scholarly journals Redefining Cirrhosis – a brief review

2013 ◽  
Vol 3 (6) ◽  
pp. 491-496 ◽  
Author(s):  
SV Pradhan
Keyword(s):  
Portal Hypertension ◽  
Liver Damage ◽  
Successful Treatment ◽  
Classification System ◽  
Vascular Remodeling ◽  
Underlying Disease ◽  
Nodule Formation ◽  
Variable Amount ◽  
Histological Features

The liver damage is associated with variable amount of fibrosis. The presence of fibrosis with nodule formation is pathognomic of cirrhosis. It is accompanied by vascular remodeling and regeneration with important functional and hemodynamic consequences that include development of portal hypertension and eventually decompensation and death. However fibrosis can regress following successful treatment of the underlying disease. The classification system followed till date does not analyze this aspect. In this brief review the histological features of fibrosis and the newer models for reclassifying cirrhosis is discussed. DOI: http://dx.doi.org/10.3126/jpn.v3i6.9000 Journal of Pathology of Nepal (2013) Vol. 3, 491-496

Telmisartan relieves liver fibrosis and portal hypertension by improving vascular remodeling and sinusoidal dysfunction

2021 ◽  
pp. 174713
Author(s):  
Lei Zheng ◽  
Zhifeng Zhao ◽  
Jiayun Lin ◽  
Hongjie Li ◽  
Guangbo Wu ◽  
...  
Keyword(s):  
Portal Hypertension ◽  
Liver Fibrosis ◽  
Vascular Remodeling

G18 : The FXR agonist PX20606 reduces liver damage, fibrosis and portal hypertension in cirrhotic rats

2015 ◽  
Vol 62 ◽  
pp. S238 ◽  
Author(s):  
P. Schwabl ◽  
E. Hambruch ◽  
B.A. Payer ◽  
T.L. Schubert ◽  
B. Strobel ◽  
...  
Keyword(s):  
Portal Hypertension ◽  
Liver Damage

scholarly journals Vaginal varices with massive hemorrhage in a patient with nonalcoholic steatohepatitis and portal hypertension: Successful treatment with liver transplantation

2008 ◽  
Vol 14 (10) ◽  
pp. 1538-1540 ◽  
Author(s):  
Patrick P. McHugh ◽  
Hoonbae Jeon ◽  
Roberto Gedaly ◽  
Thomas D. Johnston ◽  
Paul D. DePriest ◽  
...  
Keyword(s):  
Liver Transplantation ◽  
Portal Hypertension ◽  
Successful Treatment ◽  
Nonalcoholic Steatohepatitis ◽  
Massive Hemorrhage

Complications of cirrhosis and portal hypertension

2013 ◽  
pp. 251-256 ◽  
Author(s):  
Daniel Marks ◽  
Marcus Harbord
Keyword(s):  
Hepatocellular Carcinoma ◽  
Liver Transplantation ◽  
Portal Hypertension ◽  
Hepatic Encephalopathy ◽  
Spontaneous Bacterial Peritonitis ◽  
Early Stage ◽  
Nodule Formation ◽  
Architectural Distortion ◽  
Bacterial Peritonitis ◽  
Complications Of Cirrhosis

Causes and diagnosis of cirrhosis Causes and diagnosis of non-cirrhotic portal hypertension Ascites Spontaneous bacterial peritonitis Hepatorenal syndrome Variceal haemorrhage Hepatic encephalopathy Hepatopulmonary syndromes Hepatocellular carcinoma Cirrhosis occurs following progressive hepatic fibrosis, with architectural distortion of the liver and nodule formation. It is a histological diagnosis. Late-stage cirrhosis is irreversible, at which point only liver transplantation is curative. Early-stage cirrhosis has been shown to improve following treatment and may be asymptomatic....

scholarly journals Gene Ontology and KEGG Enrichment Analyses of Genes Related to Age-Related Macular Degeneration

2014 ◽  
Vol 2014 ◽  
pp. 1-10 ◽  
Author(s):  
Jian Zhang ◽  
ZhiHao Xing ◽  
Mingming Ma ◽  
Ning Wang ◽  
Yu-Dong Cai ◽  
...  
Keyword(s):  
Gene Ontology ◽  
Feature Selection ◽  
Macular Degeneration ◽  
Classification System ◽  
Underlying Disease ◽  
Age Related Macular Degeneration ◽  
Disease Genes ◽  
Kegg Pathways ◽  
Age Related ◽  
Go Terms

Identifying disease genes is one of the most important topics in biomedicine and may facilitate studies on the mechanisms underlying disease. Age-related macular degeneration (AMD) is a serious eye disease; it typically affects older adults and results in a loss of vision due to retina damage. In this study, we attempt to develop an effective method for distinguishing AMD-related genes. Gene ontology and KEGG enrichment analyses of known AMD-related genes were performed, and a classification system was established. In detail, each gene was encoded into a vector by extracting enrichment scores of the gene set, including it and its direct neighbors in STRING, and gene ontology terms or KEGG pathways. Then certain feature-selection methods, including minimum redundancy maximum relevance and incremental feature selection, were adopted to extract key features for the classification system. As a result, 720 GO terms and 11 KEGG pathways were deemed the most important factors for predicting AMD-related genes.

Histological features in western patients with idiopathic non-cirrhotic portal hypertension

2013 ◽  
Vol 62 (7) ◽  
pp. 1083-1091 ◽  
Author(s):  
Joanne Verheij ◽  
Jeoffrey N L Schouten ◽  
Mina Komuta ◽  
Frederik Nevens ◽  
Bettina E Hansen ◽  
...  
Keyword(s):  
Portal Hypertension ◽  
Histological Features

Mass Effect Alone May Not Explain Pulmonary Vascular Pathology in Severe Congenital Diaphragmatic Hernia

2015 ◽  
Vol 39 (2) ◽  
pp. 117-124 ◽  
Author(s):  
Sarkis Christopher Derderian ◽  
Christine M. Jayme ◽  
Lily S. Cheng ◽  
Roberta L. Keller ◽  
Anita J. Moon-Grady ◽  
...  
Keyword(s):  
Congenital Diaphragmatic Hernia ◽  
Diaphragmatic Hernia ◽  
Vascular Remodeling ◽  
Pulmonary Arteries ◽  
Mass Effect ◽  
Underlying Disease ◽  
Vascular Pathology ◽  
Cardiothoracic Ratio ◽  
Postnatal Mortality ◽  
Echocardiographic Parameters

Congenital diaphragmatic hernia (CDH) and congenital pulmonary airway malformation (CPAM) are diseases in which chest-occupying lesions can result in severe pulmonary hypoplasia. However, significant postnatal mortality due to pulmonary hypertension (PH) is more often seen in patients with CDH. We analyzed prenatal echocardiographic parameters of pulmonary vascular pathology in these groups to understand whether PH in patients with CDH is secondary to a mass effect or to underlying disease. We analyzed pre- and postnatal characteristics of 26 patients with severe CDH and 23 patients with severe CPAM from 2009 to 2012. Severe mediastinal compression, indicated by a low cardiothoracic ratio, was evident in both groups. However, fetuses with severe CDH had smaller pulmonary arteries bilaterally and higher pulsatility indices in the ipsilateral lung than those with severe CPAM. Prenatal modified McGoon indices were significantly lower in patients with CDH versus CPAM. Consistent with these prenatal measurements, postnatal PH was seen more frequently in patients with CDH compared to CPAM. Patients with severe CDH have prenatal evidence of pulmonary vascular remodeling compared to patients with severe CPAM. These results suggest a multifactorial origin for PH in CDH and support the idea of using prenatal medical therapies to promote vascular remodeling in these patients.

scholarly journals COX-2/sEH Dual Inhibitor PTUPB Alleviates CCl4-Induced Liver Fibrosis and Portal Hypertension

2021 ◽  
Vol 8 ◽  
Author(s):  
Zhifeng Zhao ◽  
Chihao Zhang ◽  
Jiayun Lin ◽  
Lei Zheng ◽  
Hongjie Li ◽  
...  
Keyword(s):  
Liver Cirrhosis ◽  
Portal Hypertension ◽  
Growth Factor ◽  
Liver Fibrosis ◽  
Vascular Remodeling ◽  
Mesenteric Arteries ◽  
Cytokeratin 19 ◽  
Dual Inhibitor ◽  
Bile Duct Proliferation ◽  
Cox 2

Background: 4-(5-phenyl-3-{3-[3-(4-trifluoromethylphenyl)-ureido]-propyl}-pyrazol-1-yl) -benzenesulfonamide (PTUPB), a dual cyclooxygenase-2 (COX-2)/soluble epoxide hydrolase (sEH) inhibitor, was found to alleviate renal, pulmonary fibrosis and liver injury. However, few is known about the effect of PTUPB on liver cirrhosis. In this study, we aimed to explore the role of PTUPB in liver cirrhosis and portal hypertension (PHT).Method: Rat liver cirrhosis model was established via subcutaneous injection of carbon tetrachloride (CCl4) for 16 weeks. The experimental group received oral administration of PTUPB (10 mg/kg) for 4 weeks. We subsequently analyzed portal pressure (PP), liver fibrosis, inflammation, angiogenesis, and intra- or extrahepatic vascular remodeling. Additionally, network pharmacology was used to investigate the possible mechanisms of PTUPB in live fibrosis.Results: CCl4 exposure induced liver fibrosis, inflammation, angiogenesis, vascular remodeling and PHT, and PTUPB alleviated these changes. PTUPB decreased PP from 17.50 ± 4.65 to 6.37 ± 1.40 mmHg, reduced collagen deposition and profibrotic factor. PTUPB alleviated the inflammation and bile duct proliferation, as indicated by decrease in serum interleukin-6 (IL-6), liver cytokeratin 19 (CK-19), transaminase, and macrophage infiltration. PTUPB also restored vessel wall thickness of superior mesenteric arteries (SMA) and inhibited intra- or extrahepatic angiogenesis and vascular remodeling via vascular endothelial growth factor (VEGF), von Willebrand factor (vWF), etc. Moreover, PTUPB induced sinusoidal vasodilation by upregulating endothelial nitric oxide synthase (eNOS) and GTP-cyclohydrolase 1 (GCH1). In enrichment analysis, PTUPB engaged in multiple biological functions related to cirrhosis, including blood pressure, tissue remodeling, immunological inflammation, macrophage activation, and fibroblast proliferation. Additionally, PTUPB suppressed hepatic expression of sEH, COX-2, and transforming growth factor-β (TGF-β).Conclusion: 4-(5-phenyl-3-{3-[3-(4-trifluoromethylphenyl)-ureido]-propyl}-pyrazol-1-yl)- benzenesulfonamide ameliorated liver fibrosis and PHT by inhibiting fibrotic deposition, inflammation, angiogenesis, sinusoidal, and SMA remodeling. The molecular mechanism may be mediated via the downregulation of the sEH/COX-2/TGF-β.

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