Beneficial Effect of Alcohol Withdrawal on Gut Permeability and Microbial Translocation in Patients with Alcohol Use Disorder

2017 ◽  
Vol 42 (1) ◽  
pp. 32-40 ◽  
Author(s):  
Hélène Donnadieu-Rigole ◽  
Nathalie Pansu ◽  
Thibault Mura ◽  
Stéphanie Pelletier ◽  
Régis Alarcon ◽  
...  
2020 ◽  
Author(s):  
Régis Alarcon ◽  
Margaux Tiberghien ◽  
Raphael Trouillet ◽  
Stéphanie Pelletier ◽  
Amandine Luquiens ◽  
...  

2021 ◽  
Author(s):  
Olapeju Simoyan ◽  
Krista Ulisse

The illicit use of opioids is the fastest growing substance use problem in the United States. There are three FDA- approved medications for maintenance treatment for opioid use disorder: methadone, buprenorphine and naltrexone. Stimulants include cocaine and methamphetamines. 3,4-methylenedioxymethamphetamine (MDMA or “ecstasy”) is an amphetamine derivative that also has hallucinogenic properties. Treatment of stimulant withdrawal is primarily supportive. Psychosocial interventions for stimulant use disorder may improve adherence, but they have not been shown to improve abstinence at the end of treatment. Benzodiazepines have been shown to reduce the severity and duration of symptoms related to alcohol withdrawal, in addition to reducing the risk of seizures. The Food and Drug Administration has approved disulfiram, acamprosate and naltrexone for the treatment of alcohol use disorder. This review contains 3 tables, and 31 references. Keywords: Opioid use disorder, maintenance treatment for opioid use disorder, stimulant use disorder, stimulant withdrawal, benzodiazepine overdose, benzodiazepine withdrawal, alcohol use disorder, alcohol withdrawal


2021 ◽  
Author(s):  
Rajita Sinha ◽  
Nia Fogelman ◽  
Stephanie Wemm ◽  
Gustavo Angarita ◽  
Dongju Seo ◽  
...  

2021 ◽  
Vol 10 (16) ◽  
pp. 3496
Author(s):  
Daniel Fuster ◽  
Xavier Garcia-Calvo ◽  
Oriol Farré ◽  
Paola Zuluaga ◽  
Ferran Bolao ◽  
...  

Background: The association between markers of inflammation (interleukin (IL)-6 and IL-10), monocyte activation (sCD163 and sCD14), and microbial translocation (lipopolysaccharide (LPS) and LPS binding protein) and liver fibrosis in patients with alcohol use disorder (AUD) and no overt liver disease is not well established. Methods: We studied patients admitted for treatment of AUD at two hospitals in Barcelona. Advanced liver fibrosis (ALF) was defined as FIB-4 > 3.25. Results: A total of 353 participants (76.3% male) were included and 94 (26.5%) had ALF. In adjusted correlation analyses, sCD163, sCD14, IL-6, IL-10, and LPS binding protein levels directly correlated with FIB-4 values (adjusted correlation coefficients 0.214, 0.452, 0.317, 0.204, and 0.171, respectively). However, LPS levels were inversely associated with FIB-4 (−0.283). All plasma marker levels in the highest quartile, except LPS, were associated with ALF (sCD163, sCD14, IL-6, IL-10, and LPS binding protein: adjusted odds ratio (aOR) 11.49 (95% confidence interval 6.42–20.56), 1.87 (1.11–3.16), 2.99 (1.79–5.01), 1.84 (1.11–3.16), and 2.13 (1.30–3.50), respectively). Conversely, LPS levels in the lowest quartile were associated with ALF (aOR 2.58 (1.48–4.58), p < 0.01). Conclusion: In AUD patients, plasma levels of the markers of inflammation, monocyte activation, and microbial translocation are associated with ALF.


2020 ◽  
Vol 2 (2) ◽  
Author(s):  
Alice Laniepce ◽  
Nicolas Cabé ◽  
Claire André ◽  
Françoise Bertran ◽  
Céline Boudehent ◽  
...  

Abstract In alcohol use disorder, drinking cessation is frequently associated with an alcohol withdrawal syndrome. Early in abstinence (within the first 2 months after drinking cessation), when patients do not exhibit physical signs of alcohol withdrawal syndrome anymore (such as nausea, tremor or anxiety), studies report various brain, sleep and cognitive alterations, highly heterogeneous from one patient to another. While the acute neurotoxicity of alcohol withdrawal syndrome is well-known, its contribution to structural brain alterations, sleep disturbances and neuropsychological deficits observed early in abstinence has never been investigated and is addressed in this study. We included 54 alcohol use disorder patients early in abstinence (from 4 to 21 days of sobriety) and 50 healthy controls. When acute physical signs of alcohol withdrawal syndrome were no longer present, patients performed a detailed neuropsychological assessment, a T1-weighted MRI and a polysomnography for a subgroup of patients. According to the severity of the clinical symptoms collected during the acute withdrawal period, patients were subsequently classified as mild alcohol withdrawal syndrome (mild-AWS) patients (Cushman score ≤ 4, no benzodiazepine prescription, N = 17) or moderate alcohol withdrawal syndrome (moderate-AWS) patients (Cushman score &gt; 4, benzodiazepine prescription, N = 37). Patients with severe withdrawal complications (delirium tremens or seizures) were not included. Mild-AWS patients presented similar grey matter volume and sleep quality as healthy controls, but lower processing speed and episodic memory performance. Compared to healthy controls, moderate-AWS patients presented non-rapid eye movement sleep alterations, widespread grey matter shrinkage and lower performance for all the cognitive domains assessed (processing speed, short-term memory, executive functions and episodic memory). Moderate-AWS patients presented a lower percentage of slow-wave sleep, grey matter atrophy in fronto-insular and thalamus/hypothalamus regions, and lower short-term memory and executive performance than mild-AWS patients. Mediation analyses revealed both direct and indirect (via fronto-insular and thalamus/hypothalamus atrophy) relationships between poor sleep quality and cognitive performance. Alcohol withdrawal syndrome severity, which reflects neurotoxic hyperglutamatergic activity, should be considered as a critical factor for the development of non-rapid eye movement sleep alterations, fronto-insular atrophy and executive impairments in recently detoxified alcohol use disorder patients. The glutamatergic activity is involved in sleep-wake circuits and may thus contribute to molecular mechanisms underlying alcohol-related brain damage, resulting in cognitive deficits. Alcohol withdrawal syndrome severity and sleep quality deserve special attention for a better understanding and treatment of brain and cognitive alterations observed early in abstinence, and ultimately for more efficient relapse prevention strategies.


2020 ◽  
Vol 34 (11) ◽  
pp. 1171-1175
Author(s):  
Fabio Caputo ◽  
Mauro Cibin ◽  
Antonella Loche ◽  
Roberto De Giorgio ◽  
Giorgio Zoli

About 50% of persons with an alcohol use disorder may have symptoms of alcohol withdrawal syndrome (AWS) when they reduce or discontinue their alcohol consumption. Protracted alcohol withdrawal (PAW), an underestimated and not yet clearly defined clinical condition that follows the acute stage of AWS, is characterized by the presence of substance-specific signs and symptoms (i.e. anxiety, irritability, mood instability, insomnia, craving) common to acute AWS, but persisting beyond the generally expected acute AWS time frames. Considering that PAW symptoms are mainly related to the neuro-adaptive changes of gamma-aminobutyric acid (GABA) and N-methyl-d-aspartate (NMDA) systems, naltrexone, nalmefene, and disulfiram may not be able to suppress the symptoms of PAW. After treatment of the acute phase of AWS, a more specifically pharmacological therapy able to suppress PAW symptoms could perhaps be used earlier and may be more helpful in preventing the risk of alcohol relapse, which remains higher during the first months of treatment. In light of this, medications acting on GABA and NMDA neurotransmitter systems to counterbalance the up-regulation of NMDA and the down-regulation of GABA could be employed in combination and started as soon as possible.


Alcohol ◽  
2020 ◽  
Vol 86 ◽  
pp. 93-101
Author(s):  
Daniel B. Rosoff ◽  
Katrin Charlet ◽  
Jeesun Jung ◽  
Jisoo Lee ◽  
Christine Muench ◽  
...  

2020 ◽  
Vol Publish Ahead of Print ◽  
Author(s):  
Arantza Sanvisens ◽  
Paola Zuluaga ◽  
Antoni Short ◽  
Gabriel Rubio ◽  
Antoni Gual ◽  
...  

2017 ◽  
Vol 41 (S1) ◽  
pp. S873-S873
Author(s):  
G. Pardo de Santayana ◽  
R. Landera ◽  
M. Juncal ◽  
O. Porta ◽  
L. Sánchez ◽  
...  

IntroductionAlcohol use disorder is a pressing problem in our society. However, only a small percentage of patients with alcohol use disorder are ever treated. Nalmefene acts as an antagonist of mu opioid receptors preventing the pleasurable sensation that often accompanies alcohol consumption, while its modulation of kappa opioid receptors can decrease the dysphoria associated with alcohol withdrawal.AimStudying the effect of nalmefene on patients with alcohol use disorder who are trying to reduce their daily alcohol consumption.MethodsThis is a descriptive study that pretends to assess the effect of nalmefene 18 mg/day on alcohol intake in a sample of five patients (3 men and 2 women) that came to our psychiatric consultation from March to September 2016. They all had tried in the past to stop or reduce their alcohol consumption but were unable to do so. We initiate follow-up with the patients in psychiatric consultation for the next three months with a monthly frequency.ResultsOut of the 5 patients, 4 reported to have reduced their alcohol consumption over the observation time, going from 32 drinks per week to 18 drinks per week on average. The fifth patient abandoned prematurely the treatment due to the appearance of side effects (nausea). No other relevant side effects were detected.ConclusionsNalmefene appears to be effective and safe reducing abusive alcohol intake and avoiding alcohol withdrawal syndrome. Therefore, nalmefene can be considered a good therapeutic option helping reduce alcohol consumption in patients with alcohol use disorder.Disclosure of interestThe authors have not supplied their declaration of competing interest.


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