TRALI, una amenaza enmascarada: biología y fisiopatología / TRALI, a masked menace: biology and pathophysiology

El daño pulmonar agudo ocasionado por la transfusión o TRALI (por sus siglas en inglés), definido como la aparición de un distrés respiratorio agudo en un paciente recién transfundido, pasó de ser considerado una complicación infrecuente de la terapia transfusional a ser actualmente la principal causa de mortalidad por transfusión, según sistemas de hemovigilancia de Europa y Norteamérica. Su desarrollo en forma clínicamente reconocible se atribuye a la interacción entre factores dependientes de la unidad transfundida (tipo de componente, presencia de sustancias biológicamente activas, etc.) y el estado de las respuestas celulares en el receptor. La heterogeneidad en cuanto al cuadro clínico de los pacientes afectados,la variación en el volumen infundido, el tipo de componente implicado y el tiempo desde el inicio de la transfusión hasta la aparición de los síntomas, ha hecho evolucionar la explicación a la génesis de este evento adverso, en el afán de incluir los casos sin explicación mediante las distintas hipótesis. Dos interesantes acercamientos patogénicos resultan la teoría de dos golpes y el modelo basado en el umbral que impone la relación entre los distintos factores de riesgo. La naturaleza multicausal del TRALI y el sinnúmero de variables que pueden influir en su aparición y reconocimiento, continúan haciendo de este un reto médico importante en el contexto de la medicina transfusional, donde su mejor enfoque terapéutico sigue siendo el preventivo(AU)

Transfusion-related acute lung injury (TRALI) defined as the onset of an acute respiratory distress in a recently transfused patient, has passed from been considered a rare complication of transfusion therapy to be the leading cause of transfusion-associated death, as reported by hemovigilance systems in Europe and America. In a previous paper definition, epidemiology and some clinical aspects of TRALI are reviewed. Now we focused our efforts in reviewing the incompletely understood world of its pathogenesis. Clinically recognizable TRALI´s development depends on the interaction between risk factors from both the transfused component unit (as the kind of component and substances within it) and receiver patient´s cellular response. Heterogeneity of clinical features, transfused volumes, component type and time elapsed from the beginning of transfusion to the onset of symptoms have pushed the explanations for its genesis to evolve in an effort to include as much cases as the different hypotheses allowed. Two interesting approaches to TRALI´s pathogenesis are the two hit; theory and the threshold; model imposed by risk factors interactions. The large diversity of variables and causes which can influence its onset and clinical recognition continue to make it a real challenge for clinicians, mainly within transfusion medicine, where the best therapeutic approach available is prevention(AU)

Human Neutrophil Alloantigen-3a Alloimmunization among Pregnant Korean Women / 대한수혈학회지

BACKGROUND: Alloantibodies against human neutrophil alloantigen (HNA)-3a are associated with severe and fatal transfusion related acute lung injury (TRALI). HNA-3 genotyping and HNA-3a antibody (Ab) identification are essential to diagnosis and prevention of TRALI caused by HNA-3a Ab. However there had been no laboratory for HNA-3a Ab identification in Korea. The aims of this study were to establish the HNA-3a Ab test in Korea and to estimate the incidence of HNA-3a alloimmunization among pregnant Korean women. METHODS: HNA-3a homozygotes and HNA-3b homozygotes were identified by HNA-3 genotyping. Three HNA-3a homozygotes and three HNA-3b homozygotes are included in the granulocytes panel, which consisted of 10 donors for granulocytes. Sera from 650 pregnant Korean women were tested for granulocyte Ab using a mixed passive hemagglutination assay (MPHA). When a HNA-3a Ab was detected, the woman's HNA-3 was typed to support her HNA-3a alloimmunization. RESULTS: MPHA showed positive reactions in the sera from 26 women (4.0%, 26/650). HLA Abs were detected in 18 women (2.8%, 18/650), among whom HNA Abs were identified simultaneously in 7 women. Granulocyte Abs were detected in sera from 15 women (2.3%, 15/650). The incidence of HNA-3a, HNA-1b, HNA-1a, HNA-2a, and unidentified HNA Abs among pregnant Korean women was 0.77% (5/650), 0.77% (5/650), 0.62% (4/650), 0.15 (1/650), and 0.31% (2/650), respectively. CONCLUSION: In this study, we established the HNA-3a Ab test using MPHA for diagnosis and prevention of TRALI caused by HNA-3a Ab. The incidence of HNA-3a Ab in pregnant Korean women was 0.77% (5/650).