title: Hepatic encephalopathy is associated with decreased cerebral oxygen metabolism and blood flow, not increased ammonia uptake.
abstract: Studies have shown decreased cerebral oxygen metabolism (CMRO(2)) and blood flow (CBF) in patients with cirrhosis with hepatic encephalopathy (HE). It remains unclear, however, whether these disturbances are associated with HE or with cirrhosis itself and how they may relate to arterial blood ammonia concentration and cerebral metabolic rate of blood ammonia (CMRA). We addressed these questions in a paired study design by investigating patients with cirrhosis during and after recovery from an acute episode of HE type C. CMRO(2), CBF, and CMRA were measured by dynamic positron emission tomography (PET)/computed tomography (CT). Ten patients with cirrhosis were studied during an acute episode of HE; nine were reexamined after recovery. Nine patients with cirrhosis with no history of HE served as controls. Mean CMRO(2) increased from 0.73 μmol oxygen/mL brain tissue/min during HE to 0.91 μmol oxygen/mL brain tissue/min after recovery (paired t test; P < 0.05). Mean CBF increased from 0.28 mL blood/mL brain tissue/min during HE to 0.38 mL blood/mL brain tissue/min after recovery (P < 0.05). After recovery from HE, CMRO(2) and CBF were not significantly different from values in the control patients. Arterial blood ammonia concentration decreased 20% after recovery (P < 0.05) and CMRA was unchanged (P > 0.30); both values were higher than in the control patients (both P < 0.05).
  
  
  CONCLUSIONS
  The low values of CMRO(2) and CBF observed during HE increased after recovery from HE and were thus associated with HE rather than the liver disease as such. The changes in CMRO(2) and CBF could not be linked to blood ammonia concentration or CMRA.
authors.affiliation: PET Centre & Department of Nuclear Medicine, Aarhus University Hospital, Aarhus, Denmark. dam@pet.auh.dk
authors.forename: Gitte
authors.initials: G
authors.lastname: Dam
authors.forename: Susanne
authors.initials: S
authors.lastname: Keiding
authors.forename: Ole L
authors.initials: OL
authors.lastname: Munk
authors.forename: Peter
authors.initials: P
authors.lastname: Ott
authors.forename: Hendrik
authors.initials: H
authors.lastname: Vilstrup
authors.forename: Lasse K
authors.initials: LK
authors.lastname: Bak
authors.forename: Helle S
authors.initials: HS
authors.lastname: Waagepetersen
authors.forename: Arne
authors.initials: A
authors.lastname: Schousboe
authors.forename: Michael
authors.initials: M
authors.lastname: Sørensen
mesh_terms: D000328:Adult; D000368:Aged; D000641:Ammonia / Q000378:metabolism*; D001812:Blood-Brain Barrier / Q000503:physiopathology; D002560:Cerebrovascular Circulation; D054022:Cerebrum / Q000098:blood supply / Q000378:metabolism*; D005260:Female; D006501:Hepatic Encephalopathy / Q000000981:diagnostic imaging / Q000503:physiopathology*; D006801:Humans; D008297:Male; D008875:Middle Aged; D064847:Multimodal Imaging; D010100:Oxygen / Q000378:metabolism*; D049268:Positron-Emission Tomography; D014057:Tomography, X-Ray Computed
chemical_list: D000641:Ammonia; D010100:Oxygen