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Arginase isoenzymes in human cirrhotic liver

100%
Chrzanowska A., Gajewska B., Barańczyk-Kuźma A.
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issue 3
465-469
EN
Cirrhosis leads to an inability of the liver to perform its biochemical functions. It can also lead to hepatocellular carcinoma in which, as we showed lately, arginase isoenzyme pattern changes. The present work presents our results on arginase isoenzymes and their possible role in liver cirrhosis. The study was performed on tissues obtained during liver transplantation from 60 patients with liver cirrhosis, and on samples of histologically normal liver (control) from 40 patients with benign or colorectal cancer liver metastases removed during surgery, 6-7 cm from the tumor border. Arginase isoenzymes AI (so-called liver-type arginase) and AII (called extrahepatic arginase) were identified by Western blotting and isolated by ion-exchange chromatography. Their expression on mRNA level was studied by RT-PCR. A significant decrease in arginase activity, dependent of the liver clinical stage, was observed in cirrhotic tissue. Arginase AI activity and its mRNA level were significantly decreased in cirrhotic liver, whereas the activity and expression of arginase AII were concurrently raised, as compared to normal liver. Since arginase AI is a key enzyme of the urea cycle, whereas arginase AII most probably takes part in the biosynthesis of ornithine and polyamines, the defective ammonia inactivation and increased collagen biosynthesis observed in cirrhotic liver may be related to the changes in arginase AI and AII levels, respectively.
2
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Sclerotherapy of esophageal varices in hemophilia patients with liver cirrhosis – a prospective, controlled clinical study

88%
Szczepanik A. B., Pielaciński K., Oses-Szczepanik A. M., Huszcza S., Misiak A., Dąbrowski W. P., Gajda S.
Polish Journal of Surgery
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2018
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vol. 90(1)
29-34
EN
Introduction: Bleeding from esophageal varices is a serious clinical condition in hemophilia patients due to congenital deficiency or lack of clotting factors VIII (in hemophilia A) and IX (in hemophilia B), decreased clotting factor II, VII, IX, X synthesis in the course of chronic liver disease and hipersplenic thrombocytopenia. The aim of this study was to assess the efficacy and safety of endoscopic sclerotherapy in acute esophageal variceal bleeding and in secondary prophylaxis of hemorrhage. The aim was also to investigate the optimal activity of deficiency factors VIII or IX and duration of replacement therapy required to ensure proper hemostasis after sclerotherapy procedures. Material and methods: 22 hemophilia patients (A-19, B-4) with coexistent liver cirrhosis and active esophageal variceal bleeding treated with endoscopic sclerotherapy were subjected to prospective analysis. The patients who survived were qualified to repeated sclerotherapy procedures every 3 weeks within secondary prophylaxis of bleeding (investigated group). A 3-day substitution therapy enhanced the infusion of the deficient or lacking factor in doses allowing to reach 80-100% of normal value activity of factor VIII on the 1st day and 60-80% in the next two days. The desired activity of factor IX was 60-80% and 40-60% respectively. The control group consisted of 20 non-hemophiliac patients with liver cirrhosis comparable in terms of age, sex, stage of advancement of liver cirrhosis, who underwent the same medical proceedings as the investigated group. Results: Active esophageal bleeding was stopped in 21 of 22 (95%) hemophilia patients. Complications were observed in 3 patients; 2 patients died. The rate of hemostasis, complications and deaths in the control group were comparable and no statistical differences were found. In hemophilia patients subjected to secondary prophylaxis of hemorrhage, in 18 of 20 (80%), complete eradication of esophageal varices was achieved after 4 to 7 sclerotherapy procedures in 1 patient (average 5.4). Recurrent bleeding was observed in 15% of patients, complication in 20%; 1 patient died. Time lapse from bleeding to eradication was 12-21 weeks (average 15.2). In the control group the rate of variceal eradication, complication and deaths was comparable and no statistical differences were found. The usage of factor VIII concentrates was as follows: in hemophilia A, in a severe form - 80.9 U/kg b.w./day, in hemophilia A in a severe form with an inhibitor <5 BU – 95.2 U/kg b.w./day, in mild form – 64.2 U/kg b.w./day and in severe hemophilia B – 91.6 U/kg b.w./day. Conclusions: Sclerotherapy is an effective method in the management of esophageal variceal bleeding in hemophilia patients. It is also effective for total eradication of varices when applied as a secondary prophylaxis of hemorrhage. In our opinion, a 3-day replacement therapy at the applied doses is sufficient to ensure hemostasis and avoid bleeding complications.
3
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Glutathione and GSH-dependent enzymes in patients with liver cirrhosis and hepatocellular carcinoma

75%
Czeczot H., Ścibior D., Skrzycki M., Podsiad M.
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2006
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vol. 53
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issue 1
237-242
EN
We investigated glutathione level, activities of selenium independent GSH peroxidase, selenium dependent GSH peroxidase, GSH S-transferase, GSH reductase and the rate of lipid peroxidation expressed as the level of malondialdehyde in liver tissues obtained from patients diagnosed with cirrhosis or hepatocellular carcinoma. GSH level was found to be lower in malignant tissues compared to adjacent normal tissues and it was higher in cancer than in cirrhotic tissue. Non-Se-GSH-Px activity was lower in cancer tissue compared with adjacent normal liver or cirrhotic tissue, while Se-GSH-Px activity in cancer was found to be similar to its activity in cirrhotic tissue and lower compared to control tissue. An increase in GST activity was observed in cirrhotic tissue compared with cancer tissue, whereas the GST activity in cancer was lower than in adjacent normal tissue. The activity of GSH-R was similar in cirrhotic and cancer tissues, but higher in cancer tissue compared to control liver tissue. An increased level of MDA was found in cancer tissue in comparison with control tissue, besides its level was higher in cancer tissue than in cirrhotic tissue. Our results show that the antioxidant system of cirrhosis and hepatocellular carcinoma is severely impaired. This is associated with changes of glutathione level and activities of GSH-dependent enzymes in liver tissue. GSH and enzymes cooperating with it are important factors in the process of liver diseases development.
4
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Ocena częstości występowania patologii w obrębie górnego odcinka przewodu pokarmowego u chorych ze zdekompensowaną marskością wątroby i żylakami przełyku

51%
Kowalski M. K., Cok A., Domżał-Magrowska D., Gąsiorowska A.
Annales Academiae Medicae Silesiensis
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2014
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vol. 68
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issue 1
16-22
EN
INTRODUCTION Esophageal varices are formed as a result of increased blood pressure in the portal vein. They usually develop as a result of liver cirrhosis. Liver cirrhosis may be accompanied by other endoscopic changes in the mucous mem-branes of the upper gastrointestinal tract e.g. portal gastropathy, gastric varices, as well as gastritis. AIM OF THE STUDY The aim of the paper is to evaluate the prevalence of other pathologies in upper gastrointestinal endoscopy in patients with esophageal varices and to assess the endoscopic features which indicate the risk of variceal bleeding. MATERIALS AND METHODS An analysis of 300 records of patients with endoscopic esophageal varices was conducted . Endoscopy was performed in the years 2006–2012 in the Department of Digestive Tract Diseases, Medical University of Lodz. OMED classification was used to evaluate the severity of esophageal varices. RESULTS In this research during endoscopy, esophageal varices in OMED stage I were found in 25.4% of cases, in stage II 39.3% of cases, stage III 27% of cases, and in OMED stage IV in 8.3% of cases. The mean age was 58 years (±12.6 SD), 43% of the study group were women. The most common upper GI pathology was gastritis (36.3%). Furthermore, portal gastropathy was found in 34% of cases, gastric varices in 14.3% of cases and gastric polips in 7.7% of cases. Gastric varices occurred more frequently in patients with esophageal varices in OMED stage IV (40%), than in the other groups (12%). In this group, gastric polyps were also more frequently observed than in the others (7.3%). The incidence of red spots on the mucosa of the esophagus was increased due to the severity of esophageal varices. Red spots are known to be a risk marker of bleeding. Furthermore, esophageal mucosal ulceration was observed in 4.3% of cases and oesophagitis in 1.3% of cases. CONCLUSIONS The analysis found that in patients with esophageal varices, other changes in upper gastrointestinal endoscopy were often accompanied. The most commonly reported pathologies were gastritis and portal gastropathy. The incidence of gastric fundus varices, gastric polyps or endoscopic signs of bleeding risk, was increased due to the severity of esophageal varices.
PL
WSTĘP Żylaki przełyku powstają w wyniku wzrostu ciśnienia w układzie wrotnym. Do ich rozwoju dochodzi głównie w przebiegu marskości wątroby, której mogą towarzyszyć także inne zmiany endoskopowe w obrębie błony śluzowej górnego odcinka przewodu pokarmowego (GOPP), takie m.in. jak: gastropatia wrotna, żylaki dna żołądka, zapalenie błony śluzowej żołądka. CEL PRACY Celem pracy jest ocena częstości współwystępowania innych patologii w endoskopii GOPP u chorych z żylakami przełyku, a także ocena cech endoskopowych żylaków wskazujących na ryzyko krwawienia. MATERIAŁY I METODY Dokonano analizy 300 opisów badań endoskopowych pacjentów z żylakami przełyku. Badania przeprowadzono w latach 2006–2012 w Klinice Chorób Przewodu Pokarmowego UM w Łodzi. Do oceny stopnia zaawansowania żylaków przełyku wykorzystano klasyfikację OMED. WYNIKI W przeprowadzonych badaniach endoskopowych żylaki w stopniu I według OMED stwierdzono w 25,4% przypadków, w stopniu II w 39,3%, w stopniu III w 27%, zaś w stopniu IV w 8,3%. Średni wiek badanych wynosił 58 lat (±12,6 SD), 43% grupy badanej stanowiły kobiety. Najczęstszą współwystępującą patologią GOPP było zapalenie błony śluzowej żołądka (36,3%). Ponadto stwierdzono gastropatię wrotną (34% przypadków), żylaki dna żołądka (14,3%) i polipy żołądka (7,7%). Żylaki dna żołądka współwystępowały najczęściej u pacjentów z żylakami przełyku w stopniu IV OMED (n = 40%), istotnie częściej niż w pozostałych grupach (n = 12%). W grupie tej obserwowano również częstsze niż u pozostałych (7,3%) występowanie polipów żołądka (12%). Wraz ze wzrostem zaawansowania żylaków przełyku według skali OMED obserwowano częstsze występowanie ciemnosinych znamion na błonie śluzowej przełyku, czyli endoskopowych markerów ryzyka krwawienia. Ponadto w obrębie błony śluzowej przełyku obserwowano owrzodzenia (4,3%) oraz zapalenie błony śluzowej przełyku (1,3%). WNIOSKI Przeprowadzona analiza wykazała częste współistnienie zmian endoskopowych GOPP u pacjentów z rozpoznanymi żylakami przełyku, najczęściej były to zapalenie błony śluzowej żołądka oraz gastropatia wrotna. Wzrostowi stopnia zaawansowania żylaków przełyku towarzyszyło częstsze występowanie żylaków dna żołądka, polipów żołądka i endoskopowych objawów ryzyka krwawienia.
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