Lactulose improves cognitive functions and health-related quality of life in patients with cirrhosis who have minimal hepatic encephalopathy

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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 ...

“…Prevalence of MHE in our population varies between 48% and 67.7% as shown by our previous studies using psychometric tests. 2,10,11 Patients who develop MHE are …”

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confidence: 99%

Minimal Hepatic Encephalopathy Impairs Quality of Life

Agrawal

Umapathy

Dhiman

2015

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“…The results of this study indicate that future trials with targeted prebiotics and probiotics should aim at enhancing cognition through modulation of these microbiome components. 3,11 There were no significant differences in the fecal microbiome families between the HE and no HE groups except a significantly higher abundance of Veillonellaceae in the HE group. Also, lactulose withdrawal did not change the microbiome significantly except for reduction in Faecalibacterium sp.…”

Section: Microbial Analysis Between Controls and Patients With Cirrhosismentioning

confidence: 88%

“…9,10 Current treatments for HE, such as lactulose, antiobiotics and others also rely on manipulation of the gut flora. 11,12 Culture-based techniques were used for the characterization of gut flora in prior HE studies. 9,13 Recently, Bajaj and co-workers have published 3 studies related to gut microbiota, inflammation and cognition in hepatic encephalopathy.…”

Section: Gut Flora Systemic Inflammation and Hepatic Encephalopathymentioning

confidence: 99%

Gut Microbiota, Inflammation and Hepatic Encephalopathy: A Puzzle with a Solution in Sight

Dhiman

2012

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“…23 In a randomized open label trial, lactulose therapy 30-60 mL/day was compared to no treatment in patients with cirrhosis and MHE. 24 Compared to the untreated group, there was a significant decrease in the number of abnormal psychometric tests in the group treated with lactulose (P < 0.0001). Treatment also demonstrated a significant improvement in the health-related quality of life (HRQoL) vs. those who did not receive lactulose [6.81 vs 0.17 (95% CI, 5.24-8.37) and (95% CI, À0.29 to 0.63), respectively; P < 0.001].…”

mentioning

confidence: 84%

“…Treatment also demonstrated a significant improvement in the health-related quality of life (HRQoL) vs. those who did not receive lactulose [6.81 vs 0.17 (95% CI, 5.24-8.37) and (95% CI, À0.29 to 0.63), respectively; P < 0.001]. 24 Sharma et al further reported the benefit of lactulose therapy for the primary prevention of OHE in patients with cirrhosis. A total of 120 cirrhotic patients with no prior episode of OHE were randomized to receive lactulose (55 patients, 32/55 with MHE) or no treatment (50 patients, 36/50 with MHE), with progression to OHE assessed over 12 months.…”

mentioning

confidence: 99%

Management of Covert Hepatic Encephalopathy

Waghray

Mullen

2015

Hepatic encephalopathy is a reversible progressive neuropsychiatric disorder that encompasses a wide clinical spectrum. Covert hepatic encephalopathy is defined as patients with minimal hepatic encephalopathy and Grade I encephalopathy by West-Haven Criteria. Terminology such as "sub-clinical", "latent", and "minimal" appear to trivialize the disease and have been replaced by the term covert. The lack of clinical signs means that covert hepatic encephalopathy is rarely recognized or treated outside of clinical trials with options for therapy based on patients with episodic hepatic encephalopathy. This review discusses the current available options for therapy in covert hepatic encephalopathy and focuses on non-absorbable disacharides (lactulose or lactitol), antibiotics (rifaximin), probiotics/synbiotics and L-ornithine-L-aspartate. ( J CLIN EXP HEPATOL 2015;5:S75-S81)