1,721,029 research outputs found
Failure of adrenergic system in the control of arterial pressure in cirrhosis. Role of weak neurotransmitters
No full textnot availabl
Major gastrointestinal hemorrhage during anticoagulant therapy in patients with atrial fibrillation: When should treatment be resumed? [Emorragia gastrointestinale maggiore in corso di terapia anticoagulante nei pazienti con fibrillazione atriale: quando riprendere il trattamento? ]
No full textNei pazienti con fibrillazione atriale (FA) in terapia anticoagulante orale (TAO), oltre la metà delle complicanze emorragiche si verificano nel tratto gastrointestinale (GI), con un’incidenza dell’1-4% per anno. Tale complicanza interessa prevalentemente soggetti anziani, spesso molto compromessi da un punto di vista clinico e la mortalità non è trascurabile variando nei diversi studi fra 4% e 15%. Lo scopo di questa rassegna è valutare l’utilità della ripresa della TAO dopo un’emorragia GI maggiore nei pazienti con FA. Abbiamo trovato nella letteratura quattro studi osservazionali, di cui tre con disegno retrospettivo, che hanno affrontato specificamente questo problema. In tali studi è stato utilizzato quasi esclusivamente il warfarin. La TAO veniva sospesa in tutti i pazienti all’inizio dell’emorragia GI; in circa la metà dei casi l’anticoagulante veniva poi ripristinato e nell’altra metà veniva sospeso definitivamente. I risultati di questi studi suggeriscono un beneficio della ripresa della TAO che riduceva l’incidenza degli eventi tromboembolici e della mortalità con un aumento solo modesto delle recidive emorragiche. Questi risultati, tuttavia, devono essere interpretati con molta cautela in quanto è estremamente probabile che la TAO sia stata ripristinata nei pazienti in buone condizioni cliniche – come suggerito dalla bassissima mortalità in corso di recidiva emorragica (0.7%) – e non in quelli con emorragie più gravi e/o molto compromessi da un punto di vista clinico. Per tale tipo di selezione dei pazienti non siamo in grado di definire il reale rischio emorragico legato alla ripresa della TAO dopo un’emorragia GI e ciò rappresenta un grosso limite nel processo decisionale; per acquisire tale conoscenza occorrono studi randomizzati. La valutazione sulla ripresa o meno della TAO deve essere fatta caso per caso da un team che includa il gastroenterologo (o chi gestisce la patologia GI) e il cardiologo. Aspetti clinici rilevanti come la sede e/o l’eziologia dell’emorragia GI, la severità dell’anemia e il valore dell’international normalized ratio (INR) all’inizio dell’emorragia non appaiono al momento di utilità nel “decision making”. I dati a disposizione suggeriscono che l’anticoagulante dovrebbe essere riproposto ad anziani “robusti” qualora sia stata identificata e trattata la sede del sanguinamento, mentre permangono molte perplessità sulla gestione dell’anziano “fragile” o molto compromesso da un punto di vista clinico. La letteratura non offre dati chiari su quando riprendere la TAO dopo un’emorragia GI. La valutazione deve essere fatta nel contesto clinico; tuttavia, un intervallo di tempo variabile fra 1 settimana ed 1 mese appare, di massima, adeguato. Sulla base di confronti indiretti, e pertanto con i limiti di tale tipo di valutazione, gli anticoagulanti più appropriati dopo un’emorragia GI appaiono il warfarin con uno stretto monitoraggio dell’INR, l’apixaban e l’edoxaban a basso dosaggio.In patients with atrial fibrillation (AF) under oral anticoagulant therapy (OAT), over half of the hemorrhagic complications occur in the gastrointestinal (GI) tract, with an incidence of 1-4% per year. This complication mainly involves older patients, often very compromised from the clinical point of view; mortality rates are not negligible, varying between 4% and 15%. The purpose of the present review was to evaluate the utility of resuming OAT after a major GI hemorrhage in patients with AF. Four observational studies were found in the literature that specifically investigated this issue; three of them had a retrospective design. In these studies almost exclusively warfarin was utilized. OAT was discontinued in all patients at the beginning of GI hemorrhage; in about half of the patients anticoagulation was then restarted and in the other half it was definitively stopped. The results of these studies suggest a beneficial effect of OAT resumption, since it reduced the incidence of thromboembolic events and mortality with a not marked increase in hemorrhagic recurrences. However, these results should be interpreted with caution since, very likely, OAT was resumed in patients in good clinical condition - as suggested by the very low mortality rate during hemorrhagic recurrences (0.7%) - and not in those with very severe hemorrhage and/or very compromised from the clinical point of view. Because of this type of patient selection, we do not know the real hemorrhagic risk in patients resuming OAT after GI hemorrhage. This is a strong limitation in the decision making; in order to acquire this knowledge, randomized studies should be carried out. The evaluation whether or not to restart OAT should be made in the clinical context by a team including the gastroenterologist (or the physician taking care of the GI pathology) and the cardiologist. At present, clinical variables such as site and/or cause of GI bleeding, severity of the anemia and the degree of prolongation of the international normalized ratio, do not appear useful for decision making. The available data suggest that OAT should be resumed in "robust" elderly patients, if the source of bleeding has been identified and corrected, whereas in frail patients and/or with multiple comorbidities, the doubt often remains. The available literature does not offer clear data on the optimal duration of OAT discontinuation after an episode of major GI bleeding. The evaluation should be made in the clinical context; however, therapy discontinuation between 1 week and 1 month appears to be adequate in most cases. On the basis of indirect comparisons, which show many limitations, the most appropriate anticoagulants after GI hemorrhage appear to be warfarin, apixaban and low-dose edoxaban
Use of pyridoxine-alpha-ketoglutarate (PAK) in hepatic encephalopathy
No full textPyridoxine-alpha-ketoglutarate (PAK) was administered to patients with high blood ammonia levels and with clinical signs of hepatic encephalopathy (HE). Plasma concentrations of ammonia decreased and clinical symptomatology improved. The activity of PAK was greater than that of lactulose in lowering blood ammonia levels but not significantly different in its relief of neuropsychic symptoms
Effect of arginine thiazolidinecarboxylate (ATCA)* * SULFILE is the trade name for arginine thiazolidinecarboxylate (200 mg vials) manufactured by Poli-Industria Chimica, Italy. on some clinical and functional parameters in cirrhotic patients
No full textForty patients with chronic active hepatopathy- or hepatic cirrhosis were randomly treated with arginine thiazolidinecarboxlyate (ATCA) or placebo, administered by intravenous infusion through phleboclysis. Tests for revealing the effects of the drug on liver function or liver damage were carried out. Comparison of the values of transaminases, alkaline phosphatase, total bilirubinaemia and aromatic amino acids at the end of treatment, showed significantly lower levels in the ATCA-treated patients than the placebo group. No local or general intolerance reactions, ascribable to the ATCA were observed. © 1981
Efficacy and safety of gamma hydroxybutyrate (GHB) in treating alcohol withdrawal syndrome in an alcohol-dependent in-patient with decompensated liver cirrhosis: a case report.
No full textSo far, there are no data about the
efficacy of GHB in treating AWS in inpatients
with LC. In this study, we report
a case of AWS in a hospitalized alcoholdependent
patient with decompensated LC,
successfully treated with GHB at a dosage
of 100 mg/kg administered 4 times a day
Alcohol use in adults.
Get PDFComplete abstinence is the primary goal to be
achieved in the treatment of alcohol dependence.
Unfortunately, acamprosate and naltrexone have
failed in this respect, and thus alternative drugs
warrant consideration
Gamma hydroxybutiric acid (GHB): a valid pharmacological opportunity for the treatment of alcohol dependence.
No full textGamma-hydroxybutyric acid (GHB) is a short-chain fatty acid structurally similar to the inhibitory neurotransmitter gamma-amino-butyric acid that exerts an ethanol-mimicking effect on the central nervous system, by acting on its own receptor and on the GABAB receptor. In Anglo-Saxon Countries, GHB has emerged as a recreational drug of abuse due to its euphoric effects, and several episodes of drug intoxication and withdrawal syndrome due to its non-clinical self-administration have been described in the last 10 years. However, in the United States, GHB has been employed since 2002 for the treatment of cataplexy, a symptom often manifested by patients with narcolepsy. In some European Countries, where GHB is not so widespread as a drug of abuse, this medication is currently used for the treatment of alcohol dependence with encouraging results. Indeed, clinical trials have demonstrated that 50-100 mg/kg of GHB fractioned into three or six daily doses is able to suppress alcohol withdrawal symptoms and to favor the maintenance of abstinence from alcohol. GHB has also proved to be more efficient than naltrexone in maintaining sustained abstinence from alcohol. In addition, as far as combined treatments are concerned, the combination of GHB with naltrexone is more effective than either drug alone in maintaining alcohol abstinence and, likely, in avoiding craving for GHB. As a whole, these studies have shown that episodes of craving for GHB are a very limited phenomenon (about 10-15%) in pure alcoholics, rare episodes of sedation due to GHB abuse have been reported, no cases of intoxication, coma or deaths have occurred and a withdrawal syndrome has not been observed when this drug was discontinued. On the other hand, 40-90% of alcoholics with previous heroin or cocaine dependence develop craving for and abuse of GHB during the administration of this drug. In conclusion, physicians should attribute more importance to the clinical efficacy of GHB as a valid pharmacological tool for the treatment of alcohol addiction following some simple rules of administration: GHB should be indicated in alcoholics who do not present a poly-drug dependence, its dosage should not exceed 50-100 mg/kg fractioned into three to six daily administrations, strict medical surveillance has to be planned, and, when necessary, a family member to be entrusted with the drug should be designated
- …
