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
(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
