Acamprosate

General information

Acamprosate (calcium acetylhomotaurinate) has been postulated to act by restoring the alcohol-induced neurotransmission imbalance of inhibition–excitation inputs believed to underlie alcohol dependence [ , ]. The molecular structure of acamprosate explains its specificity toward the basic molecular mechanisms involved in the pathophysiology of alcohol dependence. A competitive interaction has been described between spermidine and acamprosate, suggesting a specific binding site for acamprosate on N-methyl- d -aspartate receptors [ ].

To test the role of acamprosate as an aid in preventing relapse after detoxification, 296 alcohol-dependent patients entered a prospective, multicenter, randomized, double-blind, placebo-controlled study of acamprosate 666 mg tablets tds for 180 days [ ]. Unlike previous studies, acamprosate was prescribed from the start of alcohol withdrawal, rather than after the detoxification process. During the treatment period, 110 patients dropped out. The two treatment groups were balanced with regard to baseline values and reasons for discontinuation. There was no difference between the groups in the severity of withdrawal symptoms, as measured by the CIWA-Ar (Clinical Institute Withdrawal Assessment for Alcohol scale). Acamprosate given during withdrawal did not cause unwanted effects. The overall incidence of adverse events was similar in the two groups. The number of patients who presented at least one new adverse event (not present at baseline) during the course of the study was 99 with acamprosate and 94 with placebo. Nevertheless, there was a trend for gastrointestinal adverse events to be reported more often in the acamprosate-treated patients (n = 61) compared with placebo (n = 46). The individual adverse events that were reported more often with acamprosate were diarrhea, dyspepsia, constipation, and flatulence. Pruritus was reported by seven of those who took acamprosate and five of those who took placebo.