Probiotic Yogurt for the Treatment of Minimal Hepatic Encephalopathy

Bajaj, Jasmohan S.; Saeian, Kia; Christensen, Kenneth M.; Hafeezullah, Muhammad; Varma, Rajesh; Franco, José; Pleuss, Joan A.; Krakower, Glenn R.; Hoffmann, Raymond G.; Binion, David G.

doi:10.1111/j.1572-0241.2008.01861.x

Cited by 236 publications

(191 citation statements)

References 47 publications

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“…51 Bajaj et al further reported that probiotic yogurt treatment lead to a reversal of MHE in 71% of patients with non-alcoholic cirrhosis with no progression to OHE. 50 Consistent with prior findings, patients with MHE in this study had lower baseline HRQoL as determined by 36 item Short Form Health Survey (SF-36). However, probiotic treatment did not convey a significant difference from baseline HRQoL scores and this was likely related to the lack of sensitivity of the SF-36 in assessing HRQoL in patients with MHE.…”

Section: Probioticssupporting

confidence: 90%

“…Probiotics are not only efficacious in the treatment of OHE, but demonstrate benefit for MHE. [50][51][52][53] In a placebo controlled trial, synbiotic treatment for 30 days resulted in a decrease in intestinal pH, blood ammonia levels, and reversal of MHE compared to placebo (50.0% vs 13.3%, respectively; P < 0.05). Moreover, none of the patients developed OHE in this study.…”

Section: Probioticsmentioning

confidence: 99%

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Management of Covert Hepatic Encephalopathy

Mullen

Prakash

2012

Clinics in Liver Disease

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Section: Probioticssupporting

confidence: 90%

Section: Probioticsmentioning

confidence: 99%

Management of Covert Hepatic Encephalopathy

Mullen

Prakash

2012

Clinics in Liver Disease

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“…123 Probiotics have also been shown to restore neutrophil phagocytic activity by lowering endogenous levels of IL-10 and TLR-4 expression in patients with cirrhosis. 124 However, in other studies no changes in the reduction of the plasma proinflammatory milieu 125 or outcomes have been demonstrated. 126 …”

Section: Probioticsmentioning

confidence: 95%

Pathogenesis of Hepatic Encephalopathy: Role of Ammonia and Systemic Inflammation

Aldridge

Tranah

Shawcross

2015

Journal of Clinical and Experimental Hepatology

248

190

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The syndrome we refer to as Hepatic Encephalopathy (HE) was first characterized by a team of Nobel Prize winning physiologists led by Pavlov and Nencki at the Imperial Institute of Experimental Medicine in Russia in the 1890's. This focused upon the key observation that performing a portocaval shunt, which bypassed nitrogen-rich blood away from the liver, induced elevated blood and brain ammonia concentrations in association with profound neurobehavioral changes. There exists however a spectrum of metabolic encephalopathies attributable to a variety (or even absence) of liver hepatocellular dysfunctions and it is this spectrum rather than a single disease entity that has come to be defined as HE. Differences in the underlying pathophysiology, treatment responses and outcomes can therefore be highly variable between acute and chronic HE. The term also fails to articulate quite how systemic the syndrome of HE can be and how it can be influenced by the gastrointestinal, renal, nervous, or immune systems without any change in background liver function. The pathogenesis of HE therefore encapsulates a complex network of interdependent organ systems which as yet remain poorly characterized. There is nonetheless a growing recognition that there is a complex but influential synergistic relationship between ammonia, inflammation (sterile and non-sterile) and oxidative stress in the pathogenesis HE which develops in an environment of functional immunoparesis in patients with liver dysfunction. Therapeutic strategies are thus moving further away from the traditional specialty of hepatology and more towards novel immune and inflammatory targets which will be discussed in this review. ( J CLIN EXP HEPATOL 2015;5:S7-S20) H epatic encephalopathy (HE) is the term used to encapsulate the broad spectrum of neuropsychiatric disturbances associated with both acute and chronic liver failure (ALF and CLF, respectively), as well as porto-systemic bypass in the absence of hepatocellular disease. The clinical manifestations of HE can be extremely heterogeneous in nature, with symptoms presenting anywhere on a continuum spanning from seemingly normal cognitive performance, right the way through to states of confusion, stupor and coma. In between these extremes, patients with HE may exhibit signs such as inattentiveness, blunted affect, impairment of memory or reversal of the sleep-wake cycle, as well as physical manifestations such as tremor, myoclonus, asterixis and deep tendon hyperreflexia.ALF is defined by the onset of coagulopathy alongside any degree of encephalopathy in patients with no evidence of pre-existing liver disease. 1 The presence of HE in those with ALF is prognostic, with up to a quarter of cases developing raised intracranial pressure. 2 Patients presenting with ALF are at risk of developing its cardinal, lifethreatening feature, cerebral edema. Left untreated, cerebral edema can rapidly progress to cause herniation of the uncus through the falx cerebri, leading to compression of the brainstem and, ultimately, death. H...

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“…23 Ammonia also modulates glutamate neurotransmission and induces neurosteroid production in neurons, leading to a positive modulatory effect on the gamma-aminobutyric acid-A receptor. 24 Ammonia lowering therapies like lactulose, 11,25,26 rifaximin 27 and probiotics 28,29 have been shown to result in resolution of MHE and overt HE, thereby providing indirect evidence to ammonia's pathogenic role in HE. However, recent studies have shown the persistence of cognitive impairment in cirrhotics even after complete resolution of HE despite ammonia lowering therapy suggesting role of other factors.…”

Section: Pathogenesis Of Minimal Hepatic Encephalopathymentioning

confidence: 99%

“…49 Depression, anxiety-trait and alexithymic symptoms occurs in cirrhotics and are major determinants of impaired HRQOL. 50 Treatment of MHE with lactulose, 11 rifaximin 27,51 or probiotics 29 reverses MHE in majority of patients. Significantly HRQOL also improves with treatment of MHE.…”

Section: Effect Of Minimal Hepatic Encephalopathy On Quality Of Lifementioning

confidence: 99%

Minimal Hepatic Encephalopathy Impairs Quality of Life

Agrawal

Umapathy

Dhiman

2015

Journal of Clinical and Experimental Hepatology

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Minimal hepatic encephalopathy (MHE) is the mildest form of the spectrum of neurocognitive impairment in cirrhosis. It is a frequent occurrence in patients of cirrhosis and is detectable only by specialized neurocognitive testing. MHE is a clinically significant disorder which impairs daily functioning, driving performance, work capability and learning ability. It also predisposes to the development of overt hepatic encephalopathy, increased falls and increased mortality. This results in impaired quality of life for the patient as well as significant social and economic burden for health providers and care givers. Early detection and treatment of MHE with ammonia lowering therapy can reverse MHE and improve quality of life. ( J CLIN EXP HEPATOL 2015;5:S42-S48) H epatic encephalopathy (HE) is a neurocognitive disorder in which brain function is impaired and is associated with both acute and chronic liver dysfunction. 1 It is a major complication that develops in some form and at some stage in a majority of patients with liver cirrhosis. Minimal HE (MHE) is the mildest form of spectrum of HE which is characterized by subtle cognitive and psychomotor deficits in the absence of recognizable clinical symptoms of HE. 2 It occurs in patients with liver dysfunction and/or portosystemic shunts. In MHE, neurocognitive abnormalities primarily affect attention, speed of information processing, executive control, motor ability and coordination in an individual. 3 In 1970, Zeegen et al 4 first described this condition when they discovered that 38% of patients who had undergone portal decompression surgery scored abnormal in Reitan trail making test (number connection test). Eight years later, the term subclinical HE 5 was introduced to describe these patients. Since then, this condition was described under various names like early HE, latent HE, subclinical HE and finally minimal HE. The latest classification combines MHE and grade 1 HE into covert HE while higher grades are classified as overt HE, thus simplifying the clinical schema so that HE can be uniformly diagnosed. 6 Covert HE means that the mental defect is not detectable by the clinician using conventional testing and is not noticeable to the patient. However, it is significant because these patients usually have neuropsychiatric and neurophysiological abnormalities on advanced testing which are not enough to cause disorientation or asterixis. MHE is regarded as a preclinical stage of HE and ammonia and systemic inflammation plays an important role in its pathogenesis similar to HE. Ammonia lowering therapies were used in the treatment of MHE and found to be effective.MHE is clinically significant as it impairs daily functioning, health related quality of life (HRQOL) and driving skills, predicts the development of overt HE and is associated with poor survival. 7-11 Overt HE develops in >50% of MHE patients within three years. 10 These patients pose a significant burden to their care givers depending on the severity of cognitive dysfunction. 2,12 Considering all ...

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Probiotic Yogurt for the Treatment of Minimal Hepatic Encephalopathy

Abstract: This trial demonstrated a significant rate of MHE reversal and excellent adherence in cirrhotics after probiotic yogurt supplementation with potential for long-term adherence.

Cited by 236 publications

References 47 publications

Management of Covert Hepatic Encephalopathy

Management of Covert Hepatic Encephalopathy

Pathogenesis of Hepatic Encephalopathy: Role of Ammonia and Systemic Inflammation

Minimal Hepatic Encephalopathy Impairs Quality of Life

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