Deanna L. Oliver

Serum aminotransferase levels and platelet counts as predictors of degree of fibrosis in chronic hepatitis C virus infection.

OBJECTIVE:In patients with chronic hepatitis C virus (HCV) infection, liver fibrosis stage is a prognostic factor for therapy outcome. So far, a liver biopsy is necessary to determine disease stage accurately. We sought to develop a simple, noninvasive method of accurately predicting the degree of liver fibrosis in chronic HCV infection.METHODS:We retrospectively studied 211 consecutive patients with chronic HCV, who received a liver biopsy at the Liver Center of the University of California, San Diego. A total of 58 of these patients had a positive history of alcohol abuse, and we analyzed them separately in a sensitivity analysis. AST/ALT ratio and platelet counts were determined in all patients. Fibrosis was staged using the METAVIR score.RESULTS:Both AST/ALT ratio and platelet counts correlated significantly with the disease stage (r = 0.190, p = 0.006, and r = − 0.543, p < 0.00, respectively). In a sensitivity analysis, there was no correlation between AST/ALT ratio and disease stage for patients with a history of alcohol abuse. For patients without history of alcohol abuse, the correlation between disease stage, AST/ALT ratio, and platelet counts was r = 0.297, p < 0.00, and r = 0.560, p < 0.00, respectively. In these patients, AST/ALT ratio ≥1 in combination with a platelet count of <150,000/mm3 can identify patients with severe fibrosis or cirrhosis (stages 3 and 4) with a positive predictive value of 93.1%. Sensitivity, specificity, and negative predictive value were 41.2%, 99.1%, and 85.0%, respectively. In patients with ALT/AST ratio of <1 or platelet counts of >150,000/mm3, these laboratory parameters cannot predict liver fibrosis stage.CONCLUSION:AST/ALT ratio in combination with platelet counts may obviate a liver biopsy for fibrosis staging in some patients with chronic HCV infection.

Albumin dialysis in cirrhosis with superimposed acute liver injury: possible impact of albumin dialysis on hospitalization costs.

Abstract Albumin dialysis using the Molecular Adsorbents Recirculating System (MARS) has been found to be beneficial in the treatment of cirrhotic patients with acute decompensation to improve survival as well as reduce associated complications. The present study attempts to analyze the costs involved, and compare it to the benefit as a result of the MARS therapy, thus evaluating its cost‐effectiveness. Using the results of a study by Kim et al. (Hepatology 2001) describing the effects of complications on the cost of hospitalization in alcoholic liver disease patients, the expenditure incurred in a group of 11 patients treated with standard medical therapy (five survivors) and a group of 12 patients treated with MARS in addition (11 survivors) (Heemann et al., Hepatology 2002) were analyzed. MARS resulted in a reduction of in‐hospital deaths, as well as liver disease‐related complications. Both these factors led to a substantial reduction of costs in the MARS group, which was enough to counterbalance the extra costs associated with extra‐corporeal therapy. In the control group, the total hospitalization cost per survivor were calculated to be at

Evaluation of mental state in a clinical trial of MARS for patients with acute hepatic encephalopathy: comparison of two scales

35 904. In the MARS group, the overall expenditure per survivor including standard medical therapy plus additional MARS liver support therapy were

The effect of extracorporeal albumin dialysis on plasma phospholipid fatty acids in patients with end-stage liver disease

32 036 – a saving of nearly

Factors associated with steatosis in patients with chronic hepatitis C

4000 compared to the control group. Therefore, it appears that the benefits of MARS therapy are enough to justify the cost of treatment and safe hospital costs, at least in the described population. However, further studies are needed to confirm these results.

The Influence of HIV Coinfection on the Natural History of HCV Infection

It is important to assess the severity of hepatic encephalopathy (HE) and to quantitate improvement in HE after therapeutic interventions in a reliable and reproducible manner. The lack of a well standardized method of measurement has led to the use of different techniques by different clinical investigators, making a comparison between studies problematic. Although this issue had been noted more than 2 decades ago,1, 2 it is still unresolved and is reflected in the diversity of end-points and methods used in the assessment of acute HE in clinical trials over the last 15 years, e.g. West Haven criteria, Glasgow coma scale, PSE index with arterial or venous ammonia, and the EEG) (Table 1). Also different conditions have been classified as chronic HE (not reviewed here). The problem of how HE should be assessed, together with the considerable diversity of terms used to define different clinical settings, prompted a gathering of a panel of international experts to reach a consensus. Table 1. Clinical treatment trials of episodic hepatic encephalopathy (precipitated or spontaneous) in the last 15 years. SMT: standard medical treatment Author and Year Type of patients Therapy studied Primary End-point Measurement of HE Kramer, 200115 Stage II and III HE Cirrhosis Sorbent dialysis + SMT vs SMT only Sensory evoked potentials Clinical staging (West Haven), sensory evoked potentials automated EEG Laccetti, 200016 Stage III-IV HE Cirrhosis Flumazenil + SMT vs placebo + SMT Clin ical improvement Glasgow coma scale Barbaro, 199816 Stage IVa HE Cirrho sis Flumazenil + lactulose vs placebo + lactulose Clinical improvement and EEG. EEG and modified Glasgow coma scale (Pappas and Jones), including: verbal ability, eye-opening, pupillary light reflex, corneal reflex, spontaneous eye movements, oculocephalic reflex, motor response, respiration pattern Barbaro, 199818 Stage III-IVa HE Cirrhosis Flumazenil + lactulose vs placebo + lactulose Clinical improvement and EEG EEG and modified Glasgow coma scale (Pappas and Jones), including: verbal abilitiy, eye-opening, pupillary light reflex, corneal reflex, spontaneous eye movements, oculocephalic reflex, motor response, respiration pattern Gyr, 199614 Stage I-III HE Cirrhosis Flumazenil vs placebo (Lactulose permitted in both groups) Clinical improvement Own adapted clinical PSE score, EEG Van der Rijt, 199519 HE staged by EEG (clinical stage varied from 0 to IV) Acute or chronic liver disease Flumazenil vs placebo Clinical improvement and EEG Clinical staging asses sed by own classi ficatio n: stage I: > 2 of inverted sleep pattern, disturbed memory, impaired serial 7’s, slowness of speech, flapping tremor; stage II: > 2 of lethargy, time disorientation, asterixi s; stage III: > 2 of state that subject had to be stimulated repetitively to open eyes or execute commands, place and person disorientation; stage IV: coma. EEG Cadranel, 199520 Stage II-IV HE Cirrhosis Flumazenil vs placebo Clinical improvement and EEG Clinical grading with own classification: I: euphoria/depression, mild confusion, slowness, disordered sleep rhythm; II: drowsiness, inappropriate behaviour, accentuation of grade I; III: stupor, patient sleeps most of time but rousable, incoherent speech, marked confu sion; IVa: coma, coordinated response to pain; IVb: hyperextension and pronosupination to pain stimuli; IVc: no response to pain; V: clinica l decerebration. EEG Pomier-Layrargues, 199421 Stage IV HE Cirrhosis Flumazenil + lactulose vs placebo + lactulose Clinical improvement Modified Glasgow coma score, including: verbal ability, eyeopening, pupillary light, corneal and oculocephalic reflexes, spontaneous eye movements, motor response, respiration pattern. EEG Blanc, 199422 Acute HE Cirrhosis Lactulose + neomycin vs placebo PSE index PSE Index (mental state (West Haven), number conection test, EEG, asterixis and arterial ammonia) Strauss, 199223 Acute HE stages I-IV Cirrhosis Neomycin vs placebo Clinical improvement Clinical criteria (I to IV) but no reference or explanation. Sushma, 199224 Acute HE stages II-IV Cirrhosis Lactulose vs sodium benzoate Clinical improvement Mental state (WH), asterixis, psychometric tests, arterial ammonia, EEG, evoked potentials Vilstrup, 199025 Acute HE stages II-IV Cirrhosis BCAA iv + lactulose vs glucose iv + lactulose Clinical improvement Glasgow coma scale Klotz, 198926 Stage III HE Cirrhosis Flumazenil vs placebo Clinical improvement Coma status evaluated by reactions and reflexes to stimuli (no further explanation or reference) Uribe, 198727 Acute HE (stage II Cirrhosis Lactitol and lactose enemas vs nonacidifying enemas PSE index PSE index: mental state (WH), NCT, asterixis, EEG, fasting arterial ammonia. Morgan, 198713 Acute HE Cirrhosis Lactitol vs lactulose PSE index PSE index: mental state (WH), NCT-A, asterixis, EEG, venous ammonia

Histological improvement in patients with pegylated interferon alpha-2b plus ribavirin who were previously non-responders to rebetron

Abstract The effect of extracorporeal albumin dialysis (ECAD) using the MARS™ device on plasma phospholipid fatty acids (PLFA) in patients with end‐stage liver disease (ESLD) was examined. Phospholipids were isolated from plasma and the fatty acid (FA) composition of non‐sphingomyelin PL determined using capillary gas chromatography (GC). Plasma samples were also obtained from six patients with ESLD undergoing ECAD and from five patients with similar ESLD who were not treated, as well as from non‐fasting healthy subjects. PLFA were much lower [506 ± 62 μg/mL (M ± SD)] in patients with ESLD than in healthy subjects (2709 ± 688 μg/mL). In addition, the proportion of n3 and n6 polyunsaturated FA was much lower in patients with ESLD (n3, 1.7 ± 0.1%, n6, 19.6 ± 1.4%) than in healthy controls (n3, 4.1 ± 2.4%, n6, 31.9 ± 6.2%) ECAD caused an immediate increase in PLFA, averaging 56% in all patients, but PLFA levels decreased some hours later after treatment. ECAD also caused a small increase in the proportion of n3 and n6 of PLFA. During the 5 days of the study, PLFA rose in both ECAD‐treated and untreated patients, but the increase was significantly greater in ECAD treated patient. It is concluded that patients with ESLD have markedly decreased PLFA; these PLFA have a lower proportion of the polyunsaturated n3 and n6 FA with the result that the plasma level of these essential polyunsaturated PLFA is extremely low compared to that of healthy subjects. ECAD causes a transient increase in PLFA toward normal levels and also increases the proportion of n3 and n6 FA.

228 Extent of Recovery of Neurocognitive Dysfunction in Patients Presenting with Severe Hepatic Encephalopathy

Purpose: Steatosis is a common feature of chronic Hepatitis C (HCV). The pathophysiology of steatosis is not clear. Multiple factors may play a role in the degree of steatosis in patients with HCV infection. We investigated the correlation between pre-treatment body mass index (BMI), serum liver injury tests, and HCV viral load (HCV-RNA), and steatosis in patients with HCV.