Serum Albumin Is Inversely Associated With Portal Vein Thrombosis in Cirrhosis

We analyzed whether serum albumin is independently associated with portal vein thrombosis (PVT) in liver cirrhosis (LC) and if a biologic plausibility exists. This study was divided into three parts. In part 1 (retrospective analysis), 753 consecutive patients with LC with ultrasound-detected PVT were retrospectively analyzed. In part 2, 112 patients with LC and 56 matched controls were entered in the cross-sectional study. In part 3, 5 patients with cirrhosis were entered in the in vivo study and 4 healthy subjects (HSs) were entered in the in vitro study to explore if albumin may affect platelet activation by modulating oxidative stress. In the 753 patients with LC, the prevalence of PVT was 16.7%; logistic analysis showed that only age (odds ratio [OR], 1.024; P = 0.012) and serum albumin (OR, -0.422; P = 0.0001) significantly predicted patients with PVT. Analyzing the 112 patients with LC and controls, soluble clusters of differentiation (CD)40-ligand (P = 0.0238), soluble Nox2-derived peptide (sNox2-dp; P < 0.0001), and urinary excretion of isoprostanes (P = 0.0078) were higher in patients with LC. In LC, albumin was correlated with sCD4OL (Spearman's rank correlation coefficient [r(s)], -0.33; P < 0.001), sNox2-dp (r(s), -0.57; P < 0.0001), and urinary excretion of isoprostanes (r(s), -0.48; P < 0.0001) levels. The in vivo study showed a progressive decrease in platelet aggregation, sNox2-dp, and urinary 8-iso prostaglandin F2 alpha-III formation 2 hours and 3 days after albumin infusion. Finally, platelet aggregation, sNox2-dp, and isoprostane formation significantly decreased in platelets from HSs incubated with scalar concentrations of albumin. Conclusion: Low serum albumin in LC is associated with PVT, suggesting that albumin could be a modulator of the hemostatic system through interference with mechanisms regulating platelet activation

Comparison of Fondaparinux and Low-Molecular-Weight Heparin in the Treatment of Portal Vein Thrombosis in Cirrhosis

Background: Portal vein thrombosis is the most common thrombotic complication in cirrhosis. About 60% of anticoagulated patients can achieve recanalization. Despite fondaparinux (FPX) theoretical advantages, data are lacking about safety and efficacy for treatment of portal vein thrombosis in cirrhosis. Methods: Cirrhotic patients with portal vein thrombosis treated with FPX or low-molecular-weight heparin (LMWH) were retrospectively included. The extension of thrombosis at baseline and its evolution during anticoagulant treatment were evaluated. Patients were treated with LMWH or FPX at therapeutic dosage and reduction was considered in selected cases. Results: There were 124 patients included. Main portal vein branch, splenic, and superior mesenteric veins were involved in 84%, 13%, and 36% of cases, respectively. Forty-one patients (33%) were treated with FPX and 83 (67%) with LMWH. The probability of resolution of thrombosis at 36 months was significantly higher in patients treated with FPX than in those treated with LMWH (77% vs 51%; P = .001), particularly when prescribed at reduced dose. With multivariate analysis, the treatment with FPX (hazard ratio 2.38; P = .002) and use of a full dose (hazard ratio 1.78; P = .035) were independent predictors of portal vein full recanalization. Bleeding rate was higher in patients treated with FPX than in those treated with LMWH (27% vs 13%; P = .06). Conclusions: FPX appears to be more effective than LMWH in the treatment of portal vein thrombosis when used at reduced dose, also in complete thrombosis. FPX should be considered among possible treatments for portal vein thrombosis in cirrhosis

Central nervous system alterations in liver cirrhosis: The role of portal-systemic shunt and portal hypoperfusion

The role of portal-systemic shunting and portal liver hypoperfusion in the pathophysiology of central nervous system dysfunction of cirrhosis is not yet well defined. It is well known that one of the most important collateral vessels (CV) is a patent paraumbilical vein (PUV) but there is controversy regarding its clinical significance. We have evaluated the relationships between neuropsychological and EEG alterations, ammonia plasma level (NH4), hepatic function, and portal hemodynamics (Doppler Ultrasound) in 95 cirrhotic patients. Patency, diameter, or flow of PUV or the presence of other CV were not related to an increased prevalence of neuropsychological or EEG abnormalities. Patients with effective portal flow (EPF = portal flow - PUV flow) lower than 692 mL/min (median) had a significantly higher risk of failing the neuropsychological test, or of having an altered EEG. Low EPF and prothrombin time ( or = 51 micromol/L) were independent predictors of an abnormal EEG. Considering both low EPF and the numerosity of CV, only low EPF was found to explain EEG alterations. In conclusion, portal liver hypoperfusion and decreased liver function were associated with an increased risk of central nervous system dysfunction in cirrhotic patients, whereas PUV patency per se was not

Early Diagnosis of Type-2 Cardio-renal Syndrome by Doppler Sonographic Evaluation of Renal Vasoconstriction

Renal failure of type-2 cardio-renal syndrome is due to renal hypoperfusion secondary to heart failure and is mediated by an imbalance between vasoconstrictors and vasodilators. The decrease in glomerular filtration rate does not correlate with left ventricular ejection fraction. Aim of this study was to evaluate, by Doppler sonography, renal hemodynamic alterations in heart failure. Thirty patients (age: 51\ub115yr) with dilated cardiomyopathy (DCM) and 20 normal subjects (C) were studied. Cardiomyopathy was essential in 36.6%, post-ischemic in 36.6%, alcoholic in 16.7%, post-myocarditis in 10% of patients. All patients were hemodynamically stable. In each patient, echocardiography and renal Doppler sonography (interlobar arterial pulsatility index, PI-K) were performed the same day, together with BUN, creatinine, NT-proBNP measurement. Patients with DCM had normal kidneys morphology and volume. LVEF was 26\ub16.8%. PI-K was increased compared to C (1.74\ub10.71 vs 0.95\ub10.19, p<0.001) and also renal function was impaired (creatinine 128.5\ub184 vs 70\ub130 umol/L, p<0.01, BUN 11.6\ub15.8 vs 7\ub11.5 mmol/L, p<0.01). Prevalence of renal failure was 36.6% (NYHA 1-2: 23%, NYHA 3-4: 52.9%) while prevalence of increased PI-K was 83.3% (NYHA 1-2: 69.2%, NYHA 3-4: 94.1%). PI-K was increased already in mild heart failure (NYHA 1-2) (PI-K: 1.37\ub10.3 p<0,01), but more so in patients with more severe heart dysfunction (NYHA 3 e 4) (PI-K: 2,1\ub10,8 p<0.01) without significant correlation with LVEF or right atrial pressure. There were no differences in creatinine or BUN among patients with different severity of heart dysfunction (creatinine 105\ub123 vs 140\ub1104 umol/L, urea 10.3\ub15.7 vs 12.3\ub16 mmol/L). NT-proBNP was increased in patients with DCM (6249.61\ub13.963 ng/L) and did not correlate with LVEF, PI-K, renal function, right atrial pressure. In conclusion, in patients with chronic heart failure renal vasoconstriction can be demonstrated by Doppler-sonography in the early stage, when renal function is still normal, and increases with the worsening of heart failure. Renal Doppler resistance indices may be used for early diagnosis of type-2 cardiorenal syndrome and for prevention of acute, diuretic-induced, renal failure. Author Disclosures: D. Sacerdoti: None. S. Gaiani: None. S. Tonello: None. E. Franceschini: None. P. Pesce: None. P. Bizzotto: None. G. Bombonato: None. C. Sarais: None. M. Bolognesi: None. Key Words: Heart failure \u2022 Renal circulation \u2022 Renal function \u2022 Doppler ultrasoun

Early Diagnosis of Type-2 Cardio-renal Syndrome by Doppler Sonographic Evaluation of Renal Vasoconstriction

Renal failure of type-2 cardio-renal syndrome is due to renal hypoperfusion secondary to heart failure and is mediated by an imbalance between vasoconstrictors and vasodilators. The decrease in glomerular filtration rate does not correlate with left ventricular ejection fraction. Aim of this study was to evaluate, by Doppler sonography, renal hemodynamic alterations in heart failure. Thirty patients (age: 51\ub115yr) with dilated cardiomyopathy (DCM) and 20 normal subjects (C) were studied. Cardiomyopathy was essential in 36.6%, post-ischemic in 36.6%, alcoholic in 16.7%, post-myocarditis in 10% of patients. All patients were hemodynamically stable. In each patient, echocardiography and renal Doppler sonography (interlobar arterial pulsatility index, PI-K) were performed the same day, together with BUN, creatinine, NT-proBNP measurement. Patients with DCM had normal kidneys morphology and volume. LVEF was 26\ub16.8%. PI-K was increased compared to C (1.74\ub10.71 vs 0.95\ub10.19, p<0.001) and also renal function was impaired (creatinine 128.5\ub184 vs 70\ub130 umol/L, p<0.01, BUN 11.6\ub15.8 vs 7\ub11.5 mmol/L, p<0.01). Prevalence of renal failure was 36.6% (NYHA 1-2: 23%, NYHA 3-4: 52.9%) while prevalence of increased PI-K was 83.3% (NYHA 1-2: 69.2%, NYHA 3-4: 94.1%). PI-K was increased already in mild heart failure (NYHA 1-2) (PI-K: 1.37\ub10.3 p<0,01), but more so in patients with more severe heart dysfunction (NYHA 3 e 4) (PI-K: 2,1\ub10,8 p<0.01) without significant correlation with LVEF or right atrial pressure. There were no differences in creatinine or BUN among patients with different severity of heart dysfunction (creatinine 105\ub123 vs 140\ub1104 umol/L, urea 10.3\ub15.7 vs 12.3\ub16 mmol/L). NT-proBNP was increased in patients with DCM (6249.61\ub13.963 ng/L) and did not correlate with LVEF, PI-K, renal function, right atrial pressure. In conclusion, in patients with chronic heart failure renal vasoconstriction can be demonstrated by Doppler-sonography in the early stage, when renal function is still normal, and increases with the worsening of heart failure. Renal Doppler resistance indices may be used for early diagnosis of type-2 cardiorenal syndrome and for prevention of acute, diuretic-induced, renal failure. Author Disclosures: D. Sacerdoti: None. S. Gaiani: None. S. Tonello: None. E. Franceschini: None. P. Pesce: None. P. Bizzotto: None. G. Bombonato: None. C. Sarais: None. M. Bolognesi: None. Key Words: Heart failure \u2022 Renal circulation \u2022 Renal function \u2022 Doppler ultrasoun

Quality of life and depression in a cohort of female patient with chronic disease

Background Differences in health-related quality of life perception in patients with chronic disease may depend on pre-existing differences in personality profile. The purpose of the study was to investigate in a cohort of female patient with chronic diseases the relationship between the Quality of Life perception and the potential presence of depressive symptoms. Patients and methods: Female patients with chronic diseases were enrolled in the study. Exclusion criteria were diagnosis of psychopathological condition, treatment with psychoactive substances. Results Methodological approach was based on administration of the following test. Short Form health survey SF-36, Symptom Check List SCL-90-R, Satisfaction Profile test (SAT-P) and Beck Depression Inventory-II (BDI-II). The Pearson correlation coefficient was used to evaluate the relationship between depressive symptoms and Quality of life as assessed by psychometric test. Discussions: 57 patients, age 52(?3,4), responded to inclusion criteria. 57% of patients had a diagnosis of functional dyspepsia or gastro-oesophageal reflux not complicated, and the remaining 43% musculoskeletal diseases. The statistical analysis showed an inverse correlation between the variable Bodily Pain of the SF-36 and the variable Depression scales of the SCL-90-R

Erratum to: Portal vein thrombosis relevance on liver cirrhosis: Italian Venous Thrombotic Events Registry (Intern Emerg Med, 10.1007/s11739-016-1416-8)

In the original publication, the second author name was incorrectly published as Roberto Gino Corazza. The correct name should read as \u201cGino Roberto Corazza\u201d. Also, the PRO-LIVER Study Collaborator, Dr. Gabriella Carnevale Maff\ue8 has not been included in the Appendix by mistake. The name of Dr. Carnevale Maffe` should read in the Appendix as follows: Bergamaschi Gaetano, Carnevale Maff\ue8 Gabriella, Masotti Michela, Costanzo Filippo (I\ub0 Clinica Medica, Fondazione IRCCS Policlinico San Matteo, University of Pavia, Italy)