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1.
Ned Tijdschr Geneeskd ; 152(25): 1419-25, 2008 Jun 21.
Artigo em Holandês | MEDLINE | ID: mdl-18624005

RESUMO

OBJECTIVE: Determination of factors related to the need for transfusion in premature infants. DESIGN: Descriptive. METHOD: The need for transfusion in premature infants was determined in 2 academic centres: University Medical Center Utrecht and Leiden University Medical Center, The Netherlands. The data had been acquired in another study. The factors under study were: hospital, pregnancy duration, birth weight, gender, time of clamping of the umbilical cord, total volume of blood sampled for diagnostic purposes, number of days of mechanical ventilation, total duration of admission and duration of the admission to the Neonatal Intensive care unit. Both hospitals followed the national interdisciplinary practice guideline 'Blood transfusion'. RESULTS: The total volume ofsampled blood for diagnosis, the duration of the mechanical ventilation and the admission period were related to a greater need for transfusion. On the other hand, the chance of transfusions diminished with longer pregnancy duration or increased birth weight. The difference in need for blood transfusion between both centres was significant. The total volume of transfused erythrocytes showed a strong correlation with the volume sampled for diagnostic procedures. CONCLUSION: Anaemia in neonates is strongly related to the amount of blood taken for diagnostic procedures. Alternatives for blood transfusions in premature infants, and consequently for the reduction of the number of donors per child, are to be sought in delayed clamping of the umbilical cord, use of erythropoietin and use ofautologous umbilical cord blood.


Assuntos
Transfusão de Sangue , Eritropoetina/administração & dosagem , Sangue Fetal/fisiologia , Recém-Nascido Prematuro/sangue , Cordão Umbilical , Anemia Neonatal/sangue , Anemia Neonatal/prevenção & controle , Diagnóstico Diferencial , Feminino , Humanos , Recém-Nascido de Baixo Peso/sangue , Recém-Nascido , Masculino , Fatores de Tempo , Cordão Umbilical/cirurgia
2.
Neth J Med ; 61(1): 19-21, 2003 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-12688565

RESUMO

Although it has been long known that in theory the use of cholestyramine can cause coagulopathy due to reduced absorption of vitamin K, only a few cases have been reported. In those cases the coagulopathy occurred within a few weeks to months after the start of therapy. We report a patient with severe pruritus due to intrahepatic cholestasis, who was on cholestyramine therapy for over 25 years before haemorrhage occurred. This case demonstrates that one should be aware of the possibility of depletion of fat-soluble vitamins during the long-term use of cholestyramine.


Assuntos
Antipruriginosos/efeitos adversos , Resina de Colestiramina/efeitos adversos , Hemorragia/induzido quimicamente , Deficiência de Vitamina K/induzido quimicamente , Adulto , Antipruriginosos/administração & dosagem , Resina de Colestiramina/administração & dosagem , Humanos , Masculino , Fatores de Tempo
3.
Thromb Haemost ; 87(5): 880-7, 2002 May.
Artigo em Inglês | MEDLINE | ID: mdl-12038793

RESUMO

Low density lipoprotein (LDL) increases the sensitivity of human platelets for agonists by activating p38MAPK. Antibody 4G3 disturbs apoB100 binding to the classical apoB/E receptor and inhibits LDL-induced p38MAPK activation, whereas an antibody against a distal domain on apoB 100 has no effect. Peptide RLTRKRGLKLA mimics the binding domain of apoB 100 called the B-site and activates platelet p38MAPK. Activation by B-site peptide is dose-dependent, transient and followed by desensitization, in accordance with receptor-mediated signalling. A scrambled peptide and a partially homologous peptide RKLRKRLLRDA mimicking the apoB/E receptor binding site of apoE in high density lipoprotein (HDL) also activate p38MAPK albeit 40% weaker, but an uncharged peptide lacks p38MAPK activating capacity. LDL and B-site peptide bind to the same binding sites and initiate similar signalling to p38MAPK and cytosolic phospholipase A2. Thus, LDL and to a lesser extent HDL activate platelets via specific domains in the protein moiety that recognize receptors of the LDL receptor family.


Assuntos
Apolipoproteínas B/fisiologia , Plaquetas/metabolismo , Lipoproteínas LDL/fisiologia , Ativação Plaquetária/fisiologia , Receptores de Lipoproteínas/metabolismo , Sequência de Aminoácidos , Apolipoproteína B-100 , Apolipoproteínas B/química , Apolipoproteínas B/farmacologia , Apolipoproteínas E/farmacologia , Sítios de Ligação , Plaquetas/efeitos dos fármacos , Relação Dose-Resposta a Droga , Ativação Enzimática/efeitos dos fármacos , Humanos , Lipoproteínas HDL/química , Lipoproteínas HDL/farmacologia , Lipoproteínas HDL/fisiologia , Lipoproteínas LDL/química , Lipoproteínas LDL/farmacologia , Sistema de Sinalização das MAP Quinases/efeitos dos fármacos , Sistema de Sinalização das MAP Quinases/fisiologia , Proteínas Quinases Ativadas por Mitógeno/sangue , Dados de Sequência Molecular , Fragmentos de Peptídeos/farmacologia , Fosforilação , Processamento de Proteína Pós-Traducional/efeitos dos fármacos , Estrutura Terciária de Proteína , Receptores de Lipoproteínas/efeitos dos fármacos , Proteínas Quinases p38 Ativadas por Mitógeno
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