Use of fluoxetine in heroin addiction

Maremmani, Icro; Castrogiovanni, Paolo; Daini, L.; Zolesi, O.

doi:10.1192/bjp.160.4.570

Cited by 11 publications

(3 citation statements)

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“…In addition, two research groups have reported that fluoxetine substantially reduces heroin craving in human addicts (Gerra et al 1995;Maremmani et al 1992). These studies, together with the current findings, indicate that enhancing 5-HT transmission in opiate experienced subjects may decrease the desire for morphine.…”

Section: Discussionmentioning

confidence: 99%

Augmented Accumbal Serotonin Levels Decrease the Preference for a Morphine Associated Environment During Withdrawal

Harris

Aston‐Jones

2001

Neuropsychopharmacology

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Recent studies have found that acute morphine administration increases serotonin (5-HT) transmission within the nucleus accumbens and other forebrain regions. In contrast, 5-HT transmission is depressed during withdrawal from chronic morphine. We show that pharmacological agents that increase brain 5-HT levels In addition to gross neurological and somatic signs the abstinence syndrome associated with opiate dependence involves important subjective responses including anxiety, anhedonia, depression and drug craving (Jaffe 1990). The control and elimination of the subjective symptoms, which linger long after the physical symptoms of opiate withdrawal have dissipated, has been a major obstacle to the successful treatment of opiate dependence (Childress et al. 1994). Understanding the alterations in brain chemistry that occur during abstinence from opiate abuse may lead to improved treatments for these symptoms, and greater success in treating opiate addiction.Acute systemic administration of morphine enhances brain 5-HT synthesis (Garcia-Sevilla et al. 1980) and tryptophan hydroxylase activity (Boadle-Biber et al. 1987). Acute morphine also enhances the turnover and release of 5-HT and dopamine (DA) in widespread areas of the forebrain (Spampinato et al. 1985;Tao and Auerbach 1994). The effect of morphine on 5-HT release appears to be mediated by activation of dorsal raphe neurons (Spampinato et al. 1985;Tao and Auerbach 1994) and may reflect disinhibition caused by direct inhibition of GABA transmission. A similar mechanism has also been proposed for the excitatory effects of opiates on DA neurons in the ventral tegmental area (Bloom et al. 1972;Bonci and Williams 1997).Neurons in the nucleus accumbens have been shown to be critically involved in the reinforcing properties of opiates (Dworkin et al. 1988;Pettit et al. 1984;Zito et al. 1985). Although morphine administration enhances 5-HT and DA levels within the accumbens (Spampinato et al. 1985;Tao and Auerbach 1995;Wise et al. 1995) (Ettenberg et al. 1982;Gerrits and Van Ree 1996;Pettit et al. 1984) or morphine place preference in animals (Mackey and van der Kooy 1985; however, also see Bozarth and Wise 1981;Smith et al. 1985;Spyraki et al. 1983). On the other hand, chemical lesions of 5-HT terminals in the accumbens impair morphine self-administration without affecting responding for food or water (Smith et al. 1987), and also block the acquisition of morphine conditioned place preference (CPP) (Spyraki et al. 1988).Withdrawal from opiates decreases both dopamine and 5-HT transmission in the brain. A single dose of morphine induces measurable reductions in both 5-HT and DA levels at 24 hours post-injection (AntkiewiczMichaluk et al. 1995). Withdrawal from longer chronic opiate treatments produces profound decreases in both dopamine (Acquas et al. 1991;Pothos et al. 1991;Rossetti et al. 1992) and 5-HT transmission (Ahtee 1980;Tao et al. 1998). Reduced 5-HT levels have been linked to both depression (Maes and Meltzer 1995) and compulsive behavior (Dolberg et al. ...

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Section: Discussionmentioning

confidence: 99%

Augmented Accumbal Serotonin Levels Decrease the Preference for a Morphine Associated Environment During Withdrawal

Harris

Aston‐Jones

2001

Neuropsychopharmacology

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“…They show a satisfactory retention rate compared with uncomplicated SUD patients or non-bipolar SUD patients. The use of fluoxetine as the add-on to naltrexone maintenance has been shown to improve patients’ outcomes, suggesting that naltrexone has an anti-reward property, that is specifically reversible through fluoxetine’s antidepressant effects [63,64].…”

Section: Treatment Of Mood Disorders During Mmtmentioning

confidence: 99%

What we have learned from the Methadone Maintenance Treatment of Dual Disorder Heroin Use Disorder patients

Maremmani¹,

Pacini²,

Maremmani

2019

IJERPH

Self Cite

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Mental Disorders and Heroin Use Disorder (HUD) often co-occur and constitute correlated risk factors that the authors believe are best considered from a unitary perspective. In this article we review and discuss data collected by the V.P. Dole Research Group in Dual Disorder (V.P. Dole DD-RG) patients according to the following six discussion points: (1) Treatment of personality disorders during Methadone Maintenance Treatment (MMT); (2) Treatment of Mood Disorders during MMT; (3) Treatment of Anxiety Disorders during MMT; (4) Treatment of Psychotic Disorders during MMT; (5) Treatment of violence during MMT; (6) Treatment of Alcohol Use Disorder (AUD) during MMT. In treating Mood Disorder in HUD patients, we must bear in mind the interactions (potentiation and side effects) between psychopharmacology, used substances and agonist opioid medications; the use of psychiatric medications as an anti-craving drug, and the possible use of agonist and antagonist opioid medications in treating the other mental disorders. In treating chronic psychosis in HUD patients, we must consider the potentiation and side effects of antipsychotic drugs consequent on HUD treatment, worsening addiction hypophoria and inducing a more severe reward deficiency syndrome (RDS) in hypophoric patients. Violence and AUD during MMT can benefit from adequate dosages of methadone and co-medication with Sodium gamma-hydroxybutyrate (GHB). The experience of our V.P. Dole DD-RG suggests the following: (a) DD is the new paradigm in neuroscience in deepening our understanding of mental health; (b) To successfully treat DD patients a double competence is needed; (c) In managing DD patients priority must be given to Substance Use Disorder (SUD) treatment (stabilizing patients); (d) Antidepressant use is ancillary to SUD treatment; antipsychotic use must be restricted to acute phases; mood stabilizers must be preferred; any use of Benzodiazepines (BDZs) must be avoided.

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“…As methadone and buprenorphine are used for the maintenance of heroin addicts, they can be associated with many other drugs, especially selective serotonin reuptake inhibitors (SSRI) such as fluoxetine or fluvoxamine. It has previously been shown that these drugs are useful in the treatment of drug craving [25]. Indeed, depression is a risk factor for illicit drug-taking relapse and for failure of maintenance therapy among opioid addicts [21].…”

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confidence: 99%

In vitro interactions between fluoxetine or fluvoxamine and methadone or buprenorphine

Iribarne¹,

Picart²,

Dréano³

et al. 1998

Fundamemntal Clinical Pharma

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Methadone and buprenorphine, widely used in the treatment of opioid abuse, are metabolized by cytochrome P450 3A4, while fluoxetine and fluvoxamine, both selective serotonin reuptake inhibitors, are known to be P450 2D6 and 3A4 inhibitors in vitro. This study deals with the in vitro interactions between methadone or buprenorphine and fluoxetine or fluvoxamine. Fluoxetine inhibited methadone N-demethylation (Ki = 55 microM), but conversely did not inhibit buprenorphine dealkylation. Norfluoxetine inhibited the metabolism of both methadone and buprenorphine metabolisms (Ki 13 and 100 microM, respectively). Fluvoxamine inhibited methadone N-demethylation with a Ki of 7 microM and buprenorphine dealkylation, uncompetitively, with a Ki of 260 microM. Finally, these results suggest that care should be taken when selective serotonin reuptake inhibitors are administered in the treatment of drug craving. This is particularly true in the case of fluvoxamine which is more potent than fluoxetine in inhibiting methadone and buprenorphine metabolism.

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Use of fluoxetine in heroin addiction

Cited by 11 publications

References 1 publication

Augmented Accumbal Serotonin Levels Decrease the Preference for a Morphine Associated Environment During Withdrawal

Augmented Accumbal Serotonin Levels Decrease the Preference for a Morphine Associated Environment During Withdrawal

What we have learned from the Methadone Maintenance Treatment of Dual Disorder Heroin Use Disorder patients

In vitro interactions between fluoxetine or fluvoxamine and methadone or buprenorphine

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