CORRESPONDENCE 1291 a predictor of subsequent response to interferon-a therapy in Japthe study of Nossbaum et al. 3 ), type 1b HCV was found anese patients with chronic hepatitis C. J Med Virol 1994;44:410more frequently in older patients and was more likely 414. to be associated with acquisition vi
Proton spectroscopy of brain glutamine in acute liver failure
β Scribed by Associate Professor James R. McConnell; Dean L. Antonson; Chin Siong Ong; Wei-Kom Chu; Ira J. Fox; Thomas G. Heffron; Alan N. Langnas; Byers W. Shaw Jr.
- Publisher
- John Wiley and Sons
- Year
- 1995
- Tongue
- English
- Weight
- 571 KB
- Volume
- 22
- Category
- Article
- ISSN
- 0270-9139
No coin nor oath required. For personal study only.
β¦ Synopsis
Evidence indicates that the accumulation of glutamine in the brain plays an important role in the pathogenesis and severity of the encephalopathy of acute liver failure (ALF). This study uses in uiuo proton magnetic resonance spectroscopy ('H MRS) to assess brain glutamine (GLN) in five cases of acute liver failure. The findings are consistent with prior investigations and suggest that the alpha 'H of the GLN molecule can be used for noninvasive spectroscopic quantitation of brain GLN in patients with ALF. (HEPATOLOGY 1995;22:69-74.)
The neurologic manifestations of encephalopathy in patients with acute liver failure (ALF) can progress from mild confusion to stupor and coma. Death may result from brain edema in ALF.l,' The pathogenesis of the progressive encephalopathy and brain edema is unknown, but evidence suggests that increased brain glutamine (GLN) plays an important role.
An in viuo microdialysis study of the brain found significantly increased GLN in the cerebral cortex and in the extracellular fluid of the brain in experimental ALF.3 Research models of ALF have demonstrated that increased brain GLN is also associated with the development of brain edema.*-' Inhibition of glutamine synthetase, an enzyme in astrocytes that converts ammonia and glutamate (GLU) to GLN, can prevent the development of brain edema in experimental ALF. '-16 Investigators in 1955 demonstrated that GLN concentration was elevated in the cerebrospinal fluid of patients in hepatic coma, and later clinical studies have suggested that increased concentration of cerebrospinal fluid GLN correlates with the severity of hepatic encephalopathy (HE).l7-l'
In vivo proton magnetic resonance spectroscopy ('H
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Mortality of fulminant hepatic failure with standard supportive therapy is high (80 to 85%), but unfortunately most patients present to hospital already in Grade IV encephalopathy with severe liver dysfunction, and many have secondary organ damage. If seen earlier, during Grade III encephalopathy, r