RESUMO
The existence of a relationship between HLA and the possibility of the development of an alcoholic cirrhosis is researched in this paper. This work was done from 1982 to 1984, by the staff of four clinics of the Medicine School of the University of Uruguay. We studied 47 alcoholics with portal cirrhosis, 19 non-cirrhotic alcoholics and 250 healthy nonalcoholic controls. We confirmed with liver biopsy the cirrhosis in the first group and in the second, liver biopsy was performed in order to assure that they had no cirrhosis. Table I shows the histocompatibility antigens which were tested in the 3 groups. Levels of significance were obtained from exact Fisher test with Yates correction for discontinuity; Pc (corrected P) and RR (relative risk) were also determined. In the alcoholics with portal cirrhosis, the HLABW40 showed a Pc less than 0,005 (RR = 3,93). In the non-cirrhotic alcoholics no significative association was found. We conclude that the carrier of the genetic marker HLABW40, has almost 4 times more chances to develop a cirrhosis as consequence of chronic alcoholic abuse. The presence of this marker, in our patients, has no association with the possibility that an individual becomes an alcoholic abuser. We think that if this data are confirmed in a wider study, some guidelines for the prevention of alcoholic cirrhosis may be established.
Assuntos
Alcoolismo/imunologia , Antígenos HLA/análise , Antígenos HLA-B , Cirrose Hepática Alcoólica/imunologia , Adulto , Idoso , Alcoolismo/genética , Marcadores Genéticos , Antígenos HLA/genética , Antígeno HLA-B40 , Humanos , Fígado/patologia , Cirrose Hepática Alcoólica/genética , Pessoa de Meia-Idade , RiscoRESUMO
The aim of this work is to establish the best treatment for patients with gastric and duodenal ulcer, by measuring the effects of antiacids and H2-receptor antagonists on gastric pH. 16 patients were studied: 9 of them had a duodenal ulcer, 2 a gastric ulcer and 5 had both. All the patients remained fasting and receiving no drug for 24 hrs. During this 24 hrs., a nasogastric tube was inserted into the stomach and the gastric content was obtained by aspiration each hour from 8 A.M. to 8 P.M. Three days after, each patient received a daily dose of 1 g of Cimetidine, and the whole procedure was repeated. The same was done with 300 mg of Ranitidine daily, 150 ml of Al-Mg antiacids daily, and at last, the same procedure was performed with the association of Ranitidine and Al-Mg antiacids at the mentioned dosage. For the statistical analysis of the data, the mean ordinate of the pH was used as a representative value of each individual's pH. Individual differences (pH with treatment minus pH without treatment) were obtained. The mean effect of each treatment was obtained averaging that differences. For comparison among different drugs, the same procedure was used. Student's paired t tests were performed in a signification level. The buffering capacity was measured in the following way: The percentage of the gastric secretion samples with pH equal or higher than 4 in each treatment and in the total number of patients was confronted with the results obtained in the same patients with no treatment. All the drugs were useful for buffering the gastric acidity, but in different intensity. The association of Ranitidine and Al-Mg antiacids showed to be the most efficient statistically when compared with Cimetidine and Al-Mg antiacids; no statistical difference appeared in the comparison with Ranitidine.
Assuntos
Antiácidos/farmacologia , Úlcera Duodenal/fisiopatologia , Ácido Gástrico/metabolismo , Antagonistas dos Receptores H2 da Histamina/farmacologia , Úlcera Gástrica/fisiopatologia , Adulto , Hidróxido de Alumínio/farmacologia , Cimetidina/farmacologia , Ensaios Clínicos como Assunto , Úlcera Duodenal/tratamento farmacológico , Feminino , Determinação da Acidez Gástrica , Humanos , Hidróxido de Magnésio/farmacologia , Masculino , Pessoa de Meia-Idade , Ranitidina/farmacologia , Úlcera Gástrica/tratamento farmacológicoRESUMO
Se presenta una investigación tendiente a aclarar la posible existencia de una relación entre la estructura antígena HLA de un individuo y la eventualidad de que éste desarrolle o no una cirrosis al ingerir alcohol en forma crónica. A estos efectos se integró un equipo multidisciplinario conformado por clínicos, genetistas, psiquiatras y patólogos, integrantes de 4 Cátedras de la Facultad de Medicina. Se diseño un trabajo prospectivo de investigación que se desarrolló en el transcurso de los años 1982 a 1984. Se estudiaron 47 alcoholistas portadores de una Cirrosis Portal, 19 alcoholistas No Cirróticos y 250 testigos sanos. Los cirróticos fueron biopsiados para confirmar histopatológicamente la enfermedad y los alcoholistas no cirróticos fueron biopsiados para confirmar que no la tuvieran. En todos los grupos se determinaron los antígenos de histocompatibilidad indicados en la Tabla I. Se efectuaron los cálculos estadísticos que incluyeron X con corrección de Yates, probabilidad corregida, y el cálculo del riesgo relativo (R.R), (este último especificado en la Tabla II). En el grupo de alcoholistas cirróticos, se comprobó una asociación positiva con el HLA Bw40, con un valor estadístico muy significativo: Pc<0,005; RR=3,93. (Tabla IV). No se comprobó predominancia de este antígeno en los etilistas no cirróticos (Tabla V). Se concluye que la presencia del HLA Bw40 aumenta casi 4 veces el riesgo de desarrollar una cirrosis en los pacientes que ingieren alcohol en forma crónica. Su presencia no influye estadísticamente en nuestra serie en el riesgo de que un individuo se convierta en alcoholista. Esta investigación, de comprobarse en series mayores, que este equipo de trabajo está desarrollando, permitirá en el futuro determinar criterios de prevención de la cirrosis alcohólica