Successful use of bromocriptine in the treatment of chronic hepatic encephalopathy.

Gastroenterology (Impact Factor: 13.93). 05/1980; 78(4):663-70.
Source: PubMed

ABSTRACT Six patients with cirrhosis and severe chronic hepatic encephalopathy were treated with bromocriptine. All showed significant overall improvement clinically and in 3, the electroencephalogram became normal. The cerebral blood flow increased significantly from 32.7 +/- 2.4 (mean +/- 1 SE) to 40.5 +/- 1.5 ml/100 g brain/min (P less than 0.05). Similarly, there were significant improvements in the cerebral oxygen consumption from 2.2 +/- 0.4 to 3.3 +/- 0.4 ml/100 g brain/min (P less than 0.02) and in cerebral glucose consumption from 2.1 +/- 0.6 to 6.6 +/- 1.6 mg/100 g brain/min (P less than 0.02). Cross-over to placebo produced overall deterioration, more marked in the patients who had received the active drug for the shorter time period. No serious side effects were seen; the drug was well tolerated in doses of up to 15 mg daily and is a useful treatment for chronic hepatic encephalopathy when the response to conventional therapy has been poor.

  • [Show abstract] [Hide abstract]
    ABSTRACT: After liver resections hepatocellular failure is one of the most severe postoperative syndromes. The risk of liver failure should be evaluated preoperatively by quantitative tests of hepatic function (e. g., galactose elimination capacity, sulfobromophthalein elimination, aminopyrine breath test). Treatment of liver failure, besides supportive therapy and the usual therapy for hepatic coma, includes the administration of special amino acid mixtures. After shunt operations portasystemic encephalopathy is the most important postoperative syndrome. So far it is not possible to prevent this syndrome by patient selection or special methods of shunt surgery. Effective therapeutic modalities are available, however.
    Langenbecks Archiv fü Chirurgie 12/1980; 352(1). DOI:10.1007/BF01291989
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: The literature related to the effects of elevated plasma ammonia levels on brain energy metabolism is abundant, but heterogeneous in terms of the conclusions. Thus, some studies claim that ammonia has a direct, inhibitory effect on energy metabolism whereas others find no such correlation. In this review, we discuss both recent and older literature related to this controversial topic. We find that it has been consistently reported that hepatic encephalopathy and concomitant hyperammonemia lead to reduced cerebral oxygen consumption. However, this may not be directly linked to an effect of ammonia but related to the fact that hepatic encephalopathy is always associated with reduced brain activity, a condition clearly characterized by a decreased CMRO2. Whether this may be related to changes in GABAergic function remains to be elucidated.
    Metabolic Brain Disease 03/2014; 29(4). DOI:10.1007/s11011-014-9513-8 · 2.40 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Hepatic encephalopathy arises from the combination of hepatocellular dysfunction and portal-systemic shunting. Encephalopathy is more prominent in advanced stages of liver cirrhosis and signals the presence of fulminant hepatic failure in patients with acute liver injury. As important as the extent of shunting is the presence of large spontaneous collaterals. Ammonia continues to be a leading toxin influencing brain function. Endogenous benzodiazepines and cytokines may contribute to one of ammonia’s key effects in the brain: astrocyte swelling. The diagnosis of hepatic encephalopathy is a diagnosis of exclusion; the search for a precipitating factor should be started immediately in all cases of encephalopathy. The treatment of hepatic encephalopathy has three aims: decrease the nitrogenous load from the gut, improve the extra-intestinal elimination of ammonia and counteract central abnormalities of neurotransmission. The mainstay of treatment is directed at the colon. Newer approaches targeting the brain, such as flumazenil, have become available.
    Baillière&#x027 s Best Practice and Research in Clinical Gastroenterology 12/2000; 14(6):959-974. DOI:10.1053/bega.2000.0141 · 3.28 Impact Factor