RESUMO
Anticardiolipin and anti-beta2GP1 antibodies were measured in 50 patients with HTLV-1-associated Myelopathy-Tropical Spastic Paraparesis (HAM-TSP) and the results were compared with those obtained for 34 HTLV-1-positive and 35 HTLV-1-negative controls, as well as 128 SLE patients. aCL but not anti-beta2GP1 was associated with HTLV-I infection. aCL was more prevalent than anti-beta2GP1 (32 percent vs. 8 percent) and was not associated with anti-beta2GP1 in HAM-TSP. IgA was the dominant isotype of aCL and anti-beta2GP1. The data suggest that tin HAM-TSP, IgA aCL are frequent and are associated with HTLV-1 infection.(Au)
Assuntos
Humanos , Anticorpos Anticardiolipina/sangue , Anticorpos Antifosfolipídeos/sangue , Glicoproteínas/imunologia , Paraparesia Espástica Tropical/imunologia , Estudos de Casos e Controles , Infecções por HTLV-I/imunologia , Imunoglobulina A/sangue , Isotipos de Imunoglobulinas/sangue , Lúpus Eritematoso Sistêmico/imunologiaRESUMO
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)
Assuntos
Relatos de Casos , Humanos , Feminino , Adulto , Síndrome Antifosfolipídica/complicações , Síndrome Antifosfolipídica/genética , Marcadores Genéticos , SeguimentosRESUMO
Between October 1983 and May 1986, 17 cases of childhood acute lymphoblastic leukemia (ALL) were admitted to the General Hospital, Port of Spain, Trinidad. Fifteen of those cases were under 10 years of age, seven of whom presented with joint or bone pains. Boys outnumbered girls by almost 5:1 and the ethnic distribution showed a preponderance of patients of East Indian origin. At last follow-up (May 1989), the survival rate of the 15 under-ten-year-old patients was 71 percent. Immunophenotype studies on nine of the 17 patients revealed six carrying T cell markers and three carrying markers suggestive of a pre-B phenotype. HLA tissue typing on ten patients showed an enhanced frequency of the HLA-B40 antigen when compared with controls (p less than 0.05). This antigen was present in six of the patients typed and four carried the HLA-A2 and B40 antigens together, two of whom also carried the CW3 antigen and the other two carried untypable C antigens. Three of the four carrying HLA-A2 and B40 have died. Two of the three pre-B cases also carried the HLA-A2 and B40 antigens. HLA studies on three of the four families showed that HLA-A2 and B40 were on the same chromosome, i.e., a haplotype inherited from the mother in each case. None of the cases carried the HLA-B5 antigen although this antigen had a frequency of 37.8 percent in the control group (p less than 0.05 percent). None of the controls with the HLA-B40 antigen carried the CW3 antigen. Further evidence of a disease association must await typing of the D locus antigens but current evidence would suggest an association between HLA-B40 and childhood ALL in Trinidad. (AU)
Assuntos
Humanos , Lactente , Pré-Escolar , Criança , Masculino , Feminino , Antígenos de Diferenciação/análise , Antígenos HLA/análise , Leucemia-Linfoma Linfoblástico de Células Precursoras/imunologia , Seguimentos , Antígeno HLA-A2/análise , Antígenos HLA-B/análise , Antígenos HLA-C/análise , Leucemia-Linfoma Linfoblástico de Células Precursoras/etnologia , Leucemia-Linfoma Linfoblástico de Células Precursoras/genética , Fenótipo , Trinidad e TobagoRESUMO
Serum and urinary urate concentrations were studied in 44 patients with homozygous sickle cell (SS) disease, and in 27 controls with normal haemoglobin. Hyperuricaemia (>0.39 mmol/1(6.5 mg/100ml)) occurred in 41 percent of SS patients and inversely correlated with renal urate clearance but not with indices of bone marrow turnover. Higher serum urate concentrations occurred in patients with proteinuria, probably due to associated tubular damage. Higher serum urate concentrations and lower urate clearance occurred in males compared to females (AU)
Assuntos
Humanos , Criança , Adolescente , Adulto , Pessoa de Meia-Idade , Masculino , Feminino , Ácido Úrico/sangue , Anemia Falciforme/sangue , Ácido Úrico/urina , Fatores SexuaisRESUMO
The role of haemolysis in producing deficient complement function in homozygous sickle cell disease was studied by measuring indices of complement activation and of haemolysis in 30 asymptomatic patients. Plasma concentration of C3d (an index of increased C3 turnover) was elevated in 40 percent of patients and modest decreases in serum concentration of C3 and functionally (haemolytically) active factor B were found. There was a positive correlation between C3d and plasma haemoglobin concentration (r = 0.56, p less than 0.005). Reticulocyte count and foetal haemoglobin concentration also contributed to variation in C3d, though to a lesser extent than plasma haemoglobin. Intravascular haemolysis in sickle cell disease may produce activation of complement and thus cause partial depletion of functional factor B and C3. This may reduce the immune function of the alternative pathway. (AU)
Assuntos
Humanos , Adolescente , Adulto , Pessoa de Meia-Idade , Masculino , Feminino , Anemia Falciforme/imunologia , Ativação do Complemento , Hemoglobinas/análise , Traço Falciforme/imunologia , Proteínas do Sistema Complemento/análise , Complemento C3/análise , Testes Hematológicos , Hemólise , Análise de Regressão , Traço Falciforme/sangueRESUMO
Of 137 hypertensive black Jamaicans who took methyldopa for a mean period of 36 months, a positive ANA was found in 1.5 percent and a positive direct Coombs' test in 0.7 percent. In 36 patients in whom hydralazine was induced in the therapeutic regimen, a positive ANA was seen in only 6 percent. These results suggest that in black populations, immunologic abnormalities induced by antihypertensive drugs are less common than has been reported in white patients. (AU)
Assuntos
Humanos , Pessoa de Meia-Idade , Masculino , Feminino , Anticorpos Antinucleares , Hipertensão/tratamento farmacológico , Metildopa/farmacocinética , Teste de Coombs , Metildopa/uso terapêuticoRESUMO
Haemoglobin solutions (concentration >1.5mg/ml), prepared from lysates of erythrocytes from a normal subject and from a patient with sickle cell anaemia, caused factor B and C3 cleavage and loss of haemolytic activity of factor B when incubated with fresh autologous serum. Under the same experimental conditions, preparations of erythrocyte stroma or of buffy coat lysates did not produce factor B and C3 cleavage. This reaction required Mg++ but not Clq or C4, indicating that the alternative complement pathway was activated (Summary)