Reversal of hepatorenal syndrome in cirrhotic patients with terlipressin plus albumin. First experience in Mexico.

INTRODUCTION: Type 1 hepatorenal syndrome (HRS) is a functional renal failure that complicates end-stage cirrhosis. The vasopressin analogue terlipressin has been associated with improved renal function in patients with type 1 HRS. AIM: To evaluate the effectiveness of an infusion of terlipressin plus albumin in reversing type 1 HRS, its tolerability, and its adverse effects. METHODS: Thirteen consecutive patients with cirrhosis and type 1 HRS were included in the study. All patients received terlipressin plus albumin as treatment for HRS. The patients were divided in two groups. Group 1 contained eight patients in whom HRS was reversed with treatment, who were classified as responders. Group 2 contained five patients who were nonresponders. RESULTS: Sixty-one percent of the patients who received terlipressin plus albumin responded to therapy and underwent HRS reversal. In two patients, treatment with terlipressin was stopped because of adverse events. No relapse of HRS after terlipressin withdrawal was observed in this study. CONCLUSION: The rate of successful treatment with terlipressin plus albumin was 61%, similar to that in previously reported controlled trials. However, this is the first experience reported in Mexico. A cardiovascular evaluation is required before the start of treatment with terlipressin. This treatment appears to be an effective therapy for improving renal function in patients with type 1 HRS.

Adipokines in a group of Mexican patients with nonalcoholic steatohepatitis.

INTRODUCTION: Leptin has been implicated in the pathogenesis of nonalcoholic steatohepatitis. It has also been suggested that adiponectin plays an important role in the transition from fatty liver disease to nonalcoholic steatohepatitis. OBJECTIVE: To evaluate whether leptin and adiponectin levels are related to the degree of necroinflammatory activity and fibrosis in patients with nonalcoholic steatohepatitis. METHODS: Leptin and adiponectin levels were determined in 52 patients with nonalcoholic steatohepatitis and in 49 controls by enzyme-linked immunosorbent analysis. RESULTS: Median (interquartile range) leptin levels were higher in patients with nonalcoholic steatohepatitis than in the controls (5.75 (12.3) ng mL-1 and 2.80 (2.40) ng mL-1, respectively; P = 0.0035). Adiponectin levels were lower in patients with nonalcoholic steatohepatitis than in the controls (6.55 (5.05) mg mL-1 and 9.30 (6.70) mg mL-1, respectively; P = 0.0218). Leptin levels were lower in overweight patients than in obese patients (2.25 (6.73) and 8.0 (16.0) ng mL-1, respectively; P = 0.0025). The amount of necroinflammatory activity observed in liver biopsies correlated positively with the amount of fibrosis (P < 0.0001). Increased lactate dehydrogenase correlated with increased fibrosis in patients with nonalcoholic steatohepatitis (P = 0.0012). Necroinflammatory activity correlated with adiponectin, g-glutamyltranspeptidase, the quantitative insulin-sensitivity check index, and ferritin (P < 0.05). Risk factors for nonalcoholic steatohepatitis in the logistic regression analysis were leptin, aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, and g-glutamyltranspeptidase (P < 0.0001). Only lactate dehydrogenase (P = 0.0012) was significantly associated with advanced fibrosis on logistic regression analysis. CONCLUSIONS: Lactate dehydrogenase was associated with fibrosis and advanced fibrosis. Leptin was associated with nonalcoholic steatohepatitis but not with fibrosis or necroinflammatory activity. Adiponectin was related to necroinflammatory activity. Risk factors for nonalcoholic steatohepatitis were leptin and liver enzymes (aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, and gama-glutamyltranspeptidase).

Stem-cell transplantation into the frontal motor cortex in amyotrophic lateral sclerosis patients.

BACKGROUND AIMS: Amyotrophic lateral sclerosis (ALS) is characterized by the selective death of motor neurons. CD133(+) stem cells are known to have the capacity to differentiate into neural lineages. Stem cells may provide an alternative treatment for ALS and other neurodegenerative diseases. METHODS: Five men and five women (aged 38-62 years) with confirmed ALS were included in this study. Our institutional ethics and research committees approved the protocol. After informed consent was obtained, patients underwent Hidrogen-Magnetic Resonance Imaging (H-MRI) spectroscopy and were given scores according to an ALS functional rating scale, Medical Research Council power muscle scale and daily living activities. Bone marrow was stimulated with 300 microg filgrastim subcutaneously daily for 3 days. Peripheral blood mononuclear cells were obtained after admission by leukapheresis. The cell suspension was conjugated with anti-human CD133 superparamagnetic microbeads, and linked cells were isolated in a magnetic field. The isolated cells (2.5-7.5x10(5)) were resuspended in 300 microL of the patient's cerebrospinal fluid, and implanted in motor cortexes using a Hamilton syringe. Ten patients with confirmed ALS without transplantation were used as a control group. Patients were followed up for a period of 1 year. RESULTS: The autologous transplantation of CD133(+) stem cells into the frontal motor cortex is a safe and well-tolerated procedure in ALS patients. The survival of treated patients was statistically higher (P=0.01) than untreated control patients. CONCLUSIONS: Stem-cell transplantation in the motor cortex delays ALS progression and improves quality of life.