Chronic treatment with phentermine combined with fenfluramine lowers plasma serotonin

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Cited by (39)

  • Pulmonary Arterial Hypertension Secondary to Drugs and Toxins

    2021, Clinics in Chest Medicine
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    Fenfluramine and its enantiomer, dexfenfluramine, are appetite suppressants in the phenylethylamine class, with structural and pharmacologic properties similar to amphetamine. Like aminorex, fenfluramine is also a potent serotonergic agent that interacts with the serotonin transporter.6,11,14,15 These drugs were released in the 1970s as adjuvant therapies for obesity.

  • Fenfluramine disrupts the mitral valve interstitial cell response to serotonin

    2009, American Journal of Pathology
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    Nevertheless, the role of 5HT as a neurotransmitter in the nervous system is unique, and thus observations concerning neuronal results with Fen and Flu must also be viewed with a critical perspective when extended to other cell types. For example, Fen can deplete 5HT centrally in the nervous system.26,27 However, neuronal cells have a unique 5HT storage and reuptake capacity26–29 that is not present in fibroblasts and myofibroblasts, such as heart valve interstitial cells.

  • Drug-induced fibrotic valvular heart disease

    2009, The Lancet
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    Several hypotheses generated after the initial reports of drug-induced valvular heart disease postulated that drugs such as fenfluramine increase circulating serotonin concentrations by interfering with serotonin transporter proteins and thereby induce valvulopathy. However, several investigators have concluded that chronic fenfluramine and phentermine use lowers plasma and platelet serotonin.74,75 This finding has led researchers to question whether the valvulopathy is caused by direct drug stimulation of serotonin receptor subtypes rather than increases in serotonin.76

  • Plasma serotonin levels are normal in pulmonary arterial hypertension

    2008, Pulmonary Pharmacology and Therapeutics
    Citation Excerpt :

    Finally, it is possible that differences in laboratory assays or technique explain our findings in comparison to previous work. The highly sensitive nature of assessing platelet-free plasma 5-HT has led to studies showing great variation in plasma 5-HT levels [6–10]. We tried to take extensive precautions to prevent such variability.

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This study was supported by an unrestricted grant from SmithKline Beecham Pharmaceuticals, a grant from the American Diabetes Association, and General Clinical Research Center Grant M01-RR-00400 from the Division of Research Resources, National Institutes of Health, Bethesda, Maryland.

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