How does this occur?
"A study by Wadhera et al examined secondary MGUS that developed in patients with multiple myeloma. Of 1942 patients with multiple myeloma, 128 (6.6%) developed a secondary MGUS at a median of 12 months from the diagnosis of multiple myeloma. Overall survival was superior in patients with multiple myeloma who developed secondary MGUS compared with the rest of the cohort.["
What happens, pathophysiologically, when a patient goes from MGUS to multiple myeloma to MGUS? Was this 12 months post therapy or does it spontaneously revert from multiple myeloma to MGUS?
Forums
Re: Secondary MGUS
That's interesting suzirose. I hope one of the advisors will answer that question. It would be surprising to see multiple myeloma reverse itself to MGUS. And if it was after treatment would it really be MGUS?? Hmmm.
Thanks for the Thought Provoking Post
Art
Thanks for the Thought Provoking Post
Art
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Art - Name: Art
- Who do you know with myeloma?: Self
- When were you/they diagnosed?: 12/2011
- Age at diagnosis: 40
Re: Secondary MGUS
If the terminology is consistent, secondary MGUS almost certainly -- and logically -- pertains to the time window AFTER treatment. In the following article, for example, it refers to monoclonal gammopathies following a stem cell transplant:
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Bone Marrow Transplant. 2011 Dec 12. doi: 10.1038/bmt.2011.244. [Epub ahead of print]
Secondary MGUS after autologous hematopoietic progenitor cell transplantation in plasma cell myeloma: a matter of undetermined significance.
Manson GV, Campagnaro E, Balog A, Kaplan D, Sommers SR, Fu P, Rajkumar SV, Lazarus HM.
Department of Medicine, Division of Hematology-Oncology, Case Comprehensive Cancer Center, University Hospitals Case Medical Center, Cleveland, OH, USA.
Abstract
Plasma cell myeloma, characterized by clonally aberrant plasma cells that produce abnormal monoclonal Igs, is the most common indication for autologous hematopoietic progenitor cell transplantation (AHPCT) in North America. We observed appearance of new monoclonal gammopathies different from the original protein in the post-AHPCT setting and termed this condition 'secondary MGUS' (monoclonal gammopathy of undetermined significance). Hence, we performed a retrospective, single institution review of serum protein electrophoresis/immunofixation electrophoresis data in 92 AHPCT recipients from the period 2000-2009. In all, 22 of 92 patients (24%) undergoing AHPCT met criteria for secondary MGUS. Contrary to previous studies, often referred to as 'abnormal protein banding,' we did not observe this condition as a favorable prognostic indicator in affected patients when compared with the control group (P=0.686). However, we did note that a subgroup of the study cohort who developed secondary MGUS after a prolonged latency (>10 months) had an improved median OS compared with the remainder of the study cohort (75 months vs 41 months, P=0.005). As there have been significant advancements in understanding the pathobiology and clinical significance of MGUS, we believe that secondary MGUS merits dedication of resources for investigation to determine its true clinical relevance, prognostic value and pathophysiology.
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Bone Marrow Transplant. 2011 Dec 12. doi: 10.1038/bmt.2011.244. [Epub ahead of print]
Secondary MGUS after autologous hematopoietic progenitor cell transplantation in plasma cell myeloma: a matter of undetermined significance.
Manson GV, Campagnaro E, Balog A, Kaplan D, Sommers SR, Fu P, Rajkumar SV, Lazarus HM.
Department of Medicine, Division of Hematology-Oncology, Case Comprehensive Cancer Center, University Hospitals Case Medical Center, Cleveland, OH, USA.
Abstract
Plasma cell myeloma, characterized by clonally aberrant plasma cells that produce abnormal monoclonal Igs, is the most common indication for autologous hematopoietic progenitor cell transplantation (AHPCT) in North America. We observed appearance of new monoclonal gammopathies different from the original protein in the post-AHPCT setting and termed this condition 'secondary MGUS' (monoclonal gammopathy of undetermined significance). Hence, we performed a retrospective, single institution review of serum protein electrophoresis/immunofixation electrophoresis data in 92 AHPCT recipients from the period 2000-2009. In all, 22 of 92 patients (24%) undergoing AHPCT met criteria for secondary MGUS. Contrary to previous studies, often referred to as 'abnormal protein banding,' we did not observe this condition as a favorable prognostic indicator in affected patients when compared with the control group (P=0.686). However, we did note that a subgroup of the study cohort who developed secondary MGUS after a prolonged latency (>10 months) had an improved median OS compared with the remainder of the study cohort (75 months vs 41 months, P=0.005). As there have been significant advancements in understanding the pathobiology and clinical significance of MGUS, we believe that secondary MGUS merits dedication of resources for investigation to determine its true clinical relevance, prognostic value and pathophysiology.
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Dan D
Re: Secondary MGUS
Suzzierose
Great find, this is interesting stuff! If I understand the article correctly, it appears that secondary MGUS is completely different than traditional MGUS as most of us understand it. As I understand it, multiple myeloma is typically characterized by having cancerous plasma cells making an excess amount and clone copies of signal type of abnormal immunoglobulin protein, such as IGg, IGa, IGm that we are used to hearing us get classified into through our lab testing. What I believe they are describing in the article on secondary MGUS is that after stem cell transplantation in some patients they see a new multiple myeloma immunoglobulin protein appear in addition to the one the patient had before transplantation. For example if you had IGg myeloma like myself, then you might be IGa and IGg or another one of the multiple myeloma protein types. They are not talking about reverting from having multiple myeloma back to a state of traditional MGUS or smoldering multiple myeloma. The article also states that secondary MGUS is prognostic of improved survival, which seems counter intuitive. Hopefully a researcher or doctor can help explain this to us in terms we can understand, I could be interpreting this all wrong.
Great find, this is interesting stuff! If I understand the article correctly, it appears that secondary MGUS is completely different than traditional MGUS as most of us understand it. As I understand it, multiple myeloma is typically characterized by having cancerous plasma cells making an excess amount and clone copies of signal type of abnormal immunoglobulin protein, such as IGg, IGa, IGm that we are used to hearing us get classified into through our lab testing. What I believe they are describing in the article on secondary MGUS is that after stem cell transplantation in some patients they see a new multiple myeloma immunoglobulin protein appear in addition to the one the patient had before transplantation. For example if you had IGg myeloma like myself, then you might be IGa and IGg or another one of the multiple myeloma protein types. They are not talking about reverting from having multiple myeloma back to a state of traditional MGUS or smoldering multiple myeloma. The article also states that secondary MGUS is prognostic of improved survival, which seems counter intuitive. Hopefully a researcher or doctor can help explain this to us in terms we can understand, I could be interpreting this all wrong.
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Eric Hofacket - Name: Eric H
- When were you/they diagnosed?: 01 April 2011
- Age at diagnosis: 44
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