508
distinguished from H pylori, being larger and with 5-10 regular spirals. The PAP method detailed H pylori as dark-brown spiral bacteria but did not stain the tightly spiral organisms. The patient was prescribed an Hz-receptor antagonist but did not return for follow-up. Since the frequency of H pylori infection in Brazil is high (about 80% in patients coming to upper endoscopy4 7) it is not surprising for a patient with H pylori infection to acquire tightly spiral bacteria (or vice versa). Gastric infection caused by spiral bacteria may not protect the host from other gastric infections caused by spiral bacteria.
Laboratory of Research in Bacteriology and Department of Pathology, Faculty of Medicine, Federal University of Minas Gerais, CEP 30130 - Belo Horizonte, Minas Gerais, Brazil
DULCIENE M. M. QUEIROZ MÔNICA M. D. A. CABRAL ANA M. M. F. NOGUEIRA ALFREDO J. A. BARBOSA GIFONE A. ROCHA EDILBERTO N. MENDES
McNulty CAM, Dent JC, Curry A, et al. New spiral bacterium in gastric mucosa. J Clin Pathol 1989; 42: 585-91. 2. Lee A, Hazzell SL, O’Rourke J, Kouprach S. Isolation of a spiral-shaped bacterium from the cat stomach. Infect Immunol 1988; 56: 2843-50. 3. Dye KR, Marshall BJ, Frierson HF, Guerrant RL, McCallum RW. Ultrastructure of another spiral organism associated with human gastritis. Dig Dis Sci 1989; 34: 1.
counselled without testing or had an unknown test result, and 704 had a known result-143 of whom had already been diagnosed as seropositive. Of the 561 with an unknown serostatus when approached through the programme 118 (21%) proved HIVpositive. For all testing programmes in Sweden, apart from blood screening, fewer than 1 person in 1000 now tests positive. Thus partner notification seems to be an efficient way to identify people at high risk of HI V infection and to offer them counselling and testing. Analysis of aggregated data from partner notification might also yield information on patterns of spread and risks of transmission. An example is our finding that slightly more than half (143/261) the seropositive partners were known to be HIV carriers. On the assumption that a carrier’s probability of being notified as a partner of an index patient is independent of previous knowledge of his/her infection, this would imply that the true number of HIV carriers in Sweden is about twice the reported number-ie, around 4000. We believe our results show that partner notification can be done in all patients, provided that patient motivation and cooperation are attained by professionalism, empathy, and respect for integrity and
confidentiality. JOHAN GIESECKE
1787-91.
4. Rocha GA, Queiroz DMM, Mendes EN, Lage AP, Barbosa AJA. Simple carbolfuchsin staining for showing C pylori and other spiral bacteria in gastric mucosa. J Clin Pathol 1989; 42: 1004-05. 5. Fischer R, Samisch W, Schwenke E. "Gastrospirillum hominis": another four cases. Lancet 1989; ii: 59. 6. Wyatt J. Detection of Campylobacter pylori by histology. In: Rathbone BJ, Heatley RV, eds. Campylobacter pylon and gastroduodenal disease. Oxford; Blackwell Scientific, 1989: 63-68. 7. Barbosa AJA, Queiroz DMM, Mendes EN, Rocha GA, Lima GF Jr, Oliveira CA. Immunocytochemical identification of Campylobacter pylori gastritis and correlation with culture. Arch Pathol Lab Med 1988; 112: 523-25.
Partner notification for HIV in Sweden SIR,-Partner notification has long been used in the control of treatable sexually transmitted diseases (STD). Its applicability to HIV infection has been discussed,l,2 and the need for research Some results have been published.6-9 The ethical difficulties are considerable, and are much the same as those for the expansion of HIV testing. Prerequisites to partner notification are that carriers thus discovered are not stigmatised and that ample pre-test and post-test counselling and support are available. In Sweden HIV infection was classified in law as an STD in 1985. Cases are anonymously reported to the county Medical Officer of Health, and the patient’s doctor (or a counsellor working with him) is obliged to carry out partner notification. By placing this responsibility with the doctor or counsellor cooperation with the patient becomes part of the total sociopsychological care for the patient, and names of partners need not be known outside the doctor’s office. Patients can choose to refer partners themselves or to ask the doctor for assistance, in which case the index patient’s identity is withheld. In 1989, we initiated a study to measure the outcome of the Swedish programme, with the participation of most departments caring for patients with HIV infection. During the first years of the epidemic partner notification was not common, and even legislation did not immediately change medical routines. The participating departments (about 1500 patients) were asked to supply data only for patients for whom they had attempted partner notification, irrespective of the result. Outcomes of partner notification for 463 index patients from twenty departments were reported. Of these 210 were homosexual or bisexual men, 128 were intravenous drug users, 94 were heterosexually infected, and 31 had received blood transfusions or blood products. Only partners who could be identified were counted; anonymous contacts and partners abroad were excluded. The highest average number of seropositive partners per index patient was found in homosexual and bisexual men (0-78) and drug abusers (0-64), and the lowest was in blood recipients (0 10). A total of 1456 partners were named: 656 could not be traced, 96 were
emphasised.3-’
Department of Epidemiology, National Bacteriological Laboratory, S-105 21 Stockholm, Sweden 1. Osbome J. 444-47. 2. Potterat JJ,
KRISTINA RAMSTEDT TORVALD RIPA GUNILLA RÅDÖ GIANPAOLO SCALIA-TOMBA MIKAEL WESTRELL, for The Swedish Study Group on Partner Notification for HIV Infection
Sounding Board. AIDS: politics and science. N Engl J Med 1988. 318:
Spencer NE, Woodhouse DE, Muth JB. Partner notification in the control of human immunodeficiency virus infection. Am J Public Health 1989: 79: 874-76. 3. Adler M, Johnson A. Contact tracing for HIV infection. Br Med J 1988: 296: 1420-21. 4. Rutherford G, Woo J. Contact tracing and the control of human immunodeficiency virus infection. J AMA 1988: 259: 3609-10. 5. World Health Organisation. Report of the consultation on partner notification for preventing HIV transmission. Geneva: WHO, Jan 11-13, 1989. WHO/GPA/
ESR/89.2. 6. Wykoff R, Heath C, Hollis S, et al. Contact tracing to identify human immunodeficiency virus in a rural community. JAMA 1988: 259: 3563-66. 7. Centers for Disease Control. Partner notification for preventing HIV infection Colorado, Idaho, South Carolina, Virginia. MMWR 1988: 37: 393-96, 441-02. 8. Kristoffersen JE. Case contact tracing and testing in HIV infection. In: Proceedings and abstracts of the Fourth International Conference on AIDS, Stockholm, June 12-16, 1988. Stockholm: Swedish Ministry of Health and Social Affairs, 1988: 354. 9 Clumeck N, Taelman H, Hermans P, Piot P, Schoumacher M, De Wit S. A cluster of HIV infection among heterosexual people without apparent risk factors. N Engl J Med 1989: 321: 1460-62.
"Treating through" hypersensitivity to cotrimoxazole in children with HIV infection SiR,—Dr Putterman and his colleagues (July 7, p 52) report their experience with "treating through" hypersensitivity to cotrimoxaole in an adult with AIDS and Pneumocystis carinii pneumonia (PCP). We have successfully desensitised 7 HIVinfected children to co-trimoxazole. From 1986-88 we treated with intravenous co-trimoxazole 3 HIV-infected children (aged 3-4 years) who had PCP. Hypersensitive reactions were successfully managed with corticosteroids and antihistamines. We then started prophylaxis for PCP with co-trimoxazole (5 mg/kg daily) in 4 HIV-infected children (aged 4-13) at risk of PCP with CD4 counts below 200. In all children we noted allergic exanthema and fever 8-12 days after the start of therapy. We therefore stopped co-trimoxazole and after the skin reactions disappeared we started oral desensitisation with gradual increases in co-trimoxazole dose. The basic solution we used was co-trimoxazole suspension for children (8 mgjh) (solution A). 1 ml of this suspension was diluted with 19 ml distilled water (solution B). The desensitisation regimen was: days 1-4 solution B (day 1 =ml, 2 =2 ml, 3 = 4 ml, 4 =8 ml), days 5-9
solutionA(day5=0’6m!,6=l’2ml,7=2’5ml,8=5ml,9=10mt. From days 10 to 17 we gave 40 mg co-trimoxazole daily. After that we raised the dose every 3 days to 5 mg/kg daily. During the period of desensitisation all children had inhaled pentamidine isethionate
509
(4 mg/kg every 2 weeks). Since
we
began long-term prophylaxis
with co-trimoxazole PCP has not developed in the children so treated. We have found that PCP-prophylaxis by inhalation of pentamidine (4 mg/kg monthly) can be difficult in children under 5 years. In these cases oral PCP-prophylaxis with co-trimoxazole is necessary. To avoid drug-related allergic side-effects in prophylaxis for and treatment of PCP we therefore recommended an initial oral
the pre-disease phase Evidence for an interaction between the two retroviruses at the molecular level comes from in-vitro studies, with stimulation of HIV expression by HTLV-1 gene products.3 Dysregulation of the immune system by HTLV-I/II could also have predisposed this man to the rapid appearance of AIDS. HIV-1 and HTLV-I/Il co-infected individuals should be subject to especially close surveillance.
JEAN-JACQUES LEFRÈRE
desensitisation.
Centre of Paediatrics, Department of Haematology and Klinikum der Johann Wolfgang, 6000 Frankfurt, West Germany
Oncology,
W. KREUZ T. GÜNGÖR CHR. LOTZ M. FUNK B. KORNHUBER
Institut National de Transfusion
Sanguine,
Alexandre-Cabanel, 75015 Paris, France rue
ANNE-MARIE COUROUCÉ MARTINE MARIOTTI ERIC WATTEL ODETTE PROU FRANÇOIS BOUCHARDEAU PATRICK LAMBIN
Schaffar-Deshayes L, Chavanc M, Monplaisir N, et al. Antibodies to HTLV-I p24 sera in blood donors, elderly people and patients with hemopoietic diseases in France and in French West Indies. Int J Cancer 1984; 34: 667-70. 2. Lefrère JJ, Couroucè AM, Lambin P, Fine JM, Doinel C, Salmon C. Clinical and biological features in the 12 months preceding onset of AIDS in HIV-infected subjects.J AIDS 1989; 2: 100-01. 3. Siekevitz M, Josephs SF, Dukovich M, Peffer N, Wong-Staal F, Greene WC. Activation of the HIV-1 LTR by T cell mitogens and the trans-activator protein of 1.
Rapid progression
to AIDS in dual
HIV-1/HTLV-I infection SIR,-Dr Page and colleagues (June 16, p 1439) report that seropositivity for human T-cell leukaemia virus (HTLV) type I/II may adversely affect the clinical outcome in human immunodeficiency virus type 1 (HIV-1) infection. However, the duration of HIV-1 infection was unknown. A 50-year-old black man, bom in the French West Indies (Guadeloupe), was found to be HIV-1 seronegative (ELISA) on routine screening of blood donatons on July 24, 1987 (first donation). In July, 1988, he twice had unprotected intercourse with prostitutes. When he gave blood a second time, on December 16, 1988, he was HIV-1seropositive, this being confirmed by western blot. The patient reported no other extramarital sexual contacts for 4 years; his wife, tested in January, 1989, was HIV-1seronegative. He denied other risk factors for HIV infection (blood transfusion, homosexual acivity, and intravenous drug use). The date of HIV-1 infection could thus be established as July, 1988. During a systematic screening of people at risk for HTLV-I/Il infection, antibodies to HTLV-I/11 were found in the Dec 16,1988, sample (July, 1987, sample not available) by ELI SA and confirmed by western blot, with reactivity to the two main core proteins and to gp46. This HTLV-1/11 seropositivity was not surprising since the man had been born in and had several times visited the French West Indies, where HTLV-I/11 is endemic.1 The presence of DNA for both retroviruses was confirmed by gene amplification via the polymerase chain reaction in peripheral blood mononuclear cells with primer pairs ingag,pol, and LTR regions for HIV-1 and inpol and tax regions for HTLV-I(II. The finding of HIV-1 seropositivity prompted clinical and laboratory follow-up (table). Progression towards disease was evidenced by the decrease in CD4 count. He refused zidovudine therapy, proposed in February, 1990, to prevent AIDS, and was in stage IVA HIV infection within only 23 months of infection with this retrovirus. To date there have been no clinical manifestations of HTLV-I(II infection. The very rapid evolution of HIV-1infection in this case suggests that HTLV-1/11 co-infection may adversely affect the survival pattern of HIV-1 seropositive individuals. Serum p24 antigen remained negative during follow-up, as is sometimes observed in CLINICAL AND BIOLOGICAL FEATURES DURING FOLLOW-UP PERIOD OF PATIENT CO-INFECTED BY HIV-1 AND HTlV-I/11 WITH KNOWN DURATION OF HIV-1 INFECTION
HTLV-I. Science 1987; 238: 1575-78.
Deep venous thrombosis and antibodies to cyproterone acetate SrR,-Oestrogens and combined oral contraceptives are well known risk factors for deep venous thrombosis (DVT).1,2 An immune mechanism may be responsible for the vascular lesions induced by oral contraceptives.3 We describe here a patient with DVT associated with antibodies to cyproterone acetate. A 19-year-old woman was admitted on June 10, 1990, for an acute dyspnoea. Clinical findings revealed a typical right acute proximal DVT. The chest radiograph was normal. The electrocardiogram showed T-wave inversion on leads Vl V2 V3. Her arterial oxygen tension was decreased. Venography revealed thrombi in the right common iliac vein but not in the vena cava. A temporary vena cava filter (’Filtrethery’; Prothia, France) was inserted under fluoroscopic guidance through a right basilar approach, and intravenous streptokinase was started at a dose of 10 000 U/h for 5 days. On June 14 this therapy was changed to intravenous heparin, and this was maintained during 4 weeks. Venography on June 26 revealed no more thrombi. A ventilation perfusion lung scan on June 29 pointed to a right posterobasal defect. Risk factors for DVT4 were then sought but the inherited risks of antithrombin III, protein C, and protein S deficiency were excluded, as were acquired factors such as sepsis, lupus anticoagulant, and cancer. Because this woman had, since February, 1990, been taking the combined oral contraceptive ’Diane 35’ (cyproterone acetate 2 mg, ethinyloestradiol 35 (ig, Schering) antibodies to synthetic oestrogen-progestagen were sought (INSERM U32, Hopital Henri Mondor, Creteil). There were no antibodies to ethinyloestradiol or to progesterone but antibody to cyproterone acetate was found A test for circulating immune complexes (precipitating when serum is brought to 25% saturation in ammonium sulphate) was positive. Although we cannot be certain that cyproterone acetate antibodies caused the DVT, this case is very suggestive. O. LEROY C. BEUSCART E. SENNEVILLE Intensive Care Unit, F. VISTICOT I. TILLIE Centre Hospitalier, M. BRION 59208 Tourcoing, France G. BEAUCAIRE 1. Boston Collaborative
Drug Surveillance Program. Oral contraceptives and venous thromboembolism disease, surgically confirmed gallbladder disease, and breast tumour. Lancet 1978; i: 1399-407. 2. Stadel BV. Oral contraceptive and cardiovascular disease. N Engl J Med 1981; 305: 612-18. 3. Beaumont V, Beaumont JL. Thromboses vasculanes secondaires à la prise d’estro-progestatifs de synthèse: un mecanisme immunologique. Now Presse Méd 1981; 10: 503-07. 4. Anon. Concensus conference: prevention of embolism. JAMA 1986; 256: 744-49.
venous
thrombosis and
pulmonary
distinguished from H pylori, being larger and with 5-10 regular spirals. The PAP method detailed H pylori as dark-brown spiral bacteria but did not stain the tightly spiral organisms. The patient was prescribed an Hz-receptor antagonist but did not return for follow-up. Since the frequency of H pylori infection in Brazil is high (about 80% in patients coming to upper endoscopy4 7) it is not surprising for a patient with H pylori infection to acquire tightly spiral bacteria (or vice versa). Gastric infection caused by spiral bacteria may not protect the host from other gastric infections caused by spiral bacteria.
Laboratory of Research in Bacteriology and Department of Pathology, Faculty of Medicine, Federal University of Minas Gerais, CEP 30130 - Belo Horizonte, Minas Gerais, Brazil
DULCIENE M. M. QUEIROZ MÔNICA M. D. A. CABRAL ANA M. M. F. NOGUEIRA ALFREDO J. A. BARBOSA GIFONE A. ROCHA EDILBERTO N. MENDES
McNulty CAM, Dent JC, Curry A, et al. New spiral bacterium in gastric mucosa. J Clin Pathol 1989; 42: 585-91. 2. Lee A, Hazzell SL, O’Rourke J, Kouprach S. Isolation of a spiral-shaped bacterium from the cat stomach. Infect Immunol 1988; 56: 2843-50. 3. Dye KR, Marshall BJ, Frierson HF, Guerrant RL, McCallum RW. Ultrastructure of another spiral organism associated with human gastritis. Dig Dis Sci 1989; 34: 1.
counselled without testing or had an unknown test result, and 704 had a known result-143 of whom had already been diagnosed as seropositive. Of the 561 with an unknown serostatus when approached through the programme 118 (21%) proved HIVpositive. For all testing programmes in Sweden, apart from blood screening, fewer than 1 person in 1000 now tests positive. Thus partner notification seems to be an efficient way to identify people at high risk of HI V infection and to offer them counselling and testing. Analysis of aggregated data from partner notification might also yield information on patterns of spread and risks of transmission. An example is our finding that slightly more than half (143/261) the seropositive partners were known to be HIV carriers. On the assumption that a carrier’s probability of being notified as a partner of an index patient is independent of previous knowledge of his/her infection, this would imply that the true number of HIV carriers in Sweden is about twice the reported number-ie, around 4000. We believe our results show that partner notification can be done in all patients, provided that patient motivation and cooperation are attained by professionalism, empathy, and respect for integrity and
confidentiality. JOHAN GIESECKE
1787-91.
4. Rocha GA, Queiroz DMM, Mendes EN, Lage AP, Barbosa AJA. Simple carbolfuchsin staining for showing C pylori and other spiral bacteria in gastric mucosa. J Clin Pathol 1989; 42: 1004-05. 5. Fischer R, Samisch W, Schwenke E. "Gastrospirillum hominis": another four cases. Lancet 1989; ii: 59. 6. Wyatt J. Detection of Campylobacter pylori by histology. In: Rathbone BJ, Heatley RV, eds. Campylobacter pylon and gastroduodenal disease. Oxford; Blackwell Scientific, 1989: 63-68. 7. Barbosa AJA, Queiroz DMM, Mendes EN, Rocha GA, Lima GF Jr, Oliveira CA. Immunocytochemical identification of Campylobacter pylori gastritis and correlation with culture. Arch Pathol Lab Med 1988; 112: 523-25.
Partner notification for HIV in Sweden SIR,-Partner notification has long been used in the control of treatable sexually transmitted diseases (STD). Its applicability to HIV infection has been discussed,l,2 and the need for research Some results have been published.6-9 The ethical difficulties are considerable, and are much the same as those for the expansion of HIV testing. Prerequisites to partner notification are that carriers thus discovered are not stigmatised and that ample pre-test and post-test counselling and support are available. In Sweden HIV infection was classified in law as an STD in 1985. Cases are anonymously reported to the county Medical Officer of Health, and the patient’s doctor (or a counsellor working with him) is obliged to carry out partner notification. By placing this responsibility with the doctor or counsellor cooperation with the patient becomes part of the total sociopsychological care for the patient, and names of partners need not be known outside the doctor’s office. Patients can choose to refer partners themselves or to ask the doctor for assistance, in which case the index patient’s identity is withheld. In 1989, we initiated a study to measure the outcome of the Swedish programme, with the participation of most departments caring for patients with HIV infection. During the first years of the epidemic partner notification was not common, and even legislation did not immediately change medical routines. The participating departments (about 1500 patients) were asked to supply data only for patients for whom they had attempted partner notification, irrespective of the result. Outcomes of partner notification for 463 index patients from twenty departments were reported. Of these 210 were homosexual or bisexual men, 128 were intravenous drug users, 94 were heterosexually infected, and 31 had received blood transfusions or blood products. Only partners who could be identified were counted; anonymous contacts and partners abroad were excluded. The highest average number of seropositive partners per index patient was found in homosexual and bisexual men (0-78) and drug abusers (0-64), and the lowest was in blood recipients (0 10). A total of 1456 partners were named: 656 could not be traced, 96 were
emphasised.3-’
Department of Epidemiology, National Bacteriological Laboratory, S-105 21 Stockholm, Sweden 1. Osbome J. 444-47. 2. Potterat JJ,
KRISTINA RAMSTEDT TORVALD RIPA GUNILLA RÅDÖ GIANPAOLO SCALIA-TOMBA MIKAEL WESTRELL, for The Swedish Study Group on Partner Notification for HIV Infection
Sounding Board. AIDS: politics and science. N Engl J Med 1988. 318:
Spencer NE, Woodhouse DE, Muth JB. Partner notification in the control of human immunodeficiency virus infection. Am J Public Health 1989: 79: 874-76. 3. Adler M, Johnson A. Contact tracing for HIV infection. Br Med J 1988: 296: 1420-21. 4. Rutherford G, Woo J. Contact tracing and the control of human immunodeficiency virus infection. J AMA 1988: 259: 3609-10. 5. World Health Organisation. Report of the consultation on partner notification for preventing HIV transmission. Geneva: WHO, Jan 11-13, 1989. WHO/GPA/
ESR/89.2. 6. Wykoff R, Heath C, Hollis S, et al. Contact tracing to identify human immunodeficiency virus in a rural community. JAMA 1988: 259: 3563-66. 7. Centers for Disease Control. Partner notification for preventing HIV infection Colorado, Idaho, South Carolina, Virginia. MMWR 1988: 37: 393-96, 441-02. 8. Kristoffersen JE. Case contact tracing and testing in HIV infection. In: Proceedings and abstracts of the Fourth International Conference on AIDS, Stockholm, June 12-16, 1988. Stockholm: Swedish Ministry of Health and Social Affairs, 1988: 354. 9 Clumeck N, Taelman H, Hermans P, Piot P, Schoumacher M, De Wit S. A cluster of HIV infection among heterosexual people without apparent risk factors. N Engl J Med 1989: 321: 1460-62.
"Treating through" hypersensitivity to cotrimoxazole in children with HIV infection SiR,—Dr Putterman and his colleagues (July 7, p 52) report their experience with "treating through" hypersensitivity to cotrimoxaole in an adult with AIDS and Pneumocystis carinii pneumonia (PCP). We have successfully desensitised 7 HIVinfected children to co-trimoxazole. From 1986-88 we treated with intravenous co-trimoxazole 3 HIV-infected children (aged 3-4 years) who had PCP. Hypersensitive reactions were successfully managed with corticosteroids and antihistamines. We then started prophylaxis for PCP with co-trimoxazole (5 mg/kg daily) in 4 HIV-infected children (aged 4-13) at risk of PCP with CD4 counts below 200. In all children we noted allergic exanthema and fever 8-12 days after the start of therapy. We therefore stopped co-trimoxazole and after the skin reactions disappeared we started oral desensitisation with gradual increases in co-trimoxazole dose. The basic solution we used was co-trimoxazole suspension for children (8 mgjh) (solution A). 1 ml of this suspension was diluted with 19 ml distilled water (solution B). The desensitisation regimen was: days 1-4 solution B (day 1 =ml, 2 =2 ml, 3 = 4 ml, 4 =8 ml), days 5-9
solutionA(day5=0’6m!,6=l’2ml,7=2’5ml,8=5ml,9=10mt. From days 10 to 17 we gave 40 mg co-trimoxazole daily. After that we raised the dose every 3 days to 5 mg/kg daily. During the period of desensitisation all children had inhaled pentamidine isethionate
509
(4 mg/kg every 2 weeks). Since
we
began long-term prophylaxis
with co-trimoxazole PCP has not developed in the children so treated. We have found that PCP-prophylaxis by inhalation of pentamidine (4 mg/kg monthly) can be difficult in children under 5 years. In these cases oral PCP-prophylaxis with co-trimoxazole is necessary. To avoid drug-related allergic side-effects in prophylaxis for and treatment of PCP we therefore recommended an initial oral
the pre-disease phase Evidence for an interaction between the two retroviruses at the molecular level comes from in-vitro studies, with stimulation of HIV expression by HTLV-1 gene products.3 Dysregulation of the immune system by HTLV-I/II could also have predisposed this man to the rapid appearance of AIDS. HIV-1 and HTLV-I/Il co-infected individuals should be subject to especially close surveillance.
JEAN-JACQUES LEFRÈRE
desensitisation.
Centre of Paediatrics, Department of Haematology and Klinikum der Johann Wolfgang, 6000 Frankfurt, West Germany
Oncology,
W. KREUZ T. GÜNGÖR CHR. LOTZ M. FUNK B. KORNHUBER
Institut National de Transfusion
Sanguine,
Alexandre-Cabanel, 75015 Paris, France rue
ANNE-MARIE COUROUCÉ MARTINE MARIOTTI ERIC WATTEL ODETTE PROU FRANÇOIS BOUCHARDEAU PATRICK LAMBIN
Schaffar-Deshayes L, Chavanc M, Monplaisir N, et al. Antibodies to HTLV-I p24 sera in blood donors, elderly people and patients with hemopoietic diseases in France and in French West Indies. Int J Cancer 1984; 34: 667-70. 2. Lefrère JJ, Couroucè AM, Lambin P, Fine JM, Doinel C, Salmon C. Clinical and biological features in the 12 months preceding onset of AIDS in HIV-infected subjects.J AIDS 1989; 2: 100-01. 3. Siekevitz M, Josephs SF, Dukovich M, Peffer N, Wong-Staal F, Greene WC. Activation of the HIV-1 LTR by T cell mitogens and the trans-activator protein of 1.
Rapid progression
to AIDS in dual
HIV-1/HTLV-I infection SIR,-Dr Page and colleagues (June 16, p 1439) report that seropositivity for human T-cell leukaemia virus (HTLV) type I/II may adversely affect the clinical outcome in human immunodeficiency virus type 1 (HIV-1) infection. However, the duration of HIV-1 infection was unknown. A 50-year-old black man, bom in the French West Indies (Guadeloupe), was found to be HIV-1 seronegative (ELISA) on routine screening of blood donatons on July 24, 1987 (first donation). In July, 1988, he twice had unprotected intercourse with prostitutes. When he gave blood a second time, on December 16, 1988, he was HIV-1seropositive, this being confirmed by western blot. The patient reported no other extramarital sexual contacts for 4 years; his wife, tested in January, 1989, was HIV-1seronegative. He denied other risk factors for HIV infection (blood transfusion, homosexual acivity, and intravenous drug use). The date of HIV-1 infection could thus be established as July, 1988. During a systematic screening of people at risk for HTLV-I/Il infection, antibodies to HTLV-I/11 were found in the Dec 16,1988, sample (July, 1987, sample not available) by ELI SA and confirmed by western blot, with reactivity to the two main core proteins and to gp46. This HTLV-1/11 seropositivity was not surprising since the man had been born in and had several times visited the French West Indies, where HTLV-I/11 is endemic.1 The presence of DNA for both retroviruses was confirmed by gene amplification via the polymerase chain reaction in peripheral blood mononuclear cells with primer pairs ingag,pol, and LTR regions for HIV-1 and inpol and tax regions for HTLV-I(II. The finding of HIV-1 seropositivity prompted clinical and laboratory follow-up (table). Progression towards disease was evidenced by the decrease in CD4 count. He refused zidovudine therapy, proposed in February, 1990, to prevent AIDS, and was in stage IVA HIV infection within only 23 months of infection with this retrovirus. To date there have been no clinical manifestations of HTLV-I(II infection. The very rapid evolution of HIV-1infection in this case suggests that HTLV-1/11 co-infection may adversely affect the survival pattern of HIV-1 seropositive individuals. Serum p24 antigen remained negative during follow-up, as is sometimes observed in CLINICAL AND BIOLOGICAL FEATURES DURING FOLLOW-UP PERIOD OF PATIENT CO-INFECTED BY HIV-1 AND HTlV-I/11 WITH KNOWN DURATION OF HIV-1 INFECTION
HTLV-I. Science 1987; 238: 1575-78.
Deep venous thrombosis and antibodies to cyproterone acetate SrR,-Oestrogens and combined oral contraceptives are well known risk factors for deep venous thrombosis (DVT).1,2 An immune mechanism may be responsible for the vascular lesions induced by oral contraceptives.3 We describe here a patient with DVT associated with antibodies to cyproterone acetate. A 19-year-old woman was admitted on June 10, 1990, for an acute dyspnoea. Clinical findings revealed a typical right acute proximal DVT. The chest radiograph was normal. The electrocardiogram showed T-wave inversion on leads Vl V2 V3. Her arterial oxygen tension was decreased. Venography revealed thrombi in the right common iliac vein but not in the vena cava. A temporary vena cava filter (’Filtrethery’; Prothia, France) was inserted under fluoroscopic guidance through a right basilar approach, and intravenous streptokinase was started at a dose of 10 000 U/h for 5 days. On June 14 this therapy was changed to intravenous heparin, and this was maintained during 4 weeks. Venography on June 26 revealed no more thrombi. A ventilation perfusion lung scan on June 29 pointed to a right posterobasal defect. Risk factors for DVT4 were then sought but the inherited risks of antithrombin III, protein C, and protein S deficiency were excluded, as were acquired factors such as sepsis, lupus anticoagulant, and cancer. Because this woman had, since February, 1990, been taking the combined oral contraceptive ’Diane 35’ (cyproterone acetate 2 mg, ethinyloestradiol 35 (ig, Schering) antibodies to synthetic oestrogen-progestagen were sought (INSERM U32, Hopital Henri Mondor, Creteil). There were no antibodies to ethinyloestradiol or to progesterone but antibody to cyproterone acetate was found A test for circulating immune complexes (precipitating when serum is brought to 25% saturation in ammonium sulphate) was positive. Although we cannot be certain that cyproterone acetate antibodies caused the DVT, this case is very suggestive. O. LEROY C. BEUSCART E. SENNEVILLE Intensive Care Unit, F. VISTICOT I. TILLIE Centre Hospitalier, M. BRION 59208 Tourcoing, France G. BEAUCAIRE 1. Boston Collaborative
Drug Surveillance Program. Oral contraceptives and venous thromboembolism disease, surgically confirmed gallbladder disease, and breast tumour. Lancet 1978; i: 1399-407. 2. Stadel BV. Oral contraceptive and cardiovascular disease. N Engl J Med 1981; 305: 612-18. 3. Beaumont V, Beaumont JL. Thromboses vasculanes secondaires à la prise d’estro-progestatifs de synthèse: un mecanisme immunologique. Now Presse Méd 1981; 10: 503-07. 4. Anon. Concensus conference: prevention of embolism. JAMA 1986; 256: 744-49.
venous
thrombosis and
pulmonary
