scholarly journals Blood Ammonia Level Correlates with Severity of Cirrhotic Portal Hypertensive Gastropathy

2018 ◽  
Vol 2018 ◽  
pp. 1-9 ◽  
Author(s):  
Ferial El-Kalla ◽  
Loai Mansour ◽  
Abdelrahman Kobtan ◽  
Asmaa Elzeftawy ◽  
Lobna Abo Ali ◽  
...  
Keyword(s):  
Portal Hypertension ◽  
Cell Activation ◽  
Stellate Cell ◽  
Splenic Vein ◽  
Control Group ◽  
Portal Hypertensive Gastropathy ◽  
Blood Ammonia ◽  
Abdominal Ultrasonography ◽  
Portosystemic Shunts ◽  
Longitudinal Diameter

Background. Portal hypertensive gastropathy (PHG) is a common anomaly with potential for bleeding found in portal hypertension. Blood ammonia levels correlate well with liver disease severity and existence of portosystemic shunts. Increased ammonia results in vasodilation and hepatic stellate cell activation causing and exacerbating portal hypertension.Objective. To assess the relation of blood ammonia to the presence and severity of portal hypertensive gastropathy in cirrhosis.Methods. This cross-sectional study included 381 cirrhotics undergoing screening for esophageal varices (EV) divided into a portal hypertensive gastropathy group (203 patients with EV and PHG), esophageal varix group (41 patients with EV but no PHG), and control group (137 patients with no EV or PHG). A full clinical examination, routine laboratory tests, abdominal ultrasonography, child score calculation, and blood ammonia measurement were performed for all patients.Results. Blood ammonia, portal vein, splenic vein, and splenic longitudinal diameters were significantly higher and platelet counts lower in patients with EV and EV with PHG than controls. Patients having EV with PHG had significantly higher bilirubin and ammonia than those with EV but no PHG. Severe PHG was associated with significantly higher ammonia, EV grades, and superior location and a lower splenic longitudinal diameter than mild PHG. The PHG score showed a positive correlation with blood ammonia and a negative correlation with splenic longitudinal diameter.Conclusions. Blood ammonia levels correlate with the presence, severity, and score of portal hypertensive gastropathy in cirrhosis suggesting a causal relationship and encouraging trials of ammonia-lowering treatments for the management of severe PHG with a tendency to bleed.

scholarly journals Ultrasonographic evaluation of portal hypertnsion

Mediscope ◽  
2015 ◽  
Vol 2 (1) ◽  
pp. 27-31
Author(s):  
MS Ahamed ◽  
PK Chowdhury ◽  
AS Mohiuddin ◽  
MA Hossain ◽  
B Paik
Keyword(s):  
Portal Hypertension ◽  
Portal Vein ◽  
Splenic Vein ◽  
Cross Sectional Study ◽  
Oesophageal Varices ◽  
Deep Inspiration ◽  
Abdominal Ultrasonography ◽  
Cross Sectional ◽  
Mesenteric Veins ◽  
Diameter Variation

A descriptive type of cross-sectional study was done to measure diameters of splenic, superior mesenteric and portal veins with their variation with respiration in patients with portal hypertension. Trans-abdominal ultrasonography was used for the purpose among purposively selected 59 patients with chronic liver disease and portal hypertension using computer sonography with multiple probes having multiple frequency depending on physical built of subjects. The diameters of selected veins were measured in the course of expiration and deep inspiration. Mean age of respondents was 53.2 years with standard deviation of 11.4 years. 44 (74.6%) subjects were male, whereas 15 (25.4%) were female. In all cases oesophageal varices were present. Portal vein was clearly visualized in all cases, while splenic vein in 53 (89.8%) cases and superior mesenteric vein in 49 (83.1%) cases. During deep inspiration, diameter of portal vein was greater than 13 mm in 31 (52.5%), while ?13 mm in 28 (47.5%) of portal hypertensive cases. Of 31, lack variation in diameter during respiration was observed in 29 (93.6%) cases. Size of liver (length in mid-clavicular line) in 18 (30.5%) cases were between 96 to 115 mm, while in 19 (32.2%) cases it was within 116 to 135 mm and in 22 (37.3%) cases it was between 136 to 160 mm. In 36 (61.0%) cases surface of liver was irregular, while in 51 (86.4%) cases parenchymal echotexture of liver was coarse. Size of spleen was enlarged in 44 (74.6%) cases, and ascites was present in 47 (79.7%) cases. Diameter variation with breathing of splenic and superior mesenteric veins observed only in 5 (8.5%) patients. Lack of diameter variation of portal, splenic and superior mesenteric veins with respiration in ultrasonography is an indicator of portal hypertension.Mediscope Vol. 2, No. 1: 2015, Pages 27-31

scholarly journals Stellate Cell Activation and Imbalanced Expression of TGF-β1/TGF-β3 in Acute Autoimmune Liver Lesions Induced by ConA in Mice

2017 ◽  
Vol 2017 ◽  
pp. 1-12 ◽  
Author(s):  
Liyun Wang ◽  
Lei Tu ◽  
Jinping Zhang ◽  
Keshu Xu ◽  
Wei Qian
Keyword(s):  
Treatment Group ◽  
Liver Injury ◽  
Cell Activation ◽  
Stellate Cell ◽  
Stellate Cells ◽  
Control Group ◽  
Liver Lesions ◽  
Saline Injection ◽  
Dynamic Expression ◽  
Tgf Β1

Objective. To study the pathogenic feature of liver injury, activation of hepatic stellate cells, and dynamic expression of TGF-β1/TGF-β3 to reveal their role in liver injury induced by ConA.Methods. Mice were randomly divided into control group and ConA treatment group. ConA (20 mg/kg) was injected through vena caudalis in ConA treatment group; the controls received the same volume of saline injection. After injection for 2 h, 8 h, 24 h, and 48 h, animals were terminated. Blood, liver, and spleen were harvested. Liver function and histopathology were studied.α-SMA, vimentin, TGF-β1, and TGF-β3 were detected.Results. After ConA injection, liver damage started to increase. Expression ofα-SMA, vimentin, TGF-β1, and TGF-β3 was significantly enhanced; all above indicators reached peak at 8 h; but from 24 h after ConA injection, TGF-β3 expression began to decline, while the TGF-β1/TGF-β3 ratio at 48 h was significantly lower than control.Conclusion. (1) Autoimmune liver injury induced by ConA showed time-based features, in which the most serious liver lesions happened at 8 h after ConA injection. (2) Early activation of HSC and imbalance expression of TGF-β1 and TGF-β3 existed in ConA-induced acute autoimmune liver injury, which may be associated with liver dysfunction and the mechanisms of progression to fibrosis.

INDICATIONS FOR PANCREATODUODENAL RESECTION IN TREATMENT OF CHRONIC PANCREATITIS COMPLICATED FORMS

2020 ◽  
pp. 18-22
Author(s):  
S. E. Arutyunov ◽  
M. V. Klymenko ◽  
K. E. Shamoun
Keyword(s):  
Chronic Pancreatitis ◽  
Portal Hypertension ◽  
Magnetic Resonance ◽  
Pancreatic Fistula ◽  
Inflammatory Process ◽  
Cell Activation ◽  
Stellate Cell ◽  
Magnetic Resonance Cholangiopancreatography ◽  
Pancreas Head ◽  
Surgical Treatments

Chronic pancreatitis is a recurrent progressive disease accompanied by fibrosis and fibrocystic degeneration of the pancreatic parenchyma. There are remained the unexplored issues of progression of fibrosis in the pancreas parenchyma, which lead to a rapid enlargement of the head, the development of complications that require a resection surgery. To develop a differentiated approach to the choice of surgical treatments and indications for pancreatoduodenal resection in complicated forms of chronic pancreatitis, a study was performed in 137 patients underwent resection and drainage surgery. Pancreatoduodenal resection was accomplished in 12 patients. Instrumental research methods were used: multidetector (64−slice) computed tomography with 3D reconstruction, magnetic resonance imaging, magnetic resonance cholangiopancreatography, endoscopic retrograde cholangiopancreatography. Two clinical examples are given. Indications for pancreatoduodenal resection in patients with chronic pancreatitis were expressed fibro−inflammatory process in the area of the pancreas head, suspected development of oncological pathology. Progressive fibrotic changes in the pancreas parenchyma, mainly in the head, occurring in some patients, associated with stellate cell activation and fibrogenesis, they lead to the development of biliary and portal hypertension, stimulation of oncogenesis. It is concluded that with the progression of fibro−inflammatory process in the pancreas head with the development of complications (pancreatic, biliary and portal hypertension), as well as in case of impossibility to exclude the tumor, the surgery of choice is pancreatoduodenal resection. The presence of severe fibrosis in the pancreas parenchyma reduces the risk of developing pancreatic fistula when performing pancreatoduodenal resection. Key words: complicated forms of chronic pancreatitis, pancreatoduodenal resection, fibro−inflammatory process, pancreatic fistula

Metformin reduces hepatic resistance and portal pressure in cirrhotic rats

2015 ◽  
Vol 309 (5) ◽  
pp. G301-G309 ◽  
Author(s):  
Dinesh M. Tripathi ◽  
Eva Erice ◽  
Erica Lafoz ◽  
Héctor García-Calderó ◽  
Shiv K. Sarin ◽  
...  
Keyword(s):  
Portal Hypertension ◽  
Growth Factor ◽  
Bile Duct ◽  
Common Bile Duct ◽  
Vascular Resistance ◽  
Cell Activation ◽  
Transforming Growth Factor ◽  
Stellate Cell ◽  
Portal Pressure ◽  
Functional Components

Increased hepatic vascular resistance is the primary factor in the development of portal hypertension. Metformin ameliorates vascular cells function in several vascular beds. Our study was aimed at evaluating the effects, and the underlying mechanisms, of metformin on hepatic and systemic hemodynamics in cirrhotic rats and its possible interaction with the effects of propranolol (Prop), the current standard treatment for portal hypertension. CCl4-cirrhotic rats received by gavage metformin 300 mg/kg or its vehicle once a day for 1 wk, before mean arterial pressure (MAP), portal pressure (PP), portal blood flow (PBF), hepatic vascular resistance, and putative molecular/cellular mechanisms were measured. In a subgroup of cirrhotic rats, the hemodynamic response to acute Prop (5 mg/kg iv) was assessed. Effects of metformin ± Prop on PP and MAP were validated in common bile duct ligated-cirrhotic rats. Metformin-treated CCl4-cirrhotic rats had lower PP and hepatic vascular resistance than vehicle-treated rats, without significant changes in MAP or PBF. Metformin caused a significant reduction in liver fibrosis (Sirius red), hepatic stellate cell activation (α-smooth muscle actin, platelet-derived growth factor receptor β polypeptide, transforming growth factor-βR1, and Rho kinase), hepatic inflammation (CD68 and CD163), superoxide (dihydroethidium staining), and nitric oxide scavenging (protein nitrotyrosination). Prop, by decreasing PBF, further reduced PP. Similar findings were observed in common bile duct ligated-cirrhotic rats. Metformin administration reduces PP by decreasing the structural and functional components of the elevated hepatic resistance of cirrhosis. This effect is additive to that of Prop. The potential impact of this pharmacological combination, otherwise commonly used in patients with cirrhosis and diabetes, needs clinical evaluation.

scholarly journals Relationship between hemodynamic parameters and portal venous pressure in cirrhosis patients with portal hypertension

2020 ◽  
Vol 15 (1) ◽  
pp. 981-987
Author(s):  
Hongjuan Yao ◽  
Yongliang Wang
Keyword(s):  
Portal Hypertension ◽  
Liver Function ◽  
Portal Vein ◽  
Doppler Ultrasound ◽  
Venous Pressure ◽  
Splenic Vein ◽  
Portal Venous Pressure ◽  
Control Group ◽  
Hemodynamic Parameters ◽  
Vein Diameter

AbstractCirrhosis caused by viral and alcoholic hepatitis is an essential cause of portal hypertension (PHT). The incidence of PHT complication is directly proportional to portal venous pressure (PVP), and the clinical research of PVP and its hemodynamic indexes is of great significance for deciding the treatment strategy of PHT. Various techniques are currently being developed to decrease portal pressure but hemodynamic side effects may occur. In this article, the hemodynamic indexes of cirrhotic PHT patients were studied to explore the correlation between the index and PVP and to evaluate the clinical value of Doppler ultrasound in measuring PVP in patients with PHT. This was achieved by selecting 90 cirrhotic PHT patients who underwent transjugular intrahepatic portosystemic shunt in our hospital from June 2015 to September 2019. Fifty healthy people who had a physical examination in the hospital in the same period were selected as the control group. The liver hemodynamic parameters of two groups were measured by Doppler ultrasound, and the cirrhotic PHT patients were graded by the Child–Pugh grading method to evaluate the liver function and measure the PVP value. The results showed that both the central portal vein velocity (PVV) and splenic vein velocity (SVV) of the PHT group were lower than those of the control group. Also, the portal vein diameter (PVD), portal venous flow and splenic vein diameter (SVD) were higher than those of the control group (all Ps < 0.05). Among liver function graded PHT patients, the PVD, PVV, SVD and SVV were significantly different (all Ps < 0.05). Furthermore, the PVP of patients with liver function grades A, B and C was 38.9 ± 1.4, 40.6 ± 5.1 and 42.5 ± 4.8 cmH2O, respectively, with a significant difference. It can be concluded from this study that Doppler ultrasound can be used as a tool for clinical assessment of PHT in cirrhosis patients. Doppler ultrasound showed a good prospect in noninvasive detection of PHT in cirrhosis; however, this technique needs application on large sample population study to validate the results.

Healing gone wrong: convergence of hemostatic pathways and liver fibrosis?

2020 ◽  
Vol 134 (16) ◽  
pp. 2189-2201
Author(s):  
Jessica P.E. Davis ◽  
Stephen H. Caldwell
Keyword(s):  
Wound Healing ◽  
Liver Disease ◽  
Hepatic Fibrosis ◽  
Cell Activation ◽  
Stellate Cell ◽  
Factor Xa ◽  
Clinical Trial Data ◽  
Chronic Liver ◽  
Healing Response ◽  
Wound Healing Response

Abstract Fibrosis results from a disordered wound healing response within the liver with activated hepatic stellate cells laying down dense, collagen-rich extracellular matrix that eventually restricts liver hepatic synthetic function and causes increased sinusoidal resistance. The end result of progressive fibrosis, cirrhosis, is associated with significant morbidity and mortality as well as tremendous economic burden. Fibrosis can be conceptualized as an aberrant wound healing response analogous to a chronic ankle sprain that is driven by chronic liver injury commonly over decades. Two unique aspects of hepatic fibrosis – the chronic nature of insult required and the liver’s unique ability to regenerate – give an opportunity for pharmacologic intervention to stop or slow the pace of fibrosis in patients early in the course of their liver disease. Two potential biologic mechanisms link together hemostasis and fibrosis: focal parenchymal extinction and direct stellate cell activation by thrombin and Factor Xa. Available translational research further supports the role of thrombosis in fibrosis. In this review, we will summarize what is known about the convergence of hemostatic changes and hepatic fibrosis in chronic liver disease and present current preclinical and clinical data exploring the relationship between the two. We will also present clinical trial data that underscores the potential use of anticoagulant therapy as an antifibrotic factor in liver disease.

NCX-1000, an NO derivative of UDCA, refeases NO and protects against portal hypertension by inhibiting hepatic stellate cell contraction

2001 ◽  
Vol 120 (5) ◽  
pp. A379-A379
Author(s):  
S FIORUCCI ◽  
E ANTONELLI ◽  
O MORELLI ◽  
A MENCARELLI ◽  
B PALAZZETTI ◽  
...  
Keyword(s):  
Portal Hypertension ◽  
Hepatic Stellate Cell ◽  
Stellate Cell ◽  
Cell Contraction
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