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acute liver failure (alf)
Acute liver failure (ALF) is an uncommon disorder that leads to jaundice, coagulopathy, and multisystem organ failure.
      
Of these patients, 45 had acute liver failure (ALF), 31 had acute decompensation of chronic liver disease, eight had graft failure and four had miscellaneous conditions.
      
Acute liver failure (ALF) is a rare condition in the pediatric population.
      
Variations in the natural history and clinical features of acute liver failure (ALF) have led to a number of different classifications and subgroupings.
      
The aim of our study is to report upon the presentation of two patients with life-threatening acute liver failure (ALF) due to amoxicillin and amoxicillin/clavulanate.
      
Evidence from both clinical and experimental studies demonstrates that mild hypothermia prevents encephalopathy and brain edema in acute liver failure (ALF).
      
Glutamatergic dysfunction has been suggested to play an important role in the pathogenesis of hepatic encephalopathy (HE) in acute liver failure (ALF).
      
A growing body of evidence suggests that alterations in N-methyl-D-asparate NMDA-mediated excitatory neurotransmission may be involved in the pathophysiology of hepatic encephalopathy (HE) in acute liver failure (ALF).
      
Increased intracranial pressure in patients with acute liver failure (ALF) remains a major immediate cause of mortality.
      
Data in support of its use in acute liver failure (ALF) is still scant and difficult to assess.
      
The availability of adequate experimental models of acute liver failure (ALF) is of prime importance to provide a better understanding of this condition and allow the development and testing of new therapeutic approaches for patients with ALF.
      
It is generally accepted that astrocyte swelling forms the major anatomic substrate of the edema associated with acute liver failure (ALF) and that ammonia represents a major etiological factor in its causation.
      
 

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