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1.
Ann Cardiol Angeiol (Paris) ; 52(2): 125-8, 2003 Apr.
Artigo em Francês | MEDLINE | ID: mdl-12754971

RESUMO

PURPOSE: This retrospective stady has for objective to compare the effect of Tranexamic Acid (TA) to the low dose of aprotinin (AP) in primary mitral valve surgery in terms of blood loss and transfusion requirements. METHODS: Are included in the study operated patients of a valvulopathy mitral isolated. Two groups of 50 patients are collected. The tranexamic acid group has received 30 mg kg-1 the acid tranexamic and the aprotinin group has received a low regimen as 500,000 UIK of aprotinin. Blood loss by the chest drains are assessed to different times during first 24 hours post cardiopulmonary bypass. In the same way, we have measured the platelet and fibrinogen count. Blood products were administered according to a classic protocol. RESULTS: The two groups are comparable clinic and echocardiographic parameters what authorizes us an appariement acceptable. Various cardiopulmonary bypass times are almost similar. We noticed a tendency to excessive blood loss processed by low regimen aprotinin and a significant rate difference of platelet and the fibrinogen level. But no complication has been recorded in the two groups. CONCLUSIONS: This study demonstrates relatively different effect of the two fibrinolytics inhibitors in primary mitral valve surgery. As for the superiority of one of the two produces, it needs a confirmation by a randomised and controlled clinical trial.


Assuntos
Antifibrinolíticos/administração & dosagem , Aprotinina/administração & dosagem , Perda Sanguínea Cirúrgica/prevenção & controle , Hemostáticos/administração & dosagem , Valva Mitral/cirurgia , Ácido Tranexâmico/administração & dosagem , Adulto , Ponte Cardiopulmonar , Relação Dose-Resposta a Droga , Feminino , Fibrinogênio/análise , Doenças das Valvas Cardíacas/cirurgia , Humanos , Masculino , Contagem de Plaquetas , Estudos Retrospectivos , Resultado do Tratamento
2.
Presse Med ; 15(8): 383-6, 1986 Feb 22.
Artigo em Francês | MEDLINE | ID: mdl-2938157

RESUMO

The sera of 74 diabetic patients and of their first degree relatives were studied for 4 different types of islet cell antibodies (ICA, CFICA, ICSA, ICACT) and the results were compared according to the HLA genotype. Seventy two percent of the patients' sera were positive for at least one type of auto-antibody. Two types of auto-antibodies were observed: anticytoplasmic antibodies (ICA and CFICA), and surface antibodies (ICSA and ICACT). The different types of antibodies were not associated with any HLA-DR. These antibodies were also present in 15% of the healthy relatives. The fact that they were detected in the sera of siblings sharing no haplotype with the proband, some of them bearing neither DR3 nor DR4 antigens, suggests that non HLA linked genes and/or environmental factors partly control their secretion.


Assuntos
Autoanticorpos/classificação , Diabetes Mellitus Tipo 1/imunologia , Antígenos HLA/genética , Ilhotas Pancreáticas/imunologia , Autoanticorpos/análise , Diabetes Mellitus Tipo 1/genética , Diabetes Mellitus Tipo 1/fisiopatologia , Feminino , Humanos , Masculino , Fatores de Tempo
3.
Presse Med ; 12(36): 2247-51, 1983 Oct 15.
Artigo em Francês | MEDLINE | ID: mdl-6226964

RESUMO

Insulin-dependent diabetes results from the interaction of genetic, immunological and environmental factors. In view of the association between insulin-dependent diabetes and HLA system, it has been postulated that the diabetogenic gene(s) is (or are) located in the region of the DR locus in that system. The hypothesis of viral factors is supported by epidemiological arguments and experimental models but has only been exceptionally confirmed in man. The fact that anti-islet antibodies are frequently detected at the onset of insulin-dependent diabetes or even before the first symptoms develop suggests that an auto-immune mechanism might be involved in the destruction of beta-cells. Although the mode of inheritance of genes supposed to predispose to insulin-dependent diabetes as well as the mechanisms behind the pancreatic lesion are still poorly understood, determining "markers" of the disease should eventually make it possible to detect subjects at risk of diabetes and to prevent its development.


Assuntos
Diabetes Mellitus Tipo 1/etiologia , Formação de Anticorpos , Autoanticorpos/análise , Diabetes Mellitus Tipo 1/induzido quimicamente , Diabetes Mellitus Tipo 1/genética , Diabetes Mellitus Tipo 1/imunologia , Meio Ambiente , Humanos , Imunidade Celular , Risco , Viroses/complicações
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