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Hi David, I would like to know is this the way of things regarding pain. I was diagnosed with monoclonal gammopathy of undetermined significance (MGUS) in 2012 for the last 2 years I have been experiencing bouts of neuropathic nerve pain.
First starting in my shoulder blades then into arms, hands and now on the one side of my face, legs and feet. Sometimes the pain feels like an aching, lightening pain, quick and sharp, especially in the palms of my hands and face.
I was told that I have neuralgia and fibromyalgia as well as raised SHBG levels I’m also allergic to many foods and I have been for many years. I’ve now requested a follow up for my blood testing to be done, hopefully, my MGUS has not progressed further.
Dear Monoclonal gammopathy Patient-
You have been diagnosed with several possibly overlapping issues all of which may be contributing to your pain. I will address as many possibilities as I can.
Regarding nerve pain and monoclonal gammopathy (MGUS). As you know, MGUS is supposed to be “asymptomatic” aka you are not supposed to experience nerve pain. However, pain can be an MGUS symptom and is well documented. Further, nerve pain is well documented for fibromyalgia as well. Also as you probably know, conventional oncology considers MGUS to be a “blood disorder” and therefore can offer no therapies.
My experience is for pre-MM patients (single plasmacytoma, MGUS, and SMM) to pursue evidence-based, non-toxic therapies. Several of the therapies I take as a long-term MM survivor overlaps with supplements that I have read about helping fibromyalgia- an example would be vitamin D3- I take this for bone health and balance and I will link a study below about fibromyalgia.
Please consider the pre- MM cancer coaching program. The information provided has been shown to reduce your risk of progressing to MM. I have worked with pre-MM patients who tell me that they have slowly reduced their m-spike.
Let me know if you have any questions.
Hang in there,
Neuropathies associated with MGUS are usually demyelinating or mixed, with features of demyelination and axonal loss, and the axonal changes are usually attributed to severe or chronic demyelination. Pure axonal neuropathies in patients with MGUS are considered rare, comprising only a few cases in large series.1 3 6 10 11 14 15 21
However, a recent prospective study found 40% of patients with polyneuropathies that were associated with MGUS had electrodiagnostic features of a purely axonal process.13
Another study from the same investigators found that almost 20% of patients in their series with chronic axonal neuropathy had MGUS.22 Our experience was similar in that we found that 44% of a consecutive series with MGUS and neuropathy had primarily axonal disease.
These patients with A-MGUS had a relatively homogenous clinical presentation with modest sensory symptoms—distal leg numbness, paraesthesiae, and mild imbalance—with pain affecting one third of patients. Weakness or falling was uncommon.
A few patients with A-MGUS had unusual presentations, with severe sensory loss in the upper limbs or moderate leg weakness with bilateral foot drop. Most had an unsteady gait but all were ambulatory and disability was usually mild.
Although the degree of weakness was similar in patients with A-MGUS and D-MGUS, there were several clinical features that distinguished the groups. Falling was more common in patients with D-MGUS, reflecting leg ataxia and impaired sensation of joint position. Patients with D-MGUS also had more severe loss of large fibre sensation and more often had generalised areflexia, typical of patients with chronic inflammatory demyelinating polyneuropathy.20 20a Accordingly, they had greater disability and a worse Rankin score compared with the A-MGUS group.
There was an association between the type of MGUS and the electrophysiological features of the neuropathy. IgM-MGUS and anti-MAG antibodies occurred often in patients with D-MGUS, confirming previous reports that patients with IgM neuropathies have more prominent demyelination on EMG studies5 6 8 11 12 In the three of our patients with A-MGUS and IgM gammopathy, none had anti-MAG antibodies. This supports the notion that anti-MAG antibodies may be relatively specific for demyelinating neuropathies.8 9 23
Patients with IgM-MGUS have been traditionally distinguished from those with IgG/IgA-MGUS, in part because of greater demyelination found on nerve conduction studies in the IgM group.2 5 6 In our patients with MGUS and either axonal or demyelinating neuropathy, there were no important clinical, EMG, or treatment features that separated patients with IgM and IgG-MGUS. Thus in addition to the nature of the immunoglobulin abnormality, the predominant electrodiagnostic pattern (axonal vdemyelinating) may be helpful in differentiating the clinical features, course, and response to therapy in patients with MGUS associated neuropathies (see below).
Could the association between patients with axonal neuropathy and MGUS be chance? M proteins are present in up to 3% of the population over the age of 70, and the finding of an M protein in older patients with an “idiopathic” axonal neuropathy may be coincidental and not related to the neuropathy.24 25
None the less, there are several lines of evidence that suggest that the association between MGUS and axonal neuropathy is more than chance. In their study of patients with chronic idiopathic axonal neuropathy, Notermans et al concluded that there were no significant differences between patients with and without MGUS, but the data showed that MGUS patients had greater involvement of the arms, worse disability on the Rankin score, and a higher frequency of denervation compared with patients without MGUS.22…
Most patients with A-MGUS had a progressive course, and only one patient had a relapsing course responsive to plasma exchange. Only three of our patients with A-MGUS responded to immunotherapy, by contrast with 15 of the 20 patients with D-MGUS.
There was no difference in the response rates with IVIg or steroids, but patients with D-MGUS had a significantly greater response rate to plasma exchange and a larger change in the mean Rankin score.
The beneficial effects of plasma exchange in our patients with IgM need to be interpreted cautiously due to the limitations of a retrospective analysis; results of the small prospective trial by Dyck et al showed that their patients with IgM had a less favourable response to plasma exchange compared with patients with IgG or IgA-MGUS.37 Most of the patients with A-MGUS had only one series of five exchanges, a single course of IVIg, or a short trial of steroids.
The lack of a therapeutic response may indicate that short term immunomodulating therapy may be inadequate in patients with MGUS with prominent axonal loss, but our numbers are too small to draw definitive conclusions.
In summary, there is a subset of patients with MGUS who have a mild, predominantly sensory axonal neuropathy that can be clinically and electrophysiologically distinguished from the demyelinating or mixed neuropathies that are more consistently associated with MGUS.
The pattern of electrodiagnostic abnormalities, in addition to the nature of the M protein, may be helpful in defining the course and response to treatment. Some of these patients may improve with immune modulation.