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Los pacientes alcohólicos pueden padecer diversos trastornos hematológicos, que pueden afectar los glóbulos rojos, los leucocitos y las plaquetas siendo el resultado de múltiples factores, entre los cuales tenemos: el efecto directo del alcohol sobre la médula ósea, la presencia de una enfermedad hepática aguda o crónica, la insuficiente alimentación de estos pacientes, y el sangrado. En los estudios realizados la incidencia de trastornos hematológicos afecta de manera predominante la serie roja, en segundo término la serie blanca y por último la serie plaquetaria.

Serie roja

La principal alteración se traduce en anemia. Esta pasa por varias etapas:

• Primera etapa: se aprecia un equilibrio vitamínico negativo, secundario a la sustitución del alcohol por otros alimentos de la dieta.
• Segunda etapa: que comienza una semana después de que se comenzó a beber en exceso y una dieta inadecuada la cual se traduce en cambios megaloblásticas en la médula ósea.
• Tercera etapa: la aparición de sideroblastos en anillo en los precursores eritroides en medula ósea.

En estos pacientes alcohólicos es frecuente observar la presencia de varios tipos de anemias hemolítica. Se describe una estomatocitosis transitoria sin acantositosis ni hiperlipidemia, la cual cede cuando el paciente deja de beber pero a parece una vez que el paciente reanuda sus hábitos. Se describe una anemia hemolítica con glóbulos rojos en forma de equinocito “equinocitosis” asociado a pacientes portadores de cirrosis hepática alcohólica, ictericia, hepatomegalia y esplenomegalia. Su característica más resaltante es la poiquilocitosis dada por equinocitos lo cual es un defecto de membrana del glóbulo rojo debido a un aumento en su contenido de colesterol y de su relación colesterol-fosfolípidos.

El mecanismo de anemia se produce debido a que estos globulosa rojos así deformados son más rígidos y por ende son destruidos por el bazo. El síndrome de Zieve, es una anemia hemolítica transitoria que se caracteriza por anemia, triglicéridos elevados o hipercolesterolemia en un paciente con ingesta masiva de alcohol.

Las alteraciones megaloblásticas que se observan en la medula ósea de estos pacientes son debido a deficiencia de acido fólico más que a vitamina B12 cuyos niveles siempre están normales.

Mecanismos implicados: dieta inadecuada por carecer la misma de acido fólico, efecto directo del alcohol sobre el metabolismo del acido fólico lo que ocasiona malaabsorción de esta substancia. La manifestación morfológica de este efecto es la presencia de vacuolas en los precursores eritroides así como los cambios megaloblásticos en las tres series hematopoyéticas.

También se describe anomalías sideroblásticas reversibles en pacientes con alcoholismo grave. Se traduce en anemia, con una anisocromía en los frotis de sangre periférica, con cifras bajas de acido fólico sérico, hierro sérico elevado, y sideroblastos en anillo en los precursores eritroides en médula ósea. Estos cambios son debidos a que el alcohol impide la transformación de la piridoxina en fosfato de piridoxal lo que se traduce en un bloqueo de la enzima sintetasa de acido amino-levulínico para formar acido amino-levulínico para la síntesis del grupo Hem, con un aumento del contenido del hierro en las mitocondrias.

Serie blanca

Se describe leucopenia con neutropenia. Mecanismos implicados: A) trastornos cuantitativos: efecto directo del alcohol sobre la maduración celular, déficit de acido fólico, hiperesplenismo B) trastornos cualitativos: quimiotaxis, adherencia y actividad fagocítica disminuida, lo que impide la eliminación adecuada de las bacterias inhaladas al pulmón. C) Reducción de las células T y disminución de la transformación de los linfocitos de ahí la alta incidencia de tuberculosis en estos pacientes.

Serie plaquetaria

Se describe trombocitopenia. Mecanismos implicados: déficit de acido fólico, efecto directo del alcohol sobre los precursores de las plaquetas en la médula ósea de allí que es común observar trombocitosis a medida que el paciente se recupera de este efecto, hiperesplenismo. También se describe trombocitopatías, debido a una disminución de la agregación plaquetaria con prolongación del tiempo de sangría, disminución de la liberación de tromboxano A2 de las plaquetas, anomalías que se normalizan 1-3 semanas de suspendido la ingesta alcohólica.

Trastornos de la coagulación

No se observan cambios significados como consecuencia del consumo agudo o crónico de alcohol en la hemostasia secundaria a no ser que coexista con una hepatopatía importante (déficit de los factores vitamino K dependientes), ya que los factores de la coagulación suelen encontrarse dentro de los rangos normales. No obstante, en los alcohólicos crónicos, se aprecia una disminución de la antitrombina III, lo que explica la trombosis espontánea en algunos pacientes.

Se ha postulado que no todos las alteraciones de la coagulación en estos pacientes son el resultado de un déficit en la síntesis hepática, ya que las alteraciones en la hemostasia secundaria podría ser consecuencia de la interacción directa del acetaldehído con las diversas proteínas de la coagulación.


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