Sobrecrecimiento bacteriano intestinal un factor de riesgo de peritonitis bacteriana espontánea y mortalidad en pacientes con cirrosis hepática / Intestinal bacterial overgrowth is a risk factor for spontaneous bacterial peritonitis and mortality in patients with liver cirrhosis

Spontaneous bacterial peritonitis (SBP) is a major and serious complication of liver cirrhosis. Small intestinal bacterial overgrowth (SIBO) has been shown to occur with increased frequency in patients with cirrhosis. Studies have suggested that SIBO may contribute to the development of SBP. Aims: to assess the prevalence of SIBO and its relationship with the mortality in patients with cirrhosis. Patients and Methods: One hundred three cirrhotic patients, 62 male, mean age 56.6 (range 35-89) entered in the study in a four year period with a mean follow-up of 22.2 months (range 3-76). SIBO was evaluated by breath hydrogen test (BHT) with lactulose. A positive BHT was defined as an increase of 20 ppm during the first 60 min after lactulose ingestion. SBP was diagnosed by a polymorphonuclear leukocyte count greater than or equal to of 250 cells/mm3 in ascitic fluid. Results: A 50 percent of cirrhotic patients had SIBO at the beginning of follow-up period. The prevalence of SIBO was similar in patients with Child-Pugh class A, B, or C (48 percent 51 percent and 48 percent patients respectively). The presence of SBP was significantly higher in patients with SIBO (17/54 patients) than patients without SIBO (1/53 patients), p < 0.05. The mortality of cirrhotic patients was higher in the SIBO group than in the non-SIBO group (25/50 versus 16/35 patients. p < 0.05). Conclusions: The results of this study confirm that the presence of SIBO is a risk factor for SBP and mortality in patients with liver cirrhosis. SIBO should be investigated and treated during the follow-up in these patients.

La peritonitis bacteriana espontánea (PBE) es una complicación frecuente y grave en pacientes con cirrosis hepática. El sobrecrecimiento bacteriano intestinal (SBI) ha sido descrito con frecuencia en pacientes con cirrosis. Estudios han sugerido que el SBI puede ser un factor importante en el desarrollo de la PBE. Objetivos: Evaluar la prevalencia de SBI y su relación con la mortalidad en pacientes con cirrosis hepática. Pacientes y métodos: Ciento tres pacientes cirróticos, 67 hombres, edad promedio 58,6 (rango 35-89) entraron al estudio en un período de cuatro años con un seguimiento promedio de 22,2 meses (rango 3-76). El SBI fue evaluado por test de hidrógeno en aire espirado (THE) con lactulosa. Un examen era considerado positivo con un nivel mayor de 20 ppm después de la ingesta de lactulosa en los primeros 60 min. El diagnóstico de PBE se fundamentó en un recuento de polimorfonucleares mayor o igual que 250 células/mm3 en muestra de líquido ascítico. Resultados: El 50 por ciento de los pacientes cirróticos presentó SBI al comienzo de su seguimiento. La prevalencia de SBI fue similar en pacientes cirróticos Child-Pugh A, B, o C (48 por ciento, 50 por ciento y 50 por ciento respectivamente). La presencia de PBE fue significativamente mayor en pacientes con SBI (17/50 pacientes) que en pacientes sin SBI (1/53 pacientes). p < 0,05. La mortalidad de los pacientes cirróticos fue mayor en el grupo con SBI que en el grupo sin SBI (25/50 versus 16/53 pacientes, p < 0,05). Conclusiones: Los resultados de este estudio confirman que la presencia de SBI es un factor de riesgo de PBE y mortalidad en pacientes con cirrosis hepática. El SBI debería ser investigado y tratado durante el seguimiento de estos pacientes.

Influence of pre-exposure to temephos and pyriproxyfen on the pharmacological action of some laxatives

The aim of the present work is to study the influence of short term daily oral exposure to temephos or pyriproxyfen on the pharmacological action [percent gastric emptying and small bowel transit] of 2 laxatives [lactulose and picolax] in male adult rats. The animals were fed normal diet [1[st] main group], or diet containing 50 times the maximum human acceptable daily intake of either temephos [2[nd] main group], or pyriproxyfen [3[rd] main group] for 15 consecutive days. In the 16[st] day the control group [1[st] main group] was subdivided into 4 subgroups: - First subgroup: given orally 1.5 ml of tested meal [0.5 mg phenol red / 1ml 5% glucose solution] and the animals were sacrificed immediately. - Second subgroup: given 1.5ml of the tested meal but sacrificed after 30 min. - Third and fourth subgroup: given 0.643 or 0.2 ml of lactulose or picolax / 100gm body weight and 30 min. later, animals were given the test meal and after another 30 min. the; animals were sacrificed and the% gastric emptying and small intestine transit were determined. Second and third main groups were subdivided to 3 subgroups given orally the test meal, lactulose, picoltax, respectively and sacrificed after 30 min. Results showed that - temephos and pyriproxyfen negatively interfere with the pharmacological action of lactulose as they sharply decrease its laxative action. - Temephos decrease the laxative action of picolax while pyriproxyfen showed no detectable effects

Neostigmine for the Treatment of Acute Hepatic Encephalopathy with Acute Intestinal Pseudo-obstruction in a Cirrhotic Patient

We treated a 49-yr-old man with neostigmine, who had liver cirrhosis, acute hepatic encephalopathy, and acute intestinal pseudoobstruction. He was admitted in a state of hepatic confusion. On physical examination, the abdomen was distended; and bowel sound was absent. Plain abdomen film revealed multiple airfluid levels and distention of bowel loops. Initially, we gave him lactulose enemas every 6 hr for one day without improvement in his mental state. Furthermore, he became to a state of coma. Therefore, we gave him 0.5 mg of neostigmine subcutaneously to improve his peristaltic movement, and 2 L of polyethylene glycol electrolyte solution through a nasogastric tube for 4 hr to reduce the production and absorption of gutderived toxins of nitrogenous compounds. After these treatments, the venous ammonia level decreased to the normal range within 12 hr, and the coma disappeared after 2 days. We suggest that neostigmine may be one of the most effective treatments to initiate peristaltic movement and bowel cleansing in cirrhotic patients with acute hepatic encephalopathy and acute intestinal pseudoobstruction.

Preparo domiciliar de cólon com bisacodil e soluçäo de lactulose a 10 por cento para colonoscopia ambulatorial / Oral bowel preparation with bisacodil and 10 per cent lactulose solution for elective colonoscopy

Realizamos 2000 colonoscopias ambulatoriais de dezembro de 1994 a maio de 1998. Na véspera, o preparo consistiu de dieta sem resíduos e quatro comprimidos de bisacodil às 19 horas. Para a manhä do dia do exame, orientamos o paciente diluir 120ml de lactulose em água ou suco de laranja coado até obter um litro de soluçäo e ingerí-la em uma hora, seis horas antes do início do procedimento endoscópico. Além disso, deveriam beber água ou chá à vontade até o momento do mesmo. As principais indicaçöes foram de dor abdominal, diarréia, enterorragia, obstipaçäo e pesquisa de tumores. Consideramos o resultado como Bom em 84, 85 por cento dos casos, Regular em 9,2 por cento e Ruim em 5,9 por cento. Ocorreu intolerância ao esquema em 3,35 por cento, quando os pacientes referiram vômitos. Queixas de cólicas abdominais, em 9,75 por cento dos casos, ocorreram principalmente durante a noite, sendo creditadas ao bisacodil. Mesmo os doentes com estenose näo complicaram com obstruçäo. Concluímos que o preparo de cólon para colonoscopia com lactose é eficaz, podendo ser feito a nível domiciliar, com boa aceitaçäo e maior conforto para o paciente

Efecto de la combinación de benzoato de sodio con lactulosa en la hiperamonemia experimental / Effect of sodium benzoate plus lactulose combination in experimental hyperammonemia

El benzoato de sodio se ha utilizado en el tratamiento de la encefalopatía hepática hiperamonémica con buenos resultados. Con el objeto de investigar si la combinación de benzoato de sodio con un disacárido (lactosa, lactulosa) tiene un efecto aditivo sobre la disminución de amonio plasmático, se estudió el efecto de la combinación de benzoato de sodio con lactulosa en el modelo de anastomosis portocava en la rata, ya que éste es el modelo experimental que produce mayores elevaciones de amonio en sangre. Se utilizaron ratas Wistar de 250-300 g de peso en las que se practicó una anastomosis porto-cava terminolateral. Diez días después de la operación se inició tratamiento experimental por un periodo de siete días, dividiendo a los animales en cuatro grupos: a) solución salina, b) B.S. 500 mg/kg/día, c) lactulosa 4 g/kg/día, d) benzoato de sodio más lactulosa (dosis anotadas). También se incluyeron un grupo de ratas normales y un grupo con operación ficticia como controles. Se tomaron muestras de sangre arterial al final del periodo de estudio y se determinó amonio por el método enzimático. Resultados. El benzoato de sodio y la lactulosa disminuyeron significativamente las concentraciones de amonio plasmático (437ñ50, 433ñ85 ug/dl, respectivamente) en comparación con el grupo control (638 ñ 50 ug/dl, p = 0.05), tal como se esperaba. La combinación de benzoato de sodio con lactulosa produjo una disminución de amonio aún mayor (264 ñ 17 ug/dl, p<0.001), lo cual apoya la existencia de un efecto aditivo entre ambos fármacos. Estos hallazgos parecen reproducirse en la clínica de acuerdo a estudios clínicos preliminares en los que se ha utilizado la combinación de lactosa con benzoato de sodio. Estos resultados sugieren que puede haber un efecto aditivo entre el benzoato de sodio y disacáridos como la lactulosa, lo cual podría aumentar la eficiencia del tratamiento e incluso disminuir la dosis total de medicamentos y aumentar la tolerancia a cada uno de los fármacos. Finalmente, se plantea la posibilidad de emplear otros fármacos derivados del benzoato de sodio

Effect of lactulose and neomycin on plasma level of prostaglandin E in patients with portasystemic encephalopathy

This work aimed at the study of the relation of plasma prostaglandin E [PGE] to the development of chronic portosystemic encephalopathy [PSE] in patients with chronic liver disease and its response to treatment with either lactulose or neomycin. The study included 30 patients with chronic liver disease and PSE and 10 healthy controls. PGE plasma levels were assayed using radioimmunoassay [RIA] at the beginning of the study and 14 days after treatment with either lactulose [15 patients] or neomycin [15 patients]. PGE mean levels were higher in patients with chronic liver disease and PSE in comparison to controls [11.61 +/- 5.2 versus 1.88 +/- 1.16 ng/ml respectively, P < 0.05]. The overall result of treatment with either lactulose or neomycin was a reduction from 11.61 +/- 5.2 to 9.85 +/- 4.42 ng/ml. [P < 0.05]. Ascitic patients had higher PGE levels than non ascitic patients before [14.05 +/- 3.74 vs 8.42 +/- 4.78 respectively] and after treatment [10.99 +/- 3.74 vs 8.92 +/- 4.92]. Neomycin resulted in a decrease in PGE levels only in the ascitic group from 16.2 +/- 3.77 to 11.9 +/- 4.69 ng/ml. [P < 0.05] while lactulose did not significantly alter the PGE level in ascitic or non ascitic patients. It is concluded that PGE levels are increased in patients with PSE and that their level increases more with the degree of hepatic decompensation. Neomycin significantly decreases PGE levels in ascitic patients while lactulose did not significantly influence PGE levels. PGE may not be used as a marker of PSE since all patients showed clinical improvement with either lactulose or neomycin