St Josef Hospital Oberhausen

Oberhausen, Germany

St Josef Hospital Oberhausen

Oberhausen, Germany
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Bruix J.,University of Barcelona | Poynard T.,University Pierre and Marie Curie | Colombo M.,University of Milan | Schiff E.,University of Miami | And 14 more authors.
Gastroenterology | Year: 2011

Background & Aims: Several studies have reported that low doses of interferon can delay the development of hepatocellular carcinoma (HCC) and progression of chronic hepatitis C. We investigated the incidence of clinical events among participants of the Evaluation of PegIntron in Control of Hepatitis C Cirrhosis (EPIC)3 program. Methods: Data were analyzed from an open-label randomized study of patients with chronic hepatitis C who had failed to respond to interferon alfa plus ribavirin. All patients had compensated cirrhosis with no evidence of HCC. Patients received peginterferon alfa-2b (0.5 μg/kg/week; n = 311) or no treatment (controls, n = 315) for a maximum period of 5 years or until 98 patients had a clinical event (hepatic decompensation, HCC, death, or liver transplantation). The primary measure of efficacy was time until the first clinical event. Results: There was no significant difference in time to first clinical event among patients who received peginterferon alfa-2b compared with controls (hazard ratio [HR], 1.452; 95% confidence interval [CI]: 0.8802.396). There was no decrease in the development of HCC with therapy. The time to disease progression (clinical events or new or enlarged varices) was significantly longer for patients who received peginterferon alfa-2b compared with controls (HR, 1.564; 95% CI: 1.1302.166). In a prospectively defined subanalysis of patients with baseline portal hypertension, peginterferon alfa-2b significantly increased the time to first clinical event compared with controls (P = .016). There were no new safety observations. Conclusions: Maintenance therapy with peginterferon alfa-2b is not warranted in all patients and does not prevent HCC. However, there is a potential clinical benefit of long-term suppressive therapy in patients with preexisting portal hypertension. © 2011 AGA Institute.

Deterding K.,Klinik fur Gastroenterologie | Heidelberger S.,Klinik fur Gastroenterologie | Wiebner B.,Deutsche Leberstiftung | Meining K.,Klinik fur Gastroenterologie | And 13 more authors.
Deutsche Medizinische Wochenschrift | Year: 2012

Background and aim: Hepatitis B is a significant health burden in Germany. The aim of this study was (I) to gain more information on knowledge of hepatitis B patients and patient management considering epidemiologic and socio-economic factors, (II) to investigate the knowledge of relatives of patients with hepatitis B about liver disease, modes of infection and possibilities of prevention. Patients and methods: Structured questionnaires were sent to 1000 patients with hepatitis B as a project of the Model Region North of the German network of excellence for viral hepatitis. The patients were asked to forward additional questionnaires to their relatives and household members. Results: 312 (31 %) questionnaires were sent back and evaluated. The majority of responding patients had an immigration background (75 %). The knowledge of hepatitis B patients about their disease status was very heterogeneous. While most of them were aware of their ALT-values, only some patients knew their HBV viral loads. Patients with a low socio-economic status consulted physicians more often but did not receive medical examinations more frequently. The knowledge of relatives (384 relatives from families of 216 patients) about the mode of transmission and the possibilities of prevention were also heterogeneous. Only 84 % of the partners and children were vaccinated against hepatitis B and only 75 % of relatives knew that condoms protect against HBV infection. Conclusion: Not only patients with hepatitis B but also relatives and household members should be informed about consequences of liver disease and HBV infection. The poor vaccination coverage even of sexual partners of HBV-infected individuals requires attention and should lead to a better education. © Georg Thieme Verlag KG Stuttgart · New York.

Kamper L.,Witten/Herdecke University | Meyn H.,Witten/Herdecke University | Rybacki K.,University Hospital | Nordmeyer S.,St Josef Hospital Oberhausen | And 4 more authors.
CardioVascular and Interventional Radiology | Year: 2012

Objective In vertebrobasilar occlusion, rapid recanalization is the only substantial means to improve the prognosis. We introduced a standard operating procedure (SOP) for interventional therapy to analyze the effects on interdisciplinary time management. Methods Intrahospital time periods between hospital admission and neuroradiological intervention were retrospectively analyzed, together with the patients' outcome, before (n = 18) and after (n = 20) implementation of the SOP. Results After implementation of the SOP, we observed statistically significant improvement of postinterventional patient neurological status (p = 0.017). In addition, we found a decrease of 5:33 h for the mean time period from hospital admission until neuroradiological intervention. The recanalization rate increased from 72.2% to 80% after implementation of the SOP. Conclusion Our results underscore the relevance of SOP implementation and analysis of time management for clinical workflow optimization. Both may trigger awareness for the need of efficient interdisciplinary time management. This could be an explanation for the decreased time periods and improved postinterventional patient status after SOP implementation. © Springer Science+Business Media, LLC and the Cardiovascular and Interventional Radiological Society of Europe (CIRSE) 2011.

Yildiz Y.,University of Bonn | Hoffmann P.,University of Bonn | Vom Dahl S.,St Franziskus Hospital Cologne | Breiden B.,University of Bonn | And 16 more authors.
Orphanet Journal of Rare Diseases | Year: 2013

Background: Gaucher disease (GD) is the most common inherited lysosomal storage disorder in humans, caused by mutations in the gene encoding the lysosomal enzyme glucocerebrosidase (GBA1). GD is clinically heterogeneous and although the type of GBA1 mutation plays a role in determining the type of GD, it does not explain the clinical variability seen among patients. Cumulative evidence from recent studies suggests that GBA2 could play a role in the pathogenesis of GD and potentially interacts with GBA1. Methods. We used a framework of functional and genetic approaches in order to further characterize a potential role of GBA2 in GD. Glucosylceramide (GlcCer) levels in spleen, liver and brain of GBA2-deficient mice and mRNA and protein expression of GBA2 in GBA1-deficient murine fibroblasts were analyzed. Furthermore we crossed GBA2-deficient mice with conditional Gba1 knockout mice in order to quantify the interaction between GBA1 and GBA2. Finally, a genetic approach was used to test whether genetic variation in GBA2 is associated with GD and/ or acts as a modifier in Gaucher patients. We tested 22 SNPs in the GBA2 and GBA1 genes in 98 type 1 and 60 type 2/3 Gaucher patients for single- and multi-marker association with GD. Results: We found a significant accumulation of GlcCer compared to wild-type controls in all three organs studied. In addition, a significant increase of Gba2-protein and Gba2-mRNA levels in GBA1-deficient murine fibroblasts was observed. GlcCer levels in the spleen from Gba1/Gba2 knockout mice were much higher than the sum of the single knockouts, indicating a cross-talk between the two glucosylceramidases and suggesting a partially compensation of the loss of one enzyme by the other. In the genetic approach, no significant association with severity of GD was found for SNPs at the GBA2 locus. However, in the multi-marker analyses a significant result was detected for p.L444P (GBA1) and rs4878628 (GBA2), using a model that does not take marginal effects into account. Conclusions: All together our observations make GBA2 a likely candidate to be involved in GD etiology. Furthermore, they point to GBA2 as a plausible modifier for GBA1 in patients with GD. © 2013 Yildiz et al.; licensee BioMed Central Ltd.

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