BAP updated guidelines: evidence-based guidelines for the pharmacological management of substance abuse, harmful use, addiction and comorbidity: recommendations from BAP

Lingford‐Hughes, Anne; Welch, Sarah; Peters, Lesley; Nutt, David

doi:10.1177/0269881112444324

Cited by 275 publications

(270 citation statements)

References 588 publications

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“…Methadone and buprenorphine are effective and essential medicines for the management of opioid dependence 7, 8. Opioid substitution treatment (OST) has positive benefits across multiple outcomes on mortality risk, transmission of HIV and hepatitis C virus (HCV), HIV treatment prognosis and drug‐related crime 1, 9, 10, 11, 12, 13, 14, 15, 16.…”

Section: Introductionmentioning

confidence: 99%

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The impact of buprenorphine and methadone on mortality: a primary care cohort study in the United Kingdom

et al. 2018

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AimsTo estimate whether opioid substitution treatment (OST) with buprenorphine or methadone is associated with a greater reduction in the risk of all‐cause mortality (ACM) and opioid drug‐related poisoning (DRP) mortality.DesignCohort study with linkage between clinical records from Clinical Practice Research Datalink and mortality register.SettingUK primary care.ParticipantsA total of 11 033 opioid‐dependent patients who received OST from 1998 to 2014, followed‐up for 30 410 person‐years.MeasurementsExposure to methadone (17 373, 61%) OST episodes or buprenorphine (9173, 39%) OST episodes. ACM was available for all patients; information on cause of death and DRP was available for 5935 patients (54%) followed‐up for 16 363 person‐years. Poisson regression modelled mortality by treatment period with an interaction between OST type and treatment period (first 4 weeks on OST, rest of time off OST, first 4 weeks off OST, rest of time out of OST censored at 12 months) to test whether ACM or DRP differed between methadone and buprenorphine. Inverse probability weights were included to adjust for confounding and balance characteristics of patients prescribed methadone or buprenorphine.FindingsACM and DRP rates were 1.93 and 0.53 per 100 person‐years, respectively. DRP was elevated during the first 4 weeks of OST [incidence rate ratio (IRR) = 1.93 95% confidence interval (CI) = 0.97–3.82], the first 4 weeks off OST (IRR = 8.15, 95% CI = 5.45–12.19) and the rest of time out of OST (IRR = 2.13, 95% CI = 1.47–3.09) compared with mortality risk from 4 weeks to end of treatment. Patients on buprenorphine compared with methadone had lower ACM rates in each treatment period. After adjustment, there was evidence of a lower DRP risk for patients on buprenorphine compared with methadone at treatment initiation (IRR = 0.08, 95% CI = 0.01–0.48) and rest of time on treatment (IRR = 0.37, 95% CI = 0.17–0.79). Treatment duration (mean and median) was shorter on buprenorphine than methadone (173 and 40 versus 363 and 111, respectively). Model estimates suggest that there was a low probability that methadone or buprenorphine reduced the number of DRP in the population: 28 and 21%, respectively.ConclusionsIn UK general medical practice, opioid substitution treatment with buprenorphine is associated with a lower risk of all‐cause and drug‐related poisoning mortality than methadone. In the population, buprenorphine is unlikely to give greater overall protection because of the relatively shorter duration of treatment.

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Section: Introductionmentioning

confidence: 99%

“…Internationally, there is no consensus about which medication to use. In the United Kingdom, methadone is recommended as the first‐line treatment if there are no contraindications 8.…”

Section: Introductionmentioning

confidence: 99%

The impact of buprenorphine and methadone on mortality: a primary care cohort study in the United Kingdom

et al. 2018

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“…There is limited further evidence regarding the GABAergic system in individuals with GD, with some inconsistent evidence of greater GABA concentrations measured in the CSF in GD (Nordin and Sjodin 2007; Roy et al 1989). These observations, as well as the growing use of GABAergic medication such as baclofen and topiramate to treat addiction, indicate that it is timely and important to characterize the GABA A receptor system in GD (Lingford‐Hughes et al 2012b). …”

Section: Introductionmentioning

confidence: 99%

Evidence for GABA‐A receptor dysregulation in gambling disorder: correlation with impulsivity

et al. 2016

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As a behavioural addiction, gambling disorder (GD) provides an opportunity to characterize addictive processes without the potentially confounding effects of chronic excessive drug and alcohol exposure. Impulsivity is an established precursor to such addictive behaviours, and GD is associated with greater impulsivity. There is also evidence of GABAergic dysregulation in substance addiction and in impulsivity. This study therefore investigated GABAA receptor availability in 15 individuals with GD and 19 healthy volunteers (HV) using [11C]Ro15‐4513, a relatively selective α5 benzodiazepine receptor PET tracer and its relationship with impulsivity. We found significantly higher [11C]Ro15‐4513 total distribution volume (VT) in the right hippocampus in the GD group compared with HV. We found higher levels of the ‘Negative Urgency’ construct of impulsivity in GD, and these were positively associated with higher [11C]Ro15‐4513 VT in the amygdala in the GD group; no such significant correlations were evident in the HV group. These results contrast with reduced binding of GABAergic PET ligands described previously in alcohol and opiate addiction and add to growing evidence for distinctions in the neuropharmacology between substance and behavioural addictions. These results provide the first characterization of GABAA receptors in GD with [11C]Ro15‐4513 PET and show greater α5 receptor availability and positive correlations with trait impulsivity. This GABAergic dysregulation is potential target for treatment.

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“…Treatment for alcoholism can be highly effective, and although psychosocial approaches dominate the treatment field, pharmacotherapy can have an important adjunctive role if appropriately integrated (Lingford-Hughes et al, 2012). A wealth of evidence links dysfunction of the dopamine system with alcohol liking, self-administration, and reinforcement in animal models and also in humans under laboratory settings.…”

Section: Introductionmentioning

confidence: 99%

In Vivo Imaging of Cerebral Dopamine D3 Receptors in Alcoholism

Erritzoe

Tziortzi

Bargiela

et al. 2014

Neuropsychopharmacol

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Animal studies support the role of the dopamine D3 receptor (DRD3) in alcohol reinforcement or liking. Sustained voluntary alcohol drinking in rats has been associated with an upregulation of striatal DRD3 gene expression and selective blockade of DRD3 reduces ethanol preference, consumption, and cue-induced reinstatement. In vivo measurement of DRD3 in the living human brain has not been possible until recently owing to a lack of suitable tools. In this study, DRD3 status was assessed for the first time in human alcohol addiction. Brain DRD3 availability was compared between 16 male abstinent alcohol-dependent patients and 13 healthy non-dependent age-matched males using the DRD3-preferring agonist positron emission tomography (PET) radioligand [ 11 C]PHNO with and without blockade with a selective DRD3 antagonist (GSK598809 60 mg p.o.). In striatal regions of interest, where the [ 11 C]PHNO PET signal represents primarily DRD2 binding, no differences were seen in [ 11 C]PHNO binding between the groups at baseline. However, baseline [ 11 C]PHNO binding was higher in alcohol-dependent patients in hypothalamus (V T : 16.5±4 vs 13.7±2.9, p ¼ 0.040), a region in which the [ 11 C]PHNO signal almost entirely reflects DRD3 availability. The reductions in regional receptor binding (V T ) following a single oral dose of GSK598809 (60 mg) were consistent with those observed in previous studies across all regions. There were no differences in regional changes in V T following DRD3 blockade between the two groups, indicating that the regional fractions of DRD3 are similar in the two groups, and the increased [ 11 C]PHNO binding in the hypothalamus in alcohol-dependent patients is explained by elevated DRD3 in this group. Although we found no difference between alcohol-dependent patients and controls in striatal DRD3 levels, increased DRD3 binding in the hypothalamus of alcohol-dependent patients was observed. This may be relevant to the development of future therapeutic strategies to treat alcohol abuse.

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BAP updated guidelines: evidence-based guidelines for the pharmacological management of substance abuse, harmful use, addiction and comorbidity: recommendations from BAP

Cited by 275 publications

References 588 publications

The impact of buprenorphine and methadone on mortality: a primary care cohort study in the United Kingdom

The impact of buprenorphine and methadone on mortality: a primary care cohort study in the United Kingdom

Evidence for GABA‐A receptor dysregulation in gambling disorder: correlation with impulsivity

In Vivo Imaging of Cerebral Dopamine D3 Receptors in Alcoholism

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