[Incidence and clinical characteristics of congenital heart disease in Badajoz Province, Spain]. / Incidencia de las cardiopatías congénitas en la provincia de Badajoz.

INTRODUCTION: There is no clear consensus as regards the exact incidence of congenital heart disease. The objective of this study was to determine the incidence of congenital heart defects in Badajoz province (Spain). MATERIAL AND METHODS: This is a retrospective study based on the clinical histories of 742 patients who were seen for the first time during 1997 in the paediatric cardiology unit of Badajoz Women and Children's Hospital. The incidence of congenital Heart defects is calculated by adding the number of patients assessed in 1997 and those who will be assessed in the future, considering the population born in 1997. The last figure is inferred from the number of patients who were born before 1997 and were assessed in that year, comparing the number of newborns between 1997 and previous years. The number of patients is divided by the total newborns in 1997 and multiplied by 1,000. RESULTS: Congenital heart defects were found in 15.6 % of the patients seen during 1997. The incidence ranges from 16.1 to 5.4 new cardiac diseases per 1,000 newborn babies per year if some minor congenital heart defects that are not considered in other publications are excluded, such as interatrial communication of the ostium secundum type, interventricular communication of the small muscle, mild prolapsed mitral valve, bicuspid aortic valve, patent ductus arteriosus in prematures infants, silent ductus arteriosus and congenital arrhythmias. CONCLUSIONS: The incidence of congenital heart defects in Badajoz province range from 16.1 to 5.5 new cardiac diseases per 1,000 newborn babies per year. We consider that the incidence in the Badajoz province is reliable and similar to other recent publications.

Incidencia de las cardiopatías congénitas en la provincia de Badajoz / Incidence and clinical characteristics of congenital heart disease in Badajoz province, Spain

Introducción: Las cardiopatías congénitas son una patología sobre las que aún no hay un consenso claro respecto a su incidencia. El objetivo de este trabajo ha sido determinar su incidencia en la provincia de Badajoz. Material y métodos: Se ha realizado un estudio retrospectivo sobre las historias clínicas de los 742 pacientes vistos por primera vez en la Unidad de Cardiología Pediátrica del Hospital Materno-Infantil de Badajoz durante 1997. La incidencia de las cardiopatías congénitas se calcula sumando a los cardiópatas nacidos en 1997 y que manifestaron la patología ese mismo año, los que la presentaron en los años sucesivos respecto del total de recién nacidos en 1997. Esta última cifra se estima a partir del número de cardiópatas que nacieron antes de 1997 y que debutaron en 1997, comparando el número de recién nacidos de cada uno de esos años anteriores respecto al número de recién nacidos de 1997. Este total de cardiópatas se divide entre los recién nacidos en 1997 y se multiplica por 1.000. Resultados: El 15,6 % de los pacientes visitados en 1997 tenía patología cardíaca congénita. La incidencia sin considerar algunas cardiopatías leves (que tampoco suelen ser consideradas en otras publicaciones, como comunicación interauricular tipo ostium secundum pequeña, comunicación interventricular muscular pequeña, prolapso de la válvula mitral leve, válvula aórtica bicúspide, conducto arterial del prematuro, conducto arterial silente o arritmias congénitas) osciló entre 16,1 y 5,4 cardiópatas por 1.000 recién nacidos vivos y año. Conclusiones: La incidencia de las cardiopatías congénitas en la provincia de Badajoz oscila entre 16,1 y 5,4 por 1.000 recién nacidos vivos. Esta cifra se considera fiable y semejante a otras publicaciones recientes (AU)

Introduction: There is no clear consensus as regards the exact incidence of congenital heart disease. The objective of this study was to determine the incidence of congenital heart defects in Badajoz province (Spain). Material and methods: This is a retrospective study based on the clinical histories of 742 patients who were seen for the first time during 1997 in the paediatric cardiology unit of Badajoz Women and Children's Hospital. The incidence of congenital Heart defects is calculated by adding the number of patients assessed in 1997 and those who will be assessed in the future, considering the population born in 1997. The last figure is inferred from the number of patients who were born before 1997 and were assessed in that year, comparing the number of newborns between 1997 and previous years. The number of patients is divided by the total newborns in 1997 and multiplied by 1,000. Results: Congenital heart defects were found in 15.6 % of the patients seen during 1997. The incidence ranges from 16.1 to 5.4 new cardiac diseases per 1,000 newborn babies per year if some minor congenital heart defects that are not considered in other publications are excluded, such as interatrial communication of the ostium secundum type, interventricular communication of the small muscle, mild prolapsed mitral valve, bicuspid aortic valve, patent ductus arteriosus in prematures infants, silent ductus arteriosus and congenital arrhythmias. Conclusions: The incidence of congenital heart defects in Badajoz province range from 16.1 to 5.5 new cardiac diseases per 1,000 newborn babies per year. We consider that the incidence in the Badajoz province is reliable and similar to other recent publications (AU)

Normalization of T2 signal abnormalities in hemispheric white matter with liver transplant.

OBJECTIVE: To determine whether edema can be assessed by MRI using T2-weighted signal intensity of hemispheric white matter in cirrhotic patients. METHODS: Fast-FLAIR and magnetization transfer images were obtained before (24) and after (11) liver transplantation. T2-weighted abnormalities on baseline scans and their time-course changes were analyzed and compared with MT ratios (MTR). RESULTS: Fast-FLAIR baseline images showed faint to substantial, bilateral, symmetric increased signal intensity along the hemispheric white matter in or around the corticospinal tract in 23/24 patients. After liver transplantation the signal abnormalities gradually recovered. This gradual decrease in signal intensity correlated with an increase in MTR values. CONCLUSION: Asymptomatic symmetric high-signal intensity in the hemispheric white matter on fast-FLAIR MR images is present in cirrhosis. Normalization of this finding after successful liver transplantation and its correlation with MTR values suggest that this signal abnormality reflects mild edema.

The development of low-grade cerebral edema in cirrhosis is supported by the evolution of (1)H-magnetic resonance abnormalities after liver transplantation.

BACKGROUND/AIMS: Liver failure may cause brain edema through an increase in brain glutamine. However, usually standard neuroimaging techniques do not detect brain edema in cirrhosis. We assessed magnetization transfer ratio and (1)H-magnetic resonance (MR) spectroscopy before and after liver transplantation to investigate changes in brain water content in cirrhosis. METHODS: Non-alcoholic cirrhotics without overt hepatic encephalopathy (n=24) underwent (1)H-MR of the brain and neuropsychological tests. (1)H-MR results were compared with those of healthy controls (n=10). In a subgroup of patients (n=11), the study was repeated after liver transplantation. RESULTS: Cirrhotic patients showed a decrease in magnetization transfer ratio (31.5+/-3.1 vs. 37.1+/-1.1, P<0.01) and an increase in glutamine/glutamate signal (2.22+/-0.47 vs. 1.46+/-0.26, P<0.01). The increase in glutamine/glutamate signal was correlated to the decrease in magnetization transfer ratio and to neuropsychological function. Following liver transplantation, there was a progressive normalization of magnetization transfer ratio, glutamine/glutamate signal and neuropsychological function. Accordingly, correlations between these variables were lost after liver transplantation. CONCLUSIONS: Cirrhotic patients show reversible changes in magnetization transfer ratio that are compatible with the development of low-grade cerebral edema. Minimal hepatic encephalopathy and low-grade cerebral edema appear to be the consequences of the metabolism of ammonia in the brain.

[Clinical characteristics and prognostic criteria in alcoholic hepatitis and alcoholic hepatitis with cirrhosis]. / Características clínicas y criterios pronósticos en la hepatitis alcohólica y hepatitis alcohólica con cirrosis.

A comparative study of clinical and biological features and of the immediate prognosis was made in 46 patients with alcoholic hepatitis and 19 patients with alcoholic hepatitis with liver cirrhosis. The presence of cirrhosis has different clinical manifestations and a more intense alteration of albumin, prothrombin, total bilirubin and immunoglobulins (p less than 0.01). The development of ascites, encephalopathy and hepatorenal syndrome (p less than 0.05) and albumin, prothrombin and total bilirubin values at admission (p less than 0.01) were the best parameters to identify the patients with a poorer prognosis. There were no significant differences between both groups in mortality, frequency of encephalopathy or renal failure.