Recently Diagnosed or Relapsed? Stopping Looking For a Miracle Cure, and Use Evidence-Based Therapies To Enhance Your Treatment and Prolong Your Remission

Multiple Myeloma an incurable disease, but I have spent the last 25 years in remission using a blend of conventional oncology and evidence-based nutrition, supplementation, and lifestyle therapies from peer-reviewed studies that your oncologist probably hasn't told you about.

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Myeloma Symptoms at Diagnosis-

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“Most patients with MM present with signs or symptoms related to the infiltration of plasma cells into the bone or other organs or to kidney damage from excess light chains.”

This multiple myeloma (MM) blog post falls under the feel good category of learning about your MM. Meaning, we all have symptoms upon diagnosis of MM but often forget about them once active therapy (induction, consolidation, ASCT, maintenance, etc.) begins.

This is the type of post about MM that is educational in nature. “I remember that! I was exhausted for months before my MM diagnosis but no one could figure out why!” According to the research below, your exhaustion was probably anemia,  a common symptom of newly diagnosed MM patients that occurs when MM plasma cells crowd out your red blood cells that circulate oxygen throughout your body. Fewer red blood cells, less oxygen, you feel tired all the time…

Certain symptoms however, such as renal involvement, can have serious consequences regarding your prognosis and overall survival. It’s in your best interest to understand all you can about any renal damage at diagnosis and the health of your kidney now and in the future.

When you read the information below, try to keep a sharp eye out for symptoms that you experienced that can effect you for years if not the rest of your life.

For example, I discovered my own MM because of bone pain-cord compression-neurologic disease (Radiculopathy)-that is affects my neck and arm health. My oncologist and surgeon did as much as they could to repair and health the lesion and neck (corpectomy) but my point is that I wish I had been a part of the decision-making. For the record, this surgery was the single most effect therapy that I underwent during my three + years of conventional MM therapies.

Have you been diagnosed with multiple myeloma? What symptoms have you experienced? To learn more about conventional and evidence-based non-conventional MM therapies, scroll down the page, post a question or comment and I will reply to you ASAP.

Hang in there,

David Emerson

  • MM Survivor
  • MM Cancer Coach
  • Director PeopleBeatingCancer

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Multiple myeloma: Clinical features, laboratory manifestations, and diagnosis

Spectrum of disease — Most patients with MM present with signs or symptoms related to the infiltration of plasma cells into the bone or other organs or to kidney damage from excess light chains. As an example, a retrospective analysis of 1027 sequential patients diagnosed with MM at a single institution found the following symptoms and signs at presentation [10]:
Anemia – 73 percent
Bone pain – 58 percent
Elevated creatinine – 48 percent
Fatigue/generalized weakness – 32 percent
Hypercalcemia – 28 percent
Weight loss – 24 percent, one-half of whom had lost ≥9 kg
Anemia — A normocytic, normochromic anemia (hemoglobin ≤12 g/dL) is present in 73 percent at diagnosis and in 97 percent at some time during the course of the disease [10]. This anemia can be related to bone marrow replacement, kidney damage, and/or can be due to dilution in the case of a large M-protein. Anemia commonly results in complaints of fatigue and pallor seen on physical examination.
Macrocytosis (mean corpuscular volume [MCV] >100 fL) was present in 9 percent of 1027 patients studied [10]. In this study, 53 patients (11 percent) with an MCV >100 fL had a vitamin B12 level <200 ng/L. This finding is similar to a prevalence of vitamin B12 deficiency of 14 percent seen in a separate study of 664 consecutive patients with plasma cell dyscrasias [31]. While the mechanism for low vitamin B12 levels in these patients is not known, investigations must be done to rule out pernicious anemia.
Bone pain — Bone pain, particularly in the back or chest, and less often in the extremities, is present at the time of diagnosis in approximately 60 percent of patients [10]. The pain is usually induced by movement and does not occur at night except with change of position. The patient’s height may be reduced by several inches because of vertebral collapse. Plasmacytomas of the ribs occur and can present either as expanding costal lesions or soft tissue masses.
Renal disease — The serum creatinine concentration is increased in almost one-half of patients at diagnosis (and is >2 mg/dL [177 micromol/L] in approximately 20 percent); renal failure may be the presenting manifestation of MM [10,32]. Two major causes of renal insufficiency in patients with MM are light chain cast nephropathy (also called myeloma kidney) and hypercalcemia. Patients who do not secrete light chains are not at risk for myeloma kidney. In the absence of other causes of renal failure, a presumptive diagnosis of light chain cast nephropathy can be made in the setting of high involved free light chain (FLC) levels (typically >1500 mg/L).
In contrast, renal biopsy should be performed to document typical histologic changes in patients with suspected cast nephropathy, especially if the serum-involved FLC level is <500 mg/L [37]. (See “Clinical features, evaluation, and diagnosis of kidney disease in multiple myeloma and other monoclonal gammopathies”.)
Other causes of renal failure in a patient with MM include concurrent light chain (AL) amyloidosis, light chain deposition disease, and drug-induced renal damage. Renal disease in MM is discussed in more detail separately. (See “Epidemiology, pathogenesis, and etiology of kidney disease in multiple myeloma and other monoclonal gammopathies”.)
Hypercalcemia — Hypercalcemia is found in 28 percent of one series of patients with MM at the time of diagnosis; serum calcium was ≥11 mg/dL (2.75 mmol/liter) in 13 percent and can require emergent treatment [10]. The ionized calcium should be measured if the patient has a high serum calcium level but no symptoms of hypercalcemia. Elevation of the serum calcium may be due to binding of the monoclonal protein with calcium [38]. (See “Treatment of the complications of multiple myeloma”, section on ‘Hypercalcemia’ and “Treatment of hypercalcemia” and “Hypercalcemia of malignancy: Mechanisms”, section on ‘Osteolytic metastases’.)
Of note, severe hypercalcemia can act as an unmeasured cation and thereby result in a low anion gap. A decreased anion gap may also be due to the presence of a cationic IgG molecule. (See “Serum anion gap in conditions other than metabolic acidosis”.)
Neurologic disease — Radiculopathy, usually in the thoracic or lumbosacral area, is the most common neurologic complication of MM. It can result from compression of the nerve by a paravertebral plasmacytoma or rarely by the collapsed bone itself.
Cord compression – Spinal cord compression from an extramedullary plasmacytoma (image 2) or a bone fragment due to fracture of a vertebral body (image 3) occurs in approximately 5 percent of patients; it should be suspected in patients presenting with severe back pain along with weakness or paresthesias of the lower extremities, or bladder or bowel dysfunction or incontinence.
This set of symptoms constitutes a medical emergency; magnetic resonance imaging (MRI) or computed tomographic myelography of the entire spine must be performed immediately, with appropriate follow-up treatment by chemotherapy, radiotherapy, or neurosurgery to avoid permanent paraplegia. (See “Clinical features and diagnosis of neoplastic epidural spinal cord compression” and “Treatment and prognosis of neoplastic epidural spinal cord compression”.)
 Peripheral neuropathy– Peripheral neuropathy is uncommon in MM at the time of initial diagnosis and, when present, is usually due to amyloidosis. An exception to this general rule occurs in the infrequent subset of patients with POEMS syndrome (osteosclerotic myeloma) in which neuropathy occurs in nearly 100 percent of patients. The pathogenesis of the neuropathy is uncertain but a paraneoplastic mechanism may be important; this issue is discussed separately. (See “POEMS syndrome” and “Paraneoplastic syndromes affecting peripheral nerve and muscle”, section on ‘Association with plasma cell dyscrasias’.)
Central nervous system (CNS) involvement – Intracranial plasmacytomas are rare and almost always represent extensions of myelomatous lesions of the skull or plasmacytomas involving the clivus or base of the skull. Leptomeningeal myelomatosis along with abnormal cerebrospinal fluid findings is uncommon but is being recognized more frequently, especially in advanced stages of the disease [39-44]. When found it denotes a poor prognosis with survival historically measured in months despite treatment [43]. It is usually associated with high-risk cytogenetics; lactate dehydrogenase (LDH) levels may be elevated. Survival appears to have improved slightly since the incorporation of immunomodulatory drugs and proteasome inhibitors into first-line therapy [45,46].
Rare cases of encephalopathy due to hyperviscosity or high blood levels of ammonia, in the absence of liver involvement, have been reported [47-50]. Myeloma cell lines developed from such patients produce elevated amounts of ammonia, although the mechanism is unclear [51]. Ammonia levels and the patient’s state of consciousness return to normal if and when the underlying myeloma responds to chemotherapy.
Infection — Patients with MM are at increased risk for infection due to a combination of immune dysfunction and physical factors. Immune dysfunction results from impaired lymphocyte function, suppression of normal plasma cell function, and hypogammaglobulinemia. Physical factors include hypoventilation secondary to pathologic fractures and pain involving the rib cage and spine. Streptococcus pneumoniae and gram-negative organisms are the most frequent pathogens.”

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