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One of the most difficult aspects about an MGUS or SMM diagnosis is your oncologist telling you that your diagnosis is asymptomatic. That your memory loss, slurred speech, burning pain or even your fractured hip can’t be attributed to your pre-myeloma diagnosis.
If you’re reading this post, you may have been diagnosed with monoclonal gammopathy of undetermined significance (MGUS) and been told that your diagnosis is an asymptotic blood disorder. Yet, perhaps you’ve noticed that your memory is weakening, your vision may be blurred and perhaps your speech has slurred.
According to the study linked and excerpted below, a symptom of MGUS is hyperviscosity syndrome. Basically a thickening of a person’s blood. The presence of the MGUS plasma cell or monoclonal protein, causes a person’s blood to thicken.
If your blood thicken’s it can gum-up your brain, eye, etc. function.
Fortunately, thick blood is a relatively easy symptom to test for and identify. Talk to your doctor but there are therapies that can reduce the thickness of the blood. A relatively easy diagnosis and therapy.
The fact is, there are many evidence-based, non-toxic therapies that studies show can reduce the risk of pre-MM becoming full-blown MM. Nutrition, supplementation, lifestyle therapies, etc. all have shown the ability to reduce the risk of MM.
For more information about these non-toxic therapies, scroll down the page, send me a comment or a question and I will reply to you ASAP.
In the meantime, hang in there.
“Systemic manifestations of monoclonal gammopathies (MG) are rare but extremely varied. This general review focuses on
and biological manifestations, with the exception of amyloidosis AL and cryoglobulinemia….”
“Description of the problem- Hyperviscosity syndrome (HVS) is a combination of clinical signs and symptoms related to increased blood viscosity. It can result from abnormal plasma components such as paraproteins (seen in Waldenstrom’s macroglobulinemia [WM] and multiple myeloma [MM]) or immune complexes (systemic lupus erythematosis). HVS can also be secondary to increased cellular components due to leukemia or myeloproliferative disorders.
“A 69-year-old woman with a 3-year history of IgG monoclonal gammopathy of undetermined significance (MGUS), hypertension, idiopathic pulmonary fibrosis, and chronic kidney disease, presented for an outpatient bone marrow biopsy.
Preprocedure laboratory studies revealed a significantly elevated INR (>10), prompting presentation to a local emergency department. Upon evaluation the patient endorsed a 2–3-day history of word slurring, writing difficulty, and vision changes.
She confirmed that she was not prescribed any anticoagulants and had no history of severe bleeding. There were no signs of active bleeding. Mental status examination showed mild confusion with orientation to self and place but not to month or year. There was a detectable loss in language fluency. Neurologic examination was remarkable for mild left upper extremity drift. Computed tomography of the head showed lytic lesions of the calvarium…
A 2-procedure series of plasmapheresis was performed with the goal of decreasing serum IgG and viscosity. Albumin was used as the replacement fluid. After the first procedure on hospital day 4 the patient’s mental status and speech subjectively improved, IgG decreased from 11.6 to 3.7 g/dL, and the PT shortened to 28 s (Fig. 1). IgG further decreased to 1.7 g/dL after the second procedure on hospital day 5…
HVS is a rare but serious complication of hypergammaglobulinemia that often presents as an oncologic emergency. The viscosity, or thickness, of whole blood is modulated by multiple factors, including
Monoclonal gammopathies such as Waldenstrom’s macroglobulinemia or MM can raise serum viscosity through production of excess paraprotein, which leads to the shearing of the endothelium in small blood vessels…
Waldenstrom’s macroglobulinemia is the most common underlying cause of HVS, followed by IgA and IgG MM, respectively (5).
The incidence of HVS is higher in patients with Waldenstrom’s macroglobulinemia (10–30%) than in MM (2–6%), which is likely due to the high intrinsic viscosity of the large pentameric IgM protein (5). Our patient’s presentation is unusual in that she developed HVS in the setting of an IgG paraprotein, rather than IgM or IgA.