The cost of treatment failure: resource use and costs incurred by hepatitis C virus genotype 1-infected patients who do or do not achieve sustained virological response to therapy.

Chronic hepatitis C virus (HCV) infection places a considerable economic burden on health services. Cost-effectiveness analyses of antiviral treatment for patients with chronic HCV infection are dependent on assumptions about cost reductions following sustained virological response (SVR) to therapy. This study quantified the medium-term difference in health resource usage and costs depending on treatment outcome. Retrospective chart review of patients with HCV genotype 1 infection who had received at least 2 months pegylated interferon and ribavirin therapy, with known treatment outcome was conducted. Disease status was categorized as chronic hepatitis, cirrhosis or decompensated liver disease. Health resource use was documented for each patient in each disease state. Unit costs were from the NHS 'Payment by Results' database and the British National Formulary. One hundred and ninety three patients (108 SVR, 85 non-SVR) with mean follow-up of 3.5 (SVR) and 4.9 (non-SVR) years were enrolled. No SVR patient progressed to a more severe liver disease state. Annual transition rates for non-SVR patients were 7.4% (chronic hepatitis to cirrhosis) and 4.9% (cirrhosis to decompensated liver disease). By extrapolation of modelled data over a 5-year post-treatment period, failure of patients with chronic hepatitis to achieve SVR was associated with a 13-fold increase (roughly £2300) in costs, whilst for patients who were retreated, the increase was 56-fold, equating to more than £10 000. Achievement of an SVR has significant effects on health service usage and costs. This work provides real-life data for future cost-effectiveness analyses related to the treatment for chronic HCV infection.

MR and 1H MR spectroscopy of the brain in patients with liver cirrhosis and early stages of hepatic encephalopathy.

BACKGROUND/AIMS: Hepatic encephalopathy is a serious problem in patients with liver cirrhosis and precise pathophysiological mechanisms responsible for encephalopathy are not fully understood. Magnetic resonance imaging and magnetic resonance spectroscopy can be used to detect specific morphological and metabolic abnormalities in the brain even in patients with early stages of hepatic encephalopathy. METHODOLOGY: Twenty patients with liver cirrhosis and 14 patients with grade I-II hepatic encephalopathy were studied with magnetic resonance and proton magnetic resonance spectroscopy. Localized magnetic resonance spectra were acquired in the parietal gray/white matter regions and basal ganglia. Control group consisted of 20 healthy volunteers. RESULTS: Frequency and degree of brain atrophy and bilateral signal hyperintensities in globus pallidus were similar in groups with liver cirrhosis and with encephalopathy. Decreased myoinositol, choline and increased glutamine levels were noted in both groups whereas N-acetylaspartate levels were unchanged. The statistically significant differences between cirrhotic and encephalopathic groups were observed only in myoinositol/creatine ratio in basal ganglia. There were no significant differences in metabolic concentrations between parietal and basal ganglia regions. CONCLUSIONS: Metabolic brain alterations occur earlier than clinical evidence of hepatic encephalopathy but there is no correlation between presence of symptoms encephalopathy and magnetic resonance and magnetic resonance spectroscopy findings.

Severe respiratory distress caused by central airway obstruction treated with self-expandable metallic stents.

We investigate retrospectively the efficacy of self-expandable metallic stents (SEMS) for severe respiratory distress (SRD) in patients with central airway obstruction (CAO). Thirty three patients with CAO were treated with SEMS using fiberoptic bronchoscopy method. We found an intraluminal obstruction present in 7, extraluminal compression in 10, and combined stenosis in 16 cases. Tumor infiltration occupied more than 90% of the endoluminal diameter in 21, 70% in 9, and 50% in 3 cases. Obstruction was caused by primary cancer of lung in 23, thyroid in 5, and esophagus in 5 patients. Up to 3 stents per patient were placed. Double stenting (esophagus and trachea) was required in five patients. All patients exhibited symptomatic and arterial blood gas improvement. The mean follow-up was 65 (5 to 752) days. SEMS are useful for the treatment of SRD caused by CAO. The overall effect is related to the degree of tumor progression itself.

Beta thromboglobulin and platelet factor 4 in bronchoalveolar lavage fluid of patients with systemic sclerosis.

OBJECTIVE: To evaluate concentrations of the platelet activation markers beta thromboglobulin (BTG) and platelet factor 4 (PF4) in bronchoalveolar lavage fluid (BALF) from patients with systemic sclerosis with and without scleroderma interstitial lung disease (SLD). METHODS: BTG and PF-4 were measured by enzyme immunoassay in BALF from 37 patients with systemic sclerosis. Controls were 10 healthy subjects. BALF was collected during routine bronchoscopy from the right middle lobe. SLD was diagnosed by high resolution computed tomography of the lungs. RESULTS: BTG was detected in 11 of the patients with systemic sclerosis (29.7%) and PF4 was found in eight (21.6%). Mean (SD) concentrations of BTG and PF4 in BALF from patients with detectable levels of these platelet activation markers were 106.9 (69.8) and 35.2 (17.4) IU/ml, respectively. The BTG:PF4 ratio was more than 2:1, indicating in vivo release. Both markers were found exclusively in patients with SLD. SLD patients with detectable platelet activation markers had a significantly shorter disease duration than those with undetectable BTG/PF4. CONCLUSIONS: The study provides evidence that activation of blood platelets takes place within the lungs of patients with SLD and may contribute to the development of lung fibrosis.