There is a variety of specialized outpatient and residential Alcohol and Other Drugs (AOD) services, but research on outcomes of these services is limited. Given the chronic, relapsing nature of AOD problems, there is a need for longitudinal research on outcomes after treatment in various AOD services.

Patient-Reported Outcome Measures (PROMs) and Patient-Reported Experience Measures (PREMs) are hardly used in the AOD field but provide excellent tools and a framework to monitor progress and outcomes in these services based on experiences of service users.

The objectives of the OMER-BE study are to:

1. Assess and compare patient characteristics at baseline in various treatment modalities

2. Test and prepare the routine measurement of PROMs and PREMs in AOD services using a self-report tool

3. Assess patient-reported experiences qualitatively in various treatment modalities for AOD patients

The overall goal is to continuously assess and improve AOD services.

We have set up a naturalistic, longitudinal cohort study for which we will engage and follow up 250 AOD users as they present themselves in selected AOD services in four different treatment modalities (outpatient non-pharmacological treatment, outpatient substitution treatment, residential psychiatric treatment and therapeutic communities for addictions).

Sociodemographic and clinical factors and PROMs will be assessed at baseline. PROMs and PREMs will be assessed at 45-, 90- and 180-days follow-up. The questionnaires that will be used during the baseline and follow-up assessments are based on the ICHOM Standard Set for Addictions (ICHOM SSA, 2020), a set of brief validated questionnaires to measure and monitor treatment outcomes routinely in AOD services.

Following the 6-month follow-up we will perform a qualitative study in a subset of N=20 participants (5 per treatment modality). These participants will be invited to take part in an in-depth interview with one of the researchers, where the following topics will be discussed: treatment history, recovery experiences, helping and hindering factors in recovery, and experiences with different treatment modalities.

47 participants have been recruited in the OMER-BE study up until October 2022. 38 (81%) of the participants were born male, 9 (19%) were born female. The average age of participants is 33, with ages ranging from 19 to 47 years old.

Preliminary findings will be presented at the congress.

Further recruitment of study participants up to a total of 250 will be undertaken until the end of 2023.

The OMER-BE study aims to assess and improve AOD services by using a self-report tool, measuring PROMs and PREMs.

None Declared

Little is known about the effect of ethnicity on the response to antipsychotic medication in patients with schizophrenia.

To determine whether ethnicity moderates the response to antipsychotic medication in patients with schizophrenia, and whether this moderation is independent of confounders.

We analysed 18 short-term, placebo-controlled registration trials of atypical antipsychotic medications in patients with schizophrenia (N = 3880). A two-step, random-effects, individual patient data meta-analysis was applied to establish the moderating effect of ethnicity (White versus Black) on symptom improvement according to the Brief Psychiatric Rating Scale (BPRS) and on response, defined as >30% BPRS reduction. These analyses were corrected for baseline severity, baseline negative symptoms, age and gender. A conventional meta-analysis was performed to determine the effect size of antipsychotic treatment for each ethnic group separately.

In the complete data-set, 61% of patients were White, 25.6% of patients were Black and 13.4% of patients were of other ethnicities. Ethnicity did not moderate the efficacy of antipsychotic treatment: pooled β-coefficient for the interaction between treatment and ethnic group was −0.582 (95% CI −2.567 to 1.412) for mean BPRS change, with an odds ratio of 0.875 (95% CI 0.510–1.499) for response. These results were not modified by confounders.

Atypical antipsychotic medication is equally effective in both Black and White patients with schizophrenia. In registration trials, White and Black patients were overrepresented relative to other ethnic groups, limiting the generalisability of our findings.

Cognitive deficits may be characteristic for only a subgroup of first-episode psychosis (FEP) and the link with clinical and functional outcomes is less profound than previously thought. This study aimed to identify cognitive subgroups in a large sample of FEP using a clustering approach with healthy controls as a reference group, subsequently linking cognitive subgroups to clinical and functional outcomes.

204 FEP patients were included. Hierarchical cluster analysis was performed using baseline brief assessment of cognition in schizophrenia (BACS). Cognitive subgroups were compared to 40 controls and linked to longitudinal clinical and functional outcomes (PANSS, GAF, self-reported WHODAS 2.0) up to 12-month follow-up.

Three distinct cognitive clusters emerged: relative to controls, we found one cluster with preserved cognition (n = 76), one moderately impaired cluster (n = 74) and one severely impaired cluster (n = 54). Patients with severely impaired cognition had more severe clinical symptoms at baseline, 6- and 12-month follow-up as compared to patients with preserved cognition. General functioning (GAF) in the severely impaired cluster was significantly lower than in those with preserved cognition at baseline and showed trend-level effects at 6- and 12-month follow-up. No significant differences in self-reported functional outcome (WHODAS 2.0) were present.

Current results demonstrate the existence of three distinct cognitive subgroups, corresponding with clinical outcome at baseline, 6- and 12-month follow-up. Importantly, the cognitively preserved subgroup was larger than the severely impaired group. Early identification of discrete cognitive profiles can offer valuable information about the clinical outcome but may not be relevant in predicting self-reported functional outcomes.

To examine the mortality risk of current and life-time depressive as well as anxiety disorders, whether this risk is moderated by sex or age, and whether this risk can be explained by lifestyle and/or somatic health status.

A cohort study (Lifelines) including 141,377 participants (18–93 years) which were followed-up regarding mortality for 8.6 years (range 3.0–13.7). Baseline depressive and anxiety disorders according to Diagnostic and Statistical Manual of Mental Disorders, fourth edition criteria were assessed with the Mini International Neuropsychiatric Interview and lifetime diagnoses by self-report. All-cause mortality was retrieved from Statistics Netherlands. Cox-regression was applied to calculate proportional hazard ratios, adjusted for lifestyle (physical activity, alcohol use, smoking, and body mass index) and somatic health status (multimorbidity and frailty) in different models.

The mortality rate of depressive and anxiety disorders was conditional upon age but not on sex. Only in people below 60 years, current depressive and anxiety disorders were associated with mortality. Only depressive disorder and panic disorder independently predicted mortality when all mental disorders were included simultaneously in one overall model (hazard ratio [HR] = 2.18 [95% confidence intervals (CI): 1.56–3.05], p < 0.001 and HR = 2.39 [95% CI: 1.15–4.98], p = 0.020). Life-time depressive and anxiety disorders, however, were independent of each other associated with mortality. Associations hardly changed when adjusted for lifestyle characteristics but decreased substantially when adjusted for somatic health status (in particular physical frailty).

In particular, depressive disorder is associated with excess mortality in people below 60 years, independent of their lifestyle. This effect seems partly explained by multimorbidity and frailty, which suggest that chronic disease management of depression-associated somatic morbidity needs to be (further) improved.

Addiction is now generally regarded to be a brain disease with a chronic course and a high probability of relapse even after long periods of abstinence. Recently, attention in the pathogenesis od addictive behaviors has shifted from abnormalities in the reward and motivational systems towards co-occurring abnormalities in decision making such as conflict monitoring and impulsivity. In this presentation, new data on abnormal decision making in substance use disorders and pathological gambling are presented.

A selected review of the recent literature including data from patients with substance use disorders and pathological gambling.

The data currently available show that smokers, alcoholics, drug dependent patients and pathological gamblers all suffer from abnormalities in motor impulsivity and delay discounting problems and that these abnormalities are associated with hypoactivity of the prefrontal cortex (PFC). Data further show that these abnormalities can not be fully attributed to the presence of comorbid axis I or axis II disorders. Recent data also show that activation of the PFC is dependent on adequate error and conflict monitoring by the anterior cingulate cortex (ACC). However, currently no data are available regarding ACC functioning in addicted patients, but it can not be excluded that at least part of the decision making abnormalities are due to deficits in error/conflict monitoring.

Substance dependent patients and pathological gamblers are characterized by serious deficits in decision making and these deficits should be adressed in future treatments for example through medication, EEG- or fMRI-feedback or transcranial magnetic stimulation.

Addiction, or Substance Use Disorder (SUD), among adults with Autism Spectrum Disorders (ASD) has never been studied before, contrary to SUD in ADHD. However, we know from clinical practice that comorbid SUD in ASD can present with a considerable impairment. Distinguishing between ASD and ADHD can be challenging, but becomes increasingly so in case of comorbid SUD.

The main objective of this study was to gain insight into the aspects of comorbid SUD in ASD on three levels: a phenotypical, an endophenotypical, and a genetic level. A second objective was to determine how ASD differs from ADHD in adult patients on these three levels, with and without comorbid SUD.

We studied 130 patients with ASD (n = 75) or ADHD (n = 55) with or without SUD. We looked at risk factors for developing SUD, prevalence, and outcome. Furthermore, we studied personality profiles and autism spectrum profiles (AQ). We assembled neuropsychological and genetic data.

Comorbidity of SUD with ASD is less common than in ADHD, but the consequences are just as severe. Comorbid SUD is not always associated with a negative outcome, at least in the perception of the individual. Assessment of adults with ASD and SUD can be misleading when the neuropsychological functioning is not also taken into consideration. Finally, in the absence of SUD, ASD and ADHD in adults share many features on the (endo-)phenotypical level, but may be distinguishable at a genetic level. In the presence of SUD, differences between ASD and ADHD are more pronounced.

We describe the efficacy and safety of as-needed use of nalmefene in the subgroup of patients with a high drinking risk level (DRL; men:>60g/day; women:>40g/day); i.e. a group of patients with a great unmet medical need for.

To evaluate the 6 month efficacy and safety of as-needed use of nalmefene 18mg versus placebo in a subgroup of alcohol-dependent patients with high DRL from a randomised controlled trial [NCT00812461].

All patients received a motivational and adherence-enhancing intervention (BRENDA) in combination with either nalmefene or placebo. Number of heavy drinking days (HDDs) and total alcohol consumption (TAC) were measured using the Timeline Follow-back method. Additionally, data on clinical improvement, liver function and safety were collected throughout the study.

The study population consisted of 317 patients: placebo N=162; nalmefene N=155 (mean age 44.8±10.3 years; 69% men; mean HDDs: 22±6.2/month; mean TAC 111±47.9g/day). Mean number of HDDs decreased to 10 days/month and mean TAC decreased to 43g/day at month 6 in the nalmefene group. There was a superior effect of nalmefene compared to placebo in reducing the number of HDDs (-2.7 [95% CI: -5.0;-0.3];p=0.0253) and TAC -10.3 [-20.2;-0.5];p=0.0404). Improvements in clinical status and alanine amino transferase were greater in the nalmefene group compared to the placebo group (p< 0.05). Adverse events were more common with nalmefene; incidence of adverse events leading to dropout was at the placebo level.

As-needed nalmefene was efficacious in reducing alcohol consumption in patients with high risk for alcoholrelated harm.

There is growing evidence that cognitive deficits play an important role in the development, course and relapse of substance use disorders. In particular, functions that involve control over one's own behaviour (impulsivity), and over behaviour when confronted with motivationally relevant drug cues (craving) are related to relapse in recent studies. So far, pharmacological manipulations of cognitive deficits are rare and relapses after treatment are the rule rather than the exception.

Therefore, we performed a randomized, double-blind, placebo-controlled trial with modafinil, which is a known cognitive enhancer and a wake-promoting agent.

At first, the interaction between impulse control, overall cognitive functioning, motivational strength of drug cues, and vulnerability to relapse, will be elucidated in order to disentangle new treatment possibilities. Second, the effectiveness of a long term treatment with modafinil on impulse control and relapse will be explored.

83 abstinent alcohol dependent inpatients were randomized to a single morning dose of modafinil (300 mg/d), or matching placebo, for 10 weeks. Both neurocognitive tests (on impulsivity, craving and overall cognitive functioning) and self-report questionnaires were administered before, during and after treatment. Patients were followed up 6 months after treatment, to measure relapse rate. Primary outcome variables are test performance, craving ratings and relapse.

Data will be unblinded after finalizing the follow-up data collection. Therefore, results will be available from January 2012.

It is expected that modafinil improves cognitive functioning, increases time to first relapse and reduces relapse rates and relapse severity, compared to placebo.

Current treatments for alcohol dependence, aiming to keep patients abstinent, have shown limited treatment and success rates. Reduction of alcohol consumption is increasingly recognised as a valid and needed option that should be an integrated part of the management of alcohol-dependent patients.

The main objective was to evaluate the efficacy of as-needed use of nalmefene 18 mg (base) versus placebo in reducing the monthly number of heavy drinking days (HDDs) and the monthly total alcohol consumption (TAC; g/day) over 24 weeks in alcohol-dependent patients.

Drinking measures were derived from daily drinking estimates collected with the Timeline Followback method. Safety and additional efficacy data were collected throughout the study.

A total of 604 patients (mean age 51.6 ± 9.6 years, 67% men) were randomised (298 to placebo and 306 to nalmefene). There was a significantly superior effect (mixed model repeated measures) of nalmefene compared to placebo in reducing the number of HDDs (−2.3 ± 0.8 [95% CI −3.8; −0.8]; p = 0.002) and TAC (−11.0 ± 3.0 [95% CI −16.8; −5.1]; p < 0.001). Improvements in Clinical Global Impression - Global Improvement and Severity of Illness scores and reductions in liver enzymes gamma-glutamyltransferase and alanine aminotransferase from baseline were statistically significantly larger in the nalmefene group compared to placebo at week 24. Adverse events (generally transient; most were mild or moderate) and withdrawals were more common with nalmefene than placebo.

Nalmefene was efficacious in reducing alcohol consumption. Nalmefene was safe and well tolerated and dosing on an as-needed basis was feasible.

We describe the efficacy and safety of as-needed use of nalmefene in the subgroup of patients with a high drinking risk level (DRL; men:>60g/day; women:>40g/day); i.e. a group of patients with a great unmet medical need for treatment.

To evaluate the 1 year efficacy and safety of as-needed use of nalmefene 18mg versus placebo in a subgroup of alcohol dependent patients with high DRL from a randomised controlled trial [NCT00811941].

All patients received a motivational and adherence-enhancing intervention (BRENDA) in combination with either nalmefene or placebo. Number of heavy drinking days (HDDs) and total alcohol consumption (TAC) were measured using the Timeline Follow-back method. Additionally, data on clinical improvement, liver function and safety were collected throughout the study.

The study population consisted of 187 patients: placebo N=42; nalmefene N=145 (mean age 46.2±11.9 years; 78% men; mean HDDs 19±6.3/month; mean TAC 101±45.0 g/day). Mean number of HDDs decreased to 7 days/month and mean TAC decreased to 33g/day at 1 year in the nalmefene group. At 1 year, there was a superior effect of nalmefene compared to placebo in reducing the number of HDDs (-3.6 [95% CI:-6.5;-0.7]; p=0.0164) and TAC -17.3 [-30.9;-3.8]; p=0.0129). Improvements in clinical status and in liver enzymes from baseline were larger in the nalmefene compared to the placebo group. Adverse events and adverse events leading to dropout were more common with nalmefene than placebo.

As-needed nalmefene was efficacious in reducing alcohol consumption in patients with high risk for alcoholrelated harm.

The phase 3 programme investigating nalmefene for reduction of alcohol consumption in alcohol dependent patients comprised two 6-month studies (ESENSE1 and 2) and one 12-month study (SENSE), conducted in 19 European countries.

To investigate the tolerability and safety of as-needed use of 18 mg nalmefene.

1997 patients with a diagnosis of alcohol dependence were recruited. Adverse events (AEs) and other safety variables were recorded.

797 patients in the placebo group and 1144 patients in the nalmefene group received study medication; patients took study medication on 62% and 51% of the days, respectively. The incidence of AEs was high in both the placebo and the nalmefene group (62.7% and 74.7%, respectively), and was not dependent on the drinking risk level at baseline. While mostly mild or moderate, these AEs did lead to dropout in some patients: 47 patients (6%) in the placebo group and 149 patients (13%) in the nalmefene group. Patients continuing in the studies seemed to develop tolerance with time for the most frequent AEs. Median time to event and median duration of these AEs were generally shorter for nalmefene than for placebo (many started after 1st dose). 35 patients (4.4%) in the placebo group and 57 patients (5.0%) in the nalmefene group had serious adverse events (SAEs). The majority of SAEs were not related to study medication and no apparent trends with respect to overall incidence or distribution across organ systems were noted.

Nalmefene was well-tolerated and no major safety issues were identified.