***TASK***
the task is to simplify the input abstract of a biomedical literature

***INPUT***
the input is the abstract of a biomedical literature

***OUTPUT***
the output is the simplified abstract for the input abstract of a biomedical literature

***DOCUMENTATION***

***EXAMPLES***

Input: Five trials that randomly assigned 144 participants with overt hepatic encephalopathy that were published during 1979 to 1982 were included. Three trials assessed levodopa, and two trials assessed bromocriptine. The mean daily dose was 4 grams for levodopa and 15 grams for bromocriptine. The median duration of treatment was 14 days (range seven to 56 days). None of the trials followed participants after the end of treatment. Only one trial reported adequate bias control; the remaining four trials were considered to have high risk of bias. Random-effects model meta-analyses showed that dopamine agents had no beneficial or detrimental effect on hepatic encephalopathy in the primary analyses (15/80 (19%) versus 14/80 (18%); odds ratio (OR) 2.99, 95% confidence interval (CI) 0.09 to 100.55; two trials) or when paired data from cross-over trials were included (OR 1.04, 95% CI 0.75 to 1.43). Clear evidence of intertrial heterogeneity was identified both in the primary analysis (I2 = 65%) and when paired data from cross-over trials were included (I2 = 40%). Dopamine agents had no beneficial or harmful effect on mortality (42/144 (29%) versus 38/144 (26%); OR 1.11, 95% CI 0.35 to 3.54; five trials). Trial sequential analyses demonstrated that we lacked information to refute or recommend the interventions for all outcomes. Dopamine agonists did not seem to increase the risk of adverse events. This review found no evidence to recommend or refute the use of dopamine agents for hepatic encephalopathy. More randomised placebo-controlled clinical trials without risks of systematic errors and risks of random errors seem necessary to permit firm decisions on dopamine agents for patients with hepatic encephalopathy.
Output:

We performed the present systematic review to determine the beneficial and harmful effects of dopamine agents for patients with hepatic encephalopathy. Our analyses included five small trials published in 1982 or earlier. All trials but one had high risks of bias (i.e., risks of systematic errors or risks of overestimation of beneficial effects or risks of underestimation of harmful effects). Only 144 patients were included in the five trials, and accordingly risks of random errors (i.e., play of chance) are present. Our analyses showed no significant differences regarding symptoms of hepatic encephalopathy or mortality in patients treated with dopamine agents compared with patients who received an inactive placebo or no intervention. The number of patients with adverse events seemed comparable in the two intervention groups. Based on the available evidence, we conclude that no evidence can be found to recommend or refute the use of dopamine agents for hepatic encephalopathy. More randomised placebo-controlled clinical trials without risks of systematic errors and risks of random errors seem necessary to obtain firm evidence on dopamine agents for patients with hepatic encephalopathy.