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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What is myeloma with amyloidosis? When a person is diagnosed with a blood cancer called multiple myeloma with a complication called amyloidosis what does it mean?
According to research 15%-20% of newly diagnosed MM patients also have amyloidosis.
The MM patient’s prognosis depends largely on what, if any, is the patient’s organ involvement. According to the study linked at the bottom of this post, treatment of AL/MM is aggressive therapy in hopes of at least a VGPR.
While this is a general video about amyloidosis, I am including it as it give a good explanation of AL itself as well as it’s relation to MM.
It is unclear if there are evidence-based non-conventional therapies for AL amyloidosis and MM. My initial study of supplements indicates that curcumin and omega-3 fatty acids may help though more research is needed.
As a long-term MM survivor however, I am inclined to believe that there are non-conventional therapies that may help.
Email me at David.PeopleBeatingCancer@gmail.com if you have any questions.
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“Background: Amyloid light-chain amyloidosis (AL amyloidosis) is commonly associated with multiple myeloma. However, the clinical characteristics and prognosis of symptomatic and smoldering multiple myeloma with AL amyloidosis are not particularly clear…
Results: Compared with symptomatic multiple myeloma patients without AL amyloidosis, patients with AL amyloidosis had higher incidence of BNP≧700pg/mL (P< 0.001), ALP> 187.5IU/L (P=0.032) and ALB< 25g/L (P< 0.001).
Similarly, compared with smoldering multiple myeloma patients without AL amyloidosis, patients with AL amyloidosis had higher incidence of BNP≧700pg/mL (P=0.030) and Alb< 25g/L (P=0.024).
The existence of AL amyloidosis, especially those with the heart involvement, was related to shorter long-term survival of symptomatic and smoldering multiple myeloma according to univariate analyses.
Renal involvement and gastrointestinal tract involvement had an impact on the prognosis of smoldering multiple myeloma but not on the symptomatic multiple myeloma. Cox regression model for overall survival detected BNP≧700pg/mL in symptomatic multiple myeloma having independent poorer prognostic significance (HR=2.455, P=0.004).
Interestingly, BNP at diagnosis was significantly correlated with cardiac amyloidosis (r=0.496, P< 0.001). Cox regression model for overall survival detected the presence of AL amyloidosis in smoldering multiple myeloma having independent poorer prognostic significance (HR=8.741, P=0.002).
Conclusion: AL amyloidosis is an independent poor prognostic factor for not only symptomatic multiple myeloma but also smoldering multiple myeloma. It is mainly because of involvement of important organs, especially the heart. AL amyloidosis probably has a greater impact on the prognosis of smoldering multiple myeloma than on the symptomatic multiple myeloma.”
Conclusions
AL amyloidosis remains an incurable and devastating disease, with a still excessive diagnostic delay. Median OS is approaching five years in the last decade, despite an almost universal heart involvement.
MM is a complex and heterogeneous disease with variable outcomes. The association of both entities is not well characterized. Diagnosis should be based on current international consensus criteria. The most frequent type of association is the synchronous occurrence of both diseases.
In our series of AL pts, 18.7% fulfill the diagnostic criteria of MM, most of them with a synchronous pattern. The prognosis of AL is dominated by the heart involvement. Our Cox regression model shows that NT-proBNP ≥ 8500 pg/mL is an independent prognostic factor for OS, whereas LVEF has a marginal effect.
Besides, age is also a very strong prognostic factor for both AL and MM. Finally, ASCT is still a goal for AL pts. 21.6% underwent ASCT in our series and the great advantage in this subgroup is confirmed in terms of OS, behaving as an independent prognostic factor.”
Immunoglobulin light chain amyloidosis is a clonal, nonproliferative plasma cell disorder in which fragments of immunoglobulin light or heavy chain are deposited in tissues. Clinical features depend on organs involved but can include heart failure with preserved ejection fraction, nephrotic syndrome, hepatic dysfunction, peripheral/autonomic neuropathy, and “atypical smoldering multiple myeloma or MGUS.”
Tissue biopsy stained with Congo red demonstrating amyloid deposits with apple-green birefringence is required for the diagnosis of AL amyloidosis. Organ biopsy is not required in 85% of patients. Verification that amyloid is composed of immunoglobulin light chains is mandatory. The gold standard is laser capture mass spectroscopy.
N-terminal pro–brain natriuretic peptide (NT-proBNP or BNP), serum troponin T(or I), and difference between involved and uninvolved immunoglobulin free light chain values are used to classify patients into four stages; 5-year survivals are 82%, 62%, 34%, and 20%, respectively.
All patients with a systemic amyloid syndrome require therapy to prevent deposition of amyloid in other organs and prevent progressive organ failure. Current first-line therapy with the best outcome is daratumumab, bortezomib, cyclophosphamide, and dexamethasone. The goal of therapy is a ≥VGPR. In patients failing to achieve this depth of response options for consolidation include pomalidomide, stem cell transplantation, venetoclax, and bendamustine.
Delayed diagnosis remains a major obstacle to initiating effective therapy prior to the development of end-stage organ failure. Trials of antibodies to deplete deposited fibrils are underway.”