David S. Barnes

Cleveland Clinic, Cleveland, Ohio, United States

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Publications (31)211.63 Total impact

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    ABSTRACT: Background. Skeletal muscle loss (sarcopenia) is a major clinical complication in alcoholic cirrhosis with no effective therapy. Skeletal muscle autophagic proteolysis and myostatin expression (inhibitor of protein synthesis) are increased in cirrhosis and believed to contribute to anabolic resistance. A prospective study was performed to determine the mechanisms of sarcopenia in alcoholic cirrhosis and potential reversal by leucine.Methods. In 6 well-compensated, stable alcoholic cirrhotic patients and 8 controls, serial vastus lateralis muscle biopsies were obtained before and 7h after a single oral BCAA mixture enriched with leucine (BCAA/LEU). Primed-constant infusion of L-[ring- H ]-phenylalanine was used to quantify whole body protein breakdown (WbPB) and muscle protein fractional synthesis rate (FSR) using liquid chromatography/mass spectrometry . Muscle expression of myostatin, mTOR targets, autophagy markers, protein ubiquitination and intracellular amino acid deficiency sensor, general control of nutrition 2 (GCN2) were quantified by immunoblots and leucine transporter (SLC7A5) and glutamine exchanger (SLC38A2) by real time PCR.Results. Following oral administration, plasma BCAA concentrations showed a similar increase in cirrhosis and controls. Skeletal muscle FSR was 9.63±0.36%/h in controls and 9.05±0.68%/h in cirrhotics (p=0.54). Elevated WbPB in cirrhosis was reduced with BCAA/LEU (p=0.01). Fasting skeletal muscle molecular markers showed increased myostatin expression, impaired mTOR signaling and increased autophagy in cirrhosis compared to controls (p<0.01). BCAA/LEU did not alter myostatin expression but mTOR signaling, autophagy measures and GCN2 activation were consistently reversed in cirrhotic muscle (p<0.01). SLC7A5 expression was higher in basal state in cirrhosis than controls (p<0.05) but increased with BCAA/LEU only in controls (p<0.001).Conclusions. We demonstrate that impaired mTOR1 signaling and increased autophagy in skeletal muscle of alcoholic cirrhosis patients is acutely reversed by BCAA/LEU. This article is protected by copyright. All rights reserved.
    Hepatology 01/2015; DOI:10.1002/hep.27717 · 11.19 Impact Factor
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    ABSTRACT: Colonic configuration during insertion phase (IP) and withdrawal phase (WP) is different and some polyps seen during IP are difficult to find during WP and vice versa. To determine if polypectomy performed during both IP and WP of colonoscopy (study arm) increases adenoma detection rate (ADR) compared to WP only (control arm). In this prospective randomized controlled trial, adults undergoing out-patient colonoscopy were enrolled. The primary outcome was mean number of adenomas detected per patient. Secondary outcomes were ADR, defined as the proportion of colonoscopies with at least one adenoma, polyp detection rates (PDR), number of patients classified as high-risk group (presence of ≥3 adenomas of any size, any adenoma ≥1 cm in size, or adenoma with villous component, or high grade dysplasia), procedural times, patients discomfort, and ease of procedure. Among 772 patients enrolled, 610 were included (329 in study arm and 281 in control arm). In both arms, mean number of adenomas detected per patient were similar, 0.78 ± 1.4 vs. 0.74 ± 1.5, P = 0.75. Also, ADR (39.2 vs. 38.1 %, P = 0.77) and PDR (57.1 and 54.1 %, P = 0.45) were similar. Mean insertion time was significantly higher in study arm (10.2 ± 5.8 vs. 9.3 ± 5.6 min, p = 0.046). Proportion of patients identified as high-risk group were significantly higher in study arm (18.8 vs. 11.7 %, P = 0.016). Conclusions: Polypectomy performed during both IP and WP compared to the WP only, did not improve ADR or mean number of adenomas detected per patient. Trial registration: Clinicaltrials.gov, #NCT01025960.
    Surgical Endoscopy 07/2014; 29(3). DOI:10.1007/s00464-014-3723-3 · 3.31 Impact Factor
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    ABSTRACT: Current consensus suggests CD to be a multi-systemic disease that could affect any organ system including the liver. It remains under-diagnosed in the US and its prevalence and management in cirrhotic patients has not been studied.
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    ABSTRACT: Pre-transplant sarcopenia (reduced skeletal muscle mass) predicts poor outcome in cirrhosis. In contrast, whether muscle mass increases post orthotopic liver transplantation (OLT) is not known and was studied prospectively. Consecutive patients who underwent a comprehensive nutritional evaluation in a liver transplant nutrition clinic were included. Core abdominal muscle area was measured on abdominal CT obtained pre- and post-OLT. Age and gender based controls were used to define sarcopenia. Measures of body composition pre-transplant were correlated with CT measurements. Predictors and clinical impact of post-OLT change in muscle area were examined. In 3 subjects post-OLT and 3 controls, expression of genes regulating skeletal muscle mass were quantified. During the study period, 53 patients (M:F 41:12; age 56.9±7.5 years) were followed up after OLT for 19.3±9 months. Five patients died and another 5 had acute graft rejection. Pre-OLT sarcopenia was present in 33 (66.2%). Pre-transplant clinical characteristics including Child's score, MELD score and nutritional status or post transplantation immunosuppression regimen did not predict post transplant change in muscle mass. New onset post-OLT sarcopenia developed in 14 patients. Loss of muscle mass post-OLT increased risk of diabetes mellitus and a trend towards higher mortality. Skeletal muscle expression of myostatin was higher and that of ubiquitin proteasome proteolytic components lower post-OLT than in controls. Post transplantation sarcopenia is common and could not be attributed to pre-transplant characteristics or the type or duration of post-OLT immunosuppression. Post-transplant sarcopenia contributes to adverse consequences and strategies targeting myostatin may be beneficial.
    Journal of Gastroenterology and Hepatology 01/2014; 29(6). DOI:10.1111/jgh.12524 · 3.63 Impact Factor
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    ABSTRACT: BACKGROUND: Ascites usually occurs in the setting of end-stage liver disease and low serum albumin and is associated with increased mortality. However, some patients develop ascites despite normal serum albumin (NSA), when a higher portal pressure and/or enhanced renal sodium retention would be expected. This study investigated the relationship between the hepatic venous pressure gradient (HVPG) and serum albumin in ascitic patients with different etiologies of cirrhosis and mortality. METHODS: Records of all patients with non-malignant ascites who underwent HVPG measurement from 2005 to 2009 were reviewed. RESULTS: One hundred and thirty-eight 138 patients met inclusion criteria; 18.8% had NSA. No difference in sodium excretion or diuretic use was noted in patients with and without NSA. NASH patients were more likely to have a NSA (34.2% vs 12.4%; P=0.001) as well as lower HVPG (15 vs 17.9mmHg; P=0.009) compared to other etiologies. MELD and HVPG predicted overall survival. However, mortality did not differ by disease etiology, though NASH patients had lower CTP (7.6 vs 8.5; P<0.001) and MELD (15.6 vs 18.1; P=0.09) scores, particularly among patients who died. CONCLUSIONS: In patients with ascites and NSA, there were no increase in HVPG or urinary sodium retention. NASH patients with ascites had lower HVPG and a higher prevalence of NSA. They also had a higher mortality relative to MELD and CTP scores in other patients. In these patients, mechanisms other than portal and oncotic pressures and sodium retention play a role in ascites development, and increase mortality rate when complicated by low albumin.
    Gastroentérologie Clinique et Biologique 11/2012; DOI:10.1016/j.clinre.2012.10.006 · 1.98 Impact Factor
  • Gastrointestinal Endoscopy 04/2012; 75(4):AB167. DOI:10.1016/j.gie.2012.04.132 · 4.90 Impact Factor
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    Gastroenterology and Hepatology 02/2011; 7(2):132-4.
  • Gastroenterology 01/2011; 140(5). DOI:10.1016/S0016-5085(11)63957-7 · 13.93 Impact Factor
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    ABSTRACT: Primary biliary cirrhosis (PBC) is sometimes diagnosed based on a positive antimitochondrial antibody in the appropriate clinical setting without a liver biopsy. Although a liver biopsy can assess the extent of liver fibrosis and provide prognostic information, serum fibrosis markers avoid biopsy complications and sampling error and provide results as a continuous variable, which may be more precise than categorical histological stages. The current study was undertaken to evaluate serum fibrosis markers as predictors of clinical progression in a large cohort of PBC patients. Serial liver biopsy specimens and serum samples were collected every 2 years in 161 PBC subjects for a median of 7.3 years. Clinical progression was defined as development of one or more of the following events: varices, variceal bleed, ascites, encephalopathy, liver transplantation, or liver-related death. Serum hyaluronic acid, tissue inhibitor of metalloproteinase 1, and procollagen III aminopeptide were measured and entered into the previously validated enhanced liver fibrosis (ELF) algorithm. The ability of ELF, histological fibrosis, bilirubin, Model for End-Stage Liver Disease (MELD), and Mayo Risk Score to differentiate between individuals who would experience a clinical event from those who would not was evaluated at different time points. Event-free survival was significantly lower in those with high baseline ELF. Each 1-point increase in ELF was associated with a threefold increase in future complications. The prognostic performance of all tests was similar when performed close to the time of the first event. However, at earlier times in the disease process (4 and 6 years before the first event), the prognostic performance of ELF was significantly better than MELD or Mayo R score. CONCLUSION: The ELF algorithm is a highly accurate noninvasive measure of PBC disease severity that provides useful long-term prognostic information.
    Hepatology 11/2008; 48(5):1549-57. DOI:10.1002/hep.22517 · 11.19 Impact Factor
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    ABSTRACT: This placebo-controlled, randomized, multicenter trial compared the effects of MTX plus UDCA to UDCA alone on the course of primary biliary cirrhosis (PBC). Two hundred and sixty five AMA positive patients without ascites, variceal bleeding, or encephalopathy; a serum bilirubin less than 3 mg/dL; serum albumin 3 g/dL or greater, who had taken UDCA 15 mg/kg daily for at least 6 months, were stratified by Ludwig's histological staging and then randomized to MTX 15 mg/m2 body surface area (maximum dose 20 mg) once a week while continuing on UDCA. The median time from randomization to closure of the study was 7.6 years (range: 4.6-8.8 years). Treatment failure was defined as death without liver transplantation; transplantation; variceal bleeding; development of ascites, encephalopathy, or varices; a doubling of serum bilirubin to 2.5 mg/dL or greater; a fall in serum albumin to 2.5 g/dL or less; histological progression by at least two stages or to cirrhosis. Patients were continued on treatment despite failure of treatment, unless transplantation ensued, drug toxicity necessitated withdrawal, or the patient developed a cancer. There were no significant differences in these parameters nor to the time of development of treatment failures observed for patients taking UDCA plus MTX, or UDCA plus placebo. The trial was conducted with a stopping rule, and was stopped early by the National Institutes of Health at the advice of our Data Safety Monitoring Board for reasons of futility. In conclusion, methotrexate when added to UDCA for a median period of 7.6 years had no effect on the course of PBC treated with UDCA alone.
    Hepatology 11/2005; 42(5):1184-93. DOI:10.1002/hep.20897 · 11.19 Impact Factor
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    ABSTRACT: In an attempt to improve the efficacy of antiviral therapy for chronic hepatitis C, a three-drug combination of pegylated interferon alpha-2b, ribavirin, and amantadine has been suggested. Despite the initial enthusiasm, the role of amantadine in the treatment of chronic hepatitis C remains controversial. In a multi-center, open-label clinical trial, the potential efficacy and safety of this triple combination regimen were assessed. In this open-label pilot study, two separate patient populations with chronic hepatitis C and viremia were enrolled: treatment-naive and those who had failed a previous course of treatment. Patients were started on pegylated interferon alpha-2b at a dose of 1.5 microg/kg weekly with ribavirin, 1000-1200 mg/day, and amantadine, 200 mg/day, for 4 weeks, followed by pegylated interferon alpha-2b, 0.5 microg/kg weekly, ribavirin, 1000-1200 mg/day, and amantadine, 200 mg/day, for another 20 weeks. Patients with undetectable HCV RNA at week 24 continued this regimen for a total of 48 weeks and were followed for another 24 weeks. Patients with undetectable virus (<50 IU/mL) after 24 weeks of follow-up were considered to have SVR. Health-related quality of life and safety data were also collected. Sixty-nine treatment-naive and 99 nonresponder patients with chronic hepatitis C were enrolled in the study. Of all patients enrolled, 74% were male, aged 47.27+/-5.76 years; their body mass index (BMI) was 28.87+/-5.05 kg/m2, 79.4% were white, 85% had HCV genotypes 1 and 4, and 36% had cirrhosis. Their baseline HCV RNA was 689,242+/-698,030 IU/mL, with a baseline ALT of 107.25+/-79.08. Of the entire cohort, 35 (21%) discontinued early due to side effects or loss to follow-up. Significant anemia (hemoglobin, < 10 g/dL) occurred in 11% (19/168), while severe anemia (hemoglobin, <8.5 g/dL) occurred in 0.6% (1/168). In the treatment-naive group, sustained virologic response (SVR) was 34.3%, versus 19.4% for the group who had previously failed to respond to a course of treatment (P = 0.01). For both groups combined, virologic response after 24 weeks of therapy was 40.5%, with an end-of-treatment virologic response of 35.7% and a SVR of 26.2%. Patients with genotypes 1 and 4 had lower response rates than those with genotypes 2 and 3 (SVR, 21 vs. 46%; P = 0.001). Patients with advanced fibrosis (Metavir stages 3 and 4) tended to have lower response rates than those with minimal or mild fibrosis (Metavir stages 0-2) (SVR, 10 vs. 30%; P = 0.08). African-American patients with HCV had lower response rates than Caucasians or other ethnic groups (SVR, 4 vs. 29 vs. 20%; P = 0.04). Age, gender, and BMI did not affect SVR. The addition of amantadine to pegylated interferon alpha-2b and ribavirin does not seem to increase the efficicacy of this regimen.
    Digestive Diseases and Sciences 05/2005; 50(5):970-5. DOI:10.1007/s10620-005-2673-y · 2.55 Impact Factor
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    ABSTRACT: Superimposed non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH) may affect HCV-related fibrosis. We performed a study to determine the relationship between NAFLD and chronic hepatitis C. One hundred and twenty patients with chronic hepatitis C and available liver biopsies were included. Baseline liver biopsies were read by 1 hepatopathologist using Metavir, as well as a fatty liver pathology protocol. Patients' baseline clinical, demographic, and virologic data were associated with the extent of steatosis (>33% vs. < or =33%), the type of fatty liver (no steatosis vs. steatosis only vs. NASH), and the stage of fibrosis seen on the liver biopsy. Seventy percent of patients were men and 80% were white. The mean age was 47.48+/-5.70 years, mean BMI was 29.01 +/-5.01 kg/m, and mean waist to hip ratio (W/H) was 0.90+/-0.08. Patients with higher grade of steatosis had higher BMI (32.83+/-6.26 vs. 28.49+/-4.62, P = 0.034), more likely to have genotype 3 (21.4% vs. 5.7%, P = 0.037) and advanced fibrosis (92.9% vs. 62.3%, P = 0.033) than those with lower grade of steatosis. Of these, only HCV-genotype 3 remained independently associated with higher grade of steatosis. When patients with superimposed NASH (n = 22) were compared with those with only steatosis (n = 49) and those without steatosis (n = 49), patients with superimposed NASH had more evidence of obesity (BMI: 30.64+/-5.23 vs. 29.90+/-5.35 vs. 27.33+/-4.07, P = 0.008; W/H: 0.97+/-0.06 vs. 0.91+/-0.08 vs. 0.87+/-0.07, P < 0.001), more commonly infected with HCV genotype 3 (14% vs. 12% vs. 0%, P = 0.036) and had more advanced fibrosis (95.5% vs. 75.5% vs. 42.9%, P < 0.001). Race, gender, and age did not affect extent of steatosis or presence of superimposed NASH. In conclusion, markers of obesity (BMI and W/H) and HCV genotype 3 are associated with the extent of steatosis and type of fatty liver. Higher grade of steatosis and presence of superimposed NASH are both associated with advanced hepatic fibrosis.
    Journal of Clinical Gastroenterology 09/2004; 38(8):705-9. DOI:10.1097/01.mcg.0000135372.10846.2a · 3.19 Impact Factor
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    ABSTRACT: This study aims to quantify the risk of cardiac surgery in patients with cirrhosis. Records of all adult patients with cirrhosis undergoing cardiac surgery using cardiopulmonary bypass at the Cleveland Clinic (Cleveland, OH) from January 1992 to June 2002 were analyzed for any relationship of Child-Pugh class and/or score and Model for End-Stage Liver Disease (MELD) score with outcome measures of hepatic decompensation and death during the first 3 months after surgery. Forty-four patients underwent coronary artery bypass grafting (16 patients), valve surgery (16 patients), a combination of the 2 procedures (10 patients), or pericardiectomy (2 patients). Twelve patients (27%) developed hepatic decompensation, and 7 patients (16%) died. Proportions of hepatic decompensation were 3 of 31, 8 of 12, and 1 of 1 patients, and death, 1 of 31, 5 of 12, and 1 of 1 patients in Child-Pugh classes A, B, and C, respectively. The association of hepatic decompensation and mortality with Child-Pugh class, Child-Pugh score, and MELD score was significant (P < 0.005). Areas under the receiver operating characteristic curves for mortality were similar for Child-Pugh (0.84 +/- 0.09) and MELD scores (0.87 +/- 0.09). A cutoff Child-Pugh score >7 was found to have a sensitivity and specificity of 86% and 92% for mortality, with a negative predictive value of 97% (95% confidence interval [CI], 83-99) and positive predictive value of 67% (95% CI, 31-91), respectively. However, a similar cutoff value for MELD score could not be established. Child-Pugh score and/or class and MELD score are significantly associated with hepatic decompensation and mortality after cardiac surgery using cardiopulmonary bypass in patients with cirrhosis. Such surgery can be conducted safely in patients with a Child-Pugh score </=7. Patients with a Child-Pugh score >/=8 have a significant risk for mortality.
    Clinical Gastroenterology and Hepatology 09/2004; 2(8):719-23. DOI:10.1016/S1542-3565(04)00296-4 · 6.53 Impact Factor
  • Gastroenterology 04/2003; 124(4). DOI:10.1016/S0016-5085(03)83764-2 · 13.93 Impact Factor
  • Gastroenterology 04/2003; 124(4). DOI:10.1016/S0016-5085(03)83944-6 · 13.93 Impact Factor
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    ABSTRACT: The purpose of this study was to examine the long-term survival and causes of death in patients who survive the first year after liver transplantation. The focus of the analysis was 433 patients who survived for at least 1 year after liver transplantation between November 1, 1984, and December 31, 2001. A total of 586 liver transplants were performed in 542 patients during this time period. The overall 1-, 5-, and 10-year survivals and the 5- and 10-year survivals for those patients who lived for a year were analyzed on the basis of Kaplan-Meier survival estimates. Factors examined included diagnosis, sex, age, and retransplantation. The causes of death were also analyzed. The overall 1-, 5-, and 10-year survivals were 85%, 73%, and 55%, respectively. The 5- and 10-year survivals for those patients who lived for a year were 86% and 65%, respectively. Fifty-one percent of the causes of late death were graft-related, 71% from recurrent primary disease. Cardiovascular events and de novo malignancies were responsible for 65% of the nongraft-related deaths. The long-term survival in patients who survive for the first year after liver transplantation is excellent. Recurrent primary disease is responsible for the majority of graft-related deaths. Cardiovascular events and de novo malignancy cause most of the nongraft-related deaths.
    Surgery 11/2002; 132(4):775-80; discussion 780. DOI:10.1067/msy.2002.128343 · 3.11 Impact Factor
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    ABSTRACT: Hepatitis C virus (HCV) is a major cause of chronic liver disease worldwide, affecting 175 million people globally. Over 80% of acutely infected patients go on to develop chronicity, but only 20% to 25% will develop end-stage liver disease and its complications. The sequelae of HCV-induced chronic liver disease accounts for 8,000 to 10,000 deaths annually in the United States and is currently the leading indication for liver transplantation. To date, there are no accurate noninvasive markers of disease activity and fibrosis. Liver biopsy is indicated to exclude other forms of liver pathologies and to establish the stage of liver disease. In this study, the role of liver biopsy in chronic hepatitis C was evaluated. Additionally, we calculated a discriminant score to predict cirrhosis in chronic hepatitis C infection. Our results showed that additional diagnoses or unsuspected diagnoses are less frequent than clinicians' suspected. We confirmed that the discriminant score for predicting cirrhosis is inferior to liver biopsy. In conclusion, the majority of patients with chronic hepatitis C will require a liver biopsy, which has an important implication on staging of the liver disease, prognosis, and possibly further management options.
    Hepatology 02/2001; 33(1):196-200. DOI:10.1053/jhep.2001.20534 · 11.19 Impact Factor
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    ABSTRACT: Interferon-based regimens (alone or with ribavairin) are standard therapies for chronic hepatitis C. The aim of this study was to compare a 24-week regimen of interferon alpha-2b + ribavirin (IFN + RIBA) to interferon alpha-2b + amantadine (IFN + AMANT) in non-responders to previous interferon monotherapy. In a multi-center, double-blind clinical trial, 118 patients (non-responders to previous interferon monotherapy) were equally randomized into the two arms: interferon alpha-2b (3 MU thrice weekly) and ribavirin (800 mg daily) vs. interferon alpha-2b (3 MU thrice weekly) and amantadine (200 mg daily). After 24 weeks of therapy, HCV RNA became undetectable in 34.8% (95% CI: 23.7-49.2) of IFN + RIBA and 19.6% (95% CI: 10.6-34.7) of IFN + AMANT (P = 0.10). This response was sustained in 3.9% (95% CI: 1.0-14.9) of IFN + RIBA and 0% of IFN + AMANT (P = 0.16). Ten patients from IFN + AMANT (17%) and 12 patients (20%) from IFN + RIBA were discontinued before completion of therapy. Of these, 7% in IFN + AMANT and 12% in IFN + RIBA were discontinued due to adverse effects. Re-treatment of interferon non-responders with a 24-week course of IFN + AMANT was not associated with any sustained viral eradication. Although IFN + RIBA in this group was associated with a reasonable end of treatment response, relapses were common and sustained responses were low.
    Journal of Hepatology 02/2001; 34(1):128-33. DOI:10.1016/S0168-8278(00)00003-9 · 10.40 Impact Factor
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    ABSTRACT: In the 1990s, liver transplantations and transjugular intrahepatic portosystemic shunts (TIPS) have become the most common methods to decompress portal hypertension. This center has continued to use surgical shunts for variceal bleeding in good-risk patients who continue to bleed through endoscopic and pharmacologic treatment. This article reports this center's experience with surgical shunts and TIPS shunts from 1992 through 1999. Sixty-three patients (Child A, 43 patients; Child B, 20 patients) received surgical shunts: distal splenorenal, 54 patients; splenocaval, 4 patients; coronary caval, 1 patient; and mesocaval, 4 patients. Sixty-two patients had refractory variceal bleeding, and 1 patient had ascites with Budd-Chiari syndrome. Two hundred patients (Child A, 24 patients; Child B, 62 patients; Child C, 114 patients) received TIPS shunts. One hundred forty-nine patients had refractory variceal bleeding, and 51 patients had ascites, hydrothorax, or hepatorenal syndrome. Data were collected by prospective databases, protocol follow-up, and phone contact. The 30-day mortality rate was 0% for surgical shunts and 26% for TIPS shunts; the overall survival rate was 86% (median follow-up, 36 months) for surgical shunts and 53% (median follow-up, 40 months) for TIPS shunts. For surgical shunts, the portal hypertensive rebleeding rate was 6.3%; the overall rebleeding rate was 14.3%. For TIPS shunts, the overall rebleeding rate was 25.5% (30-day, 9.4%; late, 22.4%). There were 4 reinterventions for surgical shunts (6.3%); the reintervention rate for TIPS shunts in the bleeding group was 33%, and the reintervention rate in the ascites group was 9.5%. Encephalopathy was severe in 3.1% of the shunt group and mild in 17.5%; this was not systematically evaluated in the TIPS shunts patients. Surgical shunts still have a role for patients whose condition was classified as Child A and B with refractory bleeding, who achieve excellent outcomes with low morbidity and mortality rates. TIPS shunts have been used in high-risk patients with significant early and late mortality rates and have been useful in the control of refractory bleeding and as a bridge to transplantation. The comparative role of TIPS shunts versus surgical shunt in patients whose condition was classified as Child A and B is under study in a randomized controlled trial.
    Surgery 11/2000; 128(4):540-7. DOI:10.1067/msy.2000.108209 · 3.11 Impact Factor
  • Gastroenterology 04/2000; 118(4). DOI:10.1016/S0016-5085(00)81909-5 · 13.93 Impact Factor