I was diagnosed with multiple myeloma in June, 2007. I had an autologous SCT in April, 2008 and came out of it in nCR. I relapsed after 2 years and then participated in a pomalidomide / dex clinical trial which took my m-spike down to zero (undetectable) after 6 weeks.
After about 6 months the m-spike started climbing slowly but was still at a very low level (0.4) so I wasn't concerned about multiple myeloma symptoms (crab). But, after being on the drug about 8 months and with an m-spike of 0.4, I started getting pains in my shoulder. An MRI revealed a plasmacytoma and a PET/CT scan showed lesions in several other areas. I am now on Velcade which is bringing the m-spike back down.
My question is, how can the myeloma be so active with such a relatively low m-spike? When I had my first bout in 2007, my m-spike had reached 3.0.
Thanks,
Paul Walker,
Olathe, Kansas
Forums
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Re: Relapse with low M-spike
There are many answers to your question.
First, many patients with relatively low tumor burdens may have very focal disease that is capable of being locally destructive. Often patients will present in exactly such a fashion. They can have a local plasmacytoma that causes great harm with a bone marrow and tumor markers that are entirely negative. Sometimes when we treat multiple myeloma we will kill the diffuse disease but the local plasmacytoma will be more resistant and continue to grow, or progress more rapidly than the rest of the disease as we see a relapse. Many of us feel that we see that more often since the introduction of IMIDs [Revlimid, thalidomide, pomalidomide] than we did prior to that time.
Second are what we call oligosecretory relapses. This is disease that basically stops secreting, decreases its secretion of , or changes the nature of its M protein secretion. It is a very common problem to see a patient who made a big IgA or IgG "M" spike at presentation relapse with disease that only secretes a light chain. The "M" will go down in the blood while it is going up in the urine ("light chain escape").
Other times the multiple myeloma will stop making an "M" all together ("nonsecretory escape"). As the tumor becomes more anaplastic with time and treatment it becomes less and less effecient at making its antibody (M protein). Anaplastic is a term that means the tumor becomes less and less like the original cell from which it was derived. Often in a newly diagnosed multiple myeloma pt the tumor cells will look like normal healthy plasma cells, but as the disease survives more and more therapies it becomes "angrier" and less able to perform its normal functions, of which secreting an intact antibody is but one.
First, many patients with relatively low tumor burdens may have very focal disease that is capable of being locally destructive. Often patients will present in exactly such a fashion. They can have a local plasmacytoma that causes great harm with a bone marrow and tumor markers that are entirely negative. Sometimes when we treat multiple myeloma we will kill the diffuse disease but the local plasmacytoma will be more resistant and continue to grow, or progress more rapidly than the rest of the disease as we see a relapse. Many of us feel that we see that more often since the introduction of IMIDs [Revlimid, thalidomide, pomalidomide] than we did prior to that time.
Second are what we call oligosecretory relapses. This is disease that basically stops secreting, decreases its secretion of , or changes the nature of its M protein secretion. It is a very common problem to see a patient who made a big IgA or IgG "M" spike at presentation relapse with disease that only secretes a light chain. The "M" will go down in the blood while it is going up in the urine ("light chain escape").
Other times the multiple myeloma will stop making an "M" all together ("nonsecretory escape"). As the tumor becomes more anaplastic with time and treatment it becomes less and less effecient at making its antibody (M protein). Anaplastic is a term that means the tumor becomes less and less like the original cell from which it was derived. Often in a newly diagnosed multiple myeloma pt the tumor cells will look like normal healthy plasma cells, but as the disease survives more and more therapies it becomes "angrier" and less able to perform its normal functions, of which secreting an intact antibody is but one.
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Dr. David Siegel - Name: Dr. David Siegel, M.D., Ph.D.
Re: Relapse with low M-spike
Hello, I was diagnosed with with IgA multiple myeloma in 2008. I'm currently on Revlimid / dex / Velcade, due to the fact that I've become refractory to Revlimid and Velcade alone.
For the past four months, according to my lab results, my kappa light chains and B2 mircroglobulin levels have looked pretty good. In fact, I'm in what's termed a very good partial remission.
But during these four months I started experiencing some diffuse rib and back pain. Alas, a recent PET/CT scan revealed new bone lesions on my ribs and vertebrae; one vertebrae lesion will have to be radiated. My oncologist says this is unusual and is unsure of the cause.
Any thoughts on why I 'd be experiencing new bone destruction when my lab numbers show I'm almost in remission?
Thanks for any input.
Dean
For the past four months, according to my lab results, my kappa light chains and B2 mircroglobulin levels have looked pretty good. In fact, I'm in what's termed a very good partial remission.
But during these four months I started experiencing some diffuse rib and back pain. Alas, a recent PET/CT scan revealed new bone lesions on my ribs and vertebrae; one vertebrae lesion will have to be radiated. My oncologist says this is unusual and is unsure of the cause.
Any thoughts on why I 'd be experiencing new bone destruction when my lab numbers show I'm almost in remission?
Thanks for any input.
Dean
Re: Relapse with low M-spike
Hi Dean, my partner was diagnosed with multiple myeloma IgA in 2007. In CR since Dec 07 after SCT (own stem cells).
In 2009 he had a swelling at his cheekbone, MRI showed a pathological fracture and a weak part manifestation of the multiple myeloma. All labs still showed complete remission. He got radiation, and after a whole body MRI, which showed some other lesions, Revlimid.
Since then he had several lesions, which were treated with radiation. This year in March the IgA and light chains kappa started to climb, so now he again gets Velcade, because from the Revlimid he got a bad rash.
I think it is not so unusual when you have bone lesions without any signs of the multiple myeloma in the labs.
Greetings from Germany
Caro
In 2009 he had a swelling at his cheekbone, MRI showed a pathological fracture and a weak part manifestation of the multiple myeloma. All labs still showed complete remission. He got radiation, and after a whole body MRI, which showed some other lesions, Revlimid.
Since then he had several lesions, which were treated with radiation. This year in March the IgA and light chains kappa started to climb, so now he again gets Velcade, because from the Revlimid he got a bad rash.
I think it is not so unusual when you have bone lesions without any signs of the multiple myeloma in the labs.
Greetings from Germany
Caro
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Caro - Name: Caro
- Who do you know with myeloma?: My partner since more than 12 years
- When were you/they diagnosed?: Aug. 2007
- Age at diagnosis: 57
Re: Relapse with low M-Spike
Caro, Wie geht's? Thanks for your response. It seems like I'm hearing about more and more people in this type of situation. I think Dr. Siegel cleared it up with his explanation.
But the question then becomes, how do prevent this from happening--constant scans? And how do you treat two seemingly different types of multiple myeloma.; one that's diffuse and can be tracked and one that's focal and possibly no longer secretes M protein, because it appears one set of drugs can not treat both types effectively.
Thanks again!
Dean
But the question then becomes, how do prevent this from happening--constant scans? And how do you treat two seemingly different types of multiple myeloma.; one that's diffuse and can be tracked and one that's focal and possibly no longer secretes M protein, because it appears one set of drugs can not treat both types effectively.
Thanks again!
Dean
5 posts
• Page 1 of 1