Chemotherapy-induced peripheral neuropathy: an update on the current understanding

Addington, James E.; Freimer, Miriam

doi:10.12688/f1000research.8053.1

Cited by 101 publications

(104 citation statements)

References 49 publications

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“…This finding may be related to the receipt of two different classes of CTX drugs that have both overlapping (e.g., mitochondrial dysfunction) and differential (e.g. formation of platinum-DNA adducts, taxanes’ interference with the stabilization of microtubules (for reviews see 63,101 ) mechanisms for CIN. However, patients with CIN reported a slightly lower number of previous cancer treatments.…”

Section: Discussionmentioning

confidence: 99%

“…Rather, subjective and objective measures were used that could be easily implemented in clinical practice. While only survivors who received a platinum and/or a taxane compound were included in our study, other CTX agents induce CIN (for reviews see 63,101 ). Therefore, our findings may not generalize to survivors who received other types of neurotoxic CTX.…”

Section: Discussionmentioning

confidence: 99%

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Chemotherapy-Induced Neuropathy in Cancer Survivors

Miaskowski

Mastick

Paul

et al. 2017

Journal of Pain and Symptom Management

106

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Context Evidence suggests that chemotherapy-induced neuropathy (CIN) is a significant problem for cancer survivors. However, a detailed phenotypic characterization of CIN in cancer survivors is not available. Objectives To evaluate between group differences in demographic and clinical characteristics, as well as in measures of sensation, function, and postural control, in a sample of cancer survivors who received a platinum and/or a taxane-based CTX regimen and did (n=426) and did not (n=197) develop CIN. Methods Survivors completed self-report questionnaires and underwent objective testing (i.e., light touch, pain sensation, cold sensation, vibration, muscle strength, grip strength, Purdue Pegboard test, Timed Get Up and Go Test, Fullerton Advanced Balance test). Parametric and non-parametric statistics were used to compare between group differences in study outcomes. Results Of the 426 survivors with CIN, 4.9% had CIN only in their upper extremities, 27.0% only in their lower extremities, and 68.1% in both their upper and lower extremities. Demographic and clinical characteristics associated with CIN included: older age, lower annual income, higher body mass index, a higher level of comorbidity, being born prematurely, receipt of a higher cumulative dose of chemotherapy, and a poorer functional status. Survivors with CIN had worse outcomes for all of the following objective measures: light touch, pain, temperature, vibration, upper and lower extremity function and balance. Conclusions This study is the first to provide a detailed phenotypic characterization of CIN in cancer survivors who received a platinum and/or a taxane compound. These data can serve as a benchmark for future studies of CIN in cancer survivors.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Chemotherapy-Induced Neuropathy in Cancer Survivors

Miaskowski

Mastick

Paul

et al. 2017

Journal of Pain and Symptom Management

106

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“…Chemotherapy-induced peripheral neuropathy (CIPN) is a progressive, long-lasting condition characterized by numbness, dysesthesia, hyperalgesia and allodynia (Addington and Freimer, 2016;Avan et al, 2015). It is estimated that up to 90% of all cancer patients receiving chemotherapy will be affected by CIPN at various severity levels (Bokhari and Sawatzky, 2009).…”

Section: Clinical Aspects Of Cipnmentioning

confidence: 99%

Selective HCN1 block as a strategy to control oxaliplatin-induced neuropathy

et al. 2018

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a b s t r a c tChemotherapy-Induced Peripheral Neuropathy (CIPN) is the most frequent adverse effect of pharmacological cancer treatments. The occurrence of neuropathy prevents the administration of fully-effective drug regimen, affects negatively the quality of life of patients, and may lead to therapy discontinuation. CIPN is currently treated with anticonvulsants, antidepressants, opioids and non-opioid analgesics, all of which are flawed by insufficient anti-hyperalgesic efficacy or addictive potential. Understandably, developing new drugs targeting CIPN-specific pathogenic mechanisms would dramatically improve efficacy and tolerability of anti-neuropathic therapies. Neuropathies are associated to aberrant excitability of DRG neurons due to the alteration in the expression or function of a variety of ion channels. In this regard, Hyperpolarization-activated Cyclic Nucleotide-gated (HCN) channels are overexpressed in inflammatory and neuropathic pain states, and HCN blockers have been shown to reduce neuronal excitability and to ameliorate painful states in animal models. However, HCN channels are critical in cardiac action potential, and HCN blockers used so far in pre-clinical models do not discriminate between cardiac and non-cardiac HCN isoforms. In this work, we show an HCN current gain of function in DRG neurons from oxaliplatin-treated rats. Biochemically, we observed a downregulation of HCN2 expression and an upregulation of the HCN regulatory beta-subunit MirP1. Finally, we report the efficacy of the selective HCN1 inhibitor MEL57A in reducing hyperalgesia and allodynia in oxaliplatin-treated rats without cardiac effects. In conclusion, this study strengthens the evidence for a disease-specific role of HCN1 in CIPN, and proposes HCN1-selective inhibitors as new-generation pain medications with the desired efficacy and safety profile.

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“…Recently, chemotherapy-induced NP was recognized as a serious treatment issue that can lead to dose reduction and even discontinuation of chemotherapeutics [19]. Unfortunately, the pathomechanisms behind this type of pain have not been established, and treatment options are limited [3,4], prompting the need for additional NP research.…”

Section: Discussionmentioning

confidence: 99%

Antiallodynic Effects of Intrathecal Areca Nut for Spinal Nerve-Ligated and Chemotherapy-Induced Neuropathic Pain in Rats

et al. 2018

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This study examined the effects of intrathecal areca nut on spinal nerve-ligated and chemotherapy-induced neuropathic pain (NP), and investigated the relevance of spinal 5-hydroxytryptamine (5-HT) and α2-adrenergic receptors to those effects. For drug administration, intrathecal catheters were inserted into the subarachnoid space of male Sprague-Dawley rats. NP was induced either by spinal nerve ligation (left spinal nerves L5 and L6) or by chemotherapeutic injection (intraperitoneal cisplatin, 2 mg/kg/day, once daily for 4 days). Paw withdrawal thresholds (PWT) were mechanically assessed using von Frey filaments. The involvement of 5-HT and α2-adrenergic receptors in antiallodynia was determined using antagonists with the following receptor specificities: nonselective 5-HT (dihydroergocristine), 5-HT7 (SB269970), nonselective α2-adrenoceptor (yohimbine), α-2A (BRL 44408), α-2B (ARC 239), and α-2C (JP 1302). Intrathecal areca nut significantly increased the PWT in both spinal nerve-ligated and chemotherapy-induced NP (^‡ p < 0.001). Intrathecal dihydroergocristine, SB269970, yohimbine, BRL 44408, ARC 239, and JP 1302 significantly reversed the antiallodynic effects of areca nut in both NP states (^‡ p < 0.001). Collectively, intrathecal areca nut suppressed mechanical allodynia induced by spinal nerve ligation and cisplatin injection. Furthermore, spinal 5-HT7 receptor and α2A, α2B, and α2C-adrenoceptors contributed to the antiallodynic effects of areca nut.

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Chemotherapy-induced peripheral neuropathy: an update on the current understanding

Cited by 101 publications

References 49 publications

Chemotherapy-Induced Neuropathy in Cancer Survivors

Chemotherapy-Induced Neuropathy in Cancer Survivors

Selective HCN1 block as a strategy to control oxaliplatin-induced neuropathy

Antiallodynic Effects of Intrathecal Areca Nut for Spinal Nerve-Ligated and Chemotherapy-Induced Neuropathic Pain in Rats

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