Laparoscopic Treatment of a Giant Nonparasitic Cyst in Cirrhotic Liver

Videoscopy ◽  
2011 ◽  
Vol 21 (1) ◽  
Author(s):  
Lucio Taglietti ◽  
Luca Balestra ◽  
Nereo Vettoretto ◽  
Cristina Guadrini ◽  
Murad Odeh ◽  
...  
Keyword(s):  
Cirrhotic Liver ◽  
Laparoscopic Treatment ◽  
Nonparasitic Cyst

Emergency laparoscopic treatment of complicated parastomal hernias

2020 ◽  
Vol 75 (5) ◽  
Author(s):  
Nero Vettoretto ◽  
Michela Caprioli ◽  
Emanuele Botteri
Keyword(s):  
Laparoscopic Treatment

Laparoscopic treatment of pelvic inflammatory disease and infertility implications

2019 ◽  
Vol 2 (67) ◽  
pp. 57
Author(s):  
Anca Lesnic ◽  
Romina-Marina Sima ◽  
Cristina Moisei ◽  
Cristian Balalau ◽  
Liana Pleș
Keyword(s):  
Pelvic Inflammatory Disease ◽  
Inflammatory Disease ◽  
Laparoscopic Treatment

Novel approaches to assessing renal function in cirrhotic liver disease

2007 ◽  
Vol 37 (9) ◽  
pp. 667-672 ◽  
Author(s):  
Andrew J. Portal ◽  
Mark Austin ◽  
Michael A. Heneghan
Keyword(s):  
Renal Function ◽  
Liver Disease ◽  
Cirrhotic Liver ◽  
Novel Approaches

scholarly journals Laparoscopic treatment for celiac artery stenosis caused by median arcuate ligament compression with Adachi V type vascular anomaly: a case report

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Hiroshi Saito ◽  
Koichiro Sawada ◽  
Jyunichi Ogawa ◽  
Masashi Hashimoto ◽  
Masahiro Oshima ◽  
...  
Keyword(s):  
Epigastric Pain ◽  
Vascular Anomaly ◽  
Celiac Artery ◽  
Artery Stenosis ◽  
Laparoscopic Treatment ◽  
Median Arcuate Ligament ◽  
Case Presentation ◽  
Arcuate Ligament ◽  
Major Vascular Injury

Abstract Background Median arcuate ligament syndrome (MALS), which results from compression of the median arcuate ligament (MAL), is a rare cause of abdominal pain and weight loss. Treatment is dissection of the MAL; however, the laparoscopic procedure is not yet established and it involves the risk of major vascular injury, especially in cases with an anomaly. Case presentation A 47-year-old man was evaluated at the hospital for epigastric pain. Contrast computed tomography scan revealed stenosis of the celiac artery origin due to the MAL. An Adachi V type vascular anomaly was also observed. Laparoscopic treatment was performed to release pressure on the celiac artery. Laparoscopic ultrasonography was used to less invasively confirm the release of the MAL. Despite a concomitant Adachi V type vascular anomaly, surgery was safely performed using the laparoscopic magnification view and intraoperative ultrasonography. Follow-up ultrasonography confirmed the celiac artery stenosis has not recurred. Conclusions A rare case of MALS with an Adachi V type vascular anomaly is presented and the laparoscopic treatment is detailed.

scholarly journals Serum Amyloid Beta42 Is Not Eliminated by the Cirrhotic Liver: A Pilot Study

2021 ◽  
Vol 10 (12) ◽  
pp. 2669
Author(s):  
Reiner Wiest ◽  
Thomas S. Weiss ◽  
Lusine Danielyan ◽  
Christa Buechler
Keyword(s):  
Liver Cirrhosis ◽  
Hepatic Clearance ◽  
Protective Role ◽  
Tissue Growth ◽  
Cirrhotic Liver ◽  
Diabetic Patients ◽  
Peripheral Clearance ◽  
End Stage ◽  
The Brain

Amyloid-beta (Aβ) deposition in the brain is the main pathological hallmark of Alzheimer disease. Peripheral clearance of Aβ may possibly also lower brain levels. Recent evidence suggested that hepatic clearance of Aβ42 is impaired in liver cirrhosis. To further test this hypothesis, serum Aβ42 was measured by ELISA in portal venous serum (PVS), systemic venous serum (SVS), and hepatic venous serum (HVS) of 20 patients with liver cirrhosis. Mean Aβ42 level was 24.7 ± 20.4 pg/mL in PVS, 21.2 ± 16.7 pg/mL in HVS, and 19.2 ± 11.7 pg/mL in SVS. Similar levels in the three blood compartments suggested that the cirrhotic liver does not clear Aβ42. Aβ42 was neither associated with the model of end-stage liver disease score nor the Child–Pugh score. Patients with abnormal creatinine or bilirubin levels or prolonged prothrombin time did not display higher Aβ42 levels. Patients with massive ascites and patients with large varices had serum Aβ42 levels similar to patients without these complications. Serum Aβ42 was negatively associated with connective tissue growth factor levels (r = −0.580, p = 0.007) and a protective role of Aβ42 in fibrogenesis was already described. Diabetic patients with liver cirrhosis had higher Aβ42 levels (p = 0.069 for PVS, p = 0.047 for HVS and p = 0.181 for SVS), which is in accordance with previous reports. Present analysis showed that the cirrhotic liver does not eliminate Aβ42. Further studies are needed to explore the association of liver cirrhosis, Aβ42 levels, and cognitive dysfunction.

scholarly journals Postprandial Glycogen Content Is Increased in the Hepatocytes of Human and Rat Cirrhotic Liver

Cells ◽  
2021 ◽  
Vol 10 (5) ◽  
pp. 976
Author(s):  
Natalia N. Bezborodkina ◽  
Sergey V. Okovityi ◽  
Boris N. Kudryavtsev
Keyword(s):  
Rat Liver ◽  
Liver Tissue ◽  
Glycogen Content ◽  
Glycogen Synthase ◽  
Fibrous Tissue ◽  
Glycogen Metabolism ◽  
Liver Parenchyma ◽  
Dry Mass ◽  
Cirrhotic Liver ◽  
Liver Biopsies

Chronic hepatitises of various etiologies are widespread liver diseases in humans. Their final stage, liver cirrhosis (LC), is considered to be one of the main causes of hepatocellular carcinoma (HCC). About 80–90% of all HCC cases develop in LC patients, which suggests that cirrhotic conditions play a crucial role in the process of hepatocarcinogenesis. Carbohydrate metabolism in LC undergoes profound disturbances characterized by altered glycogen metabolism. Unfortunately, data on the glycogen content in LC are few and contradictory. In this study, the material was obtained from liver biopsies of patients with LC of viral and alcohol etiology and from the liver tissue of rats with CCl4-induced LC. The activity of glycogen phosphorylase (GP), glycogen synthase (GS), and glucose-6-phosphatase (G6Pase) was investigated in human and rat liver tissue by biochemical methods. Total glycogen and its labile and stable fractions were measured in isolated individual hepatocytes, using the cytofluorometry technique of PAS reaction in situ. The development of LC in human and rat liver was accompanied by an increase in fibrous tissue (20- and 8.8-fold), an increase in the dry mass of hepatocytes (by 25.6% and 23.7%), and a decrease in the number of hepatocytes (by 50% and 28%), respectively. The rearrangement of the liver parenchyma was combined with changes in glycogen metabolism. The present study showed a significant increase in the glycogen content in the hepatocytes of the human and the rat cirrhotic liver, by 255% and 210%, respectively. An increased glycogen content in cells of the cirrhotic liver can be explained by a decrease in glycogenolysis due to a decreased activity of G6Pase and GP.

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