Intestinal Permeability in Patients with Viral and Alcoholic Liver Disease / 대한소화기학회지

BACKGROUND/AIMS: Increased intestinal permeability has been possible contributing factors to the pathogenesis of alcoholic liver disease. Moreover, it can contribute to the development of bacterial infection and intestinal endotoxemia in patients with liver cirrhosis. This study aimed to examine the difference of intestinal barrier dysfunction between alcoholic and viral liver disease patients through the comparison of the intestinal permeabilities of patients with clinical characteristics. METHODS: Intestinal permeabilities were measured in 18 healthy controls, 41 patients with alcoholic liver disease (17 cases of alcoholic liver disease without cirrhosis and 24 cases of alcoholic liver cirrhosis) and 46 patients with viral liver disease (14 cases of chronic viral hepatitis and 32 cases of viral liver cirrhosis) by measuring 24 hour urine excretion of 51Cr-EDTA. RESULTS: The intestinal permeability was significantly increased in the patients with alcoholic liver disease without cirrhosis (5.62 +/- 2.80%), alcoholic liver cirrhosis (5.29 +/- 2.48%) and viral liver cirrhosis (3.15 +/- 1.39%) compared with that in control subjects (1.99 +/- 0.53%). On the contrary, it was not increased in the patients with chronic viral hepatitis (2.05 +/- 0.57%) versus controls. The significant correlation was not found between intestinal permeability and clinical and laboratory findings. CONCLUSIONS: The intestinal permeability was elevated in patients with alcoholic liver disease compared to those with viral liver cirrhosis. The pathophysiology of liver injury secondary to intestinal epithelial damage may be different between alcoholic and viral liver diseases.

Producción endógena de alcohol en pacientes con cirrosis hepática, alteración motora y sobrecrecimiento bacteriano / Endogenous ethanol production in patients with liver cirrhosis, motor alteration and bacterial overgrowth

BACKGROUND: Small intestinal bacterial overgrowth generates endogenous ethanol production both in experimental animals and humans. Patients with cirrhosis have small intestinal bacterial overgrowth, but endogenous ethanol production has not been studied in them. AIM: To investigate endogenous ethanol production in patients with cirrhosis, altered intestinal motility and small intestinal bacterial overgrowth. PATIENTS AND METHODS: Eight patients with cirrhosis of different etiologies and altered gastrointestinal motility, consisting in changes in the migrating motor complex, were studied. All had also small intestinal bacterial overgrowth, measured by means of the H2 breath test with lactulose. Plasma ethanol levels were measured by gas liquid chromatography in fasting conditions and 120 min after a carbohydrate rich meal. RESULTS: In fasting conditions, no patient had endogenous ethanol production. Alter the meal, ethanol in concentrations of 11.3 and 8.2 mg/del were detected in two patients. Negligible amounts of ethanol were detected in 4 patients and two patients had undetectable alcohol levels. CONCLUSIONS: A low endogenous production of ethanol was demonstrated in six of eight patients with cirrhosis.

Influência do grau de comprometimento hepático sobre a circulaçäo e excreçäo renal do ácido úrico, em pacientes cirróticos / Influence of the degreees of chronic hepatic failure on the circulation and renal excretion of uric acid in cirrhotic patients

A influência do grau de insuficiência hepatocelular (na cirrose hepática) sobre a circulaçäo e excreçäo do ácido úrico foi investigada em 12 pacientes cirróticos, de etiologia alcoólica, classificados em Child A (n=5) e Child B+C (n=7), todos do sexo masculino de 27 a 59 anos de idade, comparativamente ao grupo controle saudável (n=5), pareado por sexo e idade. A excreçäo urinária do ácido úrico e dos demais metabólitos nitrogenados (uréia, amônia e creatinina) foi estudada nas condiçöes de dieta hipoprotéica-hipoenergética (0,4g-20kcal/kg/d) e normoprotéica-normoenergética (1,14g-38kcal/kg/d). Os níveis séricos de ácido úrico, de albumina e alfa-1 antitripsina (alfa 1AT) foram determinados em amostras de sangue obtidas após jejum. A presença da doença hepática resultou na elevaçäo dos níveis de alfa 1AT, e o agravamento hepatocelular, na queda de albuminemia, sem alteraçäo significativa do ácido úrico circulante. A excreçäo urinária do ácido úrico foi semelhante entre os grupos, em ambas as dietas, porém, na dieta hipoprotéica-hipoenergética, o ácido úrico näo acompanhou o padräo de excreçäo da uréia e da creatinina, o que pode ser atribuído às quedas da ureogênese e da massa muscular (creatinogênese), com o agravamento da doença ou a maior capacidade renal em reter ácido úrico, nestas condiçöes. Isto pode ser configurado matematicamente, relacionando-se metabólitos excretados na urina com seus níveis plasmáticos, mostrando hipoexcreçäo de 45 por cento dos hepatopatas, tanto para o ácido úrico como para a creatinina. Assim, a menor produçäo hepática do ácido úrico, pelos pacientes cirróticos, seria compensada pela menor excreçäo renal do metabólito, preservando os níveis plasmáticos. A importância fisiológica deste processo adaptativo estaria fundamentada na participaçäo do estresse oxidativo, na gênese e perpetuaçäo da cirrose pelo álcool, e nas propriedades anti-oxidantes do ácido úrico.

Centellografía hepatobiliar cuantitativa con 99m Tc DISIDA en sujetos normales y en cirróticos alcohólicos / Quantitative Tc 99m - DISIDA hepatobiliary scintigraphy in normal and cirrhotic alcoholic subjects

Quantitative hepatobiliary scintigraphy (Q.H.S.), with 99m Tc-DISIDA was performed on 15 control subjects and 32 alcoholic cirrhotic patients (A.C.). We used a dynamic planar scintigraphy (30 sec/ frame, up to 45 min) technique following injection intravenously of 99m TC-DISIDA. Time/activity curves were obtained from the right upper lobe of the liver and the: 1) slope uptake, 2) half-time (T 1/2 min) uptake, 3) excretion half-time (T 1/2 min), were measured from the curve. The A.C. were divided in two groups, IIA (n = 32) and IIB (n = 6) if the excretory curve show negative slope or not respectively. Results: The mean value (+/- 1 D.S. 95 percent confidence interval) of the slope uptake of the A.C. IIB (1.2 +/- 0.40) was significantly slower than a.C. IIA (2.8 +/- 0.39) and control (4.5 +/- 1.17, p = 0,0001 respectively). The difference also was significantly when the mean of A.C. IIA was compared to control (p = 0.007). The mean of T 1/2 uptake of A.C.IIB (62.2 +/- 22.2) was significantly longer than A.C. IIA (28.4 +/- 4.4 p = 0.011) and control (17.9 +/- 3.87, p = 0.003) The mean T 1/2 excretory of the A.C. IIA (90.0 +/- 17.8) was also significant delayed compared to the mean of normal control (35.6 +/- 7.6 p = 0,001). In the A.C. IIB the excretion plateau curve was associated with visualization of the gallbladder and bowel activity suggesting that the excretion of the IDA preferentially came from the left hepatic lobe. We conclude that alcoholic cirrhotic patients have impaired the mechanism related with the uptake/excretion transport of organic anion, and suggest that noninvasive Q.H.S. with 99m TC-DISIDA, can be a useful clinical technique to be used for the quantification of hepatic function in cirrhotic alcoholic patients.

Cirrosis y embarazo: presentación de un caso clínico y consideraciones sobre el tema / Cirrhosis and pregnancy: report of a case and considerations about the theme

Se presenta el caso de una mujer de 32 años de edad con cirrosis hepática diagnosticada antes de la gestación, que cursó con embarazo complicado con retardo en el crecimiento intrauterino del producto, habiéndo sospechado inicialmente en la vigésima semana de gravidez mediante ultrasonido y se ratifica en las exploraciones subsecuentes, para confirmarse finalmente con el peso subnormal del bebé al nacer. Se analiza la metodología diagnóstica de la cirrosis, su tratamiento y la evolución del embarazo

Enfermedad alcohólica del hígado (EHA)

Alcohol consumption with all its severe organic complications has become one of the leading causes of morbidity and mortality in United States. In the metropolitan areas, alcohol consumption is the third cause of death between people aged 30 to 64. Latest estimates have shown that 20 percent of the total cost of health care is related to alcohol. Liver disease secondary to alcohol has been studied extensively and all its clinico-pathological consequences described. Alcoholic hepatitis characterized by anorexia, jaundice, hepatomegaly, fever, mental changes, leukocytosis and neutrophilia has been described associated to elevated bilirubin, low albumin, high AST levels and prolonged prothrombin time; histologically the picture has the following microscopic findings: degenerative changes of liver cells such as "ballooning" mainly around the terminal hepatic veins, acute and chronic inflammatory infiltrates and latest, pericellular fibrosis in the centrolobular area. Some patients develop sclerosing hyaline necrosis consistent in collapse of hepatocytes, alcoholic hyaline accumulation, neutrophilic inflammation and severe fibrosis leading to a functional obstruction of the hepatic veins, portal hypertension, ascitis and liver failure. A characteristic cytosqueletic abnormality is the Mallory Body that for many authorities constitutes the hallmark of alcoholic hepatitis. Recently the role of megamitochondrias in this entity has been unveiled showing that patients with increased number have better prognosis that the group with few megamitochondrias. Finally a significant role for cellular immunity, cytoquines, histocompatibility antigens and malnutrition has been found determinant in order to explain progression of disease after alcohol discontinuation, and prognosis after nutritional therapy.