Hepatic encephalopathy is associated with decreased cerebral oxygen metabolism and blood flow, not increased ammonia uptake

Gitte Dam; Susanne Keiding; Ole Lajord Munk; Peter Ott; Hendrik Vilstrup; Lasse Kristoffer Bak; Helle S Waagepetersen; Arne Schousboe; Michael Sørensen

doi:10.1002/hep.25995

Hepatic encephalopathy is associated with decreased cerebral oxygen metabolism and blood flow, not increased ammonia uptake

Gitte Dam, Susanne Keiding, Ole Lajord Munk, Peter Ott, Hendrik Vilstrup, Lasse Kristoffer Bak, Helle S Waagepetersen, Arne Schousboe, Michael Sørensen

47 Citations (Scopus)

Abstract

Studies have shown decreased cerebral oxygen metabolism (CMRO₂) 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. CMRO₂, 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 CMRO₂ 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, CMRO₂ 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). Conclusion: The low values of CMRO₂ 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 CMRO₂ and CBF could not be linked to blood ammonia concentration or CMRA. (HEPATOLOGY 2013)

Original language	English
Journal	Hepatology
Volume	57
Issue number	1
Pages (from-to)	258-65
Number of pages	8
ISSN	0270-9139
DOIs	https://doi.org/10.1002/hep.25995
Publication status	Published - Jan 2013

Keywords

Adult
Aged
Ammonia
Blood-Brain Barrier
Cerebrovascular Circulation
Cerebrum
Female
Hepatic Encephalopathy
Humans
Male
Middle Aged
Oxygen
Positron-Emission Tomography and Computed Tomography

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10.1002/hep.25995

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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 (CMRO2) 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. CMRO2, 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 CMRO2 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, CMRO2 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). Conclusion: The low values of CMRO2 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 CMRO2 and CBF could not be linked to blood ammonia concentration or CMRA. (HEPATOLOGY 2013)",

keywords = "Adult, Aged, Ammonia, Blood-Brain Barrier, Cerebrovascular Circulation, Cerebrum, Female, Hepatic Encephalopathy, Humans, Male, Middle Aged, Oxygen, Positron-Emission Tomography and Computed Tomography",

author = "Gitte Dam and Susanne Keiding and Munk, {Ole Lajord} and Peter Ott and Hendrik Vilstrup and Bak, {Lasse Kristoffer} and Waagepetersen, {Helle S} and Arne Schousboe and Michael S{\o}rensen",

note = "Copyright {\textcopyright} 2012 American Association for the Study of Liver Diseases.",

year = "2013",

month = jan,

doi = "10.1002/hep.25995",

language = "English",

volume = "57",

pages = "258--65",

journal = "Hepatology",

issn = "0270-9139",

publisher = "JohnWiley & Sons, Inc.",

number = "1",

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TY - JOUR

T1 - Hepatic encephalopathy is associated with decreased cerebral oxygen metabolism and blood flow, not increased ammonia uptake

AU - Dam, Gitte

AU - Keiding, Susanne

AU - Munk, Ole Lajord

AU - Ott, Peter

AU - Vilstrup, Hendrik

AU - Bak, Lasse Kristoffer

AU - Waagepetersen, Helle S

AU - Schousboe, Arne

AU - Sørensen, Michael

PY - 2013/1

Y1 - 2013/1

N2 - Studies have shown decreased cerebral oxygen metabolism (CMRO2) 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. CMRO2, 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 CMRO2 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, CMRO2 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). Conclusion: The low values of CMRO2 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 CMRO2 and CBF could not be linked to blood ammonia concentration or CMRA. (HEPATOLOGY 2013)

AB - Studies have shown decreased cerebral oxygen metabolism (CMRO2) 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. CMRO2, 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 CMRO2 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, CMRO2 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). Conclusion: The low values of CMRO2 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 CMRO2 and CBF could not be linked to blood ammonia concentration or CMRA. (HEPATOLOGY 2013)

KW - Adult

KW - Aged

KW - Ammonia

KW - Blood-Brain Barrier

KW - Cerebrovascular Circulation

KW - Cerebrum

KW - Female

KW - Hepatic Encephalopathy

KW - Humans

KW - Male

KW - Middle Aged

KW - Oxygen

KW - Positron-Emission Tomography and Computed Tomography

U2 - 10.1002/hep.25995

DO - 10.1002/hep.25995

M3 - Journal article

C2 - 22886493

SN - 0270-9139

VL - 57

SP - 258

EP - 265

JO - Hepatology

JF - Hepatology

IS - 1

ER -

Hepatic encephalopathy is associated with decreased cerebral oxygen metabolism and blood flow, not increased ammonia uptake

Abstract

Keywords

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