S94 Poster Session − Thursday, April 23 232 GAS EXCHANGE AND PULMONARY MICROCIRCULATION ABNORMALITIES IN CIRRHOTIC AND NON-CIRRHOTIC CHRONIC LIVER DISEASE PATIENTS FREE FROM HEPATOPULMONARY SYNDROME U. Vespasiani-Gentilucci 1 , S. Scarlata 2 , M.-E. Conte 2 , G. Galati 1 , D. D’Avola 1 , S. Spataro 1 , E. Fiori 1 , C. Mazzarelli 1 , C. Pedone 2 , R. Antonelli-Incalzi 2 , A. Picardi 1 . 1 Clinical Medicine and Hepatology, 2 Geriatry and Pneumology, University Campus Bio-Medico, Rome, Italy E-mail: u.vespasiani@unicampus.it Background and Aims: Pulmonary haemodynamic changes leading to hepatopulmonary syndrome (HPS) may complicate the advanced stages of liver cirrhosis. We aimed to determine the extent of pulmonary dysfunction in non-cirrhotic chronic liver disease (CLD) patients and cirrhotic patients free from HPS. Methods: 67 subjects were studied, divided in 3 groups: 23 patients with non-cirrhotic CLD (NC), mainly HCV-related, 24 patients with cirrhosis (CIR) from different etiologies, and 20 controls (CON). Patients with an altered alveolar-arterial oxygen gradient, suggesting HPS, were excluded. All subjects underwent: arterial-blood-gas-analysis (ABGA); spirometry and lung volume assessment; carbon monoxide diffusion capacity (DlCO) determination, at baseline and after a 6-minute-walk-test (6MWT); mem- brane diffusion capacity for CO (DmCO) and pulmonary capillary volume (cV) evaluation. Results: CIR showed a tendency towards hyperventilation and respiratory alkalosis, with reduced PaCO 2 levels with respect to CON [34 (32−35) Vs 38 (36−40), p < 0.01], but not to NC [36 (33−39), p = 0.1], and reduced bicarbonate levels compared to both NC and CON [CIR 24 (23−25) Vs 26 (24−27) in NC, p < 0.05, and 27 (26−28) in CON, p < 0.01], while the differences between NC and CON were not significant. Forced expiratory volumes, forced vital capacity, total pulmonary capacity and residual volume were not significantly different between the 3 groups. DlCO - expressed as % of predicted- and cV were significantly reduced in CIR with respect to both CON and NC, and DlCO also in NC compared to CON. DmCO was not significantly different between the 3 groups, although tended to be decreased in CLD. Post-6MWT variations in DlCO were homogeneous in the 3 groups. Conclusions: Some alterations of pulmonary microcirculation, and the relative compensation mechanisms, can be observed in cirrhotic patients free from HPS and even in non-cirrhotic CLD, while post-exercise alveolar recruiting capacity and microcirculation activation seem to be preserved. DlCO [ml/(min·mmHg)] DmCO [ml(CO)/(min·mmHg] cV (l/min) Post-exercise DlCO/ baseline DlCO CON 24 (21−28) 43 (33−53) 99 (62–135) 1.10 (1.01−1.19) NC 18 (15−20) † 28 (23−33) 98 (60–135) 1.08 (1.02−1.15) CIR 14 (12−16) †,‡ 31 (17−45) 52 (40−63)* ,‡ 1.09 (1.03−1.16) *p < 0.05 vs CON; † p < 0.01 vs CON; ‡ p < 0.05 vs NC. 233 QUANTITATIVE HISTOLOGICAL ASSESSMENT IN CIRRHOSIS: SEPTAL THICKNESS PREDICTS CLINICAL DECOMPENSATION A. Viola 1,2,3 , D. Jain 1,4 , G. Garcia-Tsao 1,2 . 1 Internal Medicine, Section of Digestive Diseases, Yale University, New Haven, 2 Internal Medicine, Section of Digestive Diseases, VA CT Healthcare System, West Haven, CT, USA; 3 Department of Clinical Medicine, S.Orsola-Malpighi Hospital, University of Bologna, Bologna, Italy; 4 Pathology, Yale University, New Haven, CT, USA E-mail: antonellaviola@yahoo.com Background and Aims: We have shown that thick septa and small nodules on liver biopsy correlate with clinically significant portal hypertension (J Hepatol 2006;44:111). More recently, using the same semiquantitative scale, we showed that thick septa predict clinical decompensation of cirrhosis (Hepatology 2007; 46:579A). Aim of this study was to confirm the latter findings using quantitative analysis by digital imaging. Methods: In a retrospective study, patients with cirrhosis in whom biopsy was performed between 1994 an 2002 were reviewed. The primary end-point was clinical decompensation, defined by the development of variceal hemorrhage, ascites, jaundice or hepatic encephalopathy. Patients who were transplanted or developed hepatocellular carcinoma without decompensation were censored at that time. Trichrome-stained slides were analyzed using digital image analysis (Bioquant). The following parameters were measured without knowledge of clinical outcome: septal width (SW) of all fibrous septa per slide and fibrosis area (FA) expressed as a percentage of the total biopsy area. Results: Of 473 patients with biopsy-proven cirrhosis 115 met inclusion criteria (compensated cirrhosis not secondary to cholestatic disorder, available chart and clearly stained liver biopsies >1 cm in length). Median age was 49 years and 76% were male; predominant etiology was hepatitis C virus infection (61 patients). In a median follow up of 49 months, 25 patients (22%) developed clinical decompensation. Median SW was greater in patients who developed decompensation (212.56 m) compared to patients who remained compensated (156.59 m) (p < 0.001). Patients with thick septa (>169.01 m) had a significantly higher probability of decompensating (figure). FA was not different between those who did (19.4%) and did not (16.8%) develop decompensation (p = 0.46). Conclusions: Using an objective, quantitative method, we confirm that in cirrhosis there is a realationship between thick septa on biopsy and development of clinical decompensation. 234 THE ROLE OF SMALL INTESTINAL BACTERIAL OVERGROWTH (SIBO) IN HEPATIC ENCEPHALOPATHY I.S. Weisberg 1,2 , A.B. Jesudian 3 , K.C. Barboza 2 , T. Liu 4 , B.P. Bosworth 1 , S.H. Sigal 1,2 . 1 Division of Gastroenterology and Hepatology, New York Presbyterian Hospital − Weill Cornell Medical Center, 2 Center for Liver Disease and Transplantation, New York Presbyterian Hospital, 3 Department of Medicine, New York Presbyterian Hospital − Weill Cornell Medical Center, New York, 4 Gastroenterology and Hepatology, New England Baptist Hospital, Boston, MA, USA E-mail: iw2104@columbia.edu Background: Hepatic encephalopathy (HE) is a frequent complication of cirrhosis characterized by reversible neurocognitive impairment. Bacteri- ally derived toxins such as ammonia are produced in the gastrointestinal tract and are believed to play a central pathogenic role. Autonomic dysfunction is also common in cirrhosis and could contribute to the development of HE by impairing intestinal motility resulting in colonic inertia and small intestinal bacterial overgrowth (SIBO). Lactulose remains the mainstay of HE treatment, however nonabsorbable antibiotics, which decrease the bacterial burden, are also employed. This study aims to