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Review of duloxetine in the management of diabetic peripheral neuropathic pain.

Smith T, Nicholson RA - Vasc Health Risk Manag (2007)

Bottom Line: This compound has no other significant receptor or channel activities other than the serotonin and norepinephrine reuptake inhibition mechanisms and works to diminish or control the symptoms of diabetic neuropathy.Duloxetine has no known neuroprotective or other effects which prevent the development of neuropathy in patients with diabetes.These findings provide support for the proposed role of serotonin and norepinephrine as key mediators of the descending pain inhibition pathways of the brain stem and spinal cord.

View Article: PubMed Central - PubMed

Affiliation: Mercy Health Research, Ryan Headache Center, St. Louis, MO 63141, USA. tsmith@stlo.mercy.net

ABSTRACT
Duloxetine is a balanced selective serotonin norepinephrine reuptake inhibitor (SNRI) which, in 2004, became the first agent to receive regulatory approval for the treatment of painful diabetic neuropathy in the US. This compound has no other significant receptor or channel activities other than the serotonin and norepinephrine reuptake inhibition mechanisms and works to diminish or control the symptoms of diabetic neuropathy. Duloxetine has no known neuroprotective or other effects which prevent the development of neuropathy in patients with diabetes. The purpose of this review article is to discuss the background of painful diabetic neuropathy, the pharmacology of duloxetine, and its safety and efficacy in clinical trials and long-term observations. The authors will also comment on its use in clinical practice. Results from controlled clinical trials reveal that duloxetine administered at 60 mg qd or 60 mg bid is efficacious in treating diabetic neuropathic pain relative to placebo. Positive treatment outcomes are also seen for other measures of pain and quality of life. A minor but statistically significant increase in blood glucose compared with placebo treated patients has been observed in controlled clinical trials. Otherwise, controlled and open-label clinical studies have demonstrated a high degree of safety and tolerability for the compound. These findings provide support for the proposed role of serotonin and norepinephrine as key mediators of the descending pain inhibition pathways of the brain stem and spinal cord.

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Related in: MedlinePlus

SF-36 scales change from baseline in long-term open label studies. *p < 0.05.
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fig7: SF-36 scales change from baseline in long-term open label studies. *p < 0.05.

Mentions: Figure 7 shows the changes in SF-36 measures from baseline to endpoint. A decrease on the SF-36 indicates a poorer QOL. Those in the routine care group showed greater decreases on all SF-36 subscales relative to change in the duloxetine 60 mg bid arm. These differences were significant for the bodily pain, physical component, and physical role subscales. In addition, those in the routine care arm had a significantly greater decrease from baseline to endpoint as measured by the European QOL (indicating a poorer QOL) scale relative to change among those in the duloxetine 60 mg bid arm. A decrease on the SF-36 scales and European QOL indicate a poorer QOL.


Review of duloxetine in the management of diabetic peripheral neuropathic pain.

Smith T, Nicholson RA - Vasc Health Risk Manag (2007)

SF-36 scales change from baseline in long-term open label studies. *p < 0.05.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2350145&req=5

fig7: SF-36 scales change from baseline in long-term open label studies. *p < 0.05.
Mentions: Figure 7 shows the changes in SF-36 measures from baseline to endpoint. A decrease on the SF-36 indicates a poorer QOL. Those in the routine care group showed greater decreases on all SF-36 subscales relative to change in the duloxetine 60 mg bid arm. These differences were significant for the bodily pain, physical component, and physical role subscales. In addition, those in the routine care arm had a significantly greater decrease from baseline to endpoint as measured by the European QOL (indicating a poorer QOL) scale relative to change among those in the duloxetine 60 mg bid arm. A decrease on the SF-36 scales and European QOL indicate a poorer QOL.

Bottom Line: This compound has no other significant receptor or channel activities other than the serotonin and norepinephrine reuptake inhibition mechanisms and works to diminish or control the symptoms of diabetic neuropathy.Duloxetine has no known neuroprotective or other effects which prevent the development of neuropathy in patients with diabetes.These findings provide support for the proposed role of serotonin and norepinephrine as key mediators of the descending pain inhibition pathways of the brain stem and spinal cord.

View Article: PubMed Central - PubMed

Affiliation: Mercy Health Research, Ryan Headache Center, St. Louis, MO 63141, USA. tsmith@stlo.mercy.net

ABSTRACT
Duloxetine is a balanced selective serotonin norepinephrine reuptake inhibitor (SNRI) which, in 2004, became the first agent to receive regulatory approval for the treatment of painful diabetic neuropathy in the US. This compound has no other significant receptor or channel activities other than the serotonin and norepinephrine reuptake inhibition mechanisms and works to diminish or control the symptoms of diabetic neuropathy. Duloxetine has no known neuroprotective or other effects which prevent the development of neuropathy in patients with diabetes. The purpose of this review article is to discuss the background of painful diabetic neuropathy, the pharmacology of duloxetine, and its safety and efficacy in clinical trials and long-term observations. The authors will also comment on its use in clinical practice. Results from controlled clinical trials reveal that duloxetine administered at 60 mg qd or 60 mg bid is efficacious in treating diabetic neuropathic pain relative to placebo. Positive treatment outcomes are also seen for other measures of pain and quality of life. A minor but statistically significant increase in blood glucose compared with placebo treated patients has been observed in controlled clinical trials. Otherwise, controlled and open-label clinical studies have demonstrated a high degree of safety and tolerability for the compound. These findings provide support for the proposed role of serotonin and norepinephrine as key mediators of the descending pain inhibition pathways of the brain stem and spinal cord.

Show MeSH
Related in: MedlinePlus