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BACKGROUND: Chronic hepatitis C is an important health problem in Chile. In 2005, the Ministry of Health started a pilot treatment program with peg interferon and ribavirin, to be developed in public hospitals all over the country. AIM: To report the results of hepatitis C treatment obtained at our institution. PATIENTS AND METHODS: Between 2005 and 2009, 63 patients were referred for treatment. In all, the viral load and genotype were determined. Peg interferon alpha-2a or alpha-2b plus ribavirin were used for therapy for up to 48 weeks in genotypes (G) 1 or 4 or 24 weeks in genotypes 2 or 3. If at the end of treatment, viral load measured by polymerase chain reaction (PCR) was negative, it was repeated 6 months later. A negative viral load at that time was considered a sustained viral response (SVR). RESULTS: Among the 51 patients who started treatment, 42 (80.4%) were G1,1 was G2,1 was G4 and 7 were G3. A SVR was reached in 51.1% of G 1 and 4 and in 87.5% in G 3 and 2. In a univariate analysis, the variables significantly associated with a positive viral response were the degree of fibrosis and body mass index. CONCLUSIONS: These results are similar to those obtained in other international series, demonstrating that Hispanic ethnicity does not influence the response to treatment. Our good results could be explained by the excellent compliance of the patients to the treatment. A higher degree of fibrosis and a higher BMI were associated with a poor response.

In previous reports we have demonstrated high plasma levels of sex hormone-binding globulin (SHBG) in asymptomatic alcoholic men. In the present work the physicochemical properties of SHBG from plasma of noncirrhotic alcoholic patients have been further compared with SHBG of control subjects. Steroid binding to SHBG was similar for the two groups: alcoholic men, K(d) of 0.62 +/- 0.07 nM and control individuals, K(d) of 0.70 +/- 0.10 nM. The structure of oligosaccharides attached to SHBG from controls and alcoholic men were determined by using serial chromatography. Our data indicated that 7% of SHBG of control individuals was not retarded by the Con-A column, whereas approximately 30% of SHBG of alcoholic men eluted in the void volume of Con A. Approximately 46% of SHBG of alcoholics applied to Con A, possessed biantennary complex oligosaccharides, as indicated by the fact that it could be eluted with methyl-alpha-D-glucopyranoside and by its retention on wheat germ agglutinin; in contrast, when SHBG from control men was analyzed, approximately 51% was eluted with methyl-alpha-D-glucopyranoside. Approximately 9% of the biantennary complex oligosaccharides on SHBG of control men and none of those on SHBG from alcoholic men were fucosylated on the chitobiose core, as determined by chromatography on Lenn culinaris lectin. Galactosylated oligosaccharides were also present on the SHBG fraction as indicated by its interaction with Ricinus communis-I. Approximately 24% of SHBG of alcoholic men and 39% of those on SHBG from control individuals applied to Con-A were retained and could be eluted with methyl-alpha-D-mannopyranoside. Evidence based on the binding on mannoside-eluted SHBG to Con-A, wheat germ agglutinin, and R. communis-I indicated that at least the SHBG in this fraction, from alcoholics or controls, contained two glycosylation sites and that the sites were differentially glycosylated.

Excessive ethanol ingestion induces hypoandrogenism in male subjects. To confirm its presence and to study its relationship with the degree of liver damage and alcohol abstinence, plasma sex hormones were measured in alcoholic patients without liver failure, after two different abstinence periods. Patients were 30 male chronic alcoholics admitted to the Alcoholism Ward for treatment of their addiction. On admission, we measured: testosterone (T), estradiol (E), follicle stimulating hormone (FSH), luteinizing hormone (LH) and sex-hormone binding globulin (SHBG). A liver biopsy was also performed. These measurements were repeated at discharge and were also done in 15 normal volunteers. On admission (mean abstinence 1.9 +/- 1.7 days) total T was similar to controls, FSH was lower (p0.02) and high levels of SHBG were found (3.5 fold increase, as compared to controls). Histologically, 9 patients had normal liver; 14 had moderate alterations and 7 showed marked alterations. Hormonal values were not different in these 3 groups. At discharge, 11.1 +/- 4.7 days after admission, T, E and FSH did not show significant changes but LH decreased (8.2 +/- 5.2 mIU/ml vs 12.9 +/- 4.1, p0.001); SHBG also decreased (65.4 +/- 21.6 nmol/l vs 117.2 +/- 33.3, p0.001) to values that still were twice those of controls. It is concluded that alcoholic patients without clinical signs of liver failure have normal plasma testosterone levels, irrespective of their histologic liver alterations and high plasma SHBG levels that decreased significantly after a short abstinence. The concomitant LH decrease suggests that hypoandrogenism is likely in these patients. Fast changes in SHBG levels rise the possibility that this protein is candidate marker of alcoholism.

Thirteen asymptomatic chronic alcoholic patients were studied to investigate the early stages of portal hypertension in alcoholic liver disease and the effects of withdrawal and ethanol on hepatic function and hemodynamic variables. None of the patients presented clinical signs of decompensated liver disease, and their liver biopsies showed normal liver or moderate alterations only. In basal conditions and after an intravenous ethanol infusion (1 g/kg body weight), hepatic venous pressure gradient and hepatic blood flow using indocyanine green were measured through hepatic vein catheterization. Hepatic sinusoidal vascular resistance and indocyanine green intrinsic clearance were also calculated. Portal blood flow measurements were obtained by Doppler ultrasound. No correlation was observed between hepatic venous pressure gradient and histologic features, (steatosis, necrosis, fibrosis, inflammation and hepatocyte surface area). In basal conditions, portal hypertension was not found in any case. After ethanol, portal pressure increased significantly (p0.001); in four cases it rose to or above 5 mmHg. Portal blood flow, hepatic blood flow and hepatic vascular resistance also increased significantly. Intrinsic indocyanine green clearance decreased slightly but significantly. No significant correlations were found between portal pressure, hepatic resistance and the histologic parameters. It was concluded that alcoholic patients, without clinical or laboratory evidence of liver failure and with minimal or moderate histologic alterations, have normal portal pressures. After an intravenous ethanol load, however, four out of 13 patients (31%) reached levels of 5 mmHg or more, irrespective of their liver histology.

Background: Varioliform gastritis (VG) is found in approximately 0.3 to 2.8% of upper gastrointestinal endoscopies. Its etiology is not known. We have observed a higher frequency of VG in patients with liver cirrhosis. Aim: To confirm if there is an association between VG and liver cirrhosis. Patients and Methods: Two case-control studies were done. A retrospective study, reviewing the endoscopy database of a gastroenterological unit. A prospective study, identifying cases with the endoscopic diagnosis of VG among all patients referred for upper gastrointestinal endoscopies. The presence of liver cirrhosis, based on clinical, laboratory, ultrasonographic and endoscopic features was registered among patients with VG. Results: VG was found in 549 of 11.659 upper gastrointestinal endoscopies. Fourteen percent of patients with VG had cirrhosis compared to 5.6% in control patients (c² 29,8; p < 0.01). The odds ratio (OR) for having cirrhosis of patients with VG was 9.3 (95% confidence intervals 3.4-25.5, p < 0,01), according to a logistic regression analysis. In the prospective study, that included 1.498 upper gastrointestinal endoscopies, VG was also significantly more common among patients with liver cirrhosis. Conclusions: A higher frequency of VG was found among patients with liver cirrhosis. Therefore, the endoscopic finding of VG should alert physicians to look for the presence of a coexistent liver cirrhosis.

A preoperative nutritional assessment including anthropometry, biochemical indices and global subjective assessment was performed for 127 patients admitted for elective gastrointestinal surgery. Of these, 24 were subjected to minor surgery, 65 to intermediate surgery and 38 to major procedures. Patients were followed postoperatively, recording complications or mortality. Intermediate and major surgery patients had lower triceps skinfold thickness and mid-arm circumference and greater weight loss than did minor surgery patients. Thirty-six percent of the patients suffered complications. No association was found between preoperative nutritional status and incidence of postoperative complications. Six patients died and they showed greater preoperative weight loss (21 +/- 6.5 vs 12 +/- 1.4%) and lower serum albumin levels (25 +/- 4 vs 35 +/- 1 g/l) than patients who survived complications. Global subjective assessment classified 43% of survivors as malnourished, compared to 100% of patients who died.

We report a 33 year-old female with a diagnosis of halothane-induce fulminant hepatic failure who was subjected to a liver transplant with an ABO-incompatible graft. The patient received a therapeutic protocol that included total plasma exchange, splenectomy and quadruple immunosuppression. After 5 years, the patient remains asymptomatic and with normal liver enzymes, while she has been treated with low dose of immunosuppressive drugs. This case demonstrates an example of how the immunological process of accommodation opens the possibility of using ABO-incompatible organs as a definitive grafts.

In recently intoxicated non-cirrhotic male alcohol-misusing and -dependent patients, we studied, during early withdrawal and more prolonged abstinence, the rate of changes of sex hormones and their binding globulin (SHBG), the prevalence of hypo-androgenism and possible determinant factors of SHBG increase. Twenty-one alcoholics and 21 controls were studied. SHBG plasma levels, sex hormones (SH), cortisol, insulin and thyroid hormones were measured at admission and discharge. SHBG and SH were also determined on days 2, 4 and 7 after admission and on weeks 2, 6 and 12 after discharge. SHBG showed a 3-fold increase, decreasing slowly during the first 10 days, but remaining above control values. Luteinizing hormone was also increased. Free testosterone (Tf) was low at admission and correlated negatively with SHBG during the first 10 days. By day 10, Tf reached normal values, despite SHBG remaining elevated. The other sex hormones were normal. Neither insulin nor thyroid hormones correlated with SHBG. Cortisol was high at admission and then normalized. Clinical hypo-androgenism was found in 33-50% of patients, but did not correlate with SHBG or SH. During follow-up, nine patients relapsed. In those remaining abstinent, SHBG continued decreasing, reaching normal levels in the 12th week. In those who relapsed, SHBG remained high or even increased further. Gamma-glutamyltransferase showed similar but faster changes. We conclude that excessive alcohol ingestion is associated with marked increases of SHBG which slowly revert during abstinence. High SHBG does not fully explain the low Tf values or the presence of clinical hypo-androgenism in alcoholics. This SHBG response to ethanol makes it a potential marker of excessive alcohol intake.

We measured suprahepatic vein and arterial partial oxygen pressure in 35 alcoholics with severe (N = 7) or mild (N = 28) histological liver damage and without evidence of clinical liver failure. The suprahepatic vein was punctured with a fine needle, using a percutaneous approach. Suprahepatic vein partial oxygen pressure was lower and arterial-suprahepatic gradient higher in alcoholics with severe liver damage compared to those with mild damage (35.1 +/- 1.7 vs 44.1 +/- 2.1 and 58.9 +/- 3.7 vs 45.9 +/- 2.4 mm Hg, respectively; P0.001). Suprahepatic puncture was well tolerated and devoid of complications. It is concluded that alcoholics with severe liver damage have lower oxygen tensions in the suprahepatic vein, a phenomenon that supports the hypoxic theory of alcoholic liver disease.

This study was designed to measure the effect of chronic alcohol intake on leucine turnover in outpatients with stable alcoholic liver cirrhosis.Protein turnover rate was measured using L [1-14C] leucine in ten outpatients with proven alcoholic cirrhosis and in five healthy controls. After the performance of the turnover, the patients were divided in two groups depending on the evidence of alcohol ingestion in the previous month.Non-abstinent patients had a significantly higher leucine flux and non-oxidative disposal (73.8 +/− 25.4 and 65.9 +/− 21.6) than abstinent cirrhotic patients (48.9 +/− 9.5 and 43.7 +/− 9.0) and normal controls 37.3 +/− 8.9 and 31.1 +/− 7.6 mumol/m2/min (p < 0.01). Leucine oxidation and serum leucine levels were similar in the three groups.Alcohol intake in alcoholic cirrhotic patients has a catabolic effect that could be associated with the nutritional imbalances observed in alcoholic liver disease.