Liver Disease in Cystic Fibrosis
Gianfranco Alpini, Domenico Alvaro, Marco Marzioni, Gene LeSage, Nicholas LaRusso in The Pathophysiology of Biliary Epithelia, 2020
In our cohort of patients, treated with UDCA since 1988, liver disease showed a relatively slow progression and its impact on growth and nutrition was negligible. Cirrhosis was already present in 5 patients at the time of diagnosis of liver disease and developed in other 12 patients during follow-up. Although most patients developed portal hypertension, only a minority developed clinically relevant events related to liver disease. During more than eight years from diagnosis of liver disease, incidence of major complications of cirrhosis (oesophageal varices, gastrointestinal bleeding, ascites) was 0.4 cases per 100 cirrhotic patient-years (95% CI: 0 to 2.0). Hepatic synthetic function was sufficiently maintained in the majority of cirrhotic patients, and only one liver transplantation was required.
Hyperfibrinolysis in Liver Cirrhosis
Pia Glas-Greenwalt in Fibrinolysis in Disease Molecular and Hemovascular Aspects of Fibrinolysis, 2019
Cirrhosis is the most common chronic disease of the liver. It is defined as a diffuse process characterized by fibrosis and a conversion of normal architecture into structurally abnormal nodules. In most patients cirrhosis is caused by chronic active viral hepatitis or long-standing alcohol abuse. Other causes or diseases are, among others, primary biliary cirrhosis, pigment cirrhosis (hemochromatosis), cirrhosis associated with Wilson’s disease, autoimmune hepatitis, α1-antitrypsin deficiency, or sclerosing cholangitis. In many patients, no cause for the cirrhosis can be found (cryptogenic cirrhosis). Cirrhosis of the liver results in a reduced protein synthesis, caused by a decrease in the number as well as the function of the hepatocytes. A reduced dietary intake of amino acids may contribute to deficient protein synthesis. As a result of nodular regeneration and of the abnormal architecture of the liver, the vascular resistance in the sinusoidal bed of the liver increases. This causes a rise of the portal venous pressure (portal hypertension). Collateral vessels increase in size, which results in portal systemic shunting. Portal hypertension is usually associated with reduced hepatic clearance of substances that are normally rapidly cleared by a healthy liver.
Genome-Based Personalized Medicine in Liver Cancer
II-Jin Kim in Cancer Genetics and Genomics for Personalized Medicine, 2017
Another characteristic of patients with liver cancer (HCC) is liver cirrhosis. It is a terminal stage of advanced fibrosis from chronic hepatitis and a potent precancerous state. About 80–90% of patients also have liver cirrhosis.6 The patients suffer from decreased liver function and portal hypertension. Jaundice, encephalopathy, decreased serum albumin, deterioration of blood coagulation system, and various metabolic changes are common complications arising from decreased liver function. Portal hypertension provokes ascites, peripheral edema, and gastroesophageal varices (protruding tortuous veins). Therefore, the coexistence of liver cancer and cirrhosis complicates the prognostic prediction and therapeutic strategies.7 Even in the early stage, curative treatment could be impossible because of underlying liver cirrhosis. Liver transplantation is only an option for the patient. For advanced liver cancer, unpredicted toxicity has been a major hurdle in many clinical trials of new multikinase inhibitors in patients with liver cirrhosis.8
Decompensation as initial presentation in patients with liver cirrhosis is associated with an increased risk of future decompensation and mortality
Published in Scandinavian Journal of Gastroenterology, 2023
Koos de Wit, Thijs Kuipers, Koen Van der Ploeg, Lubbertus C. Baak, Ulrich Beuers, R. Bart Takkenberg
Liver cirrhosis is a pathophysiologic entity resulting from chronic liver injury. The development of cirrhosis is characterized by chronic inflammation leading to fibrosis in the liver [1]. As fibrosis progresses, increased structural and functional hepatic vascular resistance is observed. As a result, cirrhosis is associated with impaired liver function and hyperdynamic circulation and splanchnic vasodilation. Subsequently increased inflow in the portal vein leads to portal hypertension. Furthermore, the risk of development of hepatocellular carcinoma (HCC) is increased [2]. Chronic alcohol misuse and chronic hepatitis C (CHC) are still the main underlying causes of liver cirrhosis in developed countries [2]. But due to effective therapeutic options in CHC on the one hand and the obesity epidemic on the other hand, the incidence of cirrhosis due to non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH) is rising alarmingly [3].
Real world for management of hepatocellular carcinoma: a large population-based study
Published in Scandinavian Journal of Gastroenterology, 2023
Supatsri Sethasine, Nitipon Simasingha, Sarita Ratana-Amornpin, Varocha Mahachai
The presence of portal hypertension is an additional crucial criterion for assessing therapeutic options. Patients in the curative-stage of HCC with signs of portal hypertension were more likely to undergo RFA than LR (52.1% vs. 28.0%, p = .001). Copayment was requested for the RFA needles according to the hospital protocol. Cost had a significant impact on the treatment decisions for individual patients. Consequently, 27.6% of patients with very early and early-stage HCC received TACE as initial therapy. After receiving curative treatment, CT scans were administered every three months for the first year and every four to six months thereafter. As shown in Table 3, 71 patients who previously underwent RFA had recurrent HCC and subsequently received alternative treatment modalities. The majority of RFA patients received one to two bouts of therapy, whereas TACE patients received an average of two sequential cycles of chemoembolization.
Oxidative stress and histopathological changes in several organs of mice injected with biogenic silver nanoparticles
Published in Artificial Cells, Nanomedicine, and Biotechnology, 2022
Shushanik Kazaryan, Lilit Farsiyan, Juleta Tumoyan, Gayane Kirakosyan, Naira Ayvazyan, Hrachik Gasparyan, Sona Buloyan, Lilit Arshakyan, Ara Kirakosyan, Ashkhen Hovhannisyan
A different morphological picture was observed in the liver with extract stabilized AgNPs. Examination revealed that AgNPs induced acute venous congestion with hyperaemia of portal veins, and dilation of sinusoids compared to the control group. The observed pathological alterations confirm the development of severe portal hypertension. In addition, there is periportal infiltration of lymphocytes in some triads. These phenomena indicate the toxic effect of nanoparticles, which causes inflammatory processes in the liver tissue. Along with inflammation, few foci of metastases were observed in some areas around the portal triads and central veins. The process of focal necrosis of hepatocytes was clearly observed (Figure 10). Statistical analysis of the liver tissue in this group indicated that only the parameter of inflammation in portal tracts was significantly higher compared with the control group (p < .05), while other parameters were not significantly different.
Related Knowledge Centers
- Ascites
- Cirrhosis
- Hematemesis
- Splenomegaly
- Peritoneal Cavity
- Liver
- Portal Venous Pressure
- Portal Vein
- Anorectal Varices
- Thrombocytopenia