Publications by authors named "Kerstin Zinober"
Background: Portal hypertension (PH) resulting from static and dynamic intrahepatic changes drives liver-related complications even after removing the underlying aetiological factor.
Objective: We investigated the impact of inflammation on the dynamic component of PH during disease regression in animal models of toxin-induced cirrhosis and patients with alcohol-related cirrhosis.
Methods: In mice, cirrhosis was induced via toxin application for 12 weeks followed by toxin-withdrawal allowing for one or 2 weeks of regression.
Article Synopsis
- Cirrhosis creates a proinflammatory environment, and the study aims to analyze specific inflammation patterns across various causes of compensated cirrhosis in both animal models and human patients.
- In rat models, inflammation differed based on the cirrhosis cause, with choline-deficient high-fat diet rats showing the highest proinflammatory gene expression, while in humans, different liver diseases exhibited varying levels of inflammatory markers.
- Despite common upregulation of proinflammatory pathways in all types of liver disease, the impact on fibrosis and portal hypertension varied based on the specific etiology of the disease.
Background And Aims: Experimental studies linked dysfunctional Farnesoid X receptor (FXR)-fibroblast growth factor 19 (FGF19) signaling to liver disease. This study investigated key intersections of the FXR-FGF19 pathway along the gut-liver axis and their link to disease severity in patients with cirrhosis.
Methods: Patients with cirrhosis undergoing hepatic venous pressure gradient measurement (cohort-I n = 107, including n = 53 with concomitant liver biopsy; n = 5 healthy controls) or colonoscopy with ileum biopsy (cohort-II n = 37; n = 6 controls) were included.
Cirrhotic patients have an increased risk of bleeding and thromboembolic events, with platelets being involved as key players in both situations. The impact of peripheral versus central blood sampling on platelet activation remains unclear. In 33 cirrhotic patients, we thus analyzed platelet function in peripheral (P) and central (C) blood samples.
View Article and Find Full Text PDFBackground: In cirrhosis, the nitric oxide-soluble guanylyl cyclase (sGC)-cyclic guanosine monophosphate (cGMP) pathway is impaired, which contributes to increased intrahepatic vascular resistance (IHVR) and fibrogenesis. We investigated if sGC stimulation (riociguat (RIO)), sGC activation (cinaciguat (CINA)) or phosphodiesterase (PDE)-5 inhibition (tadalafil (TADA)) improves portal hypertension (PHT) and liver fibrosis.
Methods: Fifty male Sprague-Dawley rats underwent bile-duct ligation (BDL) or sham operation.
Article Synopsis
- - Elastography point quantification (ElastPQ) is a new, non-invasive ultrasound method used to assess liver fibrosis in patients with chronic viral hepatitis, comparing it to the established transient elastography measurement.
- - The study analyzed data from 217 patients, determining that ElastPQ effectively identifies significant fibrosis (≥F2) and cirrhosis (F4) with high accuracy based on area under the receiver operator characteristics curve (AUROC).
- - The optimal ElastPQ cutoff values for diagnosing fibrosis stages were 6.68 kPa for F2 (with 80.7% sensitivity) and 11.28 kPa for F4 (with 86.0% sensitivity), highlighting its potential as a reliable
Background & Aims: Single nucleotide polymorphisms (SNPs) in the gene that encodes interleukin (IL)-28B predict response of patients with chronic hepatitis C to antiviral therapy. We investigated the roles of polymorphisms rs12979860 and rs8099917 on the early virologic response of treatment-naïve patients.
Methods: SNPs were identified by real-time polymerase chain reaction analysis of samples from 682 patients (genotype [GT]1=372, GT2/3=208, GT4=102) who were treated with 180 μg pegylated interferon-α2a and 400 or 800 mg (GT2/3, depending on the protocol) or 1000-1200 mg (GT1/4) ribavirin/day.
Background: Epidemiological observations suggest that cancer arises from chronically inflamed tissues. Inflammatory bowel disease (IBD) is a typical example as patients with longstanding IBD are at an increased risk for developing colorectal cancer (CRC) and mutations of the NOD2/CARD15 gene increase the risk for Crohn's disease (CD). Recently, NOD2/CARD15 has been associated with a risk for CRC in some studies, which stemmed from ethnically diverse populations.
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