scholarly journals State of Oral Mucosa as an Additional Symptom in the Course of Primary Amyloidosis and Multiple Myeloma Disease

2014 ◽  
Vol 2014 ◽  
pp. 1-5 ◽  
Author(s):  
Maciej R. Czerniuk ◽  
Artur Jurczyszyn ◽  
Grzegorz Charlinski
Keyword(s):  
Multiple Myeloma ◽  
Bone Marrow ◽  
Oral Mucosa ◽  
Blood Cells ◽  
Plasma Cells ◽  
Bone Structure ◽  
Primary Amyloidosis ◽  
Monoclonal Immunoglobulin ◽  
Multidisciplinary Therapy ◽  
Haematological Changes

Multiple myeloma (myeloma multiplex (MM)) is a malignant non-Hodgkin’s lymphoma derived from B cell. Its essence is a malignant clone of plasma cells synthesizing growth of monoclonal immunoglobulin, which infiltrate the bone marrow, destroy the bone structure, and prevent the proper production of blood cells components. The paper presents a case of 62-year-old patient who developed symptoms in addition to neurological and haematological changes in the oral mucosa in the course of multiple myeloma. The treatment resulted in partial improvement. The authors wish to draw attention not only to nonspecificity and rarity of changes in the mouth which can meet the dentist but also to the complexity of the multidisciplinary therapy patients diagnosed with MM.

scholarly journals FLAMING CELLS DI MULTIPLE MYELOMA

2018 ◽  
Vol 17 (1) ◽  
pp. 51
Author(s):  
Nursin Abd. Kadir ◽  
Hj. Darmawaty E.R, ◽  
Mansyur Arif
Keyword(s):  
Multiple Myeloma ◽  
Bone Marrow ◽  
Immune Cells ◽  
Blood Cells ◽  
Plasma Cells ◽  
Complete Blood Count ◽  
Bone Marrow Aspiration ◽  
Lytic Lesion ◽  
Lumbar Vertebral Body ◽  
M Spike

Multiple myeloma is a type of cancer on plasma cells which are system of immune cells in bone marrow that produce antibodies. A47 years old man precented with an excruciatingly painfull bone lytic lesion acompanied with compressive fracture in his Thorakal XIIand first Lumbar vertebral body since a week ago. A complete blood count on admission showed anemia normocytic normocrom withhemoglobin content of 5.3 mg/dL. The blood smear revealed clumping of red blood cells to bound "Rouleaux formations". Serum proteinelectrophoresis showed specific evidence of a M-spike. Bence-Jones proteinuria was positive and serum kreatinin arised 2.44 mg/dL.The bone marrow aspiration contained 45% plasma cells, many of which exhibited the morphology of flaming cells with an eccentricnucleus and violaceous cytoplasm. Plasma cells varied in size and shape and included flaming cells and myeloma cells. The patient wasdiagnosed as having flaming cells in multiple myeloma stage IIIB.

scholarly journals The Binding of CD38 Therapeutics to Red Blood Cells and Platelets Subverts Depletion of Target Cells

Blood ◽  
2019 ◽  
Vol 134 (Supplement_1) ◽  
pp. 3136-3136
Author(s):  
Eric Robert Fedyk ◽  
Neeraja Idamakanti ◽  
Jia Chen ◽  
Jose Estevam ◽  
Vivian Hernandez ◽  
...  
Keyword(s):  
Multiple Myeloma ◽  
Bone Marrow ◽  
Red Blood Cells ◽  
Pharmaceutical Company ◽  
Blood Cells ◽  
Plasma Cells ◽  
Target Cells ◽  
Human Antibody ◽  
Wholly Owned Subsidiary

Introduction: The CD38 antigen is a target for treating multiple myeloma and is being investigated for disorders caused by plasma cells. Therapeutics bind to CD38 on red blood cells and platelets in the vasculature, prior to myeloma and plasma cells in the bone marrow and this initial activity could compromise downstream binding to target cells. Methods: We hypothesized that selectively targeting myeloma and plasma cells by circumventing CD38 expressed on RBCs and platelets could improve the potency of next generation therapeutics. We selected the human antibody TAK-079 (IgG1) because it demonstrated relatively low binding to CD38 on RBCs and platelets, in comparison to the first-generation antibody daratumumab (IgG1) in vitro, and characterized the pharmacokinetics and pharmacodynamics in relapsed/refractory multiple myeloma (RRMM) patients (NCT03439280). Results: TAK-079 and daratumumab bind to distinct amino acids of CD38 and exhibit similar affinities to recombinant CD38 protein, immobilized on a silicon chip (e.g. KD of 0.45 & 0.69 nM, respectively) and to endogenously expressed CD38 on a clonal cell line (e.g. EC50s = 0.30 & 0.34 nM, respectively). In contrast, these antibodies bound differently to components of human blood. Daratumumab bound 610% more intensively to a subpopulation of RBCs than TAK-079. Similarly, daratumumab bound 622% more intensively to a subpopulation of platelets than TAK-079. Conversely, TAK-079 bound 181% more potently than daratumumab to CD38 expressed on blood B lymphocytes (e.g. MFI mean EC50 =3.6 & 6.6 nM, respectively) and 259% more potently to blood T lymphocytes (e.g. MFI mean EC50 = 9.3 & 24.2 nM, respectively). Consistent with these data, trough exposures of TAK-079 were approximately 200% higher than those reported for daratumumab (NCT02519452) in RRMM patients, when compared at equivalent subcutaneous doses. Furthermore, bone marrow myeloma and plasma cells were completely saturated by TAK-079 and reduced at subcutaneous doses ≥ 300mg administered weekly. Conclusion: An effective strategy for developing more potent therapeutics may be to circumvent binding to CD38 on circulating RBCs and PLTs because the magnitude of CD38 antibody binding to leukocytes is inversely related to binding of circulating RBCs and PLTs in vitro. In addition, lower binding to RBCs and PLTs is associated with higher availability of CD38 antibody for binding target cells in RRMM patients, as well as target saturation and depletion by TAK-079 when administered subcutaneously at relatively low doses (eg, 300mg). Disclosures Fedyk: Millennium, a wholly owned subsidiary of Takeda Pharmaceutical Company Ltd: Employment, Patents & Royalties. Idamakanti:Takeda: Employment. Chen:Takeda: Employment. Estevam:Takeda: Employment. Hernandez:Takeda: Employment. Wagoner:Takeda: Employment. Carsillo:Takeda: Employment. Berg:Millennium Pharmaceuticals, Inc., a wholly owned subsidiary of Takeda Pharmaceutical Company Ltd: Employment, Patents & Royalties. Allikmets:Takeda: Employment, Patents & Royalties. Lahu:Think AQ: Consultancy. Palumbo:Millennium, a wholly owned subsidiary of Takeda Pharmaceutical Company Ltd: Employment, Patents & Royalties.

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 Multiple myeloma: circulating lymphocytes that express plasma cell antigens

Blood ◽  
1984 ◽  
Vol 64 (2) ◽  
pp. 352-356
Author(s):  
GJ Ruiz-Arguelles ◽  
JA Katzmann ◽  
PR Greipp ◽  
NJ Gonchoroff ◽  
JP Garton ◽  
...  
Keyword(s):  
Multiple Myeloma ◽  
Bone Marrow ◽  
Plasma Cell ◽  
Peripheral Blood ◽  
Plasma Cells ◽  
Peripheral Blood Lymphocytes ◽  
Tumor Burden ◽  
B Cell Differentiation ◽  
Blood Lymphocytes ◽  
Bone Marrow Plasma

The bone marrow and peripheral blood of 14 patients with multiple myeloma were studied with murine monoclonal antibodies that identify antigens on plasma cells (R1–3 and OKT10). Peripheral blood lymphocytes expressing plasma cell antigens were found in six cases. Five of these cases expressed the same antigens that were present on the plasma cells in the bone marrow. Patients that showed such peripheral blood involvement were found to have a larger tumor burden and higher bone marrow plasma cell proliferative activity. In some patients, antigens normally found at earlier stages of B cell differentiation (B1, B2, and J5) were expressed by peripheral blood lymphocytes and/or bone marrow plasma cells.

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.

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