Vasodilatory effects of propylthiouracil in patients with alcoholic cirrhosis.

BACKGROUND/AIMS: An experimental study has shown that propylthiouracil increases portal blood flow in normal rats. Whether propylthiouracil has a similar effect in patients with alcoholic cirrhosis remains to be demonstrated. The aim of this study was to evaluate the effects of oral propylthiouracil (300 mg) on systemic and portal hemodynamics in patients with alcoholic cirrhosis. METHODS: Plasma propylthiouracil levels were also measured by high performance liquid chromatography in five patients with alcoholic cirrhosis. In eight patients with cirrhosis, mean arterial pressure, cardiac output and portal blood flow were evaluated before and after placebo and propylthiouracil administration. Hemodynamic measurements were performed by the Doppler technique. The plasma peak level of propylthiouracil was achieved at 1.4 +/- 0.1 h in patients with alcoholic cirrhosis. This time was chosen to express hemodynamic changes. RESULTS: Propylthiouracil administration caused a significant increase in portal blood flow (+16.5%, p < 0.05) in patients with alcoholic cirrhosis. This effect was associated with a mild and significant rise in cardiac output (from 5.8 +/- 0.2 to 6.1 +/- 0.3 l/min, p < 0.05) and a decrease in peripheral vascular resistance (from 1171 +/- 69 to 1070 +/- 67 dyn . s-1 . cm-5, p < 0.01). A significant correlation was observed between changes in portal blood flow and peripheral vascular resistance (r = 0.79, p < 0.05). No significant changes were observed after placebo. CONCLUSIONS: Our findings show that propylthiouracil has a vasodilatory effect in patients with alcoholic cirrhosis. We postulate that this effect could be the mechanism by which propylthiouracil decreases hypermetabolic state, and increases oxygen delivery to the liver, in patients with alcoholic liver diseases.

[Activity of creatine kinase and its isoenzymes in hemolytic uremic syndrome]. / Actividad de la creatina kinasa y sus isoenzimas en el síndrome urémico hemolítico.

Serum creatine kinase (CK) and CK isoenzymes (CK-MM, CK-MB and CK-BB) were measured in 35 healthy and 25 children with hemolytic uremic syndrome (HUS) at 48 h, 7 and 15 days after admittance. Total serum CK activity was measured with a commercially available kit ("CK-NAC", by Merck, cat 14327) and CK isoenzymes using the Helena laboratories method. The interassay coefficients of variation with these methods are the following: for the total CK activity, 10.95 and 9.15% for an enzyme activity of 42 and 142 U/L respectively; for the activity of the isoenzymes, 6.8, 8.0 and 15.1% for activities of 102, 67 and 30 U/L. Total CK activity at 48 h in HUS patients defined two groups, group 1 (G1) which is not different from the control group (CG) and group 2 (G2) which had a significantly higher activity, p less than 0.0005. The increase in total CK remained significant until the first week. Increase in total CK resulted from the increase in CK isoenzymes: CK-MM, CK-MB and CK-BB. Highly significant correlation coefficients (p less than 0.0005) were obtained between total CK and their isoenzymes. When we examined both groups of patients in relation to clinical parameters, no difference could be found although G2 showed higher urea and fibrinogen degradation products with significantly decreased platelet counts. Although the reasons for enzyme release are not understood, anoxia and chemical toxins have been incriminates.(ABSTRACT TRUNCATED AT 250 WORDS)

Actividad de la creatina kinasa y sus isoenzimas en el sindrome uremico hemolitico / Activity of creatine kinase and its isoenzymes in hemolytic uremic syndrome

El síndrome urêmico hemolítico (SUH) es una enfermedad sistémica. En el presente trabajo se trata de demostrar el compromiso de la musculatura esquelética a través de la determinación seriada de creatinakinasa (CK) total y sus tres isoenzimas (CK-MM, CK-MB, CK-BB). La población estudiada que comprondió 25 niños con SUH, en relación a los valores de CK total y sus isoenzimas quedó dividida en dos grupos, G1 que se comporta como el control (35 niños sanos) y G2 en el que el aumento significativo de CK total se correlaciona en forma significativa con el aumento de las tres isoenzimas, aún hasta una semana de evolución. A los 15 días, sólo en G2 se encontró aumento sostenido de CK-BB que correlacionó significativamente a los niveles de urea plasmática y al grado de plaquetopenia. Interesante fue observar que el G2 presentaba en forma significativa una mayor concentración de urea plasmática, el mayor grado de plaquetopenia y cualitativamente una mayror concentración de productos de degradación de fibrinógeno. El aumento de Ck-MM se correlacionó en forma significativa con el aumento de CK-MG y CK-BB, además el aumento de CK-MB se correlacionó al aumento de CK-BB. Estos resultados señalarían un origen común de los tres isoenzimas, esto es el músculo estriado. En favor de esta hipótesis concurren los siguientes hallazgos: a) La actividad de CK-MB fue 7,0 ñ 1,8% de la actividad de CK total lo que concuerda con la concentración presente en el músculo esquelético. b) Por la isoenzima CK-BB tiene...

Actividad de la creatina kinasa y sus isoenzimas en el sindrome uremico hemolitico / Activity of creatine kinase and its isoenzymes in hemolytic uremic syndrome

El síndrome urÛmico hemolítico (SUH) es una enfermedad sistémica. En el presente trabajo se trata de demostrar el compromiso de la musculatura esquelética a través de la determinación seriada de creatinakinasa (CK) total y sus tres isoenzimas (CK-MM, CK-MB, CK-BB). La población estudiada que comprondió 25 niños con SUH, en relación a los valores de CK total y sus isoenzimas quedó dividida en dos grupos, G1 que se comporta como el control (35 niños sanos) y G2 en el que el aumento significativo de CK total se correlaciona en forma significativa con el aumento de las tres isoenzimas, aún hasta una semana de evolución. A los 15 días, sólo en G2 se encontró aumento sostenido de CK-BB que correlacionó significativamente a los niveles de urea plasmática y al grado de plaquetopenia. Interesante fue observar que el G2 presentaba en forma significativa una mayor concentración de urea plasmática, el mayor grado de plaquetopenia y cualitativamente una mayror concentración de productos de degradación de fibrinógeno. El aumento de Ck-MM se correlacionó en forma significativa con el aumento de CK-MG y CK-BB, además el aumento de CK-MB se correlacionó al aumento de CK-BB. Estos resultados señalarían un origen común de los tres isoenzimas, esto es el músculo estriado. En favor de esta hipótesis concurren los siguientes hallazgos: a) La actividad de CK-MB fue 7,0 ñ 1,8% de la actividad de CK total lo que concuerda con la concentración presente en el músculo esquelético. b) Por la isoenzima CK-BB tiene... (AU)

Actividad de la creatina kinasa y sus isoenzimas en el síndrome urémico hemolítico. / [Activity of creatine kinase and its isoenzymes in hemolytic uremic syndrome]

Serum creatine kinase (CK) and CK isoenzymes (CK-MM, CK-MB and CK-BB) were measured in 35 healthy and 25 children with hemolytic uremic syndrome (HUS) at 48 h, 7 and 15 days after admittance. Total serum CK activity was measured with a commercially available kit ([quot ]CK-NAC[quot ], by Merck, cat 14327) and CK isoenzymes using the Helena laboratories method. The interassay coefficients of variation with these methods are the following: for the total CK activity, 10.95 and 9.15

for an enzyme activity of 42 and 142 U/L respectively; for the activity of the isoenzymes, 6.8, 8.0 and 15.1

for activities of 102, 67 and 30 U/L. Total CK activity at 48 h in HUS patients defined two groups, group 1 (G1) which is not different from the control group (CG) and group 2 (G2) which had a significantly higher activity, p less than 0.0005. The increase in total CK remained significant until the first week. Increase in total CK resulted from the increase in CK isoenzymes: CK-MM, CK-MB and CK-BB. Highly significant correlation coefficients (p less than 0.0005) were obtained between total CK and their isoenzymes. When we examined both groups of patients in relation to clinical parameters, no difference could be found although G2 showed higher urea and fibrinogen degradation products with significantly decreased platelet counts. Although the reasons for enzyme release are not understood, anoxia and chemical toxins have been incriminates.(ABSTRACT TRUNCATED AT 250 WORDS)