In your experience, and if applicable, what is the time line between amyloidosis and diagnosis of Multiple Myeloma? It has been 17 months since the diagnosis of amyloidosis, and now my M protieins are rising. Curious about how soon and with what indicators will the next diagnosis be made.
Just started cycle number 1, of my new chemo regime pomlidamide, with dexamethasone. Have already done velcade, and Revlimid neither of those did any good. To continue this new regime my pplS have to come down by 50 percent by the end of cycle 2. What I find a bit of a bind is having to inject heparin every day to prevent blood clots, my haematologist has to monitor my results very closely as I had a major stroke 12years ago.
Prior to reading my reply please realize I AM NOT A DOCTOR! I do however have experience in this area as I’ve been a multiple myeloma patient for the past ten years and have done a large back of information. I have a blog that answers questions similar to yours. I also have an up coming podcast so folks like us can share and comfort one another. So perhaps I’ll see you around.
I hope this answers some of your questions or at the very least gives you questions to ask your doctor.
Remember I AM NOT A DOCTOR!
There are several types of plasma cell neoplasms. These diseases are all associated with a monoclonal (or myeloma) protein (M protein). They include monoclonal gammopathy of undetermined significance (MGUS), isolated plasmacytoma of the bone, extramedullary plasmacytoma, and multiple myeloma.
Evaluation of patients with monoclonal (or myeloma) protein (M protein)
Idiotypic myeloma cells can be found in the blood of myeloma patients in all stages of the disease.For this reason, when treatment is indicated, systemic treatment must be considered for all patients with symptomatic plasma cell neoplasms. Patients with MGUS or asymptomatic, smoldering myeloma do not require immediate treatment but must be followed carefully for signs of disease progression.
The major challenge is to separate the stable, asymptomatic group of patients who do not require treatment from patients with progressive, symptomatic myeloma who should be treated immediately.
Patients with a monoclonal (or myeloma) protein (M protein) in the serum and/or urine are evaluated by some of the following criteria:
Measure and follow the serum M protein by serum electrophoresis or by specific immunoglobulin assays; however, specific immunoglobulin quantification always overestimates the M protein because normal immunoglobulins are included in the result. For this reason, baseline and follow-up measurements of the M protein should be done by the same method.Quantitative serum-free light chains may be helpful to follow response if an M protein is not apparent.
Measure and follow the amount of M-protein light chains excreted in the urine over 24 hours. Measure the total amount of protein excreted over 24 hours and multiply this value by the percentage of urine protein that is M protein, as determined by electrophoresis of concentrated urine protein. An easier, but less accurate, method uses a spot-urine protein electrophoresis.
Identify the heavy and light chain of the M protein by immunofixation electrophoresis.
Measure the hemoglobin, leukocyte, platelet, and differential counts.
Sometimes, determine the percentage of marrow plasma cells. Be aware that marrow plasma-cell distribution may vary in different sites.
Measure serum-free kappa and lambda light chain. This is especially useful in cases of oligosecretory plasma-cell dyscrasia or for following cases of light-chain amyloidosis.
Take needle aspirates of a solitary lytic bone lesion, extramedullary tumor(s), or enlarged lymph node(s) to determine whether these are plasmacytomas.
Evaluate renal function with serum creatinine and a creatinine clearance.
Electrophoresis of concentrated urine protein is very helpful in differentiating glomerular lesions from tubular lesions. Glomerular lesions, such as those resulting from glomerular deposits of amyloid or light-chain deposition disease, result in the nonselective leakage of all serum proteins into the urine; the electrophoresis pattern of this urine resembles the serum pattern with a preponderance of albumin.
In most myeloma patients, the glomeruli function normally allows only the small molecular weight proteins, such as light chains, to filter into the urine. The concentration of protein in the tubules increases as water is reabsorbed. This leads to precipitation of proteins and the formation of tubular casts, which may injure the tubular cells.
Sunny Jim,
Diagnosed mugis in 2004.
5 years elevated to 6 protein count.
Chemo 2years.
Stem cell transplant in Salt Lake City.
3 years semi remission…total 10 years.
In the meantime. Diagnosed with breast cancer. Double masectomy!
I am a military veteran with over 37 years experience? My wife is the warrior in our family!
Niel Gnesin said:
Prior to reading my reply please realize I AM NOT A DOCTOR! I do however have experience in this area as I've been a multiple myeloma patient for the past ten years and have done a large back of information. I have a blog that answers questions similar to yours. I also have an up coming podcast so folks like us can share and comfort one another. So perhaps I'll see you around.
I hope this answers some of your questions or at the very least gives you questions to ask your doctor.
Remember I AM NOT A DOCTOR!
There are several types of plasma cell neoplasms. These diseases are all associated with a monoclonal (or myeloma) protein (M protein). They include monoclonal gammopathy of undetermined significance (MGUS), isolated plasmacytoma of the bone, extramedullary plasmacytoma, and multiple myeloma.
Evaluation of patients with monoclonal (or myeloma) protein (M protein)
Idiotypic myeloma cells can be found in the blood of myeloma patients in all stages of the disease.For this reason, when treatment is indicated, systemic treatment must be considered for all patients with symptomatic plasma cell neoplasms. Patients with MGUS or asymptomatic, smoldering myeloma do not require immediate treatment but must be followed carefully for signs of disease progression.
The major challenge is to separate the stable, asymptomatic group of patients who do not require treatment from patients with progressive, symptomatic myeloma who should be treated immediately.
Patients with a monoclonal (or myeloma) protein (M protein) in the serum and/or urine are evaluated by some of the following criteria:
Measure and follow the serum M protein by serum electrophoresis or by specific immunoglobulin assays; however, specific immunoglobulin quantification always overestimates the M protein because normal immunoglobulins are included in the result. For this reason, baseline and follow-up measurements of the M protein should be done by the same method.Quantitative serum-free light chains may be helpful to follow response if an M protein is not apparent.
Measure and follow the amount of M-protein light chains excreted in the urine over 24 hours. Measure the total amount of protein excreted over 24 hours and multiply this value by the percentage of urine protein that is M protein, as determined by electrophoresis of concentrated urine protein. An easier, but less accurate, method uses a spot-urine protein electrophoresis.
Identify the heavy and light chain of the M protein by immunofixation electrophoresis.
Measure the hemoglobin, leukocyte, platelet, and differential counts.
Sometimes, determine the percentage of marrow plasma cells. Be aware that marrow plasma-cell distribution may vary in different sites.
Measure serum-free kappa and lambda light chain. This is especially useful in cases of oligosecretory plasma-cell dyscrasia or for following cases of light-chain amyloidosis.
Take needle aspirates of a solitary lytic bone lesion, extramedullary tumor(s), or enlarged lymph node(s) to determine whether these are plasmacytomas.
Evaluate renal function with serum creatinine and a creatinine clearance.
Electrophoresis of concentrated urine protein is very helpful in differentiating glomerular lesions from tubular lesions. Glomerular lesions, such as those resulting from glomerular deposits of amyloid or light-chain deposition disease, result in the nonselective leakage of all serum proteins into the urine; the electrophoresis pattern of this urine resembles the serum pattern with a preponderance of albumin.
In most myeloma patients, the glomeruli function normally allows only the small molecular weight proteins, such as light chains, to filter into the urine. The concentration of protein in the tubules increases as water is reabsorbed. This leads to precipitation of proteins and the formation of tubular casts, which may injure the tubular cells.