Cisplatin neuropathy. Clinical, electrophysiologic, morphologic, and toxicologic studies

Thompson, S.W.N.; Davis, Larry E.; Kornfeld, Mario; Hilgers, Robert D.; Standefer, J C

doi:10.1002/1097-0142(19841001)54:7<1269::aid-cncr2820540707>3.0.co;2-9

Cited by 381 publications

(188 citation statements)

References 11 publications

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“…17 It can detect early functional changes of the sensory nerve by exploring a large number of large sensory fibers, 18 which are specifically impaired in cisplatin-induced neuropathy. 1 This method appears to be the most sensitive, as cisplatin-treated mice did not exhibit any unambiguous invariant clinical signs or any unequivocal neuronal loss in dorsal root ganglia or sensory nerves. 19,20 One of the limitations of this treatment is that plasma NT-3 concentrations decrease with time.…”

Section: Values Are Expressed As Means ± Sem In Milliseconds the mentioning

confidence: 99%

“…Cisplatin causes a dosedependent and dose-limiting sensory neuropathy, which is often disabling and from which recovery is often slow and incomplete. 1 Neurotrophin-3 (NT-3) is a promising agent for the prevention and treatment of cisplatininduced neuropathy. Indeed, NT-3 promotes the survival of the large fiber sensory neurones 2 affected in cases of cisplatin-induced neuropathy.…”

mentioning

confidence: 99%

“…Indeed, NT-3 promotes the survival of the large fiber sensory neurones 2 affected in cases of cisplatin-induced neuropathy. 1 Circulating NT-3 can readily reach dorsal root ganglia (DRG), which are the main target of cisplatin toxicity, 3 as there is no bloodnerve barrier. 4 Neurotrophic factors can therefore easily access the large sensory neurones of DRG.…”

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confidence: 99%

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Viral and non-viral gene therapy partially prevents experimental cisplatin-induced neuropathy

Kennel²,

S³

et al. 2002

Gene Ther

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Sensory neuropathies are a frequent and dose-limiting complication resulting from treatment with cisplatin. cisplatin; neuropathy Cisplatin is an efficient antineoplastic agent. However, its use is limited by its toxicity. The associated vomiting and nephrotoxicity are currently reduced by the use of antiemetics and vigorous hydration. The most problematic complication of cisplatin treatment is its neurotoxicity in the peripheral nervous system. Cisplatin causes a dosedependent and dose-limiting sensory neuropathy, which is often disabling and from which recovery is often slow and incomplete. 1 Neurotrophin-3 (NT-3) is a promising agent for the prevention and treatment of cisplatininduced neuropathy. Indeed, NT-3 promotes the survival of the large fiber sensory neurones 2 affected in cases of cisplatin-induced neuropathy. 1 Circulating NT-3 can readily reach dorsal root ganglia (DRG), which are the main target of cisplatin toxicity, 3 as there is no bloodnerve barrier. 4 Neurotrophic factors can therefore easily access the large sensory neurones of DRG. Recombinant NT-3 can prevent experimental sensory neuropathies in rats. 5,6 However, the clinical use of recombinant neurotrophic factors is limited by their poor bioavailability after systemic administration: the plasma half-life for NT-3 is only 1.28 min after intravenous administration in the rat. 7 We recently developed a non-viral gene transfer strategy to deliver continuous low doses of NT-3 into the

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Section: Values Are Expressed As Means ± Sem In Milliseconds the mentioning

confidence: 99%

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confidence: 99%

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Viral and non-viral gene therapy partially prevents experimental cisplatin-induced neuropathy

Kennel²,

S³

et al. 2002

Gene Ther

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“…An important dose-dependent side-effect of cisplatin is the development of peripheral neuropathy, mainly affecting thick-fibre-mediated sensory qualities (Thompson et al, 1984;Roelofs et al, 1984;Gerritsen van der Hoop et al, 1990a;Vecht et al, 1991; Hilkens et al, 1994). Neuropathy has also been reported as a dose-dependent side-effect of treatment with paclitaxel (Taxol) (Lipton et al, 1989;Gerven et al, 1994).…”

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confidence: 99%

Peripheral neuropathy induced by combination chemotherapy of docetaxel and cisplatin

Hilkens

Pronk²,

Verweij³

et al. 1997

Br J Cancer

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Peripheral neuropathy induced by combination chemotherapy of docetaxel and cisplatin PHE Hilkens1, LC Pronk2, J Verweij2, CJ Vecht1, WLJ van Putten3 and MJ van den Bent1Departments of 2Medical Oncology and 3Biostatistics, Dr Daniel den Hoed Cancer Center and University Hospital, Rotterdam, The Netherlands Summary Docetaxel, a new semisynthetic taxoid that has demonstrated promising activity as an antineoplastic agent, was administered in combination with cisplatin to 63 patients in a dose-escalating study. As both drugs were known to be potentially neurotoxic, peripheral neurotoxicity was prospectively assessed in detail. Neuropathy was evaluated by clinical sum-score for signs and symptoms and by measurement of the vibration perception threshold (VPT). The severity of neuropathy was graded according to the National Cancer Institute's 'Common Toxicity Criteria'. The docetaxel -cisplatin combination chemotherapy induced a predominantly sensory neuropathy in 29 (53%) out of 55 evaluable patients. At cumulative doses of both cisplatin and docetaxel above 200 mg m-2, 26 (74%) out of 35 patients developed a neuropathy which was mild in 15, moderate in ten and severe in one patient. Significant correlations were present between both the cumulative dose of docetaxel and cisplatin and the post-treatment sum-score of neuropathy (P < 0.01) as well as the post-treatment VPT (P < 0.01). The neurotoxic effects of this combination were more severe than either cisplatin or docetaxel as single agent at similar doses.Keywords: neuropathy; docetaxel; cisplatin; neurotoxicity; peripheral nerves; chemotherapy Docetaxel (Taxotere) is a new semisynthetic taxoid that has demonstrated substantial clinical activity against a wide variety of solid tumours (Pazdur et al, 1993;Aamdal et al, 1994;Fossella et al, 1994;Francis et al, 1994a;Francis et al, 1994b;Smyth et al, 1994;Chevallier et al, 1995). Docetaxel inhibits tubulin depolymerization and promotes microtubule assembly, resulting in dysfunctional microtubules (Pazdur et al, 1993).In view of their partly non-overlapping side-effects and their activities in a wide range of tumour types, developing combination chemotherapy regimens, including both taxoids and platins, is of major interest (Rowinsky et al, 1991;Rowinsky et al, 1993;Chaudhry et al, 1994). An important dose-dependent side-effect of cisplatin is the development of peripheral neuropathy, mainly affecting thick-fibre-mediated sensory qualities (Thompson et al, 1984;Roelofs et al, 1984;Gerritsen van der Hoop et al, 1990a;Vecht et al, 1991; Hilkens et al, 1994). Neuropathy has also been reported as a dose-dependent side-effect of treatment with paclitaxel (Taxol) (Lipton et al, 1989;Gerven et al, 1994). As expected, trials on combination chemotherapy of cisplatin and paclitaxel found a high incidence of peripheral neuropathy (Rowinsky et al, 1991;Rowinsky et al, 1993;Chaudhry et al, 1994).Peripheral neurotoxicity has been reported as a frequent, but usually mild side-effect of docetaxel in several phase I and phase II studie...

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“…Polyneuropathies may develop during the treatment, and are usually considered to be caused by vinblastin, cisplatinum or a combined effect of both drugs (Casey et al, 1973;Kaplan & Wiernik, 1982;Thompson et al, 1984;Roelofs et al, 1984).…”

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confidence: 99%

Raynaud's phenomenon after combination chemotherapy of testicular cancer, measured by laser Doppler flowmetry. A pilot study

Heier

Nilsen²,

Graver³

et al. 1991

Br J Cancer

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Summary The pathophysiology of Raynaud's phenomenon after Cisplatin-Bleomycin-Vinblastine combination chemotherapy, its relationship to polyneuropathy, and response to transcutaneous nerve stimulation (TNS), was studied in eight patients previously treated for testicular cancer. Peripheral circulation in the index finger was measured by laser Doppler flowmetry before and after cold provocation. In all patients there was an exaggerated and prolonged vasoconstrictor response to cold, with a mean flux reduction of 61%, and a mean restitution time of >7 min, characteristic of Raynaud's phenomenon of the vasospastic type. The normal controls had a mean flux reduction of 24% and a restitution time of 1.5 min. Clinical examination and nerve conduction measurements revealed a mild polyneuropathy in five of the eight patients, but an etiological relationship with Raynaud's phenomenon could not be ascertained. There was no measurable effect of TNS.

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Cisplatin neuropathy. Clinical, electrophysiologic, morphologic, and toxicologic studies

Cited by 381 publications

References 11 publications

Viral and non-viral gene therapy partially prevents experimental cisplatin-induced neuropathy

Viral and non-viral gene therapy partially prevents experimental cisplatin-induced neuropathy

Peripheral neuropathy induced by combination chemotherapy of docetaxel and cisplatin

Raynaud's phenomenon after combination chemotherapy of testicular cancer, measured by laser Doppler flowmetry. A pilot study

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