Skip to main content Accessibility help

We use cookies to distinguish you from other users and to provide you with a better experience on our websites. Close this message to accept cookies or find out how to manage your cookie settings.

Close cookie message
×
Hostname: page-component-6bf8c574d5-j5c6p Total loading time: 0 Render date: 2025-03-09T16:23:29.814Z Has data issue: false hasContentIssue false

18 - Treatment of emergent peripheral neuropathy in plasma cell disorders

from Section 4 - Supportive therapies

Published online by Cambridge University Press:  18 December 2013

By
Charise Gleason ,
Melanie Watson  and
Sagar Lonial
Edited by
Stephen A. Schey ,
Kwee L. Yong ,
Robert Marcus  and
Kenneth C. Anderson
Stephen A. Schey
Affiliation:
Department of Haematology, King’s College Hospital, London
Kwee L. Yong
Affiliation:
Department of Haematology, University College Hospital, London
Robert Marcus
Affiliation:
Department of Haematology, King’s College Hospital, London
Kenneth C. Anderson
Affiliation:
Dana-Farber Cancer Institute, Boston
Get access

Summary

Introduction

Peripheral neuropathy (PN) occurs due to damage, inflammation or dysfunction to the peripheral nervous system, most likely as a result of injury to axons, myelin sheaths or the cell bodies. The extent of impaired function depends on the type of nerves affected – motor, sensory or autonomic. The onset of symptoms is variable and can present gradually or in a more rapid fashion. Symptoms range from temporary numbness, tingling, paresthesias, sensitivity to touch and weakness to more severe symptoms ranging from burning pain, muscle wasting, and to the extent of paralysis[1,2]. Typically, the longest nerves in the extremities are first affected with symmetric length dependent spreading from distal to proximal nerves[3]. The most common clinical manifestation of PN occurs in a “stocking and glove” pattern and the patients may complain of losing hand grip by dropping things or having difficulty picking up small objects. Patients with autonomic symptoms may experience labile blood pressure changes, orthostatic hypotension, irregular heart rates, changes in gastrointestinal motility, swallowing or respiratory problems[2]. PN tends to have a severe impact on quality of life and functional abilities in cancer patients and can impact overall survival or severity of full dose effective therapy[1].

Type
Chapter
Information
Myeloma
Pathology, Diagnosis, and Treatment
 , pp. 245 - 254
Publisher: Cambridge University Press
Print publication year: 2013

Access options

Get access to the full version of this content by using one of the access options below. (Log in options will check for institutional or personal access. Content may require purchase if you do not have access.)

References

Tariman, J., Love, G. et al. Peripheral neuropathy associated with novel therapies in patients with multiple myeloma: concensus statement of the IMF nurse leadership board. Clin. J. Oncol. Nurs. 2008;12(3):29–36.CrossRefGoogle Scholar
Stubblefield, M. D. et al. NCCN Task Force Report: Management of neuropathy in cancer. Natl Comp. Cancer Network 2009;7(Suppl 5):S1–26.CrossRefGoogle Scholar
Kelly, J.The evaluation of peripheral neuropathy. Part I: clinical and laboratory evidence. Rev. Neurol. Dis. 2004;1:133–40.Google ScholarPubMed
Ropper, A., Gorson, K.Neuropathies associated with paraproteinemia. N. Engl. J. Med. 1998;338:1601–7.CrossRefGoogle ScholarPubMed
Dispenzieri, A., Kyle, R. A.Neurological aspects of multiple myeloma and related disorders. Best practice & research. Clin. Haematol. 2005;18(4):673–88.Google Scholar
Kuijf, M. L. et al. Detection of anti-MAG antibodies in polyneuropathy associated with IgM monoclonal gammopathy. Neurology 2009;73(9):688–95.CrossRefGoogle ScholarPubMed
Nobile-Orazio, E. et al. Long-term prognosis of neuropathy associated with anti-mag IgM M-proteins and its relationship to immune therapies. J. Peripheral Nerv. System 2000;5(4):239–40.CrossRefGoogle Scholar
Silberman, J., Lonial, S.Review of peripheral neuropathy in plasma cell disorders. Hematol. Oncol. 2008;26(2):55–65.CrossRefGoogle ScholarPubMed
Steck, A. J. et al. Peripheral neuropathy associated with monoclonal IgM autoantibody. Annals Neurol. 1987;22(6):764–7.CrossRefGoogle ScholarPubMed
Vital, A.Paraproteinemic neuropathies. Brain Pathology 2001;11(4):399–407.CrossRefGoogle ScholarPubMed
Benson, M. D., Kincaid, J. C.The molecular biology and clinical features of amyloid neuropathy. Muscle Nerve 2007;36(4):411–23.CrossRefGoogle ScholarPubMed
Plante-Bordeneuve, V., Said, G.Transthyretin related familial amyloid polyneuropathy. Curr. Opin. Neurol. 2000;13(5):569–73.CrossRefGoogle ScholarPubMed
Kyle, R., Greipp, P.Amyloidosis (AL): clinical and laboratory features in 229 cases. Mayo Clin. Proc. 1983;58:665–83.Google ScholarPubMed
Duston, M. A. et al. Peripheral neuropathy as an early marker of AL amyloidosis. Arch. Intern. Med. 1989;149(2):358–60.CrossRefGoogle ScholarPubMed
Rajkumar, S. V., Gertz, M. A., Kyle, R. A.Prognosis of patients with primary systemic amyloidosis who present with dominant neuropathy 11 Supported in part by the Quade Amyloidosis Research Foundation and Program Project Grant No. CA 62242, National Cancer Institute (National Institutes of Health). Am. J. Med. 1998;104(3):232–7.CrossRefGoogle Scholar
Argyriou, A. A., Iconomou, G., Kalofonos, H. P.Bortezomib-induced peripheral neuropathy in multiple myeloma: a comprehensive review of the literature. Blood 2008;112(5):1593–9.CrossRefGoogle ScholarPubMed
Sanchorawala, V. AL (immunoglobulin light-chain) amyloidosis. Myeloma Therapy Pursuing the Plasma Cell, 2008:551–69.
Reilly, M. M., Staunton, H.Peripheral nerve amyloidosis. Brain Pathology 1996;6(2):163–77.CrossRefGoogle ScholarPubMed
Gertz, M. A. et al. Definition of organ involvement and treatment response in immunoglobulin light chain amyloidosis (AL): a consensus opinion from the 10th International Symposium on Amyloid and Amyloidosis. Am. J. Hematol. 2005;79(4):319–28.CrossRefGoogle ScholarPubMed
Sonneveld, P., Jongen, J. L. M.Dealing with neuropathy in plasma-cell dyscrasias. Hematology 2010;2010(1):423–30.CrossRefGoogle ScholarPubMed
Kyle, R. A., Gertz, M. A.Primary systemic amyloidosis: clinical and laboratory features in 474 cases. Semin. Hematol. 1995;32(1):45–59.Google ScholarPubMed
Hausheer, F. H. et al. Diagnosis, management, and evaluation of chemotherapy-induced peripheral neuropathy. Semin. Oncol. 2006;33(1):15–49.CrossRefGoogle ScholarPubMed
Windebank, A. J., Grisold, W.Chemotherapy-induced neuropathy. J. Peripheral Nerv. Syst. 2008;13(1):27–46.CrossRefGoogle ScholarPubMed
Mohty, B. et al. Peripheral neuropathy and new treatments for multiple myeloma: background and practical recommendations. Haematologica 2009;95(2):311–19.CrossRefGoogle Scholar
Wickham, R.Chemotherapy-induced peripheral neuropathy: a review and implications for oncology nursing practice. Clin. J. Onc. Nurs. 2007;11(3):361–76.CrossRefGoogle ScholarPubMed
Xu, Y. et al. Immunomodulatory drugs reorganize cytoskeleton by modulating Rho GTPases. Blood 2009;114(2):338–45.CrossRefGoogle ScholarPubMed
Fullerton, P. M., Kremer, M.Neuropathy after intake of thalidomide (distaval). BMJ 1961;2(5256):855–8.CrossRefGoogle Scholar
Mileshkin, L. et al. Development of neuropathy in patients with myeloma treated With thalidomide: patterns of occurrence and the role of electrophysiologic monitoring. J. Clin. Oncol. 2006;24(27):4507–14.CrossRefGoogle ScholarPubMed
Richardson, P. et al. Thalidomide for patients with relapsed multiple myeloma after high-dose chemotherapy and stem cell transplantation: results of an open-label multicenter phase 2 study of efficacy, toxicity, and biological activity. Mayo Clinic Proc. 2004;79(7):875–82.CrossRefGoogle ScholarPubMed
Tosi, P. et al. Neurological toxicity of long-term (>1 yr) thalidomide therapy in patients with multiple myeloma. Eur. J. Haematol. 2005;74(3):212–16.CrossRefGoogle ScholarPubMed
D'Amato, R. J. et al. Thalidomide is an inhibitor of angiogenesis. Proc. Natl Acad. Sci. USA, 1994;91(9):4082–5.CrossRefGoogle ScholarPubMed
Sampaio, E. P. et al. Thalidomide selectively inhibits tumor necrosis factor alpha production by stimulated human monocytes. J. Exp. Med. 1991;173(3):699–703.CrossRefGoogle ScholarPubMed
Keifer, J. A., Guttridge, D., Ashburner, B. P.Baldwin, A. S.Inhibition of NF kappa B activity by thalidomide through expression of I Kappa B kinase activity. J. Biol. Chem. 2001;276:22382–7.CrossRefGoogle Scholar
Giannini, F. et al. Thalidomide-induced neuropathy: a ganglionopathy?Neurology 2003;60(5):877–8.CrossRefGoogle ScholarPubMed
Palumbo, A. et al. Thalidomide for treatment of multiple myeloma: 10 years later. Blood 2008;111(8):3968–77.CrossRefGoogle ScholarPubMed
Barlogie, B. et al. Thalidomide and hematopoietic-cell transplantation for multiple myeloma. New Engl. J. Med. 2006;354(10):1021–30.CrossRefGoogle ScholarPubMed
Richardson, P. G. et al. A randomized phase 2 study of lenalidomide therapy for patients with relapsed or relapsed and refractory multiple myeloma. Blood 2006;108(10):3458–64.CrossRefGoogle ScholarPubMed
Dimopoulos, M. et al. Lenalidomide plus dexamethasone for relapsed or refractory multiple myeloma. New Engl. J. Med, 2007;357(21):2123–32.CrossRefGoogle ScholarPubMed
Wang, M. et al. Lenalidomide plus dexamethasone is more effective than dexamethasone alone in patients with relapsed or refractory multiple myeloma regardless of prior thalidomide exposure. Blood 2008;112(12):4445–51.CrossRefGoogle ScholarPubMed
Chen, C. et al. Expanded safety experience with lenalidomide plus dexamethasone in relapsed or refractory multiple myeloma. Br. J. Haematol. 2009;146(2):164–70.CrossRefGoogle ScholarPubMed
Lacy, M. Q. et al. Pomalidomide (CC4047) plus low-dose dexamethasone as therapy for relapsed multiple myeloma. J. Clin. Oncol. 2009;27(30):5008–14.CrossRefGoogle ScholarPubMed
Lacy, M. Q. et al. Pomalidomide (CC4047) plus low dose dexamethasone (Pom/dex) is active and well tolerated in lenalidomide refractory multiple myeloma (MM). Leukemia, 2010;24(11):1934–9.CrossRefGoogle Scholar
Favis, R. et al. Genetic variation associated with bortezomib-induced peripheral neuropathy. Pharmacogenetics Genomics 2011; 21(3):121–9.CrossRefGoogle ScholarPubMed
Chaudhry, V. et al. Characteristics of bortezomib- and thalidomide-induced peripheral neuropathy. J. Peripheral Nerv. Syst. 2008;13(4):275–82.CrossRefGoogle ScholarPubMed
Richardson, P. G. et al. Frequency, characteristics, and reversibility of peripheral neuropathy during treatment of advanced multiple myeloma with bortezomib. J. Clin. Oncol. 2006;24(19):3113–20.CrossRefGoogle ScholarPubMed
Orlowski, R. Z. et al. Phase I trial of the proteasome inhibitor PS-341 in patients with refractory hematologic malignancies. J. Clin. Oncol. 2002;20(22):4420–7.CrossRefGoogle ScholarPubMed
Aghajanian, C. et al. A phase I trial of the novel proteasome inhibitor PS341 in advanced solid tumor malignancies. Clin. Cancer Res. 2002;8(8):2505–11.Google ScholarPubMed
Papandreou, C. N. et al. Phase I trial of the proteasome inhibitor bortezomib in patients with advanced solid tumors with observations in androgen-independent prostate cancer. J. Clin. Oncol. 2004;22(11):2108–21.CrossRefGoogle ScholarPubMed
Richardson, P. G., Barlogie, B., Berenson, J. et al. A phase 2 study of two doses of bortezomib in relapsed or refractory myeloma. N. Engl. J. Med. 2003;348:2609–17.CrossRefGoogle ScholarPubMed
Jagannath, S. et al. A phase 2 study of two doses of bortezomib in relapsed or refractory myeloma. Br. J. Haematol. 2004;127(2):165–72.CrossRefGoogle ScholarPubMed
Cavaletti, G., Nobile-Orazio, E.Bortezomib-induced peripheral neurotoxicity: still far from a painless gain. Haematologica 2007;92(10):1308–10.CrossRefGoogle ScholarPubMed
El-Cheikh, J. et al. Features and risk factors of peripheral neuropathy during treatment with bortezomib for advanced multiple myeloma. Clinical Lymphoma Myeloma 2008;8(3):146–52.CrossRefGoogle ScholarPubMed
Gupta, S. et al. Life-threatening motor neurotoxicity in association with bortezomib. Haematologica 2006;91(7):1001.Google ScholarPubMed
Moreau, P. et al. A phase 3 prospective randomized international study (MMY-3021) comparing subcutaneous and intravenous administration of bortezomib in patients with relapsed multiple myeloma. ASH Annual Meeting Abstracts 2010; 116(21):312.Google Scholar
O'Connor, O. A. et al. A phase 1 dose escalation study of the safety and pharmacokinetics of the novel proteasome inhibitor carfilzomib (PR-171) in patients with hematologic malignancies. Clin. Cancer Res., 2009;15(22):7085–91.CrossRefGoogle ScholarPubMed
Wolf, J. L., Vĩj, R., Lonial, S. et al. Neurotoxic and peripheral neuropathic effects in preclinical and clinical studies of carfilzomib (CFZ), a novel proteasome inhibitor (PI). J. Clin. Oncol. 2010; abstract 8135.
Jagannath, S., Vij, R., Stewart, K. et al. Final results of PX-171–003-A0, part 1 of an open-label, single-arm, phase II study of carfilzomib (CFZ) in patients (pts) with relapsed and refractory multiple myeloma (MM). J. Clin. Oncol. 2009; Abstract 8504.
Siegel, D. S., Martin, T., Wang, M. et al. Results of PX-171–003-A1, an open-label, single-arm, phase 2 (Ph 2) study of carfilzomib (CFZ) in patients (pts) with relapsed and refractory multiple myeloma (MM). Blood 2010; ASH Annual Meeting Abstracts: p. 116:A985.
Vij, R. et al. Carfilzomib: high single agent response rate with minimal neuropathy even in high-risk patients. Blood 2010; ASH Annual Meeting Abstracts: p. 116:A1938.Google Scholar
Broyl, A., Jongen, J.Van der Holt, B, et al. Mechanisms of peripheral neuropathy associated with bortezomib and vincristine in patients with newly diagnosed multiple myeloma: a prospective analysis of data from the HOVON-65/GMMG-HD4 trial. Lancet Oncol., 2010;11(11):1057–65.CrossRefGoogle Scholar
NCCN, Common terminology cirteria for adverse events v.3.0. Retrieved July 8, 2011, from . 2006.
Cella, D. F. et al. The Functional Assessment of Cancer Therapy scale: development and validation of the general measure. J. Clin. Oncol. 1993;11(3):570–9.CrossRefGoogle ScholarPubMed
Calhoun, E. A. et al. Psychometric evaluation of the Functional Assessment of Cancer Therapy/Gynecologic Oncology Group – Neurotoxicity (Fact/GOG-Ntx) questionnaire for patients receiving systemic chemotherapy. Int. J. Gynecol. Cancer 2003;13(6):741–8.CrossRefGoogle ScholarPubMed
Cavaletti, G. et al. Chemotherapy-induced peripheral neurotoxicity assessment: a critical revision of the currently available tools. Eur. J. Cancer 2010;46(3):479–94.CrossRefGoogle ScholarPubMed
Dworkin, R. H. et al. Recommendations for the pharmacological management of neuropathic pain: an overview and literature update. Mayo Clinic Proceedings 2010; 85(3 suppl):S3–S14.CrossRefGoogle ScholarPubMed
Webster, L. R. et al. Efficacy, safety, and tolerability of NGX-4010, capsaicin 8% patch, in an open-label study of patients with peripheral neuropathic pain. Diabetes Res. Clin. Pract. (in press).
Wolf, S. et al. Chemotherapy-induced peripheral neuropathy: Prevention and treatment strategies. Eur. J. Cancer. 2008;44(11):1507–15.CrossRefGoogle ScholarPubMed
Halat, K. M., Dennehy, C. E.Botanicals and dietary supplements in diabetic peripheral neuropathy. J. Am. Board Fam. Pract. 2003;16(1):47–57.CrossRefGoogle ScholarPubMed
Pace, A. et al. Neuroprotective effect of vitamin E supplementation in patients treated with cisplatin chemotherapy. J. Clin. Oncol. 2003;21(5):927–31.CrossRefGoogle ScholarPubMed
Argyriou, A. A. et al. Vitamin E for prophylaxis against chemotherapy-induced neuropathy. Neurology 2005;64(1):26–31.CrossRefGoogle ScholarPubMed
Argyriou, A. et al. A randomized controlled trial evaluating the efficacy and safety of vitamin E supplementation for protection against cisplatin-induced peripheral neuropathy: final results. Supportive Care Cancer 2006;14(11):1134–40.CrossRefGoogle ScholarPubMed
Pace, A. et al. Vitamin E neuroprotection for cisplatin neuropathy. Neurology 2010;74(9):762–6.CrossRefGoogle ScholarPubMed
Richardson, P. G. et al. Single-agent bortezomib in previously untreated multiple myeloma: efficacy, characterization of peripheral neuropathy, and molecular correlations with response and neuropathy. J. Clin. Oncol. 2009;27(21):3518–25.CrossRefGoogle ScholarPubMed
Perrone, G. et al. Ascorbic acid inhibits antitumor activity of bortezomib in vivo. Leukemia 2009;23(9):1679–86.CrossRefGoogle ScholarPubMed
Levine, S., Saltzman, A.Pyridoxine (vitamin B6) toxicity: enhancement by uremia in rats. Food Chemical Toxicol. 2002;40(10):1449–51.CrossRefGoogle ScholarPubMed
Levine, S., Saltzman, A.Pyridoxine (vitamin B6) neurotoxicity: enhancement by protein-deficient diet. J. Appl. Toxicol. 2004;24(6):497–500.CrossRefGoogle Scholar
Gedlicka, C. et al. Effective treatment of oxaliplatin-induced cumulative polyneuropathy with alpha-lipoic acid. J. Clin. Oncol. 2002;20(15):3359–61.CrossRefGoogle ScholarPubMed
Sima, A. A. F. et al. Acetyl-L-carnitine improves pain, nerve regeneration, and vibratory perception in patients with chronic diabetic neuropathy. Diabetes Care 2005;28(1):89–94.CrossRefGoogle ScholarPubMed
Tang, J. et al. Alpha-lipoic acid may improve symptomatic diabetic polyneuropathy. Neurologist 2007;13(3):164–7.CrossRefGoogle ScholarPubMed
Ziegler, D.Treatment of diabetic neuropathy and neuropathic pain. Diabetes Care 2008;31(Suppl 2):S255–S261.Google ScholarPubMed
Smyth, J. F. et al. Glutathione reduces the toxicity and improves quality of life of women diagnosed with ovarian cancer treated with cisplatin: Results of a double-blind, randomised trial. Ann. Oncol., 1997;8(6):569–73.CrossRefGoogle ScholarPubMed
Cascinu, S. et al. Neuroprotective effect of reduced glutathione on cisplatin-based chemotherapy in advanced gastric cancer: a randomized double-blind placebo-controlled trial. J. Clin. Oncol., 1995;13(1):26–32.CrossRefGoogle ScholarPubMed
Cascinu, S. et al. Neuroprotective effect of reduced glutathione on oxaliplatin-based chemotherapy in advanced colorectal cancer: a randomized, double-blind, placebo-controlled trial. J. Clin. Oncol., 2002;20(16):3478–83.CrossRefGoogle ScholarPubMed
Wang, W. -S. et al. Oral glutamine is effective for preventing oxaliplatin-induced neuropathy in colorectal cancer patients. The Oncologist 2007;12(3):312–19.CrossRefGoogle ScholarPubMed

Save book to Kindle

To save this book to your Kindle, first ensure [email protected] is added to your Approved Personal Document E-mail List under your Personal Document Settings on the Manage Your Content and Devices page of your Amazon account. Then enter the ‘name’ part of your Kindle email address below. Find out more about saving to your Kindle.

Note you can select to save to either the @free.kindle.com or @kindle.com variations. ‘@free.kindle.com’ emails are free but can only be saved to your device when it is connected to wi-fi. ‘@kindle.com’ emails can be delivered even when you are not connected to wi-fi, but note that service fees apply.

Find out more about the Kindle Personal Document Service.

Available formats
×

Save book to Dropbox

To save content items to your account, please confirm that you agree to abide by our usage policies. If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your account. Find out more about saving content to Dropbox.

Available formats
×

Save book to Google Drive

To save content items to your account, please confirm that you agree to abide by our usage policies. If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your account. Find out more about saving content to Google Drive.

Available formats
×