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Diagnosed with SMM, SPB, or MGUS?

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SMM, MGUS, Fibromyalgia, Nerve Pain?

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I was diagnosed with MGUS in 2012 for the last 2 years I have been experiencing bouts of neuropathic nerve pain.

Hi David, I would like to know is this the way of things regarding pain, I was diagnosed with 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 face, legs and feet.

Sometimes the pains feels like a aching, lightening pain, quick and sharp, especially in the palms of my hands and face. I was told that i have neuralgia and fybromalgia as well as raised SHBG levels. 

I’m also allergic to many verity of foods which I have had for many years. I’ve now requested a follow up for my bloods to be done, hopefully my MGUS has not progressed further. Stan


Hi Stan-

You have been diagnosed with several possibly overlapping issues many/all of which may be contributing to your pain. I will address as many possibilities as I can.

Re nerve pain and MGUS. As you know, MGUS is supposed to be asymptomatic aka you are not supposed to have any nerve pain. However, pain as a possible MGUS symptom 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.

To learn more about these therapies and about Pre-Myeloma conditions management, please watch the short video below:

My experience is for pre-MM patients-

  • single plasmacytoma,
  • MGUS and
  • SMM

to pursue evidence-based, non-toxic therapies. Research cites possible reduction in monoclonal proteins and therefore possible reduction in nerve damage.

Several of the therapies I take as a long-term MM survivor overlap with supplements that I have read about helping fibromyagia- 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 will has been shown to reduce your risk of progressing to MM and I have worked with MGUS patients who tell me that they have slowly reduced their m-spike.

Let me know if you have any questions. Hang in there,

David Emerson

  • MM Survivor
  • MM Cancer Coach
  • Director PeopleBeatingCancer

Recommended Reading:


Monoclonal Gammopathy Associated Peripheral Neuropathy: Diagnosis and Management

“Monoclonal gammopathies consist of a spectrum of clonal plasma cell disorders that includes monoclonal gammopathy of undetermined significance (MGUS), multiple myeloma (MM) and Waldenstrom Macroglobulinemia (WM). In this review, we outline the epidemiology, etiology, classification, diagnosis, and treatment of monoclonal gammopathy associated peripheral neuropathy.

Monoclonal gammopathy of undetermined significance (MGUS) is relatively common in the general population, with a prevalence of 3–4% among those over the age of 50. Therefore, the presence of M protein in a patient with neuropathy does not automatically indicate a causal relationship…

In addition to a review of the literature, we present a diagnostic approach to patients with monoclonal gammopathy associated peripheral neuropathy and discuss available data and options for treatment…

DIAGNOSIS

Monoclonal gammopathy associated peripheral neuropathy should be considered when an M protein is detected during work up of unexplained neuropathy. The first step in evaluation is to determine if the monoclonal gammopathy is the likely cause of peripheral neuropathy or if it is a coincidental finding related to the frequency with which M proteins are seen in the general population (Figure 1).

Other explanations and causes of peripheral neuropathy such as genetic, diabetes mellitus, alcoholism, drugs etc, must first be considered and excluded as much as possible. There are no specific tests that can be done to distinguish between a true causal association and an incidental one…

POEMS Syndrome

POEMS syndrome is a clonal plasma cell disorder described by the acronym in its name, polyneuropathy, organomegaly, endocrinopathy, monoclonal protein, and skin changes.

POEMS syndrome is characterized by a progressive chronic demyelinating sensorimotor polyneuropathy that is either length-dependent or a polyradiculoneuropathy, and is often mistaken for CIDP.

Organomegaly (hepatomegaly or splenomegaly) and skin changes (eg., hyperpigmentation) can be seen. Other characteristics include edema, pleural effusions, ascites, and papilledema.

The bone lesions in POEMS syndrome are sclerotic (osteosclerotic myeloma) in contrast to MM where bone lesions are osteolytic.

Many patients with POEMS may present mainly with neuropathy and a lambda type M protein, with the other features not being prominent. Careful evaluation with history and examination is needed, and if POEMS is suspected, radiographic (skeletal survey or computed tomographic scans) studies looking for one or more osteosclerotic bone lesions should be performed.

The peripheral neuropathy is motor predominant but with associated sensory symptoms and often pain at initial presentation.,

The histological pattern usually shows axonal degeneration along with demyelination. EMG usually shows a demyelinating pattern with more severe axonal loss (reduction of motor amplitudes and increased fibrillation potentials) than seen in CIDP or DADS-M.

The M protein in POEMS syndrome is usually IgG or IgA. The underlying cause of the neuropathy remains unknown, although vascular endothelial growth factor may play a role in pathogenesis. Treatment of POEMS syndrome involves radiation and chemotherapy for the sclerotic plasmacytomas . This usually results in significant clinical improvement of the neuropathy as well as the other systemic features.

Conclusion

Additional studies are needed investigating new options for therapy. We recognize that many patients have disabling symptoms, and as new treatments emerge for plasma cell malignancies, some of these can be translated to the treatment of severe monoclonal gammopathy associated peripheral neuropathy.

We need a better understanding of the pathophysiologic mechanisms, and better biomarkers to assess the value and effectiveness of therapy. Further studies are also needed to determine if there is a true association between non-IgM monoclonal gammopathy and peripheral neuropathy.”

 

 

 

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