Effective Treatment of Oxaliplatin-Induced Cumulative Polyneuropathy With Alpha-Lipoic Acid

Gedlicka, Claudia; Scheithauer, Werner; Schüll, Birgit; Kornek, Gabriela

doi:10.1200/jco.2002.99.502

Cited by 69 publications

(46 citation statements)

References 9 publications

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“…Our approach compares favorably with other alternatives such as carbamazepine, glutathione, ␣ lipoïc acid, or amifostine (15)(16)(17)(18)(19), which can generate toxic side effects, can interfere with oxaliplatin efficacy, or whose results are not confirmed.…”

Section: Discussionmentioning

confidence: 99%

Prevention of Oxaliplatin-Related Neurotoxicity by Calcium and Magnesium Infusions

Gamelin

Boisdron‐Celle²,

Delva³

et al. 2004

Clinical Cancer Research

311

178

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Purpose: Oxaliplatin is active in colorectal cancer. Sensory neurotoxicity is its dose-limiting toxicity. It may come from an effect on neuronal voltage-gated Na channels, via the liberation one its metabolite, oxalate. We decided to use Ca and Mg as oxalate chelators.Experimental Design: A retrospective cohort of 161 patients treated with oxaliplatin ؉ 5-fluorouracil and leucovorin for advanced colorectal cancer, with three regimens of oxaliplatin (85 mg/m 2 /2w, 100/2w, 130/3w) was identified. Ninety-six patients received infusions of Ca gluconate and Mg sulfate (1 g) before and after oxaliplatin (Ca/Mg group) and 65 did not.Results: Only 4% of patients withdrew for neurotoxicity in the Ca/Mg group versus 31% in the control group (P ‫؍‬ 0.000003). The tumor response rate was similar in both groups. The percentage of patients with grade 3 distal paresthesia was lower in Ca/Mg group (7 versus 26%, P ‫؍‬ 0.001). Acute symptoms such as distal and lingual paresthesia were much less frequent and severe (P ‫؍‬ 10 -7 ), and pseudolaryngospasm was never reported in Ca/Mg group. At the end of the treatment, 20% of patients in Ca/Mg group had neuropathy versus 45% (P ‫؍‬ 0.003). Patients with grade 2 and 3 at the end of the treatment in the 85 mg/m 2 oxaliplatin group recovered significantly more rapidly from neuropathy than patients without Ca/Mg. Conclusions: Ca/Mg infusions seem to reduce incidence and intensity of acute oxaliplatin-induced symptoms and might delay cumulative neuropathy, especially in 85 mg/m 2 oxaliplatin dosage.

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Section: Discussionmentioning

confidence: 99%

Prevention of Oxaliplatin-Related Neurotoxicity by Calcium and Magnesium Infusions

Gamelin

Boisdron‐Celle²,

Delva³

et al. 2004

Clinical Cancer Research

311

178

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“…High-dose vitamin C is not recommended because it interferes with bortezomib. Alpha-lipoic acid has been approved in Europe for the treatment of diabetic neuropathy, and is effective in docetaxel-induced PN 55 ; however, in animal models, there are indications that it may reduce bortezomib efficacy. The evidence of supplements in multiple myeloma remains anecdotal, and is largely based on extrapolation from trials with other neurotoxic drugs in different diseases.…”

Section: Pharmacological Intervention and Pain Managementmentioning

confidence: 99%

Dealing with Neuropathy in Plasma-Cell Dyscrasias

Sonneveld¹,

Jongen

2010

Hematology

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Peripheral neuropathy (PN) is a frequent complication of plasma-cell dyscrasias such as monoclonal gammopathy of undetermined significance, multiple myeloma, Waldenströ m's disease, POEMS (polyneuropathy, organomegaly, endocrinopathy, monoclonal gammopathy, and skin changes) syndrome, Castleman's disease, and light-chain amyloidosis. PN can be associated with the underlying disease or it can related to the treatment. The novel immunomodulatory drugs thalidomide and lenalidomide and the proteasome inhibitor bortezomib have changed the standard treatment of multiple myeloma. Treatment-related PN induced by thalidomide (TiPN) or bortezomib (BiPN) has become the most frequent cause of symptomatic polyneuropathy in multiple myeloma and related diseases. Dealing with PN has become a major challenge in current clinical practice for multiple myeloma patients. This review deals with practical issues such as etiology, incidence, symptoms, and clinical management of treatment-emergent PN. The major focus of the hematologist should be on the prevention of PN, primarily by frequent monitoring of the patient and by timely and adequate dose reduction of thalidomide and bortezomib. Thalidomide should not be given for periods longer than 18 months, and if it is, then patients should be carefully monitored with a low threshold for discontinuation in the face of any emergent neuropathy. In the case of BiPN, the dose of bortezomib should be reduced and/or the administration interval should be prolonged from biweekly to weekly. Adequate pain management and supportive care require a multidisciplinary approach involving the treating physician, expert nursing staff, and a neurologist as clinically indicated.

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“…Oxidative stress has been repeatedly proposed to play a central role in the mechanism of CIPN. The effect of antioxidants, including acetyl-l-carnitine, -lipoic acid, and vitamin C, which seem to partially reverse the hyperalgesia, represents indirect proof of the role of oxidative stress in oxaliplatin-induced neuropathy [54,55]. Recently, administration of the free radicals scavenger, phenyl N-tert-butylnitrone, has been shown to reduce mechanical allodynia in paclitaxel-induced neuropathic pain in rats [56].…”

Section: Introductionmentioning

confidence: 99%

Transient Receptor Potential Channels in Chemotherapy-Induced Neuropathy

Nassini¹,

Benemei²,

Fusi³

et al. 2013

TOPAINJ

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Chemotherapy-Induced Peripheral Neuropathy (CIPN) is a common dose-limiting side effect of many chemotherapeutic drugs, including platinum-based compounds (e.g., cisplatin and oxaliplatin), taxanes (e.g., paclitaxel), vinca alkaloids (e.g., vincristine), and the first-in-class proteasome inhibitor, bortezomib. Among the various sensory symptoms of CIPN, paresthesia, dysesthesia, spontaneous pain, and mechanical and thermal hypersensitivity are prominent. Inflammation, oxidative stress, loss of intraepidermal nerve fibers, modifications of mitochondria, and various ion channels alterations are part of the several mechanisms contributing to CIPN. Because attempts to mitigate chemotherapeutic-induced acute neuronal hyperexcitability and the subsequent peripheral neuropathy have yielded unsatisfactory results, a more in-depth understanding of the mechanism(s) responsible for the neurotoxic action of anticancer drugs is required.Some members of the transient receptor potential (TRP) family of channels, as the TRPV1 and TRPV4 (vanilloid), TRPA1 (ankyrin) and TRPM8 (melastatin) are expressed on the plasma membrane of primary sensory neurons (nociceptors), where they are activated by an unprecedented series of physical and chemical stimuli. There is evidence that TRPV1, TRPV4, TRPA1 and TRPM8 are prominent contributors of mechanical and thermal hypersensitivity in models of CIPN. In particular, in vitro and in vivo studies have pointed out the unique role of TRPA1 and oxidative stress in the mechanism responsible for cold and mechanical hyperalgesia in rodent models of CIPN.

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Effective Treatment of Oxaliplatin-Induced Cumulative Polyneuropathy With Alpha-Lipoic Acid

Cited by 69 publications

References 9 publications

Prevention of Oxaliplatin-Related Neurotoxicity by Calcium and Magnesium Infusions

Prevention of Oxaliplatin-Related Neurotoxicity by Calcium and Magnesium Infusions

Dealing with Neuropathy in Plasma-Cell Dyscrasias

Transient Receptor Potential Channels in Chemotherapy-Induced Neuropathy

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