Role of determination of partial pressure of ammonia in cirrhotic patients with and without hepatic encephalopathy

Nicolao, F.; Efrati, C.; Masini, Andrea; Merli, Manuela; Attili, Adolfo Francesco; Riggio, Oliviero

doi:10.1016/s0168-8278(02)00436-1

Cited by 128 publications

(103 citation statements)

References 19 publications

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“…This suggests a direct link between hyperammonemia, brain ammonia and ICP (possibly brain edema). In CLD, HE patients often present elevated arterial ammonia concentrations; however, in contrast with ALF, the correlation between ammonia and severity of HE remains controversial , Kundra et al, 2005, Nicolao et al, 2003, Ong et al, 2003and Weissenborn et al, 2007. This infers other factors may be implicated in the pathogenesis of HE.…”

Section: Ammoniamentioning

confidence: 99%

Brain edema in acute liver failure and chronic liver disease: Similarities and differences

Bosoi

Rose

2013

Neurochemistry International

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Hepatic encephalopathy (HE) is a complex neuropsychiatric syndrome that typically develops as a result of acute liver failure or chronic liver disease. Brain edema is a common feature associated with HE. In acute liver failure, brain edema contributes to an increase in intracranial pressure, which can fatally lead to brain stem herniation. In chronic liver disease, intracranial hypertension is rarely observed, even though brain edema may be present. This discrepancy in the development of intracranial hypertension in acute liver failure versus chronic liver disease suggests that brain edema plays a different role in relation to the onset of HE. Furthermore, the pathophysiological mechanisms involved in the development of brain edema in acute liver failure and chronic liver disease are dissimilar. This review explores the types of brain edema, the cells, and pathogenic factors involved in its development, while emphasizing the differences in acute liver failure versus chronic liver disease. The implications of brain edema developing as a neuropathological consequence of HE, or as a cause of HE, are also discussed. HighlightsBrain edema is a common feature in ALF and CLD. HE is inconsistently associated with the presence of brain edema. Fibrous and protoplasmic astrocytes are differentially implicated in the pathogenesis of HE. The pathogenesis of HE is multifactorial causing an array of neurological symptoms.

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Section: Ammoniamentioning

confidence: 99%

Brain edema in acute liver failure and chronic liver disease: Similarities and differences

Bosoi

Rose

2013

Neurochemistry International

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“…Recent studies explained the role of blood ammonia level (BAL) in the pathogenesis of portosystemic collaterals (PSC). Actually, ammonia levels cannot serve as a laboratory marker for portosystemic encephalopathy, being neither specific nor highly sensitive [13], although there may be a correlation with severity [14].…”

Section: Introductionmentioning

confidence: 99%

Non-Invasive Parameters of Oesophageal Varices Diagnosis: Which Sensitive and Applicable; A Pilot Study

Hassan¹,

El-Rehim²,

Sayed³

et al. 2015

J Liver

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“…Nevertheless, whether a correlation exists between hyperammonemia and HE severity in CLF still remains controversial [11], [12], [13], [14] and [15]. A recent study demonstrated that ammonia administered intravenously to healthy volunteers did not cause any significant neuropsychological impairment [16], supporting the premise that pathogenic factors other than ammonia are involved in the pathogenesis of brain edema and HE in CLF.…”

mentioning

confidence: 99%

Systemic oxidative stress is implicated in the pathogenesis of brain edema in rats with chronic liver failure

Bosoi

Yang

Huynh

et al. 2012

Free Radical Biology and Medicine

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Chronic liver failure leads to hyperammonemia, a central component in the pathogenesis of hepatic encephalopathy (HE); however, a correlation between blood ammonia levels and HE severity remains controversial. It is believed oxidative stress plays a role in modulating the effects of hyperammonemia. This study aimed to determine the relationship between chronic hyperammonemia, oxidative stress, and brain edema (BE) in two rat models of HE: portacaval anastomosis (PCA) and bile-duct ligation (BDL). Ammonia and reactive oxygen species (ROS) levels, BE, oxidant and antioxidant enzyme activities, as well as lipid peroxidation were assessed both systemically and centrally in these two different animal models. Then, the effects of allopurinol (xanthine oxidase inhibitor, 100 mg/kg for 10 days) on ROS and BE and the temporal resolution of ammonia, ROS, and BE were evaluated only in BDL rats. Similar arterial and cerebrospinal fluid ammonia levels were found in PCA and BDL rats, both significantly higher compared to their respective sham-operated controls (p < 0.05). BE was detected in BDL rats (p < 0.05) but not in PCA rats. Evidence of oxidative stress was found systemically but not centrally in BDL rats: increased levels of ROS, increased activity of xanthine oxidase (oxidant enzyme), enhanced oxidative modifications on lipids, as well as decreased antioxidant defense. In PCA rats, a preserved oxidant/antioxidant balance was demonstrated. Treatment with allopurinol in BDL rats attenuated both ROS and BE, suggesting systemic oxidative stress is implicated in the pathogenesis of BE. Analysis of ROS and ammonia temporal resolution in the plasma of BDL rats suggests systemic oxidative stress might be an important "first hit", which, followed by increases in ammonia, leads to BE in chronic liver failure. In conclusion, chronic hyperammonemia and oxidative stress in combination lead to the onset of BE in rats with chronic liver failure. HIGHLIGHTS► Hyperammonemia does not lead independently to brain edema in chronic liver failure. ► Systemic oxidative stress plays a role in brain edema in chronic liver failure. ► Systemic oxidative stress induces brain edema synergistically with hyperammonemia. ► Systemic oxidative stress is an important "first hit" in chronic liver failure.

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Role of determination of partial pressure of ammonia in cirrhotic patients with and without hepatic encephalopathy

Cited by 128 publications

References 19 publications

Brain edema in acute liver failure and chronic liver disease: Similarities and differences

Brain edema in acute liver failure and chronic liver disease: Similarities and differences

Non-Invasive Parameters of Oesophageal Varices Diagnosis: Which Sensitive and Applicable; A Pilot Study

Systemic oxidative stress is implicated in the pathogenesis of brain edema in rats with chronic liver failure

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