Effects of liver failure on inter-organ trafficking of ammonia: implications for the treatment of hepatic encephalopathy

2004 ◽  
Vol 19 (s7) ◽  
pp. S219-S223 ◽  
Author(s):  
NICOLAS CHATAURET ◽  
ROGER F BUTTERWORTH
Author(s):  
Shaima’a Dakhel AbdulHassa

Gairdia lamblia is one of parasites that cause intestinal problems within the human body, particularly private travelers and children. In this study a total of (100) diarrheal patients, 20 patients with Giardiasis were identified by fecal antigen. 9 out of 20(20%) of them were infected by fecal antigen, while 9(9%) of them were infected by using the screening general stool examination (GSE). The stool samples were collected from patient how vested the Medical City/ Baghdad and Tikrit teaching Hospital during the period from 1 st may 2018 to 1 February 2019. The results revealing a significant difference (p andlt; 0.05) between the two methods of detection for G. lamblia (Fecal antigen method and GSE). IT has been shown that out of 20 infected individuals 12(12%) were males and 8(8%) were females, indicating regarding no significant deference in the distribution of Giardiasis among genders. In regard the age, our results showed that highest infection rate 8(3.2%) was recorded in the age group (10-19) years, followed by the age group (20-2) years which was 692.4%). In this study five mutations were recorded at position (926, 1094, 1202and 1304), by using tpiA gene sequence method, and tpiB gene was on point mutation change (G254A), in the position (85) of triose phosphate isomease.


2017 ◽  
Vol 66 (1) ◽  
pp. S559
Author(s):  
M. Sheikh ◽  
N. Arias ◽  
K. Thomsen ◽  
R. Gallego-Durán ◽  
B. Agarwal ◽  
...  

Blood ◽  
2003 ◽  
Vol 102 (4) ◽  
pp. 1525-1528 ◽  
Author(s):  
Brian J. Ruscito ◽  
Neil L. Harrison

Abstract Liver failure is often accompanied by cognitive impairment and coma, a syndrome known as hepatic encephalopathy (HE). The administration of flumazenil, a benzodiazepine (BZ) antagonist, is effective in reversing the symptoms of HE in many patients. These clinical observations gave rise to notions of an endogenous BZ-like mechanism in HE, but to date no viable candidate compounds have been characterized. We show here that the hemoglobin (Hb) metabolites hemin and protoporphyrin IX (PPIX) interact with the BZ site on the γ-aminobutyric acid (GABAA) receptor and enhance inhibitory synaptic transmission in a manner similar to diazepam and zolpidem. This finding suggests that hemin and PPIX are neuroactive porphyrins capable of acting as endogenous ligands for the central BZ site. The accumulation of these porphyrins under pathophysiologic conditions provides a potentially novel mechanism for the central manifestations of HE.


Hepatology ◽  
1990 ◽  
Vol 12 (4) ◽  
pp. 695-700 ◽  
Author(s):  
Cihan Yurdaydin ◽  
Heide Hörtnagl ◽  
Petra Steindl ◽  
Christof Zimmermann ◽  
Christian Pifl ◽  
...  

1995 ◽  
Vol 21 (3) ◽  
pp. 253-256 ◽  
Author(s):  
D. Devictor ◽  
C. Tahiri ◽  
C. Lanchier ◽  
Y. Navelet ◽  
P. Durand ◽  
...  

2020 ◽  
pp. 3089-3100
Author(s):  
Jane Macnaughtan ◽  
Rajiv Jalan

Liver failure occurs when loss of hepatic parenchymal function exceeds the capacity of hepatocytes to regenerate or repair liver injury. Acute liver failure is characterized by jaundice and prolongation of the prothrombin time in the context of recent acute liver injury, with hepatic encephalopathy occurring within 8 weeks of the first onset of liver disease. Acute-on-chronic liver failure is characterized by hepatic and/or extrahepatic organ failure in patients with cirrhosis associated with an identified or unidentified precipitating event. The commonest causes of acute liver failure are acute viral hepatitis and drugs. Acute-on-chronic liver failure is most commonly precipitated by infection, alcohol abuse, and superimposed viral infection. The main clinical manifestations are hepatic encephalopathy, coagulopathy, jaundice, renal dysfunction, and haemodynamic instability. Infection and systemic inflammation contribute to pathogenesis and critically contribute to prognosis. Specific therapy for the underlying liver disease is administered when available, but this is not possible for most causes of liver failure. Treatment is predominantly supportive, with particular emphasis on (1) correction or removal of precipitating factors; (2) if encephalopathy is present, using phosphate enemata, nonhydrolysed disaccharide laxatives, and/or rifaximin; (3) early detection and prompt treatment of complications such as hypoglycaemia, hypokalaemia, cerebral oedema, infection, and bleeding. The onset of organ failure should prompt discussion with a liver transplantation centre. The mortality of acute liver failure (without liver transplantation) is about 40%. Patients with acute liver failure who do not develop encephalopathy can be expected to recover completely. Those who recover from an episode of acute-on-chronic liver failure should be considered for liver transplantation because otherwise their subsequent mortality remains high.


2011 ◽  
Vol 10 ◽  
pp. S70-S76 ◽  
Author(s):  
Ramón A. Kobashi-Margáin ◽  
Juan G. Gavilanes-Espinar ◽  
Ylse Gutiérrez-Grabe ◽  
Ángel A. Gutiérrez-Jiménez ◽  
Norberto Chávez-Tapia ◽  
...  

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