02B. CIRRHOSIS AND COMPLICATIONS was positive in 37 episodes (47.4%), being E. coli the microorganism more frequent isolated (67.5% of cases). Although infection resolution rate was achieved in 89.7% of cases, SBP-induced renal failure appeared in 23 episodes (29.4%), and 27 patients (34.6%) died during the tirst SBP episode. The 1-year actuarial probability of survival was 43.4%, being the development of SBP-induced renal failure the only independent predictor of mortality. Conclusions: Approximately 25% of cirrhotic patients developed SBP within the first 3 years after the first ascites decompensation, mainly if they have an ascitic fluid protein concentration below 10 g/L. Although the SBP resolution is achieved in almost 90% ofcases, SBP-induced renal failure appeared in a third of the patients and it was associated with a short survival-rate.
12201 CIRRHOTIC INTRAVENOUS ALBUMIN IS NOT NECESSARY IN PATIENTS WITH SPONTANEOUS BACTERIAL PERITONITIS AND LOW-RISK OF MORTALITY M. Casas’ , G. Soriano’, E. Ayala’, C. Guarner-Argente’ , 1. Ordas’ , J. Merce’, J. Balanzo’ , C. Guarner’ . ’Liuer Unit, Department of Gastroenterology; ’Department of Biochenzistv, Hospital de la Santa Creu i Sant Pau, Barcelona, SIiain E-mail:
[email protected] Intravenous albumin decreases the incidence of renal impairment and mortality in selected cirrhotic patients with spontaneous bacterial peritonitis (SBP) (age 4 0 years without shock, gastrointestinal bleeding, previous antibiotic treatment, ileus, grade 3 or 4 hepatic encephalopathy, organic nephropathy, serum creatinine level >265 mmolil, cardiac failure, or HTV) (Sort, NEJM 1999). However, it has been suggested that intravenous albumin would not improve the outcome in patients with SBP and low-risk of mortality (bilirubin <70mmol/l and urea
70mmol/l or urea > 12 mmolil), 32 (44.4%) died during hospitalization, whereas among the 53 patients (42.4%) with low-risk, only 5 (9.4%) died (p i O . O O 1 ) . No differences were observed in mortality between patients with low-risk who received albumin and who did not (218, 25% vs 3145, 6.6%, p NS), despite clinical or analytical data were similar between both groups, except for longer TNR in albumin group. Applying the inclusion criteria of Sort study (NEJM 1999) to the low-risk group of our series, only 27 patients (51%) would be included ( 5 treated and 22 non treated with albumin) and mortality was also similar in patients treated or not with albumin (3.7% vs 0%). Conclusions: 1) Cirrhotic patients with SBP and low-risk of mortality (bilirubin 1 7 0 mmolil and urea 12 mmolil) represent near half of patients with SBP in a non-selected series. 2) Inclusion criteria of Sort study excludes half ofthe patients with SBP and low-risk ofmortality. 3) Patients with SBP and low-risk ofmortality in a selected or non-selected series have a good clinical short-term outcome that does not improve with intravenous albumin administration.
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B) CLINICAL ASPECTS
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12211 HYDROCORTISONE HEMISUCCINATE IN CIRRHOTIC PATIENTS WITH SEPTIC SHOCK MAKE THE DIFFERENCE?
- DOES IT ALWAYS
0 . Chelarescu’, D. Chelarescu*, E Crumpei3, 1. Stratan’. ’Departnzent and htensioe Care; 2Department of‘ Pharnzacology, Uniuer~xit?,o f Medicine and Pharmacy; ‘Department of‘lmagixticx, h i , Ronzania E-mail: [email protected]
of‘ Anesthesiology
Background: Previous studies have shown a beneticial effect of corticoids in low dose in cirrhotic patients with septic shock but not in all cases. Could it be a cirrhosis-related factor that might influence the response to corticoids? Method: We have studied 35 cirrhotic patients with severe sepsis. Patients were randomly assigned to 2 groups: one (17 patients) received norepinephrine (NE); the second (18 patients) received NE and hydrocortisone hemisuccinate (HHC) 50 mg/6h. We determined the liver vascular index (LVI), calculated by Doppler ultrasound as the ratio of portal venous velocity to hepatic arterial pulsatility index. Low LVT is a marker of severe portal hypertension. According to initial LVT, both groups were divided into low and high LVT (cut off value 9cmis). We assessed initially plasmatic NE and initial, at 4 h, 12 h, 3 d and 7 d renal and liver function, systemic hemodynamic [stroke volume (SV), cardiac index (CT), systemic vascular resistance (SVR), cardiac output (CO)]. mortality. Results: HHC improved the hemodynamic parameters (SVR, CO) and urinary output only in cirrhotic patients with lower LVI. In patients with higher LVI, hemodynamics did not improve significantly vs NE alone group. In NE+HHC-low LVI group, the increase in SVR was 350*35 dynes s (significantly higher than in NE alone-low LVI 0.01). In NE+HHC-high LVI group, the increase in SVR was group, p i 3 2 5 f 1 5 d y n e s ~ c m -(NS ~ vs NE-high LVI group). In NE-low LVI group, the SVR increased at 24 hours from initial values with 8 5 f 1 5 dynes ~ c m - ~ vs 280+25 in NE-high LVT group (p i0.01). The vasopressor pattern remains unchanged at 5 days. Patients with lower LVT (19cmis) had an initial higher plasmatic NE level (p 0.05) vs patients with LVT > 9 cmis. This explains the relative lack of pressor response in NE-low LVI group and also the beneticial effect of HHC (by restoring adrenoreceptors sensitivity). In NE group, hemodynamic response was seen in 7 patients (41%) with LVI 1 3 f 2 .1 cmis (in non-responders LVI 5 . 5 f 3 c d s ) vs. 16 patients (88%) in NE+HHC group. Conclusion: Corticoids proved to be beneficial in cirrhotic patients with septic shock and lower LVI. Addition of HHC to NE in patients with high LVT does not improve signiticantly hemodynamic parameters. Norepinephrine alone may be sufficient in patients with high LVI, with preserved response to exogenous catecholamine.
12221 RISK OF LIVER CIRRHOSIS ASSOCIATED WITH GENOTYPE AND MUTANTS OF HEPATITIS B VIRUS Y.L. Chen’, P.J. Chen’, H.T. Yang’.’, U.H. Tloeje3, J. Su3, CL. Ten’,’, S.H. Yeh’, S.N. Lu4, S.L. You’,’, C.J. Chen’,’. ‘National Taiwan Uniuer~xi&Taipei; Genomics Research Center: Academia Sinica, Taipei, Taiwan; Bristol-Myers Squihb Pharnzaceutical Research Institute, Wallingfbrd,CT, 7JSA; Kaohsiung Chang-Gung Memorial Hospital, Kaohsiung, Taiwan E-mail: [email protected]
’
Background and Aims: The roles of genotype, precore stop codon mutation (G1896A) and mutations (A1762TiG1764A) in the basal core promoter (BCP) of hepatitis B virus (HBV) in the progression of liver cirrhosis remain unclear. The aim of this study was to investigate the risk of cirrhosis associated with HBV genotype and mutants. Methods: A cohort of 3,644 untreated participants (aged 30-65 years), who were HBsAg-seropositive and anti-HCV-seronegative, was enrolled