Functional Capacity, Respiratory Muscle Strength, and Oxygen Consumption Predict Mortality in Patients with Cirrhosis.

Introduction. Liver diseases influence musculoskeletal functions and may negatively affect the exercise capacity of patients with cirrhosis. Aim. To test the relationship between the six-minute walk test (6MWT), maximal inspiratory pressure (MIP), and exercise capacity (VO2peak) measures and the survival rate of patients with cirrhosis. Methods. This prospective cohort study consisted of 86 patients diagnosed with cirrhosis with the following aetiology: hepatitis C virus (HCV), hepatitis B virus (HBV), and/or alcoholic cirrhosis (AC). All patients were followed up for three years and submitted to the 6MWT, pressure measurements with a compound gauge, and an exercise test (VO2peak). Results. The survival analysis showed that the individuals who covered a distance shorter than 410 m during the 6MWT had a survival rate of 55% compared with a rate of 97% for the individuals who walked more than 410 m (p = 0.0001). Individuals with MIPs below -70 cmH2O had a survival rate of 62% compared with a rate of 93% for those with MIPs above -70 cmH2O (p = 0.0001). The patients with values below 17 mL/kg had a survival rate of 55% compared with a rate of 94% for those with values above 17 mL/kg (p = 0.0001). Conclusion. The 6MWT distance, MIP, and oxygen consumption are predictors of mortality in patients with cirrhosis.

Alcoholic hepatitis: How far are we and where are we going?

 The burden of alcoholic liver disease continues to be a major public health problem worldwide. The spectrum of disease ranges from fatty liver to cirrhosis and hepatocellular carcinoma. Alcoholic hepatitis (AH) is a type of acute-on-chronic liver failure and the most severe form of alcoholic liver disease. Severe AH carries a poor short-term prognosis and its management is still challenging, with scarce advances in the last decades. Corticosteroids are still the first line of therapy in severe cases. Unfortunately, many patients do not respond and novel targeted therapies are urgently needed. Liver transplantation has shown extraordinary results in non-responders to corticosteroids however; its applicability is very low. This review summarizes the epidemiology, natural history, risk factors and pathogenesis of alcoholic liver disease with special focus on the latest advances in prognostic stratification and therapy of patients with alcoholic hepatitis.

Alcoholic liver disease presents at advanced stage and progresses faster compared to non-alcoholic fatty liver diseas.

BACKGROUND AND OBJECTIVE: Steatohepatitis is a common cause of liver disease due to alcohol (ALD) or non-alcoholic fatty liver disease (NAFLD). We performed this study to compare natural history of ALD and NAFLD. MATERIAL AND METHODS: Retrospective analysis of ALD or NAFLD patients managed at our center (2007-2011). ALD diagnosed by excluding other liver diseases (except HCV) and alcohol abuse of > 40 g/d in women and > 60 g/d in men for > 5 years. NAFLD diagnosed by excluding other liver diseases and a history of alcohol use of < 10 g/d. Cirrhosis was diagnosed using biopsy for uncertain clinical diagnosis. RESULTS: Compared to patients with NAFLD (n = 365; mean age 50 yrs; 43% males; 53% diabetic), ALD patients (n = 206; mean age 51 yrs; 68% males; 24% diabetic) presented more often with cirrhosis or complications(46vs. 12%; P< 0.0001) with a higher MELD score (13 ± 7 vs. 8 ± 8; P<0.0001). On logistic regression, ALD diagnosis was associated with presence of cirrhosis by over 4-fold (4.1 [1.8-9.1]) even after excluding 23 patients with concomitant HCV. Over median follow up of about 3 and 4 yrs among ALD and NAFLD patients respectively, ALD patients more frequently developed cirrhosis or its complications including HCC with worse transplant free survival (90 vs. 95%; P = 0.038). CONCLUSIONS: Compared to NAFLD, ALD patients present at an advanced stage of liver disease with a faster progression on follow-up. Prospective multicenter studies are needed to identify potential barriers to early referral of ALD patients as basis for development of strategies to improve outcome of patients with ALD.

Involvement of the microvasculature in the pathogenesis of terlipressin-related myocardial infarction.

We report an autopsy case of a 24-year-old man with diagnoses of advanced alcoholic liver cirrhosis, portal hypertension, and esophageal variceal bleeding that presented extensive myocardial infarction after treatment with terlipressin. On postmortem examination the cut surface of the heart presented myocardial infarction implicating the left ventricle free wall, apex of the heart and ventricular septum. Light microscopic examination revealed that the extensive area of cardiac infarction was the result of the sum of diffuse foci of microinfarction of various ages interspersed with small clusters of preserved myocytes. Moreover, the epicardial vessels were patent while the small intramyocardial vessels presented thickened wall, apparent reduction in lumen diameter and disruption of endothelial cells indicative of spasm. The observations in this case allow clear insight into the involvement of the microcirculation in the pathogenesis of myocardial infarction with the use of terlipressin.

Effects of TIPS on global end-diastolic volume and cardiac output and renal resistive index in ICU patients with advanced alcoholic cirrhosis.

The transjugular porto-systemic stent-shunt (TIPS) reduces portal pressure in cirrhotic patients and is used as a nonsurgical treatment for refractory ascites, recurrent variceal hemorrhage or hepatorenal syndrome. There are concerns regarding a negative impact on cirrhotic cardiomyopathy and deterioration of hyperkinetic circulatory dysfunction. We analyzed a prospectively maintained database containing hemodynamic data on cirrhotic ICU patients. Hemodynamic monitoring was performed using transpulmonary thermodilution (PiCCO, Pulsion Medical Systems, Munich, Germany). Renal perfusion was assessed by Doppler ultrasound during studies of portal and TIPS perfusion before and after the procedure. Complete data sets of 8 patients (4 male, 4 female, age 60 years (52-67), Child-Pugh-Turcotte score 10 (8-12)) were available. After TIPS, there was a substantial increase of GEDVI (646 ml/m2 (580-737) to 663 mL/m2 (643-792); p=0.036) that was even more pronounced at 24 hours (716 mL/m2 (663-821); P=0.012). CI increased from 3.3 L/min/m2 (3.1-4.2) to 3.9 L/min/m2 (3.6-5.3) (p=0.012) and 3.9 L/min/m2 (3.7-5.2) (p=0.017), respectively. There was a significant decrease of renal RI from 0.810 (0.781-0.864) to 0.746 (0.710-0.798) (p=0.028) and a transient increase of fractional excretion of sodium. SVRI (1737 dyn*s/cm5/m2 (1088 . 2115) vs. 1917 dyn*s/cm5/m2 (1368-2177) was not significantly altered immediately after TIPS but decreased to 1495 dyn*s/cm5/m2 (833- 1765) at 24 hours (p=0.036). There were no significant changes of mean arterial pressure (MAP). In conclusion, TIPS resulted in a pronounced increase of central blood volume. The observed hemodynamic effects are compatible with a preload driven increase of cardiac output and secondary decreases in SVRI and RI.

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.

Alcohol-induced liver disease: from molecular damage to treatment.

Although the interaction between alcohol and the liver has been the subject of intensive investigation since many years, several uncertainties remain to be solved. Good examples of what we need to learn are: The real number of patients with alcohol-induced liver disease (AILD), the dose of alcohol "safe" for the liver, the genetic predisposition to the damage or, on the other side of the coin, protecting from the damage. Rather recently, however, part of these questions started to be clarified, thus permitting a better definition of the role of each of these factors in AILD. In parallel to the clinical approach to AILD, the unveiling of the molecular and biochemical mechanisms involved in AILD has progressed and proved to be important in both a better understanding of the disease and, more important, in a more rational treatment of these disorders. This review will focus on what we currently know of AILD in clinical, biochemical and molecular terms and what we need to address in the future.

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

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.

Plasma hydroxy-metronidazole/metronidazole ratio can detect early changes in hepatic function in ethanol-induced liver injury.

AIMS: To evaluate the usefulness of plasma hydroxy-metronidazole/metronidazole (OH-MET/MET) ratios as a dynamic liver function test in ethanol abusers with or without liver cirrhosis. METHODS: Metronidazole was administered intravenously for 20 min to healthy volunteers, and to patients with alcohol-induced, non-cirrhotic hepatopathy and liver cirrhosis. Plasma concentrations of metronidazole and hydroxy-metronidazole were measured by high performance liquid chromatography in samples collected 5, 10, 20 and 30 min after the metronidazole infusion. RESULTS: Patients with non-cirrhotic alcoholic hepatopathy had significantly elevated aminotransferase levels compared to healthy volunteers and Child A patients. Child-Pugh C patients had significantly prolonged prothrombin times when compared to healthy volunteers and patients with non-cirrhotic hepatopathy. Metronidazole metabolism, as measured by the OH-MET/MET ratio following the intravenous administration of 500 mg of the drug, was significantly impaired in all ethanol-abusing individuals, including patients with non-cirrhotic alcoholic hepatopathy. CONCLUSIONS: Metronidazole metabolism was impaired in ethanol abusers, even in the absence of liver cirrhosis, indicating that ethanol was capable of affecting liver function in the early stages of alcohol-induced liver disease.

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.

Prognostic value of hepatic venous pressure gradient measurements in alcoholic cirrhosis: a 10-year prospective study.

BACKGROUND & AIMS: Different parameters are considered predictors of bleeding and death in alcoholic cirrhosis. The aim of this study was to establish the prognostic value of a prospective and sequential evaluation of portal pressure, variceal size, and Pugh's score in portal-hypertensive patients with alcoholic cirrhosis but no previous bleeding. METHODS: Thirty patients were evaluated for 42 +/- 5 months (median, 39 months). After baseline studies, 30 patients underwent an additional evaluation (follow-up 1; median, 10 months), 20 patients a second evaluation (follow-up 2; median, 25 months), and 13 patients a third evaluation (follow-up 3; median, 45 months). No prophylactic treatment for bleeding was given. End points were bleeding and/or death. RESULTS: Seventeen patients died, and 10 patients bled. At follow-up 1, portal pressure decreased both in survivors and nonbleeders (from 18.7 +/- 1.0 to 15.2 +/- 1.3 mm Hg [P < 0.01] and from 18.9 +/- 0.8 to 16.5 +/- 1.0 mm Hg [P < 0.05], respectively). On multivariate analysis (Cox model), portal pressure at follow-up 1 had the best prognostic and independent value for both bleeding and survival. Subsequent studies showed similar trends. CONCLUSIONS: Measurements of portal pressure provide unique prognostic information for predicting portal hypertensive-related bleeding and mortality in patients with alcoholic cirrhosis.

Splenic hypofunction in cirrhosis is not associated with increased risk for infections.

BACKGROUND/AIM: Pitted cell count has been described as a sensitive marker of splenic function. Recently, pitted cell count was shown to be increased in patients with alcoholic liver disease, and also to be associated with an increased susceptibility to infection. Therefore, our aim in the present study was to assess splenic function in a group of patients with cirrhosis and to determine its possible role in the development of infections. METHODS: Splenic function was assessed during hospitalization in 44 patients diagnosed as having cirrhosis, and was compared to 18 healthy subjects. Function was evaluated by counting the number of pitted cells in peripheral blood films. Results were the mean value of two independent counts and were expressed as number of pitted cells/100 erythrocytes. RESULTS: The mean percentage of pitted cells in peripheral blood of cirrhotic patients was significantly greater than that assessed in controls (3.5 +/- 3.7% vs. 1.6 +/- 0.9%, P < 0.01, Mann-Whitney U test). Eighteen patients with cirrhosis (36%) had counts greater than 3.4% (mean + 2 SD of the control group). There were no significant differences between patients with counts above or below 3.4% in terms of liver tests, platelet and reticulocyte counts, the presence of complications, Child-Pugh score and the prevalence of infections. There was no difference in pitted cell count between alcoholic and non-alcoholic cirrhotic patients (3.8 +/- 3.4% vs. 3.1 +/- 2.8% respectively, P, NS). Moreover, the mortality rate and the occurrence of infections were similar in patients with normal and increased pitted cell counts during 1-year follow-up. CONCLUSION: The increased number of pitted cells in patients with cirrhosis is not related to heptic function and does not represent a risk factor for infections.

The predictive value of serum laminin for the risk of variceal bleeding related to portal pressure levels.

BACKGROUND/AIMS: This paper presents the results of the radioimmunologic determination of laminin in serum of patients with alcoholic liver cirrhosis with a preserved hepatic function, trying to evaluate its predictive value for the risk of variceal bleeding, assessed by a portal pressure level equal to or higher than 12 mmHg. PATIENTS AND METHODS: Twenty alcoholic cirrhotic patients with a preserved hepatic function as assessed by the Child-Pugh classification, had their peripheral blood taken for radioimmunological determination of serum laminin and were submitted to hepatic vein catheterization for portal pressure measurement. RESULTS: A positive and significant correlation (r = 0.70, p < 0.001) was found between serum laminin levels (mean value + SD = 2.70 + 1.13 U/ml) and hepatic vein pressure gradient (mean HVPG + SD = 16.30 + 6.06 mmHg). Such correlation prompted us to find a value for the level of laminin that more closely represented a HVPG of 12 mmHg, a well known threshold pressure for esophageal varices bleeding. At a cut-off concentration for laminin of 2.19 U/ml, sensitivity was 73%, specificity 60%, the positive predictive value was 85% and the negative predictive value 43%. In this study population, with a prevalence of 75% of a HVPG > or = 12 mmHg, the diagnostic accuracy for such levels of serum laminin was 70%. CONCLUSIONS: Although a valid attempt in having a non invasive parameter for the investigation of portal hypertension, peripheral serum laminin alone doesn't seem to be a reliable marker for predicting portal hypertension and to assess the risk of variceal bleeding in patients with alcoholic cirrhosis.

[Hepatopulmonary syndrome in decompensated cirrhotic patients]. / Sindrome hépatopulmonar en pacientes cirróticos descompensados.

Hypoxemia is common in cirrhotic patients and, when obvious pulmonary or cardiac causes are discarded, it is attributed to the so-called hepatopulmonary syndrome. The aim of this work was to assess the frequency of hypoxemia and orthodeoxia and its relationship with the degree of liver failure, in cirrhotic alcoholic patients. We studied 30 alcoholic cirrhotics. In all, arterial blood gases were measured in supine and standing positions, in 26 a chest X ray examination was done and in 20 a spirometry. Twelve patients had a subnormal PaO2 and this parameter fell more than 105 when assuming the standing position in one of these. The same reduction was observed in two subjects with normal supine PaO2. In the chest X ray examinations, pleural effusions were observed in five hypoxemic subjects and four with normal PaO2. Likewise minimal athelectasis was found in six and seven subjects and intestinal infiltrates in one of the two subjects. A significant association between hypoxemia and Pugh score was observed. Similarly, subjects with hypoxemia is frequent in alcoholic cirrhotic patients and, since it is not associated to obvious pulmonary causes, it may be attributed to the hepatopulmonary syndrome.

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

UNLABELLED: 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 seg/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 (T1/2 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% coinfidence 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 T1/2 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 T1/2 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.

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.

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.(AU)

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