Sindrome de Atra / Atra syndrome

La leucemia promielocítica aguda (APL) es el subtipo de leucemia mieloide aguda de mejor pronóstico en niños. Su incidencia es menor a 10%. Desde el punto de vista citogenético se observa una translocación t (15;17). En la terapéutica la incorporación del ácido transretinoico ha logrado altas tasas de remisión completa debido a la rápida desaparición de la coagulopatía y, en consecuencia, disminución de la tasa de recaídas, en comparación con el tratamiento de monoterapia. En general es un fármaco bien tolerado pero puede tener reacciones adversas; el más grave es el síndrome de ácido transretinoico (ATRA), potencialmente mortal. Las manifestaciones clínicas son: fiebre, ganancia de peso, infiltrados pulmonares, síndrome de dificultad respiratoria, derrame pleural o pericárdico, hipotensión, insuficiencia hepática y renal. El tratamiento es con suspensión del ácido transretinoico, medidas de apoyo y altas dosis de esteroides. Se presenta un caso clínico del hospital del Niño DIF con APL y Síndrome de ATRA.

The leukemia promyelocytic acute (APL) is the subtype of leukemia myeloid acute of better prognosis in children. Its incidence is less than 10%. From the point of view cytogenetic is observed a translocation t (15; 17). The addition of the acid transretinoico has achieved high rates of complete remission because of the rapid disappearance of the coagulopathy and, consequently, decrease in the rate of relapses, compared with monotherapy treatment. In general it is a well-tolerated drug but can have adverse reactions; the most serious is transretinoico acid (ATRA), potentially fatal syndrome. The manifestations are: fever, weight gain, pulmonary infiltrates, syndrome of shortness of breath, hypotension, pleural effusion or pericardial, hepatic and renal insufficiency. The treatment is with suspension of the acid transretinoico, measures of support and high doses of steroids. It presents a case clinical of the Hospital del Niño DIF with APL and syndrome of ATRA.

Efecto hepatoprotector del extracto hidroetanólico atomizado del maíz morado (Zea mays L) en lesiones hepáticas inducidas en ratas / Hepatoprotective effect of atomized hydroethanolic extract from Andean purple corn (Zea mays L) in induced hepatic injury in rats

Evaluar el efecto hepatoprotector del extracto hidroetanólico atomizado de Zea mays variedad morado sobre lesiones hepáticas inducidas en ratas. Diseño: Experimental. Institución: Laboratorio de Farmacología Experimental, Facultad de Medicina Humana, Universidad Nacional Mayor de San Marcos, Lima, Perú. Material biológico: Extracto hidroetanólico atomizado de maíz morado (EAM). Intervenciones: Se formó seis grupos de ratas machos (n=10, por cada grupo), se les administró fenobarbital a concentración de 0,5 g/L en agua potable ad líbitum por 15 días; posteriormente se administró tetracloruro de carbono (CCl4) a una dosis de 0,2 mL/kg, por vía oral. El diseño experimental fue el siguiente: G1: suero fisiológico (SSF); G2: CCl4 0,2 mL/kg (T); G3: T+ silimarina 25 mg/kg; G4: T + EAM 500 mg/kg; G5: T + EAM 1 000 mg/kg; G6: T + EAM 2 000 mg/kg. Principales medidas de resultados: Perfil hepático, especies reactivas al ácido tiobarbitúrico (TBARS) en suero, índice hepático, observación histológica. Resultados: Se observó aumento significativo (p<0,05) en la actividad de alanina amino transferasa (ALT) entre el grupo G2 y los grupos G3 y G4 (p<0,001). Hubo disminución significativa (p<0,05) de fosfatasa alcalina (FAL) en el grupo G2 con respecto G1. El nivel de TBARS fue menor en el grupo que recibió 1 000 mg/kg de EAM con respecto al control. Las actividades de HDL-C y triglicéridos no mostraron diferencias significativas. Se ha observado la reducción de 60 por ciento de la lesión hepática, evidenciado con menor daño del hepatocito al estudio histológico. Conclusiones: El extracto hidroetanólico atomizado de maíz morado a la dosis de 1 000 mg/kg disminuyó las lesiones hepáticas inducidas en ratas...

To evaluate the hepatoprotector effect of hydroalcoholic extract atomized of Zea mays against hepatic injuries induced in rats. Design: Experimental. Institution: Laboratory of Experimental Pharmacology, Faculty of Human Medicine, Universidad Nacional Mayor de San Marcos, Lima, Peru. Biological material: Hydroethanolic extract atomized of purple corn (EAM). Interventions: To six groups of male rats (n = 10, for each group) phenobarbital 0.5 g/L in drinkable water ad libitum was administered for 15 days, followed by carbon tetrachloride 0.2 mL/kg p.o. The experimental design was a follow: G1: normal; G2: CCl4 0.2 mL/kg (T); G3:T+ silimarina 25 mg/kg; G4: T+ EAM 500 mg/kg; G5: T + EAM 1 000 mg/kg; G6 T + EAM 2 000 mg/kg. Main outcome measures: Hepatic profile, reactive species to thiobarbituric acid (TBARS), liver index, and histological observation. Results: Significant increase (p<0.05) in ALT activity was observed between group G2 in comparison to groups G3 and G4 (p<0.001). There was significant decrease (p<0.05) of alkaline phosphatase (AP) in group G2 with respect to G1. TBARS level was less in the group that received 1 000 mg/kg of EAM regarding to control. HDL-C and triglycerides activities did not show significant differences. Reduction in 60 per cent of hepatic injury was observed, evidencing less damage of the hepatocyte by histological study. Conclusions: The purple corn atomized hydroethanolic extract at 1 000 mg/kg dose decreased induced hepatic injuries in rats...

Hepatic manifestations in chronic arsenic toxicity.

OBJECTIVE: The hepatotoxic action of arsenic, when used as a therapeutic agent, has long been recognized. Data on liver involvement following chronic exposure to arsenic-contaminated water are scanty. We report the nature and degree of liver involvement on the basis of hospital-based and cohort follow-up studies in patients who consumed arsenic-contaminated drinking water for 1 to 15 years. METHODS: 248 patients with evidence of chronic arsenic toxicity underwent clinical and laboratory examinations including liver function tests and HBsAg status. Liver biopsy was done in 69 cases; in 29 patients, liver arsenic content was estimated by neutron activation analysis. A cohort follow up of 23 patients who took arsenic-free water for 2-12 years was also carried out. RESULTS: Hepatomegaly was present in 190 of 248 patients (76.6%). Noncirrhotic portal fibrosis (91.3%) was the predominant lesion in liver histology. The maximum arsenic content in liver was 6 mg/Kg (mean 1.46 [0.42], control value 0.16 [0.04]; p < 0.001); it was undetected in 6 of 29 samples studied. Cohort follow-up studies showed elevation of globulin in four cases and development of esophageal varices in one case. CONCLUSION: We report the largest number of patients with liver disease due to chronic arsenicosis from drinking arsenic-contaminated water. Noncirrhotic portal fibrosis is the predominant lesion in this population.