139 IMPACT OF RELATIVE ADRENAL INSUFFICIENCY ON CIRCULATORY FUNCTION AND MORTALITY IN ADVANCED CIRRHOSIS

139 IMPACT OF RELATIVE ADRENAL INSUFFICIENCY ON CIRCULATORY FUNCTION AND MORTALITY IN ADVANCED CIRRHOSIS

POSTERS Poster Session – Thursday, March 31 02b: CIRRHOSIS AND ITS COMPLICATIONS: CLINICAL ASPECTS 138 THE EFFECT OF SYSTEMIC INFLAMMATORY RESPONSE...

143KB Sizes 0 Downloads 42 Views

POSTERS

Poster Session – Thursday, March 31

02b: CIRRHOSIS AND ITS COMPLICATIONS: CLINICAL ASPECTS

138 THE EFFECT OF SYSTEMIC INFLAMMATORY RESPONSE SYNDROME ON THE COURSE OF LIVER CIRRHOSIS E. Abdel-Khalek1 , A. El-Fakhry1 , M. Helaly1 , M. Hamed1 , O. Elbaz2 . 1 Internal Medicine Department, 2 Clinical Pathology Department, Faculty of Medicine, Mansoura University, Mansoura, Egypt E-mail: [email protected] Background and Aims: Patients with liver cirrhosis present an increased susceptibility to the systemic inflammatory response syndrome (SIRS), which is considered the cause of hospital admission in about 10% of patients and is present in about 40% of those admitted for ongoing complications. We tried to assess the prevalence of SIRS with the possible effects on the course of the disease during the hospital stay. Methods: 203 patients with liver cirrhosis were examined and investigated with close monitoring during hospital stay. The main clinical endpoints were death and the development of portal hypertension-related bleeding Results: 81 patients met the criteria of SIRS (39.9%). We found significant correlations between SIRS and jaundice (P = 0.005), bacterial infection (P = 0.008), high white blood cell count (P < 0.001), low hemoglobin concentration (P = 0.004), high serum creatinine levels (P < 0.001), high alanine aminotransferase levels (P < 0.001), high serum bilirubin levels (P < 0.001), high international normalized ratio (P < 0.001), low serum albumin levels (P = 0.033), high Child–Pugh score (P < 0.001). During the follow-up period, 26 patients died (12.8%), 15 developed portal hypertensionrelated bleeding (7.3%), 30 developed hepatic encephalopathy (14.7%), and 9 developed hepatorenal syndrome type-1 (4.4%). SIRS showed significant correlations both to death (P < 0.001) and to portal hypertension-related bleeding (P < 0.001). Conclusions: The systemic inflammatory response syndrome occurs more frequently in patients with advanced cirrhosis and is associated with a bad prognosis. 139 IMPACT OF RELATIVE ADRENAL INSUFFICIENCY ON CIRCULATORY FUNCTION AND MORTALITY IN ADVANCED CIRRHOSIS 1,2,3,4 J. Acevedo1,2,3,4 , J. Fernandez ´ , M. Castro1,2,4 , D. Roca1,2,4 , P. Gines ´ 1,2,3,4 , V. Arroyo1,2,3,4 . 1 Liver Unit, Hospital Cl´ınic de Barcelona, 2 University of Barcelona, 3 IDIBAPS, 4 CIBER de Enfermedades Hep´ aticas y Digestivas (CIBERehd), Barcelona, Spain E-mail: [email protected] Relative adrenal insufficiency (RAI) is frequent in cirrhotic patients with severe sepsis or septic shock and is associated with poor prognosis. However, its clinical impact on other decompensations of cirrhosis is poorly known.

Objectives: To evaluate the prevalence and prognostic value of RAI in advanced cirrhosis. Methods: Prospective study that evaluated the presence of RAI, defined as delta cortisol <9 mg/dl after corticotropin stimulation test (250 mg IV at 8–9:00 AM within 24 hours after decompensation) in a consecutive series of patients with decompensated cirrhosis hospitalized in our Liver Unit between February 2007 and July 2010. Development of clinical events during hospitalization was recorded. Patients with severe sepsis or septic shock were excluded. Results: A total of 166 patients were included. RAI was observed in 43 patients (26%). Its prevalence was similar between different decompensations. At inclusion, patients with RAI presented a higher degree of circulatory dysfunction [mean arterial pressure: 77±11 vs. 82±13 mmHg, p = 0.04; plasma renin activity: 6.7±9.3 vs. 4.0±7.4 ng/mL*h, p = 0.09, serum noradrenaline: 548±385 vs. 448±369 pg/mL, p = 0.13]; a higher prevalence of systemic inflammatory response syndrome (SIRS): 51% vs. 27%, p = 0.01 and hyponatremia (serum sodium <130 mEq/L: 44% vs. 21%, p = 0.01) and lower levels of total (86±30 vs. 100±36 mg/dL, p = 0.04) and LDL cholesterol (52±22 vs. 62±28 mg/dL, p = 0.04). During hospitalization patients with RAI presented a higher probability of developing severe infections (23% vs. 9%, p = 0.01) and septic shock (17% vs. 2%, p = 0.01). Hospital mortality was significantly higher in patients with RAI (19% vs. 7%, p = 0.04). Conclusions: Prevalence of RAI is relatively high in decompensated cirrhosis and is associated with the presence of circulatory dysfunction and SIRS. RAI increases the probability of developing severe infections, septic shock and hospital mortality. 140 RELATIONSHIP BETWEEN CIRCULATORY DYSFUNCTION AND SEVERITY OF CARDIOMYOPATHY IN PATIENTS WITH CIRRHOSIS L. Achecar, ´ A. Gonzalez-Tall ´ on, ´ F. Mesonero, R. Serradilla, ´ J.M. Milicua, L. Ruiz-del-Arbol. Gastroenterology, Hospital Ram´ on y Cajal, Universidad de Alcal´ a de Henares, Madrid, Spain E-mail: [email protected] Left ventricle diastolic dysfunction (LVDD) is the most prominent characteristic of cirrhotic cardiomyopathy but its clinical relevance had not been defined. Aim of study: To assess whether LVDD is actively involved in the clinical outcome of patients with cirrhosis. Methods: 80 cirrhotic patients with portal hypertension (67 men; age <60 years), Child–Pugh A 12, B 30 and C 38, model for end-stage liver disease (MELD) score 16, without cardiac, renal, and pulmonary diseases, diabetes, and hypertension were prospectively evaluated between 2007–2009. Echocardiography 2D and tissue Doppler imaging were performed to assess diastolic and systolic function by: the ratio of transmitral flow velocity to early diastolic annular velocity (E/E’) and E’, E/A ratio, isovolumetric relaxation time, deceleration time of E wave, left ventricular ejection fraction (EF). Systemic and hepatic hemodynamics, and plasma neurohumoral systems were also measured. Patients were followed up for 12 months.

Journal of Hepatology 2011 vol. 54 | S61–S208 © 2011 All rights reserved.