[Experimental cirrhosis induced by carbon tetrachloride inhalation: adaptation of the technique and evaluation of lipid peroxidation]. / Cirrose experimental induzida pela inalação de tetracloreto de carbono: adaptação da técnica e avaliação da peroxidação lipídica.

BACKGROUND: Long-term administration of carbon tetrachloride is an accepted experimental model to produce hepatic fibrosis. Oxidative stress has been postulated as a major molecular mechanism involved in carbon tetrachloride hepatotoxicity, where the reactive oxygen species play an important role in the pathogenesis of liver fibrosis. AIMS: This study was conducted to evaluate the effectiveness of an experimental model of hepatic cirrhosis induced by carbon tetrachloride inhalation as well as the importance of lipid peroxidation and the characteristics of the ascitic fluid in this model. METHODS: At first the hepatic histologic findings were assessed using the hematoxilineosin technique in different moments of carbon tetrachloride inhalation (5th, 7th, 9th, 12th weeks). Later, at the end of 15 weeks of the study the rats were divided in three groups (control; control + phenobarbital; and carbon tetrachloride + phenobarbital) for lipid peroxidation, ascitic fluid and histologic characteristics evaluation. For the lipid peroxidation analysis, thiobarbituric acid and QL techniques were used. Cytologic and bacteriologic parameters were analysed in the ascitic fluid. RESULTS: Cirrhosis was established in 100% of carbon tetrachloride rats between the 12th and 15th weeks with an elevation in the lipid peroxidation carbon tetrachloride rats' livers. Ascitic fluid infection was observed in one of seven rats who has developed ascites. CONCLUSIONS: The carbon tetrachloride inhalation method developed in this study is effective in cirrhosis induction and ascites formation, and the carbon tetrachloride cirrhosis physiopathogenesis is probably related to the oxidative stress installation.

Flow cytometry in the diagnosis of peritoneal carcinomatosis.

OBJECTIVES: Peritoneal carcinomatosis is the second major cause of ascites. Because of its frequency and poor prognosis, it is important to establish an accurate diagnosis. The aim of this study was to analyze the use of a DNA index, detemined by flow cytometry in the differential diagnosis of ascites, and to compare it to the cytopathological examination. METHODS: A prospective analysis was carried out on 67 patients (39 female, 28 male; mean age, 53+/-14 yr [range, 5-82]) with ascites of various etiologies. Peritoneal carcinomatosis was detected in 21 patients, whereas in 46 the ascites was of noncarcinomatosis origin. RESULTS: The sensitivity of the cytopathological examination for the diagnosis of peritoneal carcinomatosis was 42.9%, and the specificity was 100%. The mean DNA index determined by flow cytometry was similar for peritoneal carcinomatosis and noncarcinomatosis patients, being 1.28 versus 1.01, respectively, in the preparations without control lymphocytes and 1.28 versus 1.04, respectively, when control lymphocytes were added. The sensitivity of DNA index cytometry was 57.1% and specificity, 93.5%. The combined use of the DNA index and cytopathological examination did not show an advantage over the use of any of the tests individually, although the DNA index was able to detect half of the cases of peritoneal carcinomatosis in which cytopathological examination was negative. Although the sensitivity was higher when the parameters were associated, the DNA index did not offer a statistically significant advantage over the use of cytopathological examination alone, which in turn had higher specificity. CONCLUSION: The DNA index presented lower sensitivity for the diagnosis of peritoneal carcinomatosis when used alone, showing no advantage over conventional cytopathological examination. However, the DNA index was able to detect 50.0% of peritoneal carcinomatosis cases whose conventional cytopathological examinations were negative, and could be valuable in these situations.

The value of serum-ascites albumin gradient for the determination of portal hypertension in the diagnosis of ascites.

BACKGROUND/AIMS: The aim of the present study was to evaluate the correlation between serum-ascites albumin gradient and portal pressure gradient in a population with ascites related to multiple conditions. METHODOLOGY: Thirty-seven patients were divided into two groups: group 1: 30 patients with cirrhosis as the cause of ascites, and group 2: 7 patients with ascites due to other causes. All patients were submitted to paracentesis and blood examination to determine the serum-ascites albumin gradient and the hepatic venous pressure gradient was measured. RESULTS: Mean serum-ascites albumin gradient was 2.0 g/dL in group 1 and 0.6 g/dL in group 2. Mean hepatic venous pressure gradient was 14.7 mm Hg in group 1 and 1.3 mm Hg in group 2. CONCLUSIONS: There was a significant correlation between the serum-ascites albumin gradient and the hepatic venous pressure gradient (r = 0.502), indicating the reliability of the serum-ascites albumin gradient in demonstrating the presence of portal hypertension and its relationship with the origin of ascites.