RESUMO
A retrovirus human T cell lymphotropic virus type I (HTLV-I), is an essential but not a sufficient aetiological factor for tropical spastic paraparesis (TSP). Because some TSP patients have biological false positive tests for trepomemal infections (BFP-STS), we used EISA to study BFP-STS and anticardiolipin antibodies in 42 Jamaican TSP patients. The data indicate that in TSP anticardiolipin antibodies accur in about 26 percent of patients, are associated with biological false positive treponemal serology, are relatively restricted to the IgA isotype and may be induced by HTLV-I or other non-treponemal infections. (Au)
Assuntos
Adulto , Humanos , Feminino , Masculino , Técnicas In Vitro , Imunoglobulina A , Anticorpos Antifosfolipídeos , Paraparesia Espástica Tropical , Vírus Linfotrópico T Tipo 1 Humano , Retroviridae , Manifestações Neurológicas , Vírus Linfotrópico T Tipo 1 Humano/patogenicidade , Infecções por Treponema/epidemiologia , Ensaio de Imunoadsorção Enzimática , Sífilis/diagnóstico , Região do CaribeRESUMO
Antibodies against phopholipids are associated with recurrent arterial and venous thromboses, thrombocytopenia and pregnancy loss. This antiphospholipid antibody syndrome is most commonly seen in systemic lupuis erythematosus (SLE); in previous studies we demonstrated that deficiency alleles of the fourth component of the complement system are associated with the presence of antiphospholipid antibodies in SLE. A primary antiphospholipid antibody syndrome is also known to occur in the absence of evidence of a defined connective tissue disorder; the aetiological relationship of this primary antiphospholipid antibody syndrome to SLE is unclear, but previous studies have suggested a genetic basis for some components of this syndrome. We investigated a 26-year-old woman who presented in 1986 with all the features of primary anti-phospholipid antibody syndrome. During the previous 4 years she had developed one episode of deep venous thrombosis and two pregnancy losses during the second trimester. On presentation, she was thrombocytopenic, had a false positive test for syphilis, a circulating lupus anticoagulant and persistently very high levels of IgG anticardiolipin antibody. However, antinuclear antibodies were repeatedly absent from serum. She subsequently developed two episodes of stroke, with radiological evidence of cerebral infarction. The anticardiolipin antibody levels were incompletely suppressed by plasmaphaeresis and intravenous cyclophosphamide, but she improved clinically after anticoagulation with warfarin was instituted. Studies of plasma and of DNA from this patient revealed the presence of a large heterozygous gene deletion at one of loci of the fourth component of the complement system (C4A) and the adjacent 21 hydroxylase-A gene. This deletion was present in only 7 percent of a control normal population. We and others have shown this deletion to be a risk factor for systemic lpus erythematosus. We are continuing long-term follow-up of this patient and studies among her family members to further elucidate the relationship of this and other genetic factors to the antiphospholipid antibody syndrome. This is the first report of the presence of a C4A gene deletion in a patient with the primary antiphospholipid antibody syndrome and it supports the idea that there is a close genetic relationship between this syndrome and systemic lupus erythematosus (AU)