“This issue of adverse effects in (MM) survivors goes beyond peripheral neuropathy. There are other effects that need to be considered while patients are making treatment decisions.”
I am a long-term survivor of multiple myeloma. I began feeling the symptoms of peripheral neuropathy about a year after I underwent a chemotherapy cocktail called V.A.D. (vincristine, adriamycin, dexamethasone). I’m pointing this out because:
- Peripheral neuropathy is a common side effect of multiple myeloma therapy particularly velcade and thalidomide
- Though I am a long-term MM survivor with CIPN, I didn’t undergo either thalidomide or velcade. I’m putting my money on vincristine…
If I read the article linked and excerpted below the authors of the study are saying that conventional oncology needs to “ask questions” about adverse events especially when they are talking about “small therapeutic benefits with the risk of long-term adverse events.”
For the record chemotherapy-induced peripheral neuropathy (CIPN) does not simply cause patients to feel “discomfort” or “experience a lower quality of life.” The vast majority of patients and survivors with CIPN live with intense pain for the rest of their lives. This is a clear example of the cure being worse than the disease.
If you are reading this blog post before you are to undergo any platinum-based chemo or a number of chemo regimes such as thalidomide or velcade, please read and consider supplementing with evidence-based, non-conventional therapies that can reduce the severity to this awful side effects.
According to the article linked here, omega 3 fatty acids and exercise may reduce or prevent CIPN.
I use and recommend Life Extension Omega 3 fatty acids as this formula is cancer preventative, heart and brain healthy and has been evaluated and approved by Consumerlab.com.
To Learn More about Chemotherapy-induced Peripheral Neuropathy- click now
I am a long-term multiple myeloma survivor and MM cancer coach. Have you been diagnosed with multiple myeloma? Please scroll down the page, post a question or comment and I will reply to you ASAP.
Thank you,
David Emerson
- Multiple MyelomaSurvivor
- MM Cancer Coach
- Director PeopleBeatingCancer
Recommended Reading:
Bortezomib- Bortezomib is a more recent addition to cancer chemotherapeutics approved by the FDA in 2003 for the treatment of advanced myeloma. Bortezomib exerts its mechanism of action by inhibiting the 26S ribosome subunit and preventing protein degradation, leading to cell cycle arrest and apoptosis 39.
In patients treated with bortezomib, a severe, painful, sensory neuropathy commonly develops 40, 41. Bortezomib has been shown to affect polymerization of α-tubulin and result in microtubule stabilization, similar to that of the taxane class 42.
Mitochondria in the dorsal root ganglia of treated patients have shown vacuolation, presumed secondary to mitochondrial enlargement, which leads to activation of pro-apoptotic pathways 43. Inflammation and oxidation stress have also been implicated in the development of neuropathic pain associated with the administration of bortezomib.
Inhibition of NFκB by bortezomib leads to increased TNFα and the production of reactive oxygen species, both of which have been associated with neuropathic pain 44, 45.
Another mechanism of neuropathic pain in patients treated with bortezomib is activation of TRP channels. As mentioned earlier, increased levels of TRPV1 in the dorsal root ganglion of patients treated with bortezomib have been felt to be causative of some of the neuropathic pain appreciated by patients 17….”
“Results- In total, 9 GWASs were identified from the literature on CIPN caused by different drugs (4 paclitaxel, 2 bortezomib, 1 vincristine, 1 docetaxel, and 1 oxaliplatin). Data were extracted for 526 SNPs in 109 loci. One hundred fourty-eight patients in our study population were CIPN cases (102/646 bortezomib, 17/63 thalidomide and 29/274 vincristine).
In total, 13 SNPs in 9 loci were replicated in our population (p-value< 0.05). The four smallest P-values relevant to the nerve function were 0.0006 for rs8014839 (close to the FBXO33gene), 0.004 for rs4618330 (close to the INTU gene), 0.006 for rs1903216 (close to the BCL6 gene) and 0.03 for rs4687753 (close to the IL17RB gene).
“Peripheral neuropathy, which causes pain, numbness, and tingling in hands and/or feet, can bother early-stage breast cancer patients years after completing chemotherapy. New research has found only a handful of studies that tracked long-term peripheral neuropathy, leaving little data for patients and clinicians to make informed decisions…
“I think we’ve reached the point now where we need to ask questions about the adverse effects that come along after curative treatments. We need to balance what are sometimes small therapeutic benefits with the risk of long-term adverse events….”
“And these studies report a wide range of frequency for peripheral neuropathy, from as low as 11 percent to more than 80 percent of patients at one to three years after treatment...”
Overall, two years after the start of treatment, 42 percent of patients experienced neuropathy symptoms and 10 percent reported severe discomfort. In addition, women experiencing more severe neuropathy symptoms reported much worse quality of life…
For example, patients who received the lower-dose docetaxel combinations were less affected by long-term neuropathy…
Since we don’t have an effective treatment, ideally it would be best to prevent it from happening by not administering chemotherapy if it is likely to have minimal additional benefit. Alternatively, this class of drugs could be avoided in patients who are at higher risk for persistent neuropathy…
This issue of adverse effects in survivors goes beyond peripheral neuropathy. There are other effects that need to be considered while women are making treatment decisions.”
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