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How Long Does Acamprosate Take To Work?

• Renato Leandro
• 26.07.2023
• 0
• 14

How long does it take for acamprosate to work?

How long do the tablets take to work? Campral takes about a week to work. These tablets are time-released, which means that small amounts of the drug is released over time.

What is the success rate of acamprosate?

Is There Evidence for Effectiveness of Acamprosate in Maintaining Abstinence in Alcohol Dependent Patients? Ninety percent of all United States (US) residents have had an alcoholic drink at least once in their lifetime. About 51 percent of US adult population are current users of alcohol. Alcohol-related disorders constitute the third largest health problem in US. It is estimated that around 200,000 deaths each year could be attributed to alcohol-related disorders. Around 30 to 45 percent of adults in US have had an alcohol-related health problem during their lifetime. Around 20 percent of men and 10 percent of the women have met the diagnostic criteria of alcohol abuse in their lifetime and 3 to 5 percent of the women and 10 precent of the men have met the diagnostic criteria for alcohol dependence. Alcohol has been estimated to cost US economy $185 million in lost productivity, healthcare costs, and damages due to alcohol-related accidents. The treatment of alcohol can be divided into multiple stages: intervention, withdrawal, detoxification, rehabilitation, and interventions to maintain long-term abstinence. The interventions to maintain abstinence can be further subdivided into psychosocial and pharmacological methods. Multiple medications have been used in the past to help patients maintain abstinence like disulfiram, naltrexone, and serotonin reuptake inhibitors. Acamprosate had been available in Europe for many years but has only recently been approved by the Food and Drug Administration (FDA) for use in US (Campral ®, Merck). Acamprosate is a drug that promotes abstinence, but the mechanism of action of acamprosate still remains obscure. Various hypotheses have been proposed. Acamprosate has a chemical structure similar to endogenous amino acid homotaurine, which is the structural analogue of γ-amino butyric acid and the amino acid neuromodulator taurine. Chronic alcohol use has been hypothesized to lead to alterations in the normal balance between neuronal excitation and inhibition. Acamprosate is thought to interact with glutamate and GABA neurotransmitter systems in the central nervous system and restore this balance. Following chronic exposure to alcohol, there is an up regulation of the glutamatergic system in the central nervous system (CNS). This leads to excess glutamatergic activity on sudden withdrawal of alcohol. These changes persist for months after stopping intake of alcohol. Acamprosate attenuates this surge in glutamic acid release. Glutamatergic neurotransmission has been postulated to be involved in the acquisition of cue-related drinking behaviors and hence can be modulated by acamprosate. Paille, et al., in a 12-month, prospective, placebo-controlled, randomized, double-blind trial, studied the efficacy of acamprosate at two dose levels in maintaining abstinence in alcohol-dependent patients. Five-hundred and thirty-eight patients took part in this study. After detoxification, the patients included were randomly assigned to one of three groups: 177 patients received placebo, 188 received acamprosate at 1.3g/day (low dose group), and 173 received 2.0g/day (high-dose group) for 12 months. Craving was not substantially reduced by acamprosate. The study showed a dose-dependent relationship, with the higher dosage of acamprosate showing a better response than the lower dosage. The patients showed good tolerance to acamprosate with only diarrhea being reported more frequently. Sass, et al., studied the effectiveness of acamprosate in a randomized, double-blind, placebo-controlled study. After detoxification, 272 patients received routine counseling and either acamprosate or placebo for 48 weeks. They were followed for another 48 weeks without medications. It was shown that patients who were receiving acamprosate showed a significantly higher abstinence rate and also had significantly higher mean abstinence duration of 224 days vs.163 days for placebo-treated patients. Acamprosate was shown to be a very safe medication with minimal side effects. Pelc, et al., compared the efficacy of acamprosate in maintaining abstinence in recently detoxified alcoholic patients in a double-blind study. The double-blind trial was conducted using two dosages of acamprosate (1,332mg/day and 1,998mg/day). Acamprosate was shown to be significantly superior to placebo. Better effect was seen with higher dosage. Acamprosate was shown to be safe in recently detoxified alcoholic patients. Palmer, et al., performed a computer-aided study looking at the long-term cost effectiveness of improving abstinence from alcohol using adjuvant acamprosate. Despite the high acquisition costs, the authors concluded that adjuvant acamprosate therapy was both clinically and economically attractive. Rychlik, et al., performed an open, prospective, cohort study to evaluate the costs of treating alcohol dependence under real-world conditions. Eight-hundred and fourteen recently detoxified alcohol-dependent patients were provided with psychosocial rehabilitation support. In addition, 540 alcohol-dependent patients treated with adjuvant acamprosate therapy were compared with 274 patients without pharmacotherapy. Real costs were assessed over a period of one year. Of the patients who were treated with acamprosate, 33.6 percent remained abstinent compared to 21.1 percent in the standard cohort. The mean total costs per patient treated with acamprosate were EUR 1,631.49 per year, whereas that in the standard cohort, total costs were EUR 2,068.83, and the difference was shown to be highly significant ( p =0.012). Mann, et al., did a comprehensive meta-analysis of randomized, placebo-controlled studies assessing the efficacy of acamprosate in the maintenance of abstinence in alcohol-dependent subjects. They studied the evidence from 17 trials including 4087 patients from 13 countries. The primary endpoint was continuous abstinence rate at six months. Thirty-six percent of the patients receiving acamprosate and 23.4 percent of patients receiving placebo were abstinent at six months ( p <0.001). Statistically significant differences in rates were noted at three months and 12 months also. Pelc, et al., in a 26-week study, evaluated the benefits of a follow-up by a community nurse when treating alcohol dependence with acamprosate. The cumulative abstinence duration was significantly longer in subjects, who received community nurse support. Basu, et al., in a 2005 study compared the efficacy of Acamprosate and naltrexone to that of placebo in maintaining abstinence from alcohol. Seventy-seven of the patients taking Acamprosate remained abstinent compared to that of 36 percent of patients taking naltrexone and 50 percent of the patients taking placebo. Follow-up studies showed that patients on acamprosate had better functioning in several areas. De Sousa, et al., in an open-label, eight-month study conducted in western India, compared the efficacy of acamprosate and disulfiram in maintaining abstinence from alcohol. Eight-eight percent of the patients on disulfiram remained abstinent compared to 46 percent of patients on acamprosate. This study concluded that disulfiram is superior to acamprosate for preventing relapse in alcohol-dependent men with good family support. Poldrugo, et al., did a critical review of pharmacoeconomics studies of acamprosate and concluded that acamprosate enhances abstinence rate, reduces the costs of treatment, and was found to be better than other rehabilitation strategies not involving pharmacotherapy. Acamprosate has only recently been introduced in US, but it has been in use in Europe and other parts of the world for many years. Acamprosate has proved to be a safe and cost-effective treatment modality in the treatment of alcohol dependence. Studies in Europe and Asia have shown that it is more effective in alcohol-dependent patients with good family support and in those patients who are followed in the community by health professionals.1. Sadock BJ, Sadock VA. Synopsis of Psychiatry. Philadelphia, PA: Lippincott Williams and Wilkin; 2003.2. Ensuring Solutions to Alcohol Problems., Available at:,3. Garbutt JC, West SL, Carey TS, et al. Pharmacological treatment of alcohol dependence: A review of the evidence. J Am Med Assoc.1999; 281 (14):1318–25.4. Campral Drug Description., Available at:,5. De Witte P, Littleton J, Parot P, Koob G. Neuroprotective and abstinence-promoting effects of acamprosate: elucidating the mechanism of action. CNS Drugs.2005; 19 (6):517–37.6. Paille FM, Guelfi JD, Perkins AC, et al. Double-blind, randomized, multicenter trial of acamprosate in maintaining abstinence from alcohol. Alcohol Alcohol.1995; 30 (2):239–47.7. Sass H, Soyka M, Mann K, Zieglgansberger W. Relapse prevention by acamprosate. Results from a placebo-controlled study on alcohol dependence. Arch Gen Psychiatry.1996; 53 (8):673–80.8. Pelc I, Verbanck P, Le Bon O, et al. Efficacy and safety of acamprosate in the treatment of detoxified alcohol-dependent patients: A 90-day placebo-controlled dose-finding study. Br J Psychiatry.1997; 171 :73–7.9. Palmer AJ, Neeser K, Weiss C, et al. The long-term cost-effectiveness of improving alcohol abstinence with adjuvant acamprosate. Alcohol Alcohol.2000; 35 (5):478–92.10. Rychlik R, Siedentop H, Pfeil T, Daniel D. Cost-effectiveness of adjuvant treatment with acamprosate in maintaining abstinence in alcohol dependent patients. Eur Addict Res.2003; 9 (2):59–64.11. Mann K, Lehert P, Morgan MY. The efficacy of acamprosate in the maintenance of abstinence in alcohol-dependent individuals: Results of a meta-analysis. Alcohol Clin Exp Res.2004; 28 (1):51–63.12. Pelc I, Hanak C, Baert I, et al. Effect of community nurse follow-up when treating alcohol dependence with acamprosate. Alcohol Alcohol.2005; 40 (4):302–7.13. Basu D, Jhirwal OP, Mattoo SK. Clinical characterization of use of acamprosate and naltrexone: data from an addiction center in India. Am J Addict.2005; 14 (4):381–95.14. de Sousa A, de Sousa A. An open randomized study comparing disulfiram and acamprosate in the treatment of alcohol dependence. Alcohol Alcohol.2005; 40 (6):545–8. Epub 2005 Jul 25.15. Poldrugo F, Haeger DA, Comte S, et al. A critical review of pharmacoeconomics studies of acamprosate. Alcohol Alcohol.2005; 40 (5):422–30. : Is There Evidence for Effectiveness of Acamprosate in Maintaining Abstinence in Alcohol Dependent Patients?

How does acamprosate make you feel?

Precautions and Contraindications – Taking acamprosate can cause drowsiness, dizziness, and decreased alertness in some people. For this reason, it is important to determine how the medication will affect you before operating a motor vehicle. Acamprosate should not be taken if you have any of the following conditions:

Allergic reaction to Campral, sulfites, or other medicinesAllergic reaction to foods, dyes, or preservativesBreastfeedingDepressionKidney diseasePregnant or trying to get pregnantSuicidal thoughts

Why is acamprosate 666 mg?

Dosing – The dose of this medicine will be different for different patients. Follow your doctor’s orders or the directions on the label. The following information includes only the average doses of this medicine. If your dose is different, do not change it unless your doctor tells you to do so.

For oral dosage form (tablets):

To help overcome drinking problems:

Adults—Two tablets (666 mg per dose) taken three times daily. Children—Use and dose must be determined by your doctor.

What does acamprosate do to your brain?

What Is Acamprosate And What Does It Treat? – Acamprosate is a medication that works in the brain to treat alcohol use disorder. Acamprosate works by decreasing cravings and urges to use alcohol. This allows people who take the medication to control urges to drink and help to continue to not use alcohol.

Being unable to quit using alcohol despite problems with health and relationships. Requiring more alcohol to achieve the same effect. Presence of withdrawal symptoms (sweating, shaking, nausea, vomiting, confusion, anxiety) when unable to use alcohol. Spending the majority of time using or finding a way to use alcohol. Having a desire but an inability to decrease the amount of alcohol used. Giving up enjoyable activities in order to use alcohol.

Does acamprosate help with sleep?

Discussion and Future Directions – To date, this is the first systematic review evaluating the sleep-related effects of disulfiram, acamprosate, naltrexone, or nalmefene reviewed together. As reported by Snyder et al. (1981), disulfiram decreases REM sleep in acute abstinent alcoholics.

1. Interestingly, disulfiram inhibits the production of noradrenaline by blocking the dopamine β-hydroxylase enzyme ( Goldstein et al., 1964 ), and this may underlie the decreased REM sleep.
2. In fact, although noradrenergic neurons show only minimal activity during REM sleep, it is recognized that minimal brain stem level of NA is necessary for the occurrence of REM sleep ( Gottesmann, 2008 ), as REM sleep can be suppressed by lesioning the noradrenergic nucleus, locus coeruleus ( Jouvet and Delorme, 1965 ).

The disulfiram-induced reduction of REM sleep is quite interesting if we consider that during alcohol withdrawal, the REM sleep is usually increased ( Brower, 2001 ). In addition, other psychiatric disorders often associated with AUD and withdrawal, such as depressive disorders, are characterized by increased REM sleep, while on the contrary, antidepressant drugs reduce REM sleep (see Wichniak et al., 2017 ).

In this framework, it could be tempting to suggest that the reduced REM sleep may play an important role in the therapeutic effects of disulfiram, contributing maybe to mood improvements during abstinence, but unfortunately, there are no additional studies on disulfiram to further corroborate this hypothesis.

Acamprosate shows some beneficial effects on sleep, reducing insomnia in some studies ( Boeijinga et al., 2004 ; statistics not known), in line with a recent meta-analysis reporting lowered insomnia after 6 months of treatment with acamprosate versus placebo ( Perney and Lehert, 2018 ).

However, in this systematic review, we haven’t included most of the studies that were analyzed in Perney and Lehert (2018) meta-analysis, mainly for lack of sleep outcomes ( Pelc et al., 1992 ; Whitworth et al., 1996 ; Geerlings et al., 1997 ; Pelc et al., 1997 ; Poldrugo, 1997 ; Chick et al., 2000 ; Tempesta et al., 2000 ; Mason et al., 2006 ).

In fact, Perney and Lehert (2018) analyzed the raw sleep data collected from those trials. Moreover, two articles on acamprosate were excluded because they were not in English ( Barrias et al., 1997 ; Ladewig et al., 1993 ) and another two studies were excluded because there was concomitant administration of other, potentially biasing, drugs ( Besson et al., 1998 ; Chick et al., 2000 ).

• Finally, due to the high level of methodological heterogeneity across the included studies, we estimated that it was not appropriate to pool the data in a meta-analysis.
• But the results summarized in this review suggest beneficial effects of acamprosate ( Table 3 ), particularly on parameters of sleep continuity and architecture that are usually affected by AUD, giving less fragmented sleep, increased deep sleep (stage 3), and increased REM sleep latency ( Staner et al., 2006 ).

Acamprosate, by reducing the glutamatergic neurotransmission ( Mason and Crean, 2007 ; Frye et al., 2016 ), supports abstinence, and this might explain the reduced insomnia and the trend to reduce REM sleep ( Jones, 2019 ). Glutamate is the major excitatory neurotransmitter in the brain and plays an essential role in regulating wakefulness and REM sleep ( Jones, 2019 ).

Indeed, glutamatergic system dysregulation in AUD is a likely substrate for several sleep disturbances ( Koob and Colrain, 2019 ). Naltrexone alters the sleep–wake cycle giving increased insomnia and somnolence in some studies, although statistical significance was present only in few studies reported in Table 3 ( Anton et al., 1999 ; Anton et al., 2006 ; O’Malley et al., 2008 ; Oslin et al., 2008 ).

The higher risk of insomnia and somnolence with naltrexone compared to placebo is further confirmed by the results showed in the meta-analyses ( Figures 5A, B, respectively). Despite the lack of evidence on the effect of naltrexone on sleep architecture, preliminary results from a recent polysomnography study on six healthy males demonstrated that a single dose of naltrexone significantly increased stage 2 sleep and decreased REM sleep ( Sramek et al., 2014 ).

The observed effects on REM sleep seem to mimic other drugs such as benzodiazepines, tricyclic antidepressants, selective serotonin reuptake inhibitors, trazodone, and opioids ( Kay et al., 1969 ; Cronin et al., 1995 ; Obermeyer and Benca, 1996 ; Gursky and Krahn, 2000 ; Foldvary-Schaefer et al., 2002 ; Barbanoj et al., 2005 ; Shaw et al., 2005 ), all known to affect the central neurotransmitters involved in the sleep–wake cycle, such as catecholamines, acetylcholine, GABA, and histamine ( Jones, 2019 ).

Interestingly, it must be noted that there is a common signature across these three drugs (disulfiram, acamprosate, and naltrexone) in the alteration of sleep architecture. In fact, from the few polysomnography studies available, it seems that all these drugs decrease the REM sleep ( Snyder et al., 1981 ; Staner et al., 2006 ; Sramek et al., 2014 ), similarly to antidepressants (see Wichniak et al., 2017 ), although with different mechanisms of action.

• Finally, similar trends for increased insomnia were observed with nalmefene, although much less evidence was available, and the statistical significance was null or not reported.
• These results are not surprising, given that both naltrexone and nalmefene act on opioid receptors, although with different mechanisms.

Opioids modulate various neurotransmitters including acetylcholine ( Illes, 1989 ; Mulder and Schoffelmeer, 1993 ), catecholamines ( Gunne, 1959 ; Moore et al., 1965 ), and GABA ( Jalabert et al., 2011 ; Horsfall and Sprague, 2017 ), and these neurotransmitters are well known to regulate the sleep–wake cycle (see Jones, 2019 ).

More studies are required to establish the exact mechanisms of the opioid-induced effects on sleep–wake cycle. A growing body of literature shows frequent association of AUD with sleep disorders ( Brower, 2003 ; Arnedt et al., 2007 ; Angarita et al., 2016 ). Given that sleep disturbances could have a crucial role in the risk of relapse ( Brower, 2001 ), an appropriate treatment of sleep problems may support the treatment of AUD.

The sedative-hypnotic benzodiazepines have been widely used to treat sleep problems as well as acute alcohol withdrawal ( Gensburger and Ghuysen, 2019 ); however, the use of these drugs is not appropriate for people with AUD, for the risk of dangerous interactions with alcohol, and for their potential to induce dependence ( Ashton, 2005 ).

It would be unsafe to prescribe benzodiazepines to a population that is clearly more prone to developing drug dependence and can relapse into concomitant heavy drinking, with the risk of drug-alcohol interaction. Recent alternatives to treat sleep disorders in AUD patients involve the newer GABA agonist, well known as Z-hypnotics or Z-drugs (zolpidem, zopiclone, and zaleplon).

These Z-drugs enhance GABA A receptor currents via a mechanism that differs from that proposed for benzodiazepines ( Dixon et al., 2015 ) and are indicated for the treatment of insomnia characterized by difficulties with sleep initiation. Although these drugs show lower dependence than benzodiazepines, there is still concern over the non-negligible potential of abuse of the “Z” hypnotics, which would be unsafe in people with history of drug addiction ( Hajak et al., 2003 ), and could also interact with alcohol.

Recent clinical trials have demonstrated that suvorexant, a dual hypocretin/orexin receptor, normalizes sleep in patients with primary insomnia. More recent studies suggest its potential for the treatment of sleep pathology associated with AUD ( Sanchez-Alavez et al., 2019 ). Campbell et al. (2018) suggested that suvorexant may also address key physiological components related with alcohol abstinence and withdrawal, such as sleep disorders, which should in turn help decrease or inhibit relapse ( Campbell et al., 2018 ).

Although these therapeutic approaches seem promising, there is increasing concern around the concomitant use of too many drugs in healthcare. Patients with AUD are at high risk of pharmacological interactions, due to the incidence of comorbidities, the concomitant intake of numerous drugs, and the pharmacodynamic and pharmacokinetic interferences of alcohol ( Guerzoni et al., 2018 ).

On the other hand, the use of hypnotic drugs among people with AUD could contribute to overdose mortality, a serious public health concern ( Foulds et al., 2018 ). The combination of drugs, called polypharmacy, exposes the patients to a dangerous vicious circle, as more drugs means more side effects often requiring additional treatments, thus increasing the risk of drug interactions ( Marengoni and Onder, 2015 ).

Moreover, a recent systematic review with meta-analysis reported that the additional pharmacotherapy of insomnia in patients with AUD doesn’t improve alcohol abstinence ( Miller et al., 2017 ). Therefore, it is particularly important to elucidate the effects of the pharmacotherapy for AUD on sleep quality, as this may help tailor the treatment based on the sleep profile of AUD patients.

A thorough choice of the appropriate pharmacotherapy for AUD with the lowest negative impact (or the highest positive impact) on sleep may better support the crucial phase of the acute withdrawal from alcohol and result in higher success. In this respect, it appears that acamprosate is the most beneficial (or less detrimental) drug for patients with AUD with history of sleep disturbances.

However, as highlighted by this review, there is no sufficiently detailed data to corroborate this. In addition, this systematic review has important limitations, such as the inclusion of limited number of articles that are sometimes outdated, especially on disulfiram (as this is a relatively old drug).

• Most importantly, as sleep measures were almost always reported as adverse effects, it was not possible to determine at what point in the study these were assessed and how was the sleep quality before the treatment, and this represents a potential bias.
• In conclusion, given the high burden that sleep disturbances pose on AUD patients, further polysomnography studies to elucidate the effects of these drugs on sleep architecture are long overdue.

More robust evidences on the effect of these drugs on sleep architecture may suggest a more holistic approach to treat AUD that takes into consideration sleep as a crucial element of the therapy, with benefits for the patients and maybe higher success.

Does acamprosate really work?

pronounced as (a kam’ pro sate) Acamprosate is used along with counseling and social support to help people who have stopped drinking large amounts of alcohol (alcoholism) to avoid drinking alcohol again. Drinking alcohol for a long time changes the way the brain works.

1. Acamprosate works by helping the brains of people who have drunk large amounts of alcohol to work normally again.
2. Acamprosate does not prevent the withdrawal symptoms that people may experience when they stop drinking alcohol.
3. Acamprosate has not been shown to work in people who have not stopped drinking alcohol or in people who drink large amounts of alcohol and also overuse or abuse other substances such as street drugs or prescription medications.

Acamprosate comes as a delayed-release (releases the medication in the intestine) tablet to take by mouth. It is usually taken with or without food three times a day. To help you remember to take acamprosate, take it around the same times every day. Taking acamprosate with breakfast, lunch, and dinner may help you to remember all three doses.

Follow the directions on your prescription label carefully, and ask your doctor or pharmacist to explain any part you do not understand. Take acamprosate exactly as directed. Do not take more or less of it or take it more often than prescribed by your doctor. Swallow the tablets whole; do not split, chew, or crush them.

Acamprosate helps to prevent you from drinking alcohol only as long as you are taking it. Continue to take acamprosate even if you do not think you are likely to start drinking alcohol again. Do not stop taking acamprosate without talking to your doctor.

Does acamprosate reduce anxiety?

Acamprosate reduced anxiety symptoms (mean HAM-A score reduction to 8.87 from a baseline of 20). Sixty-two percent of patients receiving acamprosate achieved remission (HAM-A score ≤7).

Is acamprosate hard on the liver?

ANNOTATED BIBLIOGRAPHY – References updated: 07 September 2021

Zimmerman HJ. Drugs used in aversion therapy. In, Zimmerman HJ. Hepatotoxicity: the adverse effects of drugs and other chemicals on the liver.2nd ed. Philadelphia: Lippincott, 1999, pp.724-6. (Expert review of hepatotoxicity published in 1999: discussion of hepatotoxicity of alcohol aversion pharmacotherapy is limited to disulfiram). Mihic SJ, Koob GF, Mayfield J, Harris RA. Ethanol. In, Brunton LL, Hilal-Dandan R, Knollman BC, eds. Goodman & Gilman’s the pharmacological basis of therapeutics.13th ed. New York: McGraw-Hill, 2018, pp.421-31. (Textbook of pharmacology and therapeutics). Paille FM, Guelfi JD, Perkins AC, Royer RJ, Steru L, Parot P. Double-blind, randomized multicentre trial of acamprosate in maintaining abstinence from alcohol. Alcohol Alcohol.1995; 30 :239–47. (Controlled trial of 2 doses of acamprosate vs placebo in 538 patients with alcohol abuse; only side effect that was more frequent with drug compared to placebo was diarrhea ; no mention of ALT levels and no cases of jaundice or hepatitis). Whitworth AB, Fischer F, Lesch OM, Nimmerrichter A, Oberbauer H, Platz T, Potgieter A, et al. Comparison of acamprosate and placebo in long-term treatment of alcohol dependence. Lancet.1996; 347 :1438–42. (Randomized controlled trial of 1 year course of acamprosate vs placebo in 448 recently abstinent alcoholic patients; only 40% of patients finished 1 year of therapy, abstinent rates were higher with acamprosate than placebo ; “Acamprosate had no effect on haematology or serum biochemistry”). Chick J, Howlett H, Morgan MY, Ritson B. United Kingdom Multicentre Acamprosate Study (UKMAS): a 6-month prospective study of acamprosate versus placebo in preventing relapse after withdrawal from alcohol. Alcohol Alcohol.2000; 35 :176–87. (Randomized controlled trial of 6 month course of acamprosate vs placebo in 581 recently abstinent alcoholic patients, found decrease in alcohol craving with acamprosate but no differences in rates of relapse; “No changes which could be attributed to the drug occurred in, biochemistry test results”). Bouza C, Angeles M, Muñoz A, Amate JM. Efficacy and safety of naltrexone and acamprosate in the treatment of alcohol dependence: a systematic review. Addiction.2004; 99 :811–28. (Systematic review of 33 studies of acamprosate and naltrexone; compliance rates were low, but acamprosate was associated with increased abstinence rates and had a “good safety pattern”; no mention of hepatotoxicity). Verheul R, Lehert P, Geerlings P, Koeter MW, van den Brink W. Predictors of acamprosate efficacy: results from a pooled analysis of seven European trials including 1485 alcohol-dependent patients. Psychopharmacology.2005; 178 :167–73. (Combined analysis of 7 controlled trials of acamprosate in 1485 patients; no discussion of side effects). Rosenthal RN, Gage A, Perhach JL, Goodman AM. Acamprosate; safety and tolerability in the treatment of alcohol dependence. J Addict Med.2008; 2 :40–50. (Analysis of 13 controlled trials of acamprosate in 4234 patients ; no clinically meaningful differences in clinical chemistry results were reported). Kranzler HR, Gage A. Acamprosate efficacy in alcohol-dependent patients: summary of results from three pivotal trials. Am J Addict.2008; 17 :70–6. (Reanalysis of 3 pivotal trials conducted in Europe in support of the US approval of acamprosate including 998 patients treated for 13-52 weeks; on reanalysis, complete abstinence rates were higher with acamprosate in all 3 studies ; no discussion of side effects or hepatotoxicity). Kennedy WK, Leloux M, Kutscher EC, Price PL, Morstad AE, Carnahan RM. Acamprosate. Expert Opin Drug Metab Toxicol.2010; 6 :363–80. (Review of biochemistry, pharmacology, metabolism, efficacy and safety of acamprosate; no evidence of hepatotoxicity; indeed, abstinence is usually associated with decreases in liver enzymes). Rösner S, Hackl-Herrwerth A, Leucht S, Lehert P, Vecchi S, Soyka M. Acamprosate for alcohol dependence. Cochrane Database Syst Rev.2010;(9):CD004332. (Systematic analysis of efficacy and safety of acamprosate for alcohol dependence, states that diarrhea is the only side effect occurring more frequently with acamprosate therapy; does not mention ALT elevations or hepatotoxicity). Witkiewitz K, Saville K, Hamreus K. Acamprosate for treatment of alcohol dependence: mechanisms, efficacy, and clinical utility. Ther Clin Risk Manag.2012; 8 :45–53. (Review of safety and efficacy of acamprosate; “pharmavigilance data from over 1.5 million patients has revealed no serious health risks”). Yahn SL, Watterson LR, Olive MF. Safety and efficacy of acamprosate for the treatment of alcohol dependence. Subst Abuse.2013; 6 :1–12. (Review of safety and efficacy of acamprosate; no mention of hepatotoxicity or ALT elevations). Jonas DE, Amick HR, Feltner C, Bobashev G, Thomas K, Wines R, Kim MM, et al. Pharmacotherapy for adults with alcohol use disorders in outpatient settings: a systematic review and meta-analysis. JAMA.2014; 311 :1889–900. (Systematic review of the safety and efficacy of pharmacotherapies of alcohol dependence and abuse concludes that acamprosate helps to decrease alcohol relapse; no mention of hepatototixicity or ALT elevations). Chalasani N, Bonkovsky HL, Fontana R, Lee W, Stolz A, Talwalkar J, Reddy KR, et al. United States Drug Induced Liver Injury Network. Features and outcomes of 899 patients with drug-induced liver injury: The DILIN Prospective Study. Gastroenterology.2015; 148 :1340–1352. (Among 899 cases of drug induced liver injury enrolled in a US prospective study between 2004 and 2013, none were attributed to acamprosate). Goh ET, Morgan MY. Review article: pharmacotherapy for alcohol dependence – the why, the what and the wherefore. Aliment Pharmacol Ther.2017; 45 :865–882. (Review of medical therapies for alcohol dependence mentions that acamprosate is not metabolized in the liver and is generally safe in persons with impaired hepatic function, and that despite 30 years of clinical use it has not been reported to have serious adverse effects). Antonelli M, Ferrulli A, Sestito L, Vassallo GA, Tarli C, Mosoni C, Rando MM, et al. Alcohol addiction – the safety of available approved treatment options. Expert Opin Drug Saf.2018; 17 :169–177. (Review of current pharmacologic treatments of alcohol addiction mentions that acamprosate has not been reported to be hepatotoxic and can be used safely in persons with mild liver disease).

What are the problems with acamprosate?

Precautions – If you will be taking this medicine for a long time, it is very important that your doctor check you at regular visits for any problems or unwanted effects that may be caused by this medicine. This medicine may cause some people to be agitated, irritable or display other abnormal behaviors.

Can you stop acamprosate abruptly?

Treatment Duration and Discontinuing Acamprosate – The effectiveness and safety of acamprosate have been evaluated for up to 1 year. The length of time a particular patient takes acamprosate will be determined, ideally, with input from the prescribing professional, the specialty treatment provider, and the patient.

• Discontinuation of acamprosate may be considered once a patient has achieved stable abstinence from alcohol, reports diminished craving, and has established a sound plan and support for ongoing recovery.
• Acamprosate therapy also may be discontinued if a patient is not adhering to the medication regimen.

Acamprosate should not be discontinued just because a patient returns to alcohol use. There is no withdrawal syndrome associated with discontinuing acamprosate, and it is not necessary to taper the dose.

Does acamprosate make you hungry?

Does acamprosate cause weight gain? Weight gain is frequently reported as a side effect of by people taking this medication to control alcohol cravings associated with, Acamprosate can also cause weight loss, but this is reported infrequently. Weight gain and weight loss are more commonly reported by patients who take both acamprosate and antidepressant medications at the same time.

• Weight gain linked to acamprosate is thought to be caused by the increase in appetite that some people taking this medication experience.
• It is not clear whether increased appetite is caused by the medication itself or from stopping drinking alcohol.
• Acamprosate is also known by the name Campral, which is a discontinued brand name of the drug.

Various generic versions of acamprosate are currently available. : Does acamprosate cause weight gain?

How does acamprosate reduce cravings?

Benefits of Acamprosate –

Absorbed through the digestive tract rather than the liver, improving effectiveness and reducing side effects for patients with liver damage. Fewer, generally less severe, and less prevalent side effects than other medications. No known drug interactions with other medications or substances. Actively reduces cravings for and dependence on alcohol, by reacting with neurotransmitters in the brain, rather than reducing the pleasurable impacts of alcohol or creating negative side effects from alcohol use.

How long is the treatment for acamprosate?

My Account Area – 1. Name of the medicinal product Acamprosate 333 mg Gastro-resistant Tablets.2. Qualitative and quantitative composition Each gastro-resistant tablet contains acamprosate calcium 333.0 mg as the active ingredient. For the full list of excipients, see section 6.1.3. Pharmaceutical form Gastro-resistant tablet. White, round, biconvex coated tablet plain on both sides.4. Clinical particulars 4.1 Therapeutic indications Acamprosate is indicated as therapy to maintain abstinence in alcohol-dependent patients. It should be combined with counselling.4.2 Posology and method of administration Posology Adults within the age range 18-65 years – 2 tablets three times daily with meals (2 tablets in the morning, noon and night) in subjects weighing 60kg or more. – In subjects weighing less than 60kg, 4 tablets divided into three daily doses with meals (2 tablets in the morning, 1 at noon and 1 at night). Paediatric population and older people Acamprosate should not be administered to children, adolescents and the elderly. Duration of treatment The recommended treatment period is one year. Treatment with acamprosate should be initiated as soon as possible after the withdrawal period and should be maintained if the patient relapses. Acamprosate does not prevent the harmful effects of continuous alcohol abuse. Continued alcohol abuse negates the therapeutic benefit; therefore acamprosate treatment should only be initiated after weaning therapy, once the patient is abstinent from alcohol. Method of administration For oral use. Swallow this tablet whole. Do not chew or crush the tablet as this may damage the gastro-resistant coating.4.3 Contraindications Hypersensitivity to the active substance or to any of the excipients listed in section 6.1. Breast-feeding women (see section 4.6) Patients with renal impairment (serum creatinine >120 micromol/l) 4.4 Special warnings and precautions for use The safety and efficacy of acamprosate has not been established in patients younger than 18 years or older than 65 years. Acamprosate is therefore not recommended for use in these populations. The safety and efficacy of acamprosate has not been established in patients with severe liver insufficiency (Childs-Pugh Classification C). Because the interrelationship between alcohol dependence, depression and suicidality is well-recognised and complex, it is recommended that alcohol-dependent patients, including those treated with acamprosate, be monitored for such symptoms. Abuse and dependence Non-clinical studies suggest that acamprosate has little or no abuse potential. No evidence of dependence on acamprosate was found in any clinical study thus demonstrating that acamprosate has no significant dependence potential.4.5 Interaction with other medicinal products and other forms of interaction The concomitant intake of alcohol and acamprosate does not affect the pharmacokinetics of either alcohol or acamprosate. Administering acamprosate with food diminishes the bioavailability of the drug compared with its administration in the fasting state. In clinical trials, acamprosate has been safely administered in combination with antidepressants, anxiolytics, hypnotics and sedatives, and non-opioid analgesics. No change in the frequency of clinical and/or biological adverse reactions has been shown when acamprosate is used concomitantly with disulfiram, oxazepam, tetrabamate or meprobamate. Pharmacokinetic studies have been completed and show no interaction between acamprosate and diazepam, imipramine. There is no information available on the concomitant administration of acamprosate with diuretics.4.6 Fertility, pregnancy and lactation Pregnancy There are no adequate data from the use of acamprosate in pregnant women. Animal studies do not indicate any evidence of foetotoxicity or tetragenicity. Acamprosate must therefore only be used during pregnancy after a careful benefit/risk assessment, when the patient cannot abstain from drinking alcohol without being treated with acamprosate and when there is consequently a risk of foetotoxicity or teratogenicity due to alcohol. Breast-feeding It is known that acamprosate is excreted in the milk of lactating animals. It is not known whether acamprosate is excreted in human milk. There are no adequate data from the use of acamprosate in infants. Acamprosate must therefore not be used in breastfeeding women. If a breastfeeding woman cannot abstain from drinking alcohol without being treated with acamprosate, a decision must be made whether to discontinue breast-feeding or to discontinue Acamprosate, taking into account the importance of the medicinal product to the woman. Fertility In animal studies, no adverse effects on fertility were observed. Whether or not acamprosate affects the fertility in humans is unknown.4.7 Effects on ability to drive and use machines Acamprosate has no influence on the ability to drive and use machines.4.8 Undesirable effects According to information collected during clinical trials and spontaneous reports since marketing authorisation, the following adverse reactions may occur under treatment with Acamprosate. The following definitions apply to the frequency terminology used hereafter: very common (≥ 1/10), common (≥ 1/100 to < 1/10), uncommon (≥ 1/1,000 to < 1/100), rare (≥ 1/10,000 to < 1/1,000), very rare (< 1/10,000), not known (cannot be estimated from the available data).

Immune system disorders:

Very rare: Hypersensitivity reactions including urticaria, angio-oedema or anaphylactic reactions.

Psychiatric disorders:

Common: Decreased libido.

Uncommon: Increased libido.

Gastrointestinal disorders:

Very common: Diarrhoea.

Common: Abdominal pain, nausea, vomiting, flatulence.

Skin and subcutaneous tissue disorders:

Common: Pruritus, maculo-papular rash.

Not known: Vesiculo-bullous eruptions.

Reproductive system and breast disorders:

Common: Frigidity or impotence.

Reporting of suspected adverse reactions Reporting suspected adverse reactions after authorisation of the medicinal product is important. It allows continued monitoring of the benefit/risk balance of the medicinal product. Healthcare professionals are asked to report any suspected adverse reactions via Yellow Card Scheme at: www.mhra.gov.uk/yellowcard or search for MHRA Yellow Card in the Google Play or Apple App Store.4.9 Overdose Acute overdose is usually mild.

• In the reported cases, the only symptom which can be reasonably related to overdose is diarrhoea.
• No case of hypercalcaemia has ever been reported.
• Treatment of overdose is directed to symptoms.5.
• Pharmacological properties 5.1 Pharmacodynamic properties Pharmacotherapeutic group: Drugs used in addictive disorders, drugs used in alcohol dependence, ATC code: N07BB03 Mechanism of action Acamprosate (calcium acetylhomotaurinate) has a chemical structure similar to that of amino acid neuromediators, such as taurine or gamma-amino-butyric acid (GABA), including an acetylation to permit passage across the blood brain barrier.

Pharmacodynamic effects Acamprosate may act by stimulating GABAergic inhibitory neurotransmission and antagonising excitatory amino-acids, particularly glutamate. Animal experimental studies have demonstrated that acamprosate affects alcohol dependence in rats, decreasing the voluntary intake of alcohol without affecting food and total fluid intake.5.2 Pharmacokinetic properties Absorption Acamprosate absorption across the gastrointestinal tract is moderate, slow and sustained and varies substantially from person to person.

• Food reduces the oral absorption of acamprosate.
• Steady state levels of acamprosate are achieved by the seventh day of dosing.
• Oral absorption shows considerable variability and is usually less than 10% of the ingested drug in the first 24 hours.
• Distribution Acamprosate is not protein bound.
• Biotransformation The drug is not metabolised significantly.

Elimination The drug is excreted in the urine. Linearity There is a linear relationship between creatinine clearance values and total apparent plasma clearance, renal clearance and plasma half-life of acamprosate. Hepatic impairment The kinetics of acamprosate are not modified in group A or B of the Child-Pugh classification of impaired liver function, a population which is likely to be part of the target population for acamprosate.

This is in accordance with the absence of hepatic metabolism of the drug.5.3 Preclinical safety data In the preclinical studies, signs of toxicity are related to the excessive intake of calcium and not to acetylhomotaurine. Disorders of phosphorus/calcium metabolism have been observed including diarrhoea, soft tissue calcification, renal and cardiac lesions.

Acamprosate had no mutagenic or carcinogenic effect, nor any teratogenic or adverse effects on the male or female reproductive systems of animals. Detailed in vitro and in vivo research on acamprosate to detect genetic and chromosomal mutations has not produced any evidence of potential genetic toxicity.6.

Pharmaceutical particulars 6.1 List of excipients Tablet Core: Glycerol dibehenate Cellulose, microcrystalline Hypromellose Silica, Colloidal anhydrous Magnesium stearate Tablet seal coating: Hypromellose Tablet gastro-resistant coating: Methacrylic acid-ethyl acrylate copolymer Talc Propylene glycol 6.2 Incompatibilities Not applicable.6.3 Shelf life 3 years.6.4 Special precautions for storage This medicinal product does not require any special storage conditions.6.5 Nature and contents of container PVC blister in packs of 84, 168 and multipacks containing 168 (2 packs of 84) tablets.

Not all pack sizes may be marketed.6.6 Special precautions for disposal and other handling No special requirements for disposal. Any unused medicinal product or waste material should be disposed of in accordance with local requirements.7. Marketing authorisation holder Generics Limited t/a Mylan Station Close Potters Bar Hertfordshire EN6 1TL United Kingdom 8.

Does acamprosate increase GABA?

Acamprosate enhances N-methyl-D-apartate receptor-mediated neurotransmission but inhibits presynaptic GABA (B) receptors in nucleus accumbens neurons.

Does Campral make you sleepy?

Before using this medication, tell your doctor or pharmacist your medical history, especially of: kidney disease. This drug may make you dizzy or drowsy. Alcohol or marijuana (cannabis) can make you more dizzy or drowsy. Do not drive, use machinery, or do anything that needs alertness until you can do it safely.

What is the benefit of acamprosate?

Acamprosate In Treating Alcoholism – Acamprosate helps reduce the urge to to drink so people in recovery can focus on their sobriety and getting better. Unlike other medications used to treat alcoholism, this drug is non-habit forming and will not lead to prescription drug abuse.

• Within the first few days and weeks after a person quits drinking, they’re likely to experience uncomfortable withdrawal symptoms.
• Since withdrawal symptoms can range from mild to severe, it’s highly recommended to undergo detox in an inpatient rehab facility.
• In this type of setting, patients receive around-the-clock care from treatment providers.

Once a patient is no longer physically dependent on alcohol, a treatment professional may administer acamprosate. This drug helps people stay abstinent and prevents them from falling back into old habits. In the event of a relapse, the medication will not cause an adverse reaction or exacerbate withdrawal symptoms.

Is acamprosate similar to GABA?

ACAMPROSATE – Acamprosate is a compound with a chemical structure similar to that of the neurotransmitter GABA and the neuromodulator taurine. Its mechanism of action is not completely understood but most likely involves a functional antagonism or modulation of the glutamate NMDA receptor, which is upregulated in chronic alcoholism.

In double-blind, placebo-controlled trials, mostly conducted in Europe, acamprosate effectively maintained complete abstinence in detoxified alcohol-dependent patients ( Swift, 2007 ). When used as an adjunct to psychosocial interventions, acamprosate improves drinking outcomes such as the length and rate of abstinence.

Three European multicenter, randomized, double-blind studies of acamprosate as an adjunct to psychosocial treatment supported the FDA approval of acamprosate as an effective agent in the maintenance of abstinence from alcohol ( Paille et al., 1995 ; Pelc et al., 1997 ; Sass, Soyka, Mann, & Zieglgansberger, 1996 ).

• Meta-analyses that compare acamprosate statistically across several studies have supported the efficacy of acamprosate in improving the rates of abstinence and increasing the time to first drink, with small effect sizes ( Bouza et al., 2004 ; Mann, Lehert, & Morgan, 2004 ).
• Interestingly, the efficacy of acamprosate seems most strong only in those trials conducted in Europe; two U.S.

trials, a 6-month multisite study ( Mason, Goodman, Chabac, & Lehert, 2006 ) and the COMBINE study ( Anton et al., 2006 ), failed to find similar efficacy. Reasons for the differences in the effectiveness of acamprosate between European and U.S. studies are unclear.

How often is acamprosate dosing?

Adult – 666mg 3 times daily. Renal impairment (CrCl 30–50mL/min): initially 333mg 3 times daily. Begin therapy during abstinence; continue during relapse.

What sleep medication do recovering alcoholics take?

Trazodone – Trazodone is a sedating antidepressant which acts predominantly on the serotonergic system. It is one of the most commonly prescribed sleep aids in patients with alcohol dependence ( Friedmann et al,, 2003 ). It is not habit forming and has no abuse potential which might explain why it is frequently prescribed in patients with alcohol addiction.

Our search revealed two studies of trazodone used to treat sleep problems following cessation of alcohol use. A small, placebo-controlled trial of 16 patients following detoxification and a 2-week washout period revealed an improvement in some polysomnographic (PSG) sleep measures ( Le Bon et al,, 2003 ).

Trazodone was started at 50 mg and gradually increased to a dose of 200 mg. In cases where this was not tolerated, a dose of 150 mg was used. A polysomnogram was performed on Days 1, 2 (prior to receiving trazodone), Day 3 (first dose of trazodone, 50 mg) and on Day 28.

No drinking measures were used in this study. Wake-time after sleep onset (WASO) was improved on Days 3 and 28. Sleep efficiency was improved on Day 3, but on Day 28 the difference between the trazodone group and the placebo group was not significant. The total non-rapid eye movements sleep percentage was also improved on Day 3 but not on Day 28.

Clinical global impression (CGI), a clinician rating of the severity of the patient’s illness and Hamilton Depression Rating Scale (HAM-D) scores were significantly improved in the trazodone group ( Guy, 1976). A large, NIAAA-supported, placebo-controlled trial conducted over a period of 24 weeks in 173 patients right after detoxification revealed that trazodone significantly improved sleep.

Patients were prescribed trazodone in the range of 50–150 mg (average of 100 mg) for 12 weeks and following this the trazodone was discontinued ( Friedmann et al,, 2008 ). Trazodone improved sleep as measured by the Pittsburgh Sleep Quality Index (PSQI) at 1 month (Cohen’s d : 0.5) and at 3 months (Cohen’s d : 0.93).

Following discontinuation, sleep measures reverted to placebo level. Abstinence rates were no different between the trazodone and the placebo groups, both being low at 9.1 vs.14.1%, respectively. However, only 25.3% of patients in this trial reported having received formal alcohol treatment following detoxification.

What are the precautions for acamprosate?

You should not use acamprosate if you are allergic to it, or if you have severe kidney disease. Tell your doctor if you have ever had kidney problems. Some people have thoughts about suicide while taking acamprosate. Your doctor will need to check your progress at regular visits.

How does acamprosate reduce cravings?

Benefits of Acamprosate –

Absorbed through the digestive tract rather than the liver, improving effectiveness and reducing side effects for patients with liver damage. Fewer, generally less severe, and less prevalent side effects than other medications. No known drug interactions with other medications or substances. Actively reduces cravings for and dependence on alcohol, by reacting with neurotransmitters in the brain, rather than reducing the pleasurable impacts of alcohol or creating negative side effects from alcohol use.

Does acamprosate need to be taken with food?

Acamprosate comes as a delayed-release (releases the medication in the intestine) tablet to take by mouth. It is usually taken with or without food three times a day. To help you remember to take acamprosate, take it around the same times every day.

Does acamprosate reduce anxiety?

Acamprosate reduced anxiety symptoms (mean HAM-A score reduction to 8.87 from a baseline of 20). Sixty-two percent of patients receiving acamprosate achieved remission (HAM-A score ≤7).

Does acamprosate make you drowsy?

Precautions – If you will be taking this medicine for a long time, it is very important that your doctor check you at regular visits for any problems or unwanted effects that may be caused by this medicine. This medicine may cause some people to be agitated, irritable or display other abnormal behaviors.