Analyses of prognostic indices of chronic liver failure caused by hepatitis virus
ABSTRACT To analyze the related indices about the prognoses of chronic liver failure caused by hepatitis virus.
Retrospectively reviewed 320 cases of chronic liver failure caused by hepatitis viruses. An improved group and an ineffective group (IG) were made to compare and analyze their clinical manifestations, laboratory examination indices and complications. Logistic regression was also carried out.
There were significant differences (P<0.05) between the improved group and the IG upon such indices as age, bilirubin, prothrombin time, albumin, alpha fetoprotein, the size of liver and complications (P<0.05). The regression formula was as follows: P = 1/(1+e(-y)) (y = 1.7262-0.0948X(1)+2.9846X(2)+0.6992X(3)+1.6019X(4)+ 2.0398X(5)). (Note: X(1)-Prothrombin activity; X(2)-digestive tract hemorrhage; X(3)-hepatic encephalopathy; X(4)-hepatorenal syndrome; X(5)-pulmonary infection.).
Laboratory examination such as bilirubin, prothrombin time and alpha fetoprotein can be regarded as indices of the prognoses of chronic liver failure caused by hepatitis. Moreover, the regression equation can evaluate prognoses more comprehensively and direct our treatments.
Full-textDOI: · Available from: Zhongjie Shi, Sep 29, 2015
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- "In order to improve the study efficiency and control for confounding factors, the case and control subjects were matched by sex, age, and MELD score (frequency matching). In China, as a result of the high prevalence of hepatitis B virus (HBV), chronic HBV infection is the most common cause of liver failure (17, 18). Inclusion criteria included: 1) Hepatitis B virus-related acute-on-chronic liver failure 2) Patients who had their first episode of Grade II-IV HE in the hospital for at least six days were included in the study. "
ABSTRACT: Hepatic encephalopathy (HE) is an important neuropsychiatry complication of acute-on-chronic liver failure (ACLF). PPI therapy may increase the intestinal bacterial overgrowth and infections. The aim of this study was to assess whether PPI use in ACLF is associated with HE. A retrospective case-control study was performed. Fifty five admitted patients with hepatitis B virus (HBV)-related ACLF complicated by Stage II-IV HE developed after admission between January 2008 and December 2012 were matched (by sex, age, and MELD score) with comparable HBV-related ACLF patients (n = 110) who did not develop this complication during hospitalization. We excluded combined HE upon admission and other neurological disorders in patients with ACLF. Univariate and multivariate analyses of 30 variables (laboratory examination, predisposition, treatment, etc.) before the occurrence of HE were carried out to identify the factors predictive of HE. In univariate analysis, patients with HE in ACLF had a significantly higher rate of PPI use (89.1%) compared with non-HE (63.6%, P = 0.001). In addition, clinical and standard laboratory variables were significantly different between the two groups regarding the infection rate, hyponatremia, alpha-fetoprotein (AFP), Arginine Hydrochloride use and Lactulose use. Logistic regression analysis was used to examine the combined effects of the variables with HE as the outcome. HE in ACLF was associated with hyponatremia (odds ratio (OR) = 6. 318, 95% confidence interval (CI) = 2. 803-14.241; P = 0. 000), PPI use was independently associated with HE (OR = 4. 392, CI = 1. 604-12.031; P = 0. 004), and lactulose use was protective (OR = 0. 294, CI = 0. 136-0.675; P = 0. 003). The occurrence of HE is associated with hyponatremia and PPI use in patients with ACLF.Hepatitis Monthly 04/2014; 14(4):e16258. DOI:10.5812/hepatmon.16258 · 1.93 Impact Factor
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ABSTRACT: Unlike most other countries, in China, liver failure is termed as severe hepatitis. However, there are two differences between liver failure and severe hepatitis: the interval of acute and sub-acute severe hepatitis and the etiology. The aims of this study were to assess the best cutoff time-point to distinguish between acute and sub-acute severe hepatitis caused mainly by hepatitis B virus (HBV; 67.5%) in China and to determine whether the Chinese classifications of severe hepatitis can meet the international criteria based on pathological features and clinical characteristics. A total of 157 patients with acute, sub-acute and chronic severe hepatitis were involved in the study. Their clinical findings, laboratory data and liver biopsies were retrospectively analyzed. The different incidences of complications between acute and sub-acute severe hepatitis were significant if the cutoff point was set at 15 days or 4 weeks (P < 0.01), but there is no significant differences if the cutoff was 8 weeks. Identifying the better cutoff point with a receiver-operator characteristic curve showed that 28 days was better than 15 days (sensitivity 100%vs 92%; specificity 75%vs 53%). The major differences in histopathology between acute and sub-acute severe hepatitis were: (i) there was a single hepatic necrosis in acute severe hepatitis, but repeated and continuous hepatic necrosis in sub-acute severe hepatitis; and (ii) survivors of acute severe hepatitis had full hepatocyte regeneration in the native liver architecture. Regeneration in survivors with sub-acute severe hepatitis indicated the destruction of nodular architecture; new and old necrosis appeared at the same time. When the cutoff point for acute and sub-acute severe hepatitis was set at 15 days, some sub-acute severe hepatitis cases (full hepatocyte regeneration and one massive necrosis) had an overlap in pathological features with acute severe hepatitis. If the cutoff time-point was set at 4 weeks, the clinical features between acute and sub-acute, as well as the pathological changes, were clearly distinguished. The best cutoff time-point to distinguish between acute and sub-acute severe hepatitis is 4 weeks. This classification meets the international criteria based on the present clinical and pathological results.Journal of Gastroenterology and Hepatology 12/2007; 22(12):2101-6. DOI:10.1111/j.1440-1746.2006.04362.x · 3.50 Impact Factor
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ABSTRACT: To evaluate portalsystemic hemodynamic changes in chronic severe hepatitis B. Hemodynamic parameters included portal vein diameter (PVD), portal vein peak velocity (PVPV), portal vein volume (PVV), spleen length (SPL), spleen vein diameter (SPVD), spleen vein volume (SPVV) and umbilical vein recanalization. They were measured by Color Doppler ultrasonography in 36 patients with chronic severe hepatitis B, compared with 51 normal controls, 61 patients with chronic hepatitis B, 46 patients with compensable cirrhosis, and 36 patients with decompensable cirrhosis. In the group of chronic severe hepatitis B, PVD (12.38 +/- 1.23 mm) was significantly different from the normal control, compensable cirrhosis and decompensable cirrhosis groups (P = 0.000-0.026), but not significantly different from the chronic hepatitis group. PVPV (16.15 +/- 3.82 cm/s) dropped more significantly in the chronic severe hepatitis B group than the normal control, chronic hepatitis B and compensable cirrhosis groups (P = 0.000-0.011). PVV (667.53 +/- 192.83 mL/min) dropped significantly as compared with the four comparison groups (P = 0.000-0.004). SPL (120.42 +/- 18.36 mm) and SPVD (7.52 +/- 1.52 mm) were longer in the normal control and chronic hepatitis B groups (P = 0.000-0.009), yet they were significantly shorter than those in the decompensable cirrhosis group (P = 0.000). SPVV (242.51 +/- 137.70 mL/min) was also lower than the decompensable cirrhosis group (P = 0.000). The umbilical vein recanalization rate (75%) was higher than the chronic hepatitis B and compensable cirrhosis groups. In the course of progression from chronic hepatitis to decompensable cirrhosis, PVD, SPL and SPVD gradually increased and showed significant differences between every two groups (P = 0.000-0.002). Patients with chronic severe hepatitis B have a tendency to develop acute portal hypertension, resulting in significantly reduced portal vein perfusion. Observation of the portalsystemic hemodynamic changes may be contributed to the disease progression of chronic liver disease.World Journal of Gastroenterology 03/2008; 14(5):795-9. DOI:10.3748/wjg.14.795 · 2.37 Impact Factor