Smyth W, Reid D. A system for surveillance of voluntary HIV testing; results of the first 2 years, 1989-1990. AIDS 1992, 6: 495-500. 5. Bird AG, Gore SM, Jolliffe DW, Burns SM. Anonymous HIV surveillance in Saughton Prison, Edinburgh AIDS 1992; 6: 725-33. 1. Gore
anaphylactoid reactions during venom immunotherapy
ACE inhibitors and
StR,—Severe allergic reactions to hymenoptera stings are usually to hypersensitivity to hymenoptera venom, and require specific immunotherapy.’ Since systemic reactions could occur during immunotherapy protocols, (3-blockers are contraindicated in patients treated with venom desensitisation and should be replaced for systemic hypertension by alternative drugs such as angiotensinconverting enzyme (ACE) inhibitors. ACE inhibitors, however, can related
induce
cough, angio-oedema, and anaphylactoid reactions in high-flux membrane dialysis,2 which may be related to allergic mechanisms.’ We report two cases of enalapril-induced anaphylactoid reactions during venom immunotherapy. Patient 1--(M/52, history of life-threatening reactions after wasp stings, immediate hypersentitivity to yellow jacket wasp venom). When admitted for immunotherapy, the patient had been treated for hypertension with enalapril (20 mg daily) for 2 years. started without Desensitisation was discontinuing the antihypertensive treatment. A few minutes after the first administration of pure venom solution, the patient had generalised pruritus with a severe fall in blood pressure. He received intravenous dextran and recovered quickly. Enalapril was stopped achieved without further adverse effect. maintained with 100 jig wasp venom then Immunotherapy every month, provided that enalapril had been stopped 24 h before the venom injection. On the third month of desensitisation, the patient had a severe anaphylactoid reaction 30 min after injection, and needed oxygen, dextran infusion, and 05 mg subcutaneous and desensitisation
was
was
undergoing venom immunotherapy. Department of Respiratory Diseases, Allergy Unit, Haut- Lévêque Hospital,
MRC Biostatistics Unit, Institute of Public Health, University Forvie Site, Cambridge CB2 2SR, UK
HIV
adrenaline. He had forgotten to stop enalapril the day before. No reactions were observed after enalapril was consistently discontinued before venom administration. Patient 2-(M/34, treated with p-blockers for hypertension, generalised reaction to wasp venom). Immunotherapy was proposed after (3-blockers had been changed to enalapril. Desensitisation was started but an anaphylactoid reaction occurred after the second injection of pure venom solution. The ACE inhibitor was discontinued and replaced by calcium antagonists so that venom immunotherapy could be achieved. Since nifedipine was not well tolerated enalapril was reintroduced a few months later, but subsequent venom administration induced an anaphylactoid reaction. Enalapril was stopped again and desensitisation could be maintained without advise effect. A common mechanism of ACE inhibitor anaphylactoid reaction is thought to be a decrease in the breakdown of bradykinin, which is a potent vasodilator: During immunotherapy with venom, serum histamine increased up to the third hour after venom administration.s Since histamine induces vasodilatation, an increase in its serum concentration combined with an alteration of the kinin/killikrein system could elicit anaphylactoid reactions. Therefore, ACE inhibitors should be used with caution in allergic patients treated with desensitisation, and avoided in those more
33604 Pessac, France, and Respirology Service, Centre Hospitalier De Libourne
MANUEL TUNON-DE-LARA PASCALE VILLANUEVA MICHEL MARCOS ANDRÉ TAYTARD
J.
1. Hunt KJ, Valentine MD, Sobotka AK, Benton AW, Amodio FJ, Lichtenstein LM. A controlled trial of immunotherapy m insect hypersensitivity. N Eugl J Med 1978;
299: 157-61 L, Waer M, Vanrenterghem Y, Michielsen P Angiotensin-convertingenzyme inhibitors and anaphylactoid reactions to high-flux membrane dialysis. Lancet 1990; 336: 1360-62. 3. O’Hollaren MT, Porter GA Angiotensin converting enzyme inhibitors and the allergist Ann Allergy 1990; 64: 503-06. 4. Wood SM, Mann RD, Rawlins MD. Anglo-oedema and urticaria associated with angiotensin converting enzyme inhibitors. BMJ 1987, 294: 91-92. 5. Philip-Joet F, Anfosso-Capra, Reynaud-Gaubert, Arnaud A. Efficacité et tolérance d’accoutumance au venin d’hyménoptères en 3 heures 30 Rev Fr Allergol 1990; 30: 221-24. 2. Verresen
Anaphylactoid reactions, LDL apheresis with dextran sulphate, and ACE inhibitors SiR,—Treatment of patients with severe hypercholesterolaemia by low-density lipoprotein (LDL) apheresis with dextran sulphate adsorption is widely used in Europe and Japan. After plasma separation by a polysulphone filter, LDL-cholesterol is adsorbed to low-molecular-weight dextran sulphate covalently bound to cellulose. We did 556 treatments in 14 patients. During the initial 5 min of their first treatments, patients 10 and 12 had flushing, dyspnoea, blood pressure below 60/30 mm Hg, and bradycardia
(42-46/min). An immediate stop of treatment and administration of large fluid volumes restored the vital indices. Further LDL apheresis by other methods was uneventful in patient 12, but was accompanied by slight hypotension in patient 10. Anaphylactoid reactions induced by dextran or by ethylene oxide (ETO), the sterilant of the system, were excluded by the absence of significant dextran and ETO antibody titres. Both patients received angiotensin-converting enzyme (ACE) inhibitors (enalapril 10 mg or captopril 25 mg). The other 12 patients were not on ACE inhibitors, and their 554 treatments with dextran sulphate adsorption were without serious side-effects.’1 Because of its strong negative charges dextran sulphate is a potent activator of the contact activation system, including Hageman factor (HF), high-molecular-weight kininogen, prekallikrein, and coagulation factor XI. As a result, kallikrein generates bradykinin from high-molecular-weight kininogenLDL apheresis with dextran sulphate is associated with increased bradykinin generation.3 Bradykinin is rapidly inactivated by kinases I and II. Kinase II and ACE are identical, and bradykinin catabolism is decreased by ACE inhibitors,.-’ Diminished generation and
