IgM Multiple Myeloma: A Rare Subtype Highly Sensitive to Lenalidomide

Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. 5220-5220
Author(s):  
Alvaro Moreno-Aspitia ◽  
Antony Charles ◽  
Tejal Patel ◽  
Celine Bueno ◽  
Abba Zubair ◽  
...  
Keyword(s):  
Multiple Myeloma ◽  
Transient Response ◽  
Low Dose ◽  
Plasma Cells ◽  
Poor Response ◽  
Response To Therapy ◽  
Bone Lesions ◽  
Best Response ◽  
M Spike

Abstract Background: IgM multiple myeloma (MM) are very rare plasmaproliferative disorders representing 0.5–1.2% of all cases of MM and < 0.2% of all IgM monoclonal gammopathies. Clinical criterion are not always helpful in differentiating IgM MM from Waldenstrom macroglobulinemia. However, the presence of lytic bone lesions, absence of lymphadenopathy and/or hepatosplenomegaly, presence of translocation of the immunoglobulin heavy chain locus at 14q32 [t(11;14), t(14;16), t(4;14)], and strong expression of CD138 by the plasma cells are useful in the diagnosis of IgM MM. It has been our experience and of others that these cases have an aggressive behavior at presentation, shorter survival than IgG and IgA MM and poor response to therapy for lymphoplasmacytoid lymphomas. We present here 2 cases of IgM MM with a dramatic response to Lenalidomide and low dose dexamethasone (Rev/Dex) Results: Baseline patient characteristics at time of diagnosis of IgM MM and therapy outcome are presented in the following 2 tables: Table 1. Case 1 2 Age and sex 72 (F) 73 (F) Serum M-spike (g/dL) 5.3 6.2 Urine M-spike (mg/dl/24 hrs) 72 412 Serum IgM (mg/dL) 8,590 11,000 BM plasma cells percentage 90 20 Plasma cell immunophenotyping CD138+++, partial CD20, CD56− CD138+++, partial CD20, CD56− Cytogenetics (Standard and/or FISH) Standard: normal FISH: not done on initial biopsy. On follow up there were insufficient number of plasma cells to perform test Standard: of 20 metaphases, 6 had a complex hypotetraploid karyotype with relative loss of 13q, 14, 15, 16, 20, and 22, and numerous unbalanced rearrangements. FISH: a plasma cell clone with monosomy 13 and IGH/c-MAF fusion, t(14;16). In addition, approximately 60% of plasma cells had a tetraploid clone with the same anomalies as well as relative loss of p53 Bone lesions Multiple non-traumatic spinal fractures and of stenum Several lytic lesions of long bones Renal insufficiency No No Anemia (Hbg g/dL) Yes (8.7) Yes (8.1) Hypercalcemia (Ca mg/dL) Yes (12.5) Yes (11.4) Beta 2 microglobulin (mg/dL) 5.79 8.51 Serum viscosity (cpoise) 5.9 4.8 Table 2. Best Response to therapy Case Therapy Best Response Comments 1 Rituxan, then Fludarabine based therapy Transient response Rapid progression after partial and transient response to each therapy 1 Lenalidomide + LD-Dex sCR after cycle #6. Currently on CR 18 months later IgM declined from 8,590 to 43 mg/dL after 4 cycles of Rev/Dex. 2 Lenalidomide + LD-Dex VGPR after cycle #2 IgM declined from 11,000 to 463 mg/dL after cycle 3. Complete disappearance of M-spike in serum; BM to be done after cycle #4 Conclusions: This is the first report that we are aware of a rapid and dramatic response to lenalidomide and low dose dexamethasone in these rare cases of IgM MM with poor response to NHL-type treatment. Lenalidomide-based therapy might abrogate poor prognosis cytogenetics in this unusual subtype of MM (case #2), however, follow up for this patient is still very short.

The benefit of whole-body low-dose unenhanced multidetector computer tomography (WBLD-MDCT) for follow up and therapy response monitoring in patients with multiple myeloma: Correlation with hematologic parameters

2006 ◽  
Vol 24 (18_suppl) ◽  
pp. 7607-7607
Author(s):  
M. S. Horger ◽  
C. Driessen ◽  
C. Brodoefel ◽  
C. Faul ◽  
P. Pereira ◽  
...  
Keyword(s):  
Multiple Myeloma ◽  
Computer Tomography ◽  
Low Dose ◽  
Laboratory Data ◽  
Whole Body ◽  
Acquisition Time ◽  
Bone Lesions ◽  
Appendicular Skeleton ◽  
Multidetector Computer Tomography

7607 Background: To assessthe value of whole-body low-dose multidetector computer tomography (WBLD-MDCT) as diagnostic and survey modality in multiple myeloma (MM), and as a one-stop alternative (Horger et al. EJR 2005;54:289–297) to established imaging techniques (e.g. x-ray and MRI). Methods: Between 7/2001 and 2/2005, WBLD-MDCT scans were obtained in 90 consecutive patients with histologically proven stage II-III MM, all patients having 2 or more scans (mean = 3,8; range = 2–6). CT-scans were performed using a standardized low-dose protocol and the number, size and density of focal or diffuse medullary (in the appendicular skeleton and pelvis) and extra-medullary lesions as well as osteolysis were analysed for each examination and at follow up. Results were correlated with current standard MM laboratory data and at follow up in order to assess correct temporal recognition of significant myeloma changes by both methods. Results: Detection and follow up of medullary and extra-medullary MM lesions and osteolysis by WBLD-MDCT resulted in a sensitivity of 92%, a specificity of 93%, a NPV of 95%, a PPV of 85% and a likelihood ratio for patients with CT-abnormalities to present changes in the course of their disease of 12. Results of radiologic and hematologic analysis showed high agreement at follow up (median, 3 mo). However, agreement of both techniques at the time of investigation was only moderate (κ = 0.629), with CT being correct in 60% of mismatching cases. Thus, CT enabled earlier detection of MM changes. WBLD-MDCT assessed correctly the course of disease in all 4 patients with nonsecretory MM. Evaluation of stability was optimal in all patients. Conclusions: WBLD-MD represents a reliable, widespread, quick (75s acquisition time), and cost-effective imaging technique in MM, allowing detection of bone marrow involvement, extra-medullary tumors and lytic bone lesions in different clinical settings (staging, follow up, therapy monitoring, evaluation of stability). WBLD-MDCT repeatedly allowed detection of changes in the course of the disease prior to laboratory data, especially in extramedullary MM relapse and nonsecretory MM. No significant financial relationships to disclose.

Skeletal Survey in Multiple Myeloma: Role of Imaging

2021 ◽  
Vol 17 ◽  
Author(s):  
Paolo Spinnato ◽  
Giacomo Filonzi ◽  
Alberto Conficoni ◽  
Giancarlo Facchini ◽  
Federico Ponti ◽  
...  
Keyword(s):  
Multiple Myeloma ◽  
Low Dose ◽  
Imaging Modality ◽  
Bone Marrow Involvement ◽  
Conventional Radiography ◽  
Response To Therapy ◽  
Whole Body ◽  
Initial Assessment ◽  
Bone Lesions ◽  
Pet Ct

: Bone disease is the hallmark of multiple myeloma. Skeletal lesions are evaluated to establish the diagnosis, to choose the therapies and also to assess the response to treatments. Due to this, imaging procedures play a key-role in the management of multiple myeloma. For decades, conventional radiography has been the standard imaging modality. Subsequently, advances in the treatment of multiple myeloma have increased the need for accurate evaluation of skeletal disease. The introduction of new high performant imaging tools, such as whole-body low dose computed tomography, different types of magnetic resonance imaging studies, and 18F-fluorodeoxyglucose positron emission tomography, replaced conventional radiography. In this review we analyze the diagnostic potentials, indications of use, and applications of the imaging tools nowadays available. Whole body low-dose CT should be considered as the imaging modality of choice for the initial assessment of multiple myeloma lytic bone lesions. MRI is the gold-standard for detection of bone marrow involvement, while PET/CT is the preferred technique in assessment of response to therapy. Both MRI and PET/CT are able to provide prognostic information.

The Natural History of Smoldering (Asymptomatic) Multiple Myeloma.

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 3396-3396 ◽  
Author(s):  
Robert Kyle ◽  
Ellen Remstein ◽  
Terry Therneau ◽  
Angela Dispenzieri ◽  
Paul Kurtin ◽  
...  
Keyword(s):  
Multiple Myeloma ◽  
Bone Marrow ◽  
Plasma Cell ◽  
Light Chain ◽  
Plasma Cells ◽  
M Protein ◽  
Cell Content ◽  
Bone Marrow Plasma ◽  
M Spike

Abstract Smoldering multiple myeloma (SMM) is characterized by a serum M protein ≥ 3g/dL and/or 10% or more of plasma cells in the bone marrow. However, the definition is not standardized, and it is not known whether both serum M protein levels and bone marrow plasma cell counts are necessary for diagnosis or if one parameter is sufficient. We reviewed the medical records and bone marrows of all patients from Mayo Clinic seen within 30 days of recognition of an IgG or IgA M protein ≥ 3g/dL or a bone marrow containing ≥ 10% plasma cells from 1970 to 1995. This allows for a minimum potential follow-up of 10 years. Patients with end-organ damage at baseline from plasma cell proliferation, including active multiple myeloma (MM) and primary amyloidosis (AL) and those who had received chemotherapy were excluded. A differential of the bone marrow aspirate coupled with the bone marrow biopsy morphology and immunohistochemistry using antibodies directed against CD138, MUM-1 and Cyclin D1 were evaluated in every case in order to estimate the plasma cell content. In all, 301 patients fulfilled either of the criteria for SMM. Their median age was 64 years and only 3% were less than 40 years of age; 60% were male. The median hemoglobin value was 12.9 g/dL; 7% were less than 10 g/dL, but the anemia was unrelated to plasma cell proliferation. IgG accounted for 75%, IgA 22%, and biclonal proteins were found in 3%. The serum light-chain was κ in 67% and λ in 33%. The median serum M spike was 2.9 g/dL; 11% were at least 4.0 g/dL. Uninvolved serum immunoglobulins were reduced in 81%; only 1 immunoglobulin was reduced in 31% and both were decreased in 50%. The urine contained a monoclonal κ protein in 36% and λ in 18% and 46% were negative. The median size of the urine M spike was 0.04 g/24h; only 5 (3%) were > 1 g/24h. The median bone marrow plasma cell content was 15 – 19%; 10% had less than 10% plasma cells, while 10% had at least 50% plasma cells in the bone marrow. Cyclin D-1 was expressed in 17%. Patients were categorized into 3 groups: Group 1, serum M protein ≥ 3g/dL and bone marrow containing ≥ 10% plasma cells (n= 113, 38%); Group 2, bone marrow plasma cells ≥ 10% but serum M protein < 3g/dL (n= 158, 52%); Group 3, serum M protein ≥ 3g/dL but bone marrow plasma cells < 10% (n= 30, 10%). During 2,204 cumulative years of follow-up 85% died (median follow-up of those still living 10.8 years), 155 (51%) developed MM, while 7 (2%) developed AL. The overall rate of progression at 10 years was 62%; median time to progression was 5.5 yrs. The median time to progression was 2.4, 9.2, and 19 years in groups 1, 2, and 3 respectively; correspondingly at 10 years, progression occurred in 76%, 59%, and 32% respectively. Significant risk factors for progression with univariate analysis were serum M spike ≥ 4g/dL (p < 0.001), presence of IgA (p = 0.003), presence of urine light chain (p = 0.006), presence of λ urinary light chain (p = 0.002), bone marrow plasma cells ≥ 20% (p < 0.001) and reduction of uninvolved immunoglobulins (p < 0.001). The hemoglobin value, gender, serum albumin, and expression of cyclin D-1 were not of prognostic importance. On multivariate analysis, the percentage of bone marrow plasma cells was the only significant factor predicting progression to MM or AL.

Discrepancies in Serum Free Light Chain Assays and Immunofixation for Response Evaluation and Prognostication in Plasma Cell Proliferative Disorders

Blood ◽  
2011 ◽  
Vol 118 (21) ◽  
pp. 5099-5099
Author(s):  
Nasir Bakshi ◽  
Nahlah AlGhasham ◽  
Maha Alharbi ◽  
Jalaluddin Bhuiyan ◽  
Ghada Elgohary ◽  
...  
Keyword(s):  
Multiple Myeloma ◽  
Complete Remission ◽  
Plasma Cell ◽  
Light Chain ◽  
Free Light Chain ◽  
Response To Therapy ◽  
Oligoclonal Bands ◽  
M Spike ◽  
Serial Samples

Abstract Abstract 5099 Plasma cell proliferative disorders are monitored by a variety of methods. Serum protein electrophoresis (SPE), M-spike quantitation and Immunoelectrophoresis (IFE) are commonly assessed in patients with monoclonal gammopathy of undetermined significance (MGUS), smoldering multiple myeloma (SMM), and multiple myeloma (MM) to determine disease progression, response, or relapse. sFLC quantitation provides a rapid indicator of response, detects the rare occurrence of FLC escape, and also allows disease monitoring in the absence of a measurable serum or urine M-spike. To improve sensitivity of response assessment in MM, the International Myeloma Working Group (IMWG) has recently introduced the stringent CR category. However, no formal studies have validated this criterion. Indeed, the role of the sFLC assay has recently been questioned because of the presence of discordant abnormal sFLC ratios in a significant proportion of patients in CR. This could be at least partly explained by the presence of oligoclonal bands in response to therapy, potentially leading to false-positive results. Accordingly it has been recommended that the serum M-spike be used to monitor disease, and that FLC quantitation be used only if there is no measurable disease by electrophoresis and if the monoclonal sFLC concentration is greater than 10 mg/dL in the context of an abnormal FLC ratio. By analyzing serial samples in our patient population we aim to help usefully interpret the sFLC results and in the long run validate the prognostic impact of attaining CR versus CR plus normal sFLC ratio (stringent CR) after therapy in MM. From a total of 566 samples submitted for FLC analysis over 24-month period at our institution, 94 cases were monoclonal (abnormal FLC ratio) with kappa being the involved chain in 63 and lambda in 31 cases. Serial data from 35 multiple myeloma patients were identified by the availability of 3 serum test results (SPE/IFE/sFLC) in at least 3 serial samples that were obtained 3 months to 6 months apart along with treatment outcome details. Kappa and lambda FLC were quantitated using a Siemens BNII® nephelometer and Freelite® reagent sets from The Binding Site, Birmingham, UK; M-spikes were quantitated Capillarys® system and reagent sets (Sebia Electrophoresis, Norcross, GA). The FLC data was analyzed as the involved FLC concentration (iFLC), the difference between the involved and uninvolved FLC concentration (dFLC), and the FLC K/L ratio (rFLC). Treatment modalities included allogeneic, or autologous stem cell transplantation, conventional, bortezomib or lenalidomide containing chemotherapy. There were 16 (45%) cases in which discordance was observed between the three techniques (sFLC/SPE/IFE) during the follow-up. 11/16 (68%) patients were found to have abnormal sFLC with both abnormal FLC ratio and involved chain (FLCi), while no M-band was detected by SPE/IFE. In two cases (13%) the pattern of discrepancy was opposite with IFE found to be positive while rFLC results were within normal range of 0.26 – 1.65 mg/l. In three cases (19%) abnormal FLC ratio was detected with SPE/IFE being normal but the sFLC ratio did not match the myeloma isotype (sFLC ratio <0.26 for kappa and >1.65 for lambda isotype). In a subgroup of patients (n = 4) who relapsed during follow-up from complete remission sequential monitoring of immunofixation and free light chain assays revealed normalization of SPE/IFE with only faint/ doubtful band detected in one while FLC results were abnormal. The variability of the serum M-spike, IFE and FLC measurements confirm the IMWG recommendations for patient monitoring. The free light chain assay ratio is widely reported as a useful marker for a faster detection of remission or progression in myeloma patients. These techniques in reality complement each other and the FLC results need to be interpreted with caution in context of the electrophoresis results in order to determine the status of remission. More sensitive methods such as multiparametric imunophenotyping analysis for minimal residual disease by multiparametric flowcytometry or molecular primer assays may be useful to determine the depth of complete remission as choosing the type of screening test will likely have a relevant impact in clinical decision making in MM. Disclosures: No relevant conflicts of interest to declare.

Effect Of Low Dose Bortezomib On Bone Formation In Smoldering Myeloma Patients

Blood ◽  
2013 ◽  
Vol 122 (21) ◽  
pp. 3204-3204 ◽  
Author(s):  
Maurizio Zangari ◽  
Tamara Berno ◽  
Mohamed E Salama ◽  
Sherjeel Sana ◽  
Giampaolo Talamo ◽  
...  
Keyword(s):  
Bone Density ◽  
Research Funding ◽  
Low Dose ◽  
Plasma Cells ◽  
Bone Lesions ◽  
T Score ◽  
Score Improvement ◽  
Grade 3 ◽  
Smoldering Myeloma

Abstract Background Bortezomib has been shown to produce an anabolic bone effect (increase bone ALP and osteocalcin) in relapsed/refractory patients. This study examined the bone anabolic effect in patients with smoldering multiple myeloma (SMM) who, with a historical median age of 67 years, have frequent evidence of osteopenia not associated with lytic bone disease. SMM is usually followed expectantly without therapy. The overall risk of progression to active MM has been estimated up to 20% in the first year from diagnosis (Kyle et al, 2007). The primary aim of this trial is to determine the effect of a course of low-dose Bortezomib on bone remodeling and on disease progression. Methods The dose of bortezomib used in this trial of 0.7mg/m² is the lowest dose which has shown efficacy in the 3 largest monotherapy trials with bortezomib. Patients enrolled in this study had serum M protein ≥ 3 g/dL and/or bone marrow plasma cells ≥ 10% with absence of anemia, renal failure, hypercalcemia, and lytic bone lesions. Patients received 9 cycles of bortezomib given on days 1, 8, 15, 22 every 42 days. No bisphosphonates were allowed during the trial, Vitamin D supplements were allowed. Results Seventeen patients (9 males) with a median age of 61 years were enrolled in the study. Fourteen had IgG paraprotein and 3 had an IgA. Two participants did not complete the treatment; the first because of development of a skin rash and the second for personal reasons. A total of 11 patients completed the protocol. Four are still receiving treatment. At the time of this analysis with a median follow-up of 20 months, all patients are alive and none has progressed (Figure 1). The mean M component at baseline, end-of-study, and at most recent follow-up are shown in Figure 2. The treatment was well tolerated by the patients. One patient developed reversible grade 3 neuropathy and a drug related rash and only 3 grade 3 hematological adverse events were recorded (15%). Bone densities by DEXA scan were obtained at baseline, end of study, and yearly thereafter. Out of 17 patients, 13 had bone density T-scores before and after treatment. Six patients (46%) showed an improvement in hip T-score (mean T-score improvement 0.41, range 0.1-1.35). In the overall group, mean T scores improved by 38% (range, 3-200%). T score in lumbar spine improved in 3 patients (23%), who had a mean T-score improvement of 0.2 (range, 0.05-0.43). Conclusions The use of low dose Velcade in smoldering myeloma patients was well tolerated and produces significant increases in bone density in 46% of participants. Disclosures: Zangari: Millenium Pharm.: Research Funding. Off Label Use: Use of Bortezomib in smoldering myeloma. Salama:Eli Lilly and Co: Research Funding.

scholarly journals Cold Agglutinin Disease Secondary to Multiple Myeloma in a Psoriatic Patient

2014 ◽  
Vol 15 (2) ◽  
pp. 141-143
Author(s):  
Hazera Khatun ◽  
Salma Afrose ◽  
Mohiuddin Ahmed Khan ◽  
Tasneem Ara ◽  
Md. Sirajul Islam
Keyword(s):  
Multiple Myeloma ◽  
Plasma Cells ◽  
Clinical Symptoms ◽  
Restriction Pattern ◽  
Cold Agglutinin ◽  
Cold Agglutinin Disease ◽  
Erythrodermic Psoriasis ◽  
M Spike ◽  
Progressive Weakness

Cold agglutinin disease (CAD) is a chronic compensated hemolytic anemia. We report a case of cold agglutinin disease secondary to multiple myeloma (MM) in a patient of erythrodermic psoriasis. The patient presented with acral cyanosis, progressive weakness and generalized desquamating scaly lesions. After confirming the diagnosis (80-90% plasma cells in bone marrow, M- spike in serum protein electrophoresis, G-ë restriction pattern in immune electrophoresis) he was given chemotherapy with CTD (cyclophosphamide, thalidomide and dexamethasone) protocol. His clinical symptoms improved and he has now completed 4 cycles of chemotherapy. The interim follow up showed achievement of PR (partial response).DOI: http://dx.doi.org/10.3329/jom.v15i2.20688 J MEDICINE 2014; 15 : 141-143

Bone disease as the first manifestation of systemic AL-amyloidosis

2020 ◽  
Vol 92 (7) ◽  
pp. 85-89
Author(s):  
L. P. Mendeleeva ◽  
I. G. Rekhtina ◽  
A. M. Kovrigina ◽  
I. E. Kostina ◽  
V. A. Khyshova ◽  
...  
Keyword(s):  
Multiple Myeloma ◽  
Bone Marrow ◽  
Bone Disease ◽  
Plasma Cells ◽  
Interventricular Septum ◽  
Bone Destruction ◽  
Amyloid Deposition ◽  
Bone Lesions ◽  
Al Amyloidosis ◽  
Linear Type

Our case demonstrates severe bone disease in primary AL-amyloidosis without concomitant multiple myeloma. A 30-year-old man had spontaneous vertebral fracture Th8. A computed tomography scan suggested multiple foci of lesions in all the bones. In bone marrow and resected rib werent detected any tumor cells. After 15 years from the beginning of the disease, nephrotic syndrome developed. Based on the kidney biopsy, AL-amyloidosis was confirmed. Amyloid was also detected in the bowel and bone marrow. On the indirect signs (thickening of the interventricular septum 16 mm and increased NT-proBNP 2200 pg/ml), a cardial involvement was confirmed. In the bone marrow (from three sites) was found 2.85% clonal plasma cells with immunophenotype СD138+, СD38dim, СD19-, СD117+, СD81-, СD27-, СD56-. FISH method revealed polysomy 5,9,15 in 3% of the nuclei. Serum free light chain Kappa 575 mg/l (/44.9) was detected. Multiple foci of destruction with increased metabolic activity (SUVmax 3.6) were visualized on PET-CT, and an surgical intervention biopsy was performed from two foci. The number of plasma cells from the destruction foci was 2.5%, and massive amyloid deposition was detected. On CT scan foci of lesions differed from bone lesions at multiple myeloma. Bone fragments of point and linear type (button sequestration) were visualized in most of the destruction foci. The content of the lesion was low density. There was no extraossal spread from large zones of destruction. There was also spontaneous scarring of the some lesions (without therapy). Thus, the diagnosis of multiple myeloma was excluded on the basis based on x-ray signs, of the duration of osteodestructive syndrome (15 years), the absence of plasma infiltration in the bone marrow, including from foci of bone destruction by open biopsy. This observation proves the possibility of damage to the skeleton due to amyloid deposition and justifies the need to include AL-amyloidosis in the spectrum of differential diagnosis of diseases that occur with osteodestructive syndrome.

scholarly journals An Unprecedented Case of p190 BCR-ABL Chronic Myeloid Leukemia Diagnosed during Treatment for Multiple Myeloma: A Case Report and Review of the Literature

2018 ◽  
Vol 2018 ◽  
pp. 1-5
Author(s):  
Kosuke Miki ◽  
Naoshi Obara ◽  
Kenichi Makishima ◽  
Tatsuhiro Sakamoto ◽  
Manabu Kusakabe ◽  
...  
Keyword(s):  
Multiple Myeloma ◽  
Bone Marrow ◽  
Chronic Myeloid Leukemia ◽  
Myeloid Leukemia ◽  
Plasma Cells ◽  
Bone Marrow Examination ◽  
Bone Lesions ◽  
Dexamethasone Treatment ◽  
Lytic Bone Lesions

We report the case of a 76-year-old man who was diagnosed as having chronic myeloid leukemia (CML) with p190 BCR-ABL while receiving treatment for symptomatic multiple myeloma (MM). The diagnosis of MM was based on the presence of serum M-protein, abnormal plasma cells in the bone marrow, and lytic bone lesions. The patient achieved a partial response to lenalidomide and dexamethasone treatment. However, 2 years after the diagnosis of MM, the patient developed leukocytosis with granulocytosis, anemia, and thrombocytopenia. Bone marrow examination revealed Philadelphia chromosomes and chimeric p190 BCR-ABL mRNA. Fluorescence in situ hybridization also revealed BCR-ABL-positive neutrophils in the peripheral blood, which suggested the emergence of CML with p190 BCR-ABL. The codevelopment of MM and CML is very rare, and this is the first report describing p190 BCR-ABL-type CML coexisting with MM. Moreover, we have reviewed the literature regarding the coexistence of these diseases.

scholarly journals The Evolution in The Treatment of Multiple Myeloma Towards Targeted Magnetic Molecularly Imprinted Nanomedicines

2015 ◽  
pp. 1-2
Author(s):  
Edgar Pérez-Herrero
Keyword(s):  
Multiple Myeloma ◽  
Bone Marrow ◽  
Bacterial Infections ◽  
Plasma Cells ◽  
The Body ◽  
Western World ◽  
Bone Lesions ◽  
Non Hodgkin Lymphoma ◽  
Clonal Proliferation ◽  
Tract Infections

Multiple myeloma is the second more frequently haematological cancer in the western world, after non-Hodgkin lymphoma, being about the 1-2 % of all the cancers cases and the 10-13% of hematologic diseases. The disease is caused by an uncontrolled clonal proliferation of plasma cells in the bone marrow that accumulate in different parts of the body, usually in the bone marrow, around some bones, and rarely in other tissues, forming tumor deposits, called plasmocytomas. This uncontrolled clonal proliferation of plasma cells produces the secretion of an abnormal monoclonal immunoglobulin (paraprotein or M-protein) and prevents the formation of the other antibodies produced by the normal plasma cells that are destroyed. The anormal secretion of paraproteins unbalance the osteoblastosis and osteoclastosis processes, leading to bone lesions that cause lytic bone deposits and the release of calcium from bones (hypercalcemia) that may produce renal failure. Regions affected by bone lesions are the skull, spine, ribs, sternum, pelvis and bones that form part of the shoulders and hips. The substitution of the healthy bone marrow by infiltrating malignant cells and the inhibition of the normal production of red blood cells produce anaemia, thrombocytopenia and leukopenia. Multiple myeloma patients are immunosuppressed because of leukopenia and the abnormal immunoglobulin production caused by the uncontrolled clonal proliferation of plasma cells, being susceptible to bacterial infections, like pneumonias and urinary tract infections. The interaction of immunoglobulin with hemostatic mechanisms may lead to haemorrhagic diathesis or thrombosis. Also, disorders of the central and peripheral nervous system are part of the disease, being the more common neurological manifestations the spinal cord compressions and the peripheral neuropathies.

scholarly journals Multiple Myeloma with Suspected Non-Secretory Type

2020 ◽  
Vol 27 (1) ◽  
Author(s):  
Annisa Ginar Indrarsi ◽  
Usi Sukorini
Keyword(s):  
Multiple Myeloma ◽  
Bone Marrow ◽  
Monoclonal Gammopathy ◽  
Plasma Cells ◽  
Immunoglobulin A ◽  
Protein Electrophoresis ◽  
Palpebral Conjunctiva ◽  
General Weakness ◽  
M Spike ◽  
G Ratio

Multiple Myeloma (MM) is a hematological malignancy characterized by clonal plasma cell in bone marrow that produceabnormal globulin, which resulted in monoclonal gammopathy. Multiple Myeloma Non-Secretory (MMNS) is a very rareform of multiple myeloma with monoclonal plasmocytic proliferation in bone marrow supported by clinical manifestationand radiological findings. However, plasma cells fail to secrete immunoglobulin. A 44-year-old female came to SardjitoGeneral Hospital with main complaints of weakness and back pain. General weakness and pale palpebral conjunctiva were6 observed (+/+), liver and spleen were not palpable. Blood test results were as follows: Hb 3.0 g/dL, RBC 1.07 x 10 / μL, WBC3 3 562 x 10 /μL, PLT 114 x 10 /μL, A/G ratio 1.07, BUN 51.5 mg/dL, creatinine 4.62 mg/dL, and calcium 3.1 mmol/L. Skeletalsurvey suggested a multiple osteolytic. Protein electrophoresis revealed hypogammaglobulinemia with no M-spike. Therewere 66% of plasma cells in bone marrow. Patient was diagnosed by MMNS. Diagnosis MMNS can be established if clonalplasmacytes is accompanied with renal insufficiency and hypercalcemia. However, monoclonal gammopathy was not foundin serum protein electrophoresis. A case reported of 44-year-old female diagnosed as MMNS with 'punched out' multipleosteolytic, increased plasma cells in bone marrow without evidence of paraprotein in circulation proved by low A/G ratio andnegative M-spike.

Sign in / Sign up

Export Citation Format

Share Document