Meta-analysis of duloxetine vs. pregabalin and gabapentin in the treatment of diabetic peripheral neuropathic pain

Quilici, S; Chancellor, Jeremy; Löthgren, Mickael; Simon, Dominique; Saïd, Gérard; Le, Trong Kim; Garcia-Cebrian, A; Monz, Brigitta U.

doi:10.1186/1471-2377-9-6

Cited by 196 publications

(168 citation statements)

References 33 publications

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“…Gabapentinoids can effectively relieve many types of peripheral neuropathic pain in patients, including painful diabetic peripheral neuropathy [40,41] and post-herpetic neuralgia [40,42,43]. GBP and pregabalin are also effective in relieving pain associated with spinal cord injury, a type of central neuropathic pain [44][45][46].…”

Section: Gabapentinoid Insensitivity In Central Neuropathic Pain Of Tmentioning

confidence: 99%

Gabapentinoid Insensitivity after Repeated Administration is Associated with Down-Regulation of the α2δ-1 Subunit in Rats with Central Post-Stroke Pain Hypersensitivity

Yang

et al. 2016

Neurosci. Bull.

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The a 2 d-1 subunit of the voltage-gated Ca 2? channel (VGCC) is a molecular target of gabapentin (GBP), which has been used as a first-line drug for the relief of neuropathic pain. GBP exerts its anti-nociceptive effects by disrupting trafficking of the a 2 d-1 subunit to the presynaptic membrane, resulting in decreased neurotransmitter release. We previously showed that GBP has an antiallodynic effect in the first two weeks; but this is followed by insensitivity in the later stage after repeated administration in a rat model of central post-stroke pain (CPSP) hypersensitivity induced by intra-thalamic hemorrhage. To explore the mechanisms underlying GBP insensitivity, the cellular localization and time-course of expression of the a 2 d-1 subunit in both the thalamus and spinal dorsal horn were studied in the same model. We found that the a 2 d-1 subunit was mostly localized in neurons, but not astrocytes and microglia. The level of a 2 d-1 protein increased in the first two weeks after injury but then decreased in the third week, when GBP insensitivity occurred. Furthermore, the a 2 d-1 down-regulation was likely caused by later neuronal loss in the injured thalamus through a mechanism other than apoptosis. In summary, the present results suggest that the GBP receptor a 2 d-1 is mainly expressed in thalamic neurons in which it is up-regulated in the early stage of CPSP but this is followed by dramatic down-regulation, which is likely associated with GBP insensitivity after long-term use.Keywords Central post-stroke pain Á Calcium channel a 2 d subunit Á Gabapentinoid Á Thalamic hemorrhagic stroke Á Thalamus Á Spinal dorsal horn

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Section: Gabapentinoid Insensitivity In Central Neuropathic Pain Of Tmentioning

confidence: 99%

Gabapentinoid Insensitivity after Repeated Administration is Associated with Down-Regulation of the α2δ-1 Subunit in Rats with Central Post-Stroke Pain Hypersensitivity

Yang

et al. 2016

Neurosci. Bull.

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“…Gabapentin, like pregabalin, also binds the calcium channel a2-d subunit and has shown efficacy in a number of clinical trials for treating the pain associated with DSPN (15, 86,96,[105][106][107][108][109][110][111]. However, not all painful DSPN studies, some of which are unpublished, have been positive (15,107).…”

Section: Anticonvulsantsmentioning

confidence: 99%

“…Doses of 60 and 120 mg/day showed efficacy in the treatment of pain associated with DSPN in multicenter randomized trials, although some of these had a rather high drop-out rate (15, 86,94,96,[98][99][100][101]. Duloxetine was also suggested to induce improvement in neuropathy-related quality of life (100).…”

Section: Approved Medicationsmentioning

confidence: 99%

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Diabetic Neuropathy: A Position Statement by the American Diabetes Association

et al. 2016

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“…One of the most considered endpoints for the development of a therapeutic for this diabetic complication is the treatment of pain associated with the neuronal deterioration. As a result, there have been several candidate therapies using oral and topically applied pain relievers ranging from pregabalin [10,11] to capsaicin [12].…”

Section: Introductionmentioning

confidence: 99%

Efficient Transdermal Delivery of Benfotiamine in an Animal Model

2015

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We designed a transdermal system to serve as a delivery platform for benfotiamine utilizing the attributes of passive penetration enhancing molecules to penetrate through the outer layers of skin combined with the advance of incorporating various peripherally-acting vasodilators to enhance drug uptake. Benfotiamine, incorporated into this transdermal formulation, was applied to skin in an animal model in order to determine the ability to deliver this thiamine pro-drug effectively to the sub-epithelial layers. In this proof of concept study in guinea pigs, we found that a single topical application of either a solubilized form of benfotiamine (15 mg) or a microcrystalline suspension form (25 mg) resulted in considerable increases of the dephosphorylated benfotiamine (S-benzoylthiamine) in the skin tissue as well as in significant increases in the thiamine and thiamine phosphate pools compared to control animals. The presence of a ~8000x increase in thiamine and increases in its phosphorylated derivatives in the epidermis

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Meta-analysis of duloxetine vs. pregabalin and gabapentin in the treatment of diabetic peripheral neuropathic pain

Cited by 196 publications

References 33 publications

Gabapentinoid Insensitivity after Repeated Administration is Associated with Down-Regulation of the α2δ-1 Subunit in Rats with Central Post-Stroke Pain Hypersensitivity

Gabapentinoid Insensitivity after Repeated Administration is Associated with Down-Regulation of the α2δ-1 Subunit in Rats with Central Post-Stroke Pain Hypersensitivity

Diabetic Neuropathy: A Position Statement by the American Diabetes Association

Efficient Transdermal Delivery of Benfotiamine in an Animal Model

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