sample was confirmed positive if it demonstrated immunoreactivity to gag product p24 and to env product gp46 and/or gp61/68 on one or both confirmatory assays. None of these tests distinguishes antibodies to HTLV-1 and HTLV-11. The prevalence (0-011%) is one of the


known in


The 5 positive donors-2 women aged 21 and 45, 2 men aged 41, and a man of unknown age--were negative for HBs antigen and for antibodies to HBc and HIV. Further information could be obtained on 1 white female donor. She had received blood transfusions before 1974 and had frequent sexual intercourse with men from the French West Indies. Since May, 1984, the French Ministry of Health has recommended, for continental France, the testing of donors from endemic zones or to use only plasma for fractionation. These measures seem incomplete since 3 of the HTLV-I/II positive donors were French whites. Centre Régional de Transfusion Sanguine, 34000 Montpellier, France


Virology Laboratory, Centre Hospitalier Bretonneau, Tours


BBAb = antibodies to B burgdorferi. *Intrathecal synthesis of IgG expressed as percentage of total CSF tSpeciflc intrathecal activity/specific serum response 5

The differentiation of active neuroborreliosis from previous and fortuitous exposure to the organism may thus be very difficult. Intrathecal antibody production seems to be a useful marker of active CNS infection by B burgdorferi.9 The patients referred to by Bouma et all may have had GBS related to B burgdorferi antibodies but a diagnosis of active neuroborreliosis remains open. We agree with Mancardi et al2 on the need to differentiate GBS associated with serological response to B burgdorferi from true neuroborreliosis. Nevertheless, in the absence of specific CSF antibodies and pleocytosis, seropositivity for B burgdorferi in a patient with neurological disease (including GBS) could be fortuitous.10

A. M. COUROUCE, Institut National de Transfusion Paris 1.


and the Retrovirus Study Group, French National Society of Blood Transfusion

Schaffar-Deshayes L, Chavance M, Montplaisir N, et al. Antibodies to HTLV-I p24 in sera of blood donors, elderly people and patients with homopoietic diseases in France and the French West Indies. Int J Cancer 1984; 34: 667-70.

2. Lee

H, Burczak J, Laitila V,

al. HTLV-I and HTLV-II infection in US blood donors. Vth International Conference on AIDS (Montreal, 1989): 77. 3. Okochi K, Sato H. Transmission of adult T-cell leukemia virus (HTLV-I) through blood transfusion and its prevention. AIDS Res 1986; 2 (suppl 1): 157-61. 4. van der Poel C, Lelie N, Reesink H, et al. Prevalence of HTLV-I antibodies in blood donors in the Netherlands. Vth International Conference on AIDS (Montreal, 1989): 248. 5. Derivianaki A, Malliaraki-Pinetidou E, Georgoulias Y. Prevalence of HTLV-I in Greek blood donors. Vth International Conference on AIDS (Montreal, 1989): 145. 6. Leinikki P, Manila J, Koistinen J, et al. Screening for HTLV-I antibodies among Finnish blood donors, haemophiliacs and HIV suspected. Vth International Conference on AIDS (Montreal, 1989): 141. et

Antibodies to Borrelia burgdorferi in Guillain-Barré syndrome SIR,-Four cases of Guillain-Barre syndrome (GBS) thought to be related to Borrelia burgdorferi infection have been reported,1,2 and Bourdel et aP deal with this issue too. We present our experience in four cases meeting diagnostic criteria for GBS4 with seropositivity (by indirect immunofluorescence) to B burgdorferi (table). Patient 4 has had three relapses in the past 7 years. Only in patient 2 could we demonstrate intrathecal synthesis5 of specific antibodies. In this patient ceftriaxone had no effect on the expected natural course of the illness. An acute demyelinating polyneuropathy related to B burgdorferi infection and presenting as GBS but with cerebrospinal fluid (CSF) pleocytosis, has been described.6 Unlike typical GBS neurological involvement due to B burgdorferi infection is usually associated with CSF lymphocytic pleocytosis. Comparison of the CSF findings in idiopathic GBS and in Bannwarth syndrome due to B burgdorferi infection suggests that the features which indicate a diagnosis of neuroborreliosis are mononuclear pleocytosis, severe blood-brain barrier damage, a very high CSF IgM index, and oligoclonal IgG bands.’ The significance of high titre specificIgG in serum is uncertain, and we do not know whether this indicates active disease or not. Titres may remain high for a long time after recovery.s Positive antibody titres to B burgdorferi could be common in endemic areas.


Sections of Neurology and Microbiology, Hospital Ntra Sra de Aránzazu, San Sebastián 20080, Spain


1. Bouma PAD, Carpay HA, Rijpkema SGT. Antibodies to Borrelia burgdorferi in Guillain-Barré syndrome. Lancet 1989; ii: 739. 2. Mancardi GL, Del Sette M, Primavera A, Farinelli M, Fumarola D. Borrelia burgdorferi infection and Guillain-Barré syndrome. Lancet 1989; ii. 985-86. 3. Bourdel A, Viader F, Dupuy B, Courtheoux F, Chapon F, Thenint JP, Lechevalier B Maladie de Lyme révélée par une polyradiculonéurite sans hypercytose du liqude céphalorachidien. Presse Med 1988; 17: 1214-15. 4. Asbury AK. Diagnostic considerations in Guillain-Bitré syndrome. Ann Neurol 1981, 9 (suppl): 1-5. 5. Castaigne P, Schuller E. Les protéines du liquide cephalorachidien du benjoin colloidal a nos jours: l’étude de l’immunité intrathécale. Rev Neurol (Pans) 1988; 144: 409-15. 6. Sterman AB, Nelson S, Barclay P. Demyelinating neuropathy accompanying Lyme disease. Neurology 1982; 32: 1302-05. 7. Henriksson A, Link H, Cruz M, Stiemstedt G. Immunoglobulin alnomalities in cerebral fluid and blood over the course of lymphocytic meningoradiculitis (Bannwarth’s syndrome). Ann Neurol 1986; 20: 337-45. 8. Craft JE, Grodzicki RL. Antibody response in Lyme disease, evaluation of diagnostic tests. J Infect Dis 1984; 149: 789-95. 9. Halperin JJ, Luft BJ, Anand AK, et al. Lyme neuroborreliosis: central nervous system manifestations. Neurology 1989; 39: 753-59. 10. Mauch E, Vogel P, Kornhuber HH. Borrelia antibody titres: course in neurological diseases. Lancet 1989; ii: 332.

Urinary thromboxane metabolites in pre-eclampsia SIR,-Dr Fitzgerald and colleagues (March 31, p 751) demonstrated that the urinary excretion of both 2,3-dinorthromboxane B2 (TxB2) and 11-dehydro-TxBz, reflecting largely platelet thromboxane generation, is greater in patients with pregnancy-induced hypertension than in normotensive pregnant women.

We have studied the urinary excretion of 2,3-dinor-TxB2 in primigravidae at a gestational age of 31-32 weeks.1 Women at risk of pregnancy-induced hypertension were defined by the loss of refractoriness to the pressor effect of angiotensin 11.2 10 angiotensin-sensitive primigravid women and 10 non-sensitive primigravidae were compared. 2,3-dinor-Txb2 was extracted, purified by high-pressure liquid chromatography, and assayed.’ Urinary 2,3-dinor-TxB, was about three times higher in the pregnant women at risk (1524 [SE 493] vs 528 [87] pgmg

Antibodies to Borrelia burgdorferi in Guillain-Barré syndrome.

1168 SEROLOGICAL AND CSF FINDINGS sample was confirmed positive if it demonstrated immunoreactivity to gag product p24 and to env product gp46 and/o...
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