Colchicine‐induced myopathy and neuropathy

Younger, David S.; Mayer, S. A.; Weimer, L.H.; Alderson, Lloyd M.; Seplowitz, A. H.; Lovelace, Robert E.

doi:10.1212/wnl.41.6.943

Cited by 27 publications

(9 citation statements)

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“…Along the last decades, great effort has been made to further investigate the underlying physiopathological mechanisms and additional evidences emerged [9, 35–38] suggesting several alternative mechanisms [6, 39]. Among those, extensive research has been dedicated to chemotherapy-induced inflammation as the potential common driver of CIPN.…”

Section: Discussionmentioning

confidence: 99%

CXCR1/2 pathways in paclitaxel-induced neuropathic pain

et al. 2017

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Chemotherapy-induced peripheral neuropathy (CIPN) is a type of neuropathic pain that represents a frequent and serious consequence of chemotherapy agents. Over the last years, significant progress has been achieved in elucidating the underlying pathogenesis of CIPN. The interference of taxanes with microtubule has been proposed as a mechanism that leads to altered axonal transport and to permanent neurological damages. The inflammatory process activated by chemotherapeutic agents has been considered as a potential trigger of nociceptive process in CIPN.In this study we investigated the effect of reparixin, an inhibitor of CXCR1/CXCR2, in suppressing the development of paclitaxel-induced nociception in rats. Moreover, reparixin activity in reversing the neurotoxic effects induced by paclitaxel or GRO/KC in F11 cells was also analyzed.Reparixin administered by continuous infusion ameliorated paclitaxel-induced mechanical and cold allodynia in rats. In F11 cells, reparixin was able to inhibit the increase of acetyladed α-tubulin induced both by paclitaxel and GRO/KC. The subsequent experiments were performed in order to dissect the signal transduction pathways under GRO/KC control, eventually modulated by paclitaxel and/or reparixin. To this aim we found that reparixin significantly counteracted p-FAK, p-JAK2/p-STAT3, and PI3K-p-cortactin activation induced either by paclitaxel or GRO/KC.Overall the present results have identified IL-8/CXCR1/2 pathway as a mechanism involved in paclitaxel-induced peripheral neuropathy. In particular, the obtained data suggest that the inhibition of CXCR1/2 combined with standard taxane therapy, in addition to potentiating the taxane anti-tumor activity can reduce chemotherapy-induced neurotoxicity, thus giving some insight for the development of novel treatments.

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Section: Discussionmentioning

confidence: 99%

CXCR1/2 pathways in paclitaxel-induced neuropathic pain

et al. 2017

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“…The second resulted from acute intoxication [12]. At present, all cases of colchicine myoneuropathy described in the literature, not due to intoxication, occurred in the elderly with elevated plasma drug levels due to chronic renal insuciency [3±5, 7,10,14,15,16]. This is easily explained since the drug and its metabolites are partly excreted by the kidneys and may accumulate when correct dose adjustments are not made.…”

Section: Discussionmentioning

confidence: 99%

Colchicine-induced myoneuropathy in childhood

Harel

Mukamel

Amir

et al. 1998

European Journal of Pediatrics

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Colchicine is used in the treatment of gouty arthritis, familial Mediterranean fever, amyloidosis, Behcet disease and dermatoses. Myoneuropathy is a rare side-eect reported either with intoxication or in elderly patients with chronic renal insuciency causing elevated plasma drug levels. We report the ®rst two cases of myoneuropathy in children, both taking appropriate doses of colchicine, and having normal renal function. The myoneuropathic changes were reversible after stopping treatment. The cause of colchicine myoneuropathy is unclear. Conclusion In children treated with colchicine, neuromuscular phenomena of unknown aetiology may be related to the drug, even with a lack of intoxication or renal insuciency.

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“…However changes in axonal architecture were not apparent in rats with taxol-induced hyperalgesia 51 and axonal transport was not impaired in dorsal root ganglia (DRG) neurons exposed to paclitaxel in vitro at chemotherapeutic doses 28 . Reagents that disrupt the functions of microtubules such as TZT-1027 (a derivative of dolastatin) or colchicine 4,17 do not induce any morphological change in sensory nerves or hyperalgesia 47,73 . Although direct application of colchicine to the sciatic nerve blocks neurogenic plasma extravasation, changes of heat or mechanical withdrawal thresholds or the development of deafferentation-induced hyperalgesia have not been observed 33 .…”

Section: Introductionmentioning

confidence: 99%

Induction of Monocyte Chemoattractant Protein-1 (MCP-1) and Its Receptor CCR2 in Primary Sensory Neurons Contributes to Paclitaxel-Induced Peripheral Neuropathy

Zhang

Boyette-Davis

Kosturakis

et al. 2013

The Journal of Pain

128

153

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The use of paclitaxel (Taxol®), a microtubule stabilizer, for cancer treatment is often limited by its associated peripheral neuropathy (chemotherapy-induced peripheral neuropathy, CIPN) which predominantly results in sensory dysfunction including chronic pain. Here we show that paclitaxel CIPN was associated with an induction of chemokine monocyte chemoattractant protein-1 (MCP-1) and its cognate receptor CCR2 in primary sensory neurons of dorsal root ganglia (DRG). Immunostaining revealed that MCP-1 was mainly expressed in small nociceptive neurons while CCR2 was expressed in large and medium-sized myelinated neurons. Direct application of MCP-1 consistently induced intracellular calcium increases in DRG large and medium-sized but not small neurons mainly dissociated from paclitaxel- but not vehicle-treated animals. Paclitaxel also induced increased expression of MCP-1 in spinal astrocytes but no CCR2 signal was detected in spinal cord. Local blockade of MCP-1/CCR2 signaling by anti-MCP-1 antibody or CCR2 antisense oligodeoxynucleotides significantly attenuated paclitaxel CIPN phenotypes including mechanical hypersensitivity and loss of intraepidermal nerve fibers (IENFs) in hindpaw glabrous skin. These results suggest that activation of paracrine MCP-1/CCR2 signaling between DRG neurons plays a critical role in the development of paclitaxel CIPN and targeting MCP-1/CCR2 signaling could be a novel therapeutic approach.

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Colchicine‐induced myopathy and neuropathy

Cited by 27 publications

References 0 publications

CXCR1/2 pathways in paclitaxel-induced neuropathic pain

CXCR1/2 pathways in paclitaxel-induced neuropathic pain

Colchicine-induced myoneuropathy in childhood

Induction of Monocyte Chemoattractant Protein-1 (MCP-1) and Its Receptor CCR2 in Primary Sensory Neurons Contributes to Paclitaxel-Induced Peripheral Neuropathy

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