[Free radicals and cytotoxicity of ethanol over human leucocytes in peripheral blood]. / Radicales libres y citotoxicidad del etanol en los leucocitos humanos de sangre venosa periférica.

INTRODUCTION: The ingestion of alcohol produces oxydative stress generating free radicals of oxygen and ethanol. These free radicals have a molecular reactive ability and, therefore, they play an important role in the production of the injury which appears in the liver and in other organs and tissues. We have done an "in vitro" study where we analyse the oxydative status at rest and the respiratory explosion produced by ethanol at final concentrations of 50 and 25 mM and by the phagocytosis of a previously opsonized concentrate of bacteria (E.coli) in human leucocytes taken from peripheral blood of six healthy persons. METHOD: We have used 1.2.3. dihydrorhodamine (non-fluorescent) as the oxydative marker because it is transformed in rhodamine (fluorescent), which is quantitatively studied by Flow Cytometry. RESULTS: The peak of oxydative stress is reached with the bacteria in the phagocytes (monocytes 50% and granulocytes 90%) and it has a significant difference with the control group. By adding ethanol at 50 mM we have seen an statistic significant difference in oxydative stress in the cells of all three types (lymphocytes 9.19%, monocytes 32% and granulocytes 36%). With a concentration of 25 mM of ethanol the oxydative stress is increased but without a significant difference (lymphocytes 2.39%, monocytes 9.22% and granulocytes 4.46%). We have also seen toxic cellular effect which reaches the 40.75% of cells with ethanol at 50 mM, the 10.7% with ethanol at 25 mM and the 5.65% with bacteria. CONCLUSION: The oxydative stress caused by the production of oxygen and ethanol free radicals in the leucocytes, and the proved cytotoxic effect of ethanol may play an important role over the qualitative and the quantitative leucocyte disorder on different organs and tissues of the alcoholic patient.

Radicales libres y citotoxicidad del etanol en los leucocitos humanos de sangre venosa periférica / Free radicals and cytotoxicity of ethanol over human leucocytes in peripheral blood

Introducción: La ingesta de alcohol desencadena stress oxidativo generador de radicales libres de oxígeno y de etanol que, por su capacidad reactiva molecular, juegan un importante papel en la producción de las lesiones que aparecen en el hígado y en otros órganos y tejidos. Hemos realizado un estudio "in vitro" analizando el estado oxidativo en reposo y la explosión respiratoria desencadenada por Etanol, a concentraciones finales de 50 y 25 mM y por la fagocitosis de un concentrado de bacterias (E.coli) previamente opsonizadas, en los leucocitos humanos de sangre periférica de seis donantes sanos. Método: Como marcador oxidativo hemos utilizado la 1.2.3. dihidrorodamina,(no fluorescente) cuya oxidación la transforma en rodamina que es fluorescente y se examina cuantitativamente por Citometría de flujo. Resultados: El stress oxidativo máximo se alcanza con las bacterias en las células fagocíticas (monocitos 50 por ciento y granulocitos 90 por ciento) con diferencia significativa con respecto al grupo control. Con Etanol 50 mM se comprueba stress oxidativo con diferencia estadísticamente significativa en los tres tipos de células (linfocitos 9,19 por ciento, monocitos 32 por ciento y granulocitos 36 por ciento). A concentración 25 mM, aunque aumenta el estado oxidativo, no alcanza diferencia significativa (linfocitos 2,39 por ciento, monocitos 9,22 por ciento y granulocitos 4,46 por ciento). También hemos comprobado toxicidad celular que alcanza el 40,75 por ciento de las células con Etanol 50 mM, el 10,7 por ciento con Etanol 25 mM y el 5,65 por ciento con bacterias. Conclusión: El stress oxidativo con producción de radicales libres de oxígeno y de etanol en los leucocitos y la citotoxicidad comprobada, pueden jugar un papel importante en el trastorno cualitativo y cuantitativo de estas células en los enfermos alcohólicos y en las lesiones producidas por este tóxico en otros órganos y tejidos. (AU)

Hidatidosis intraportal como causa de hipertensión portal / Intraportal hydatidosis as manifestation of portal hypertension

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[Chronic autoimmune type II hepatitis with various extrahepatic clinical manifestations]. / Hepatitis crónica autoimmune tipo II con diversas manifestaciones clínicas extrahepáticas.

We present the case of a patient with autoimmune chronic hepatitis and anti-LKM antibodies, who developed associated autoimmune diseases, cyclic nodose erythema, bilateral peripheric paralysis, idiopathic thrombocytopenic purpura and diabetes mellitus. We describe the first signs of the disease and how three different forms can be differentiated depending on the type of autoantibodies present in the patients' serum. Finally, we list several forms of presentation of the disease, the potential clinical associations with other autoimmune processes and the potential immunological basis for the development of the hepatic lesion.

[Cardiac arrhythmia in patients with chronic obstructive pulmonary disease]. / Arritmias cardíacas en pacientes con enfermedad pulmonar obstructiva crónica.

A retrospective study of all patients diagnosed as having obstructive pulmonary disease (POD), who were admitted to our department during 1989, was carried out. The presence of cardiac arrhythmia (CA) in standard ECG having been correlated to clinical and laboratory parameters on admission. Out ot 101 admissions, 67.3% had a type of CA, the most frequent being sinus tachycardia (54.4%). 71.9% of the patients who had cardio-respiratory decompensation, 72.8% of those admitted in basal situation III/IV and 86% who were regularly taking theophylline (p less than 0.01), had a type of CA. Our data suggests that patients with worst functional situation and those with cardiorespiratory decompensation had a higher incidence of CA and that regular theophylline intake can play a role in the etiopathogenesis of CA.