eMedicine Specialties > Radiology > Musculoskeletal

Multiple Myeloma

Steven M Sorenson, MD, Consulting Staff, Department of Radiology, Coast Radiology Imaging and Intervention
Amilcare Gentili, MD, Professor of Clinical Radiology, University of California at San Diego; Consulting Staff, Department of Radiology, Thornton Hospital; Chief of Radiology, San Diego VA Health Care System; Sulabha Masih, MD, Associate Professor of Diagnostic Radiology, University of California at Los Angeles; Consulting Staff, Department of Radiology, Section of Musculoskeletal Radiology, West Los Angeles Veterans Affairs Medical Center; Carol L Andrews, MD, Consulting Musculoskeletal Radiologist, Mink Radiologic Imaging; Consulting Staff, Department of Radiology, Antelope Valley Medical Center

Updated: Aug 14, 2009

Introduction

Background

Multiple myeloma is the most common primary neoplasm of the skeletal system. The disease is a malignancy of plasma cells. Radiologically, multiple destructive lesions of the skeleton as well as severe demineralization characterize multiple myeloma. The etiology of the disease is the monoclonal proliferation of B cells, with a resultant increase of a single immunoglobulin and its fragments in the serum and urine. Electrophoretic analysis shows increased levels of immunoglobulins in the blood as well as light chains (Bence-Jones protein) in the urine (see Pathophysiology).

Lateral radiograph of the skull. This image demonstrates numerous lytic lesions, which are typical for the appearance of widespread myeloma.

Lateral radiograph of the lumbar spine. This image shows deformity of the L4 vertebral body that resulted from a plasmacytoma.

A T1-weighted magnetic resonance image of the humerus. This image demonstrates a predominantly hypointense to isointense myelomatous lesion in the medullary space of the diaphysis. The lesion extends through the anterior aspect of the cortex.

The marrow infiltration process may involve any bone, but the predominant sites include the vertebral column, ribs, skull, pelvis, and femora (axial skeleton). Although the osseous structures may appear radiographically normal or simply osteopenic, the classic appearance is of multiple, discrete, small, lytic lesions. Occasionally, a single lytic lesion is discovered and is termed a plasmacytoma (solitary myeloma). Patients with a single focus of disease often progress to multiple sites of myelomatous involvement.^1,2,3,4,5,6

Recent studies

Shortt et al compared FDG PET, whole-body MRI, and bone marrow aspiration and biopsy in multiple myeloma in 24 patients (13 women, 11 men; mean age, 67.1 years; range, 44-83 years) with multiple myeloma proven by bone marrow biopsy. Whole-body MRI had a higher sensitivity and specificity than PET, and the positive predictive value of whole-body MRI was 88%. When used in combination and with concordant findings, PET and whole-body MRI had a specificity and positive predictive value of 100%.⁷

Dimopoulos et al reviewed the literature of all imaging modalities used in multiple myeloma and provided recommendations for each modality. Conventional radiography, according to the authors, remains the gold standard for staging newly diagnosed cases and in cases of relapse. MRI can provide information that is complementary to a skeletal survey and was recommended for use in patients with normal radiographic images and in all patients with an apparently solitary plasmacytoma of bone.

According to Dimopoulos et al, urgent MRI or CT (if MRI is not available) is the diagnostic procedure of choice to assess suspected cord compression; however, bone scintigraphy should play no role in the routine staging of myeloma, and sequential dual-energy radiographic absorptiometry scans are not recommended, according to the authors. PET/CT or MIBI imaging are also not recommended for routine use, according to the study findings, although both techniques may be useful in selected cases that warrant clarification of previous imaging findings.⁸

Agool et al studied somatostatin receptor scintigraphy (SRS) in multiple myeloma patients and compared the results with radiographic findings. A positive SRS was demonstrated in 44% of newly diagnosed patients; 83% of the relapsed patients; and both of the patients with plasmacytoma. In 40% of the patients, the SRS findings corresponded with radiographic abnormalities, but in 60% of relapsed patients, SRS uptake was demonstrated in areas without new radiographic abnormalities.⁹

Pathophysiology

Plasma cells are a subset of B cells, which are the producers of humoral immunity factors termed antibodies. Antibody molecules are composed of 2 polypeptide chains: a light chain and a heavy chain. Cleavage results in the production of Fab and Fc fragments; the Fab fragment is termed the Bence-Jones protein and is found in the urine of patients with myeloma.

An individual plasma cell can produce antibody molecules of only a single immunoglobulin to combine with a single antigen. As such, a plasma cell is termed monoclonal. Most infections produce a polyclonal response because multiple antigens are present on a single bacillus or virus and activate multiple plasma cells. Electrophoresis during infections demonstrates an increase in multiple types of proteins as a result of the multiple humoral and cellular products that are produced to combat the invading organism.

However, if malignant transformation occurs in a single plasma cell, its clones produce only a single type of immunoglobulin, and electrophoresis demonstrates a monoclonal peak that corresponds to this particular immunoglobulin. Infection, as well as collagen vascular disorders, rheumatoid arthritis, and ulcerative colitis, can also produce diffuse hypergammaglobulinemia. Waldenström macroglobulinemia, leukemia, lymphoma, and myeloma produce monoclonal peaks.

If a monoclonal protein elevation is discovered in a patient and additional tests do not reveal an underlying etiology (as they often do not), the condition is termed monoclonal gammopathy of undetermined significance. Most of these patients do not progress to multiple myeloma, but they must be followed up regularly to evaluate for an increase in monoclonal protein levels or the development of lytic bone lesions.

The cause of multiple myeloma is unknown. One theory is chronic antigenic stimulation of a plasma cell, which results in transformation and the development of myeloma. However, once a plasma cell is transformed, it is known to produce innumerable clones, which spread hematogenously to other myelogenous areas. Once there, these neoplastic cells form sheets that replace the normal bone marrow. In addition, the myeloma cells produce osteoclast-stimulating factor, a cytokine that results in bone destruction.

The plasma cell activating factor interleukin-6 (IL-6) is found within bone marrow, resulting in plasma cell proliferation. The osteoblastic response in myeloma tends to be suppressed, resulting in the severe demineralization and bone destruction that are characteristic of the disease. Secondary hypercalcemia is present.

Frequency

United States

The annual incidence of multiple myeloma is approximately 4.4 cases per 100,000 persons.^10,11 Multiple myeloma is responsible for 10-20% of hematologic malignancies.^10,11

International

No exact figures are available internationally. The incidence of multiple myeloma is believed to be the same as in the United States, but this disease is diagnosed less frequently elsewhere.

Mortality/Morbidity

In 1975, Durie and Salmon proposed the initial clinical staging system for multiple myeloma.¹² Measured myeloma cell mass was correlated with 5 clinical features as follows:

• Hemoglobin level
• Serum calcium level
• Number of bone lesions on a radiographic skeletal survey
• Immunoglobulin level
• Serum creatinine level

Using these 5 features, a 3-stage system was proposed that divided patients into those with low, intermediate, and high myeloma cell burden.¹²

• Stage I consists of all the following:
  • Hemoglobin >10 g/dL
  • Serum calcium <12 mg/dL
  • Plasmacytoma to no lytic lesions on a skeletal survey
  • Low immunoglobulin production (immunoglobulin G [IgG] <5 g/dL or IgA <3 g/dL)
• Stage II patients are defined as fitting into neither stage I nor stage III.
• Stage III patients demonstrate one or more of the following:
  • Hemoglobin <8.5 g/dL
  • Serum calcium >12 mg/dL
  • More than one lytic bone lesion on a bone survey
  • High immunoglobulin production (IgG >7 g/dL or IgA >5 g/dL)

In constructing this staging system, researchers found that stage I patients had a median survival of 191 months, stage II patients survived 11-54 months, and stage III patients survived 5-34 months.

In the United States, approximately 10,000 persons per year die of multiple myeloma. Without treatment, most patients die in less than 1 year; with treatment, life expectancy may be extended 2-3 years.

Race

Multiple myeloma accounts for 10% of all hematologic malignancies in whites and 20% in blacks.¹⁰ The reason for the apparent racial predilection for blacks is unknown.

Sex

Men appear to be at an increased risk of multiple myeloma. The male-to-female ratio is estimated to be 1.4:1.^10,11

Age

Multiple myeloma is a disease of older people. The majority of patients are older than 65 years.¹³ Only 1% of patients with multiple myeloma are younger than 40 years.¹³ The disease is rare in children.

Anatomy

Multiple myeloma is a diffuse disease of the bone marrow. Almost 90% of patients with myeloma have osseous involvement. Although any bone can be affected, 4 distinct radiographic patterns of involvement are seen, including (1) normal bone mineralization without a discrete lytic lesion, (2) diffuse demineralization and no lytic lesion, (3) a single lesion (plasmacytoma), and (4) widespread lytic lesions.

The predominant sites of involvement are within the axial skeleton and include the vertebral column, ribs, skull, pelvis, and femora. Most patients have either a number of lytic foci or diffuse demineralization at diagnosis. Fewer than 10% of patients with multiple myeloma are diagnosed with only a plasmacytoma found on radiography. Interestingly, extraosseous myeloma deposits are occasionally found, most commonly in the lungs, nasopharynx, or paranasal sinuses.

Presentation

The underlying pathology of multiple myeloma is expansion of a single line of plasma cells that replace normal bone marrow and produce monoclonal immunoglobulins. As a result, in more than 80% of patients, the disease manifests with bone destruction and pain. Because bone loss occurs mostly in the axial skeleton, patients with myeloma are at risk for compression fractures of the spine and pathologic fractures of the major weight-bearing bones of the body.

The classic presentation is low back pain in an older man, with resultant discovery of demineralization or a myelomatous deposit. The classic presentation has dropped to a frequency of 37% from a high of almost 70% in the 1960s, which may be related to increased surveillance for other diseases and the incidental discovery of myeloma or may be a result of increased awareness of the nonclassic manifestations of the disease.

Patients with myeloma develop disorders relating to replacement of myelogenous marrow by plasma cells. In particular, anemia is a primary manifestation of the disease (>90% of patients). Patients may also develop frequent unexplained infections that result from an inability to mount an immune response by normal plasma cells (decreased in number by the favored production of malignant myeloma cells). Generalized weakness as a result of anemia is a frequent finding, as are the neurologic symptoms believed to be related to disruption in calcium homeostasis. More than 40% of patients with myeloma develop weight loss that is related to their disease. Finally, as many as 13% of myeloma patients have bleeding disorders, mostly related to low platelet production.

The diagnostic laboratory finding in myeloma is monoclonal hypergammaglobulinemia. IgG myeloma is the most common, followed by IgA myeloma. As a result of bone destruction, hypercalcemia is a common manifestation and can be difficult to manage. Other laboratory abnormalities include hyperuricemia (as a result of elevated cell turnover), elevated erythrocyte sedimentation rate (ESR), and increased levels of alkaline phosphatase.

Renal disorders are a common manifestation of multiple myeloma. Myeloma cells produce large numbers of proteins. Fragmentation of some of these immunoglobulins produces a special protein (ie, Bence-Jones protein) that was elucidated in the original description of the disease. This protein, as well as others produced by the malignant plasma cells, may be deposited in the kidney tubules. The proteinemia in myeloma often exceeds the resorptive ability of the kidney, resulting in proteinuria — in particular, spillage of Bence-Jones protein. In addition, amyloidosis is a frequent finding (8-15%) in patients with myeloma and further contributes to parenchymal dysfunction. Calculi are often found because of elevated uric acid and calcium levels. All of these factors can eventually result in renal failure and death.

The unequivocal diagnosis of myeloma is made when the following 3 criteria are satisfied:

• A minimum 10-15% of a bone marrow aspirate demonstrates plasma cells
• Radiographic survey demonstrates lytic lesions
• Monoclonal immunoglobulins present in the urine or blood

Note that as many as 37% of cases are discovered in asymptomatic patients. Most commonly, examination of the blood for an unrelated reason reveals an elevated protein level and leads to the eventual diagnosis of myeloma. These patients may not always meet all 3 diagnostic criteria. Other laboratory studies have been proposed to provide an unequivocal diagnosis of myeloma, including the use of special stains and the detection of nuclear abnormalities. Beta-2 microglobulin has been shown to be the peripheral marker most associated with the activity and progression of this disease.

Preferred Examination

The preferred initial radiographic examination for the staging and diagnosis of myeloma remains the skeletal survey. Patients suspected of having multiple myeloma based on bone marrow aspirate results or hypergammaglobulinemia should undergo a radiographic skeletal survey. Conventionally, this skeletal survey has consisted of a lateral radiograph of the skull, anteroposterior (AP) and lateral views of the spine, and AP views of the pelvis, ribs, femora, and humeri. Inclusion of these bones is important for both staging and diagnosis.

The finding of more than one lytic lesion in a patient with myeloma indicates stage III disease. Focused examinations of newly painful bones are of value in assessing for impending pathologic fracture.

Limitations of Techniques

The skeletal survey has limitations. Most importantly, a large number of patients diagnosed with asymptomatic myeloma may have radiographically occult myeloma deposits. At least 30% cortical bone loss is required to visualize a destructive process, such as myeloma, with radiographs. In addition, myeloma is a disease of older patients; the disease can present with diffuse demineralization, which may be indistinguishable from the pattern found in patients with osteoporosis.

Magnetic resonance imaging (MRI) has been suggested as an additional imaging examination in patients with myeloma. MRI has the advantage of rapidity and sensitivity for the presence of disease; however, specificity is limited. Some reports have suggested that an MRI examination of the spine may be of value in staging patients with myeloma because radiographically occult lesions may be found that can change therapeutic intervention.

Differential Diagnoses

Acute Lymphoblastic Leukemia
Chronic Lymphocytic Leukemia
Non-Hodgkin Lymphoma
Osteoporosis, Involutional
Waldenstrom Hypergammaglobulinemia

Other Problems to Be Considered

Metastases
Nodular histiocytic lymphoma

Radiography

Lateral radiograph of the skull. This image demonstrates numerous lytic lesions, which are typical for the appearance of widespread myeloma.

Lateral radiograph of the lumbar spine. This image shows deformity of the L4 vertebral body that resulted from a plasmacytoma.

Radiograph of the right femur. This image demonstrates the typical appearance of a single myeloma lesion as a well-circumscribed lucency in the intertrochanteric region. Smaller lesions are seen at the greater trochanter.

Radiograph of the right humerus. This image demonstrates a destructive lesion of the diaphysis. Pathologic fracture is seen.

Anteroposterior radiograph of the left shoulder. This image shows an expansile process in the glenoid.

Findings

The classic radiographic appearance of multiple myeloma is that of multiple, well-circumscribed, lytic, punched-out, round lesions within the skull, spine, and pelvis (see Images 1 and 3). The lesions tend to vary slightly in size. In addition, the bones of myeloma patients are, with few exceptions, diffusely demineralized. Because myeloma is a disease of the medullary compartment of the bone, more subtle lesions can be detected by the appearance of endosteal scalloping that is seen as slight undulation to the inner cortical margin of bone. This finding is suggestive of myelomatous involvement.

Although patients with advanced and extensive myeloma tend to have a number of circumscribed lytic lesions, some may simply have diffuse osteopenia on radiography. Fewer than 10% of patients present with a single myelomatous lesion, a plasmacytoma, found on radiographs (see Image 1). These lesions are bubbly expansions of a single bone, often the ribs or posterior elements of the spine, and are occasionally associated with a soft-tissue mass.

A rare form of myeloma known as POEMS syndrome (polyneuropathy, organomegaly, endocrinopathy, monoclonal gammopathy, and skin changes) may demonstrate sclerotic lesions on radiographs, but this condition is responsible for fewer than 1% of myeloma cases. Radiographs of treated myeloma lesions may also show areas of abnormal bone architecture with sclerosis. Usually, little periosteal reaction is seen.

Degree of Confidence

As many as 79% of patients with myeloma demonstrate skeletal involvement. The finding of multiple lytic lesions on a skeletal survey involves 2 primary differential considerations, including myeloma and metastases. However, when these lesions are found together with bone marrow plasmacytosis and elevated blood gamma-globulins, the diagnosis of myeloma is certain. If tests for these 2 parameters have not been performed (ie, bone marrow plasmacytosis, blood gamma-globulins), the finding of multiple lytic lesions statistically represents widespread metastatic disease in 60-70% of patients, with the remainder representing myeloma. In diffuse osteopenia found on radiography, consider the diagnosis of myeloma and perform additional tests; however, most of these patients only have age-related osteoporosis.

False Positives/Negatives

Diffuse osteopenia that is found on radiographs is often a source of false-negative examinations because a substantial amount of cortex must be destroyed before it becomes visible radiographically.

False-positive examinations are encountered when multiple lytic lesions are found. In these patients, perform additional studies because the most likely source of this pattern is metastatic disease, not myeloma.

Computed Tomography

Axial computed tomography (CT) scan of the glenoid. This image shows a well-defined lesion, with the typical CT scan appearance of myeloma. The cortex is intact. (See also Images 10-13.)

Axial computed tomography scan of the glenoid (same patient as in Images 9 and 11-13). One year later, the myeloma lesion had grown significantly, extending to the coracoid process and through the cortex of the glenoid.

Axial computed tomography (CT) scan through the left shoulder during a CT-guided biopsy (same patient as in Images 9-12). This image shows a core biopsy needle has been advanced through the coracoid process to obtain a tissue sample.

Findings

Computed tomography (CT) scanning depicts osseous involvement in myeloma. However the usefulness of this modality has not been well studied, and CT scanning is not required in most patients because the standard skeletal surveys usually depict most of the lesions that CT scans can detect.

The single clinical situation in which CT scan studies may be of value is in cases in which the patient has bone pain and a negative radiograph.¹⁴ In this scenario, demonstration of a myeloma lesion may alter therapy significantly. CT scanning can also guide percutaneous biopsies, especially of osseous or extraosseous lesions that are suspected of being plasmacytomas (see Image 13).

The literature also shows that the use of fluorine-18 fluorodeoxyglucose (¹⁸ F FDG) positron emission tomography (PET)/CT scanning can be helpful in the staging and post-therapeutic monitoring of multiple myeloma by providing functional detection of high metabolic lesions.^15,16 However, a preliminary report by Nanni et al in a small population of patients indicates that carbon-11 (¹¹ C)-choline PET/CT scanning may be more sensitive than¹⁸ F FDG PET/CT scanning for detecting myeloma lesions. The authors cautioned that more large-scale studies are needed to verify their results.¹⁶

Magnetic Resonance Imaging

Coronal T1-weighted magnetic resonance image through a myeloma lesion of the humerus. This image shows that the lesion has a low signal intensity. The outer cortical margin is eroded but intact; however, the lesion has transgressed the inner cortex.

A T1-weighted magnetic resonance image of the humerus. This image demonstrates a predominantly hypointense to isointense myelomatous lesion in the medullary space of the diaphysis. The lesion extends through the anterior aspect of the cortex.

A T2-weighted, fat-suppressed magnetic resonance image of a myeloma lesion of the humerus. This image demonstrates the lesion is hyperintense on this sequence, a typical finding.

A T1-weighted magnetic resonance image of the shoulder (same patient as in Images 9-10 and 12-13). This image shows the full extent of myelomatous involvement within the glenoid and coracoid process.

A T2-weighted, fat-suppressed magnetic resonance image of the shoulder (same patient as in Images 9-11 and 13). This image demonstrates the myeloma lesion is hyperintense.

Findings

MRI is potentially useful for imaging multiple myeloma because of this modality's superior soft-tissue resolution. The typical MRI appearance of a myeloma deposit is a round, low signal intensity (relative to muscle) focus on T1-weighted images, which becomes high in signal intensity on T2-weighted sequences. Images 5-7 demonstrate the appearance of a typical myeloma lesion in the proximal humerus. Myeloma lesions tend to enhance somewhat with gadolinium administration. In addition, diffuse areas of replacement of the normal fatty marrow may be seen, resulting in large regions of low T1-weighted signal.

Gadolinium-based contrast agents (gadopentetate dimeglumine [Magnevist], gadobenate dimeglumine [MultiHance], gadodiamide [Omniscan], gadoversetamide [OptiMARK], gadoteridol [ProHance]) have been linked to the development of nephrogenic systemic fibrosis (NSF) or nephrogenic fibrosing dermopathy (NFD). For more information, see the eMedicine topic Nephrogenic Fibrosing Dermopathy. The disease has occurred in patients with moderate to end-stage renal disease after being given a gadolinium-based contrast agent to enhance MRI or MRA scans. 

NSF/NFD is a debilitating and sometimes fatal disease. Characteristics include red or dark patches on the skin; burning, itching, swelling, hardening, and tightening of the skin; yellow spots on the whites of the eyes; joint stiffness with trouble moving  or straightening the arms, hands, legs, or feet; pain deep in the hip bones or ribs; and muscle weakness. For more information, see the FDA Public Health Advisory or Medscape.

Degree of Confidence

Unfortunately, almost any musculoskeletal tumor has the same signal-intensity profile and enhancement pattern as myeloma. MRI, although sensitive to the presence of disease, is not disease specific. Additional tests must be employed to diagnose myeloma, such as measurement of gamma-globulin levels and direct aspiration of bone marrow to assess for plasmacytosis. Because of this, MRI may understage or overstage patients with myeloma.

In patients with extraosseous lesions, MRI may be useful to define the degree of involvement and to evaluate for cord compression.

Nuclear Imaging

Findings

Myeloma is a disease that results in overactivity of osteoclasts and the resultant liberation of bone. Nuclear medicine bone scans rely on osteoblastic activity (bone formation) for diagnosis. As such, historically, bone scans have underestimated the extent and severity of disease and have not been used routinely.¹⁷

However, a study by Erten et al appeared to demonstrate that whole-body scintigraphy with technetium-99m 2-methoxy-isobutyl-isonitrile (^99m Tc-MIBI) uptake scintigraphy may be a useful adjunct for the diagnostic imaging of multiple myeloma.¹⁸ The authors reported that^99m Tc-MIBI seemed to demonstrate the extent and intensity of bone marrow infiltration equally as well as MRI and suggested that^99m Tc-MIBI may serve as an alternative to MRI in cases in which MRI is not readily available or when its use is limited.

Degree of Confidence

The false-negative rate of bone scintigraphy in diagnosing multiple myeloma is high. Scans may be positive with normal radiographs, requiring another test for confirmation.

Angiography

Findings

Angiographic findings are nonspecific. Tumors may have a peripheral zone of increased vascularity. Generally, this technique is not used for the diagnosis of myeloma.

Intervention

Myeloma is treated with chemotherapy and, possibly, radiation. CT scanning may be used for percutaneous biopsy. Vertebroplasty has been suggested as a treatment for pathologic fractures within the spine. 

Images 8-12 show a myeloma lesion in the left glenoid that expanded over the course of 1 year. Because the coracoid process was involved, it was selected for biopsy (see Image 13).

Medicolegal Pitfalls

• Failure to diagnose impending pathologic fractures
• Failure to appreciate subtle myeloma lesions. If a patient presents only with a plasmacytoma, the discovery of only one additional myeloma lesion on a skeletal survey changes the staging from I to III.

Multimedia

Media file 1: Lateral radiograph of the skull. This image demonstrates numerous lytic lesions, which are typical for the appearance of widespread myeloma.

Media file 2: Lateral radiograph of the lumbar spine. This image shows deformity of the L4 vertebral body that resulted from a plasmacytoma.

Media file 3: Radiograph of the right femur. This image demonstrates the typical appearance of a single myeloma lesion as a well-circumscribed lucency in the intertrochanteric region. Smaller lesions are seen at the greater trochanter.

Media file 4: Radiograph of the right humerus. This image demonstrates a destructive lesion of the diaphysis. Pathologic fracture is seen.

Media file 5: Coronal T1-weighted magnetic resonance image through a myeloma lesion of the humerus. This image shows that the lesion has a low signal intensity. The outer cortical margin is eroded but intact; however, the lesion has transgressed the inner cortex.

Media file 6: A T1-weighted magnetic resonance image of the humerus. This image demonstrates a predominantly hypointense to isointense myelomatous lesion in the medullary space of the diaphysis. The lesion extends through the anterior aspect of the cortex.

Media file 7: A T2-weighted, fat-suppressed magnetic resonance image of a myeloma lesion of the humerus. This image demonstrates the lesion is hyperintense on this sequence, a typical finding.

Media file 8: Anteroposterior radiograph of the left shoulder. This image shows an expansile process in the glenoid.

Media file 9: Axial computed tomography (CT) scan of the glenoid. This image shows a well-defined lesion, with the typical CT scan appearance of myeloma. The cortex is intact. (See also Images 10-13.)

Media file 10: Axial computed tomography scan of the glenoid (same patient as in Images 9 and 11-13). One year later, the myeloma lesion had grown significantly, extending to the coracoid process and through the cortex of the glenoid.

Media file 11: A T1-weighted magnetic resonance image of the shoulder (same patient as in Images 9-10 and 12-13). This image shows the full extent of myelomatous involvement within the glenoid and coracoid process.

Media file 12: A T2-weighted, fat-suppressed magnetic resonance image of the shoulder (same patient as in Images 9-11 and 13). This image demonstrates the myeloma lesion is hyperintense.

Media file 13: Axial computed tomography (CT) scan through the left shoulder during a CT-guided biopsy (same patient as in Images 9-12). This image shows a core biopsy needle has been advanced through the coracoid process to obtain a tissue sample.

References

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Keywords

multiple myeloma, plasma cell myeloma, myeloma, Bence-Jones protein, light chains, heavy chains, monoclonal gammopathy of unknown significance, MGUS, plasmacytoma, hypergammaglobulinemia, POEMS syndrome

Contributor Information and Disclosures

Author

Steven M Sorenson, MD, Consulting Staff, Department of Radiology, Coast Radiology Imaging and Intervention
Steven M Sorenson, MD is a member of the following medical societies: Radiological Society of North America
Disclosure: Nothing to disclose.

Coauthor(s)

Amilcare Gentili, MD, Professor of Clinical Radiology, University of California at San Diego; Consulting Staff, Department of Radiology, Thornton Hospital; Chief of Radiology, San Diego VA Health Care System
Amilcare Gentili, MD is a member of the following medical societies: American Roentgen Ray Society, Radiological Society of North America, and Society of Skeletal Radiology
Disclosure: Nothing to disclose.

Sulabha Masih, MD, Associate Professor of Diagnostic Radiology, University of California at Los Angeles; Consulting Staff, Department of Radiology, Section of Musculoskeletal Radiology, West Los Angeles Veterans Affairs Medical Center
Sulabha Masih, MD is a member of the following medical societies: American Roentgen Ray Society, Radiological Society of North America, and Society of Skeletal Radiology
Disclosure: Nothing to disclose.

Carol L Andrews, MD, Consulting Musculoskeletal Radiologist, Mink Radiologic Imaging; Consulting Staff, Department of Radiology, Antelope Valley Medical Center
Carol L Andrews, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Forensic Sciences, American Association for Women Radiologists, American College of Radiology, American Medical Association, American Roentgen Ray Society, California Radiological Society, North American Spine Society, Radiological Society of North America, and Society of Skeletal Radiology
Disclosure: AMIRSYS publishing Royalty Independent contractor

Pharmacy Editor

Bernard D Coombs, MB, ChB, PhD, Consulting Staff, Department of Specialist Rehabilitation Services, Hutt Valley District Health Board, New Zealand
Disclosure: Nothing to disclose.

Managing Editor

Wilfred CG Peh, MD, MBBS, FRCP(Glasg), FRCP(Edin), FRCR, Clinical Professor, Faculty of Medicine, National University of Singapore; Senior Consultant Radiologist, Alexandra Hospital, Singapore
Wilfred CG Peh, MD, MBBS, FRCP(Glasg), FRCP(Edin), FRCR is a member of the following medical societies: American Roentgen Ray Society, British Institute of Radiology, International Skeletal Society, Radiological Society of North America, Royal College of Physicians, and Royal College of Radiologists
Disclosure: Nothing to disclose.

CME Editor

Robert M Krasny, MD, Resolution Imaging Medical Corporation
Robert M Krasny, MD is a member of the following medical societies: American Roentgen Ray Society and Radiological Society of North America
Disclosure: Nothing to disclose.

Chief Editor

Felix S Chew, MD, MBA, EdM, Professor, Department of Radiology, Vice Chairman for Radiology Informatics, Section Head of Musculoskeletal Radiology, University of Washington
Felix S Chew, MD, MBA, EdM is a member of the following medical societies: American Roentgen Ray Society, Association of University Radiologists, and Radiological Society of North America
Disclosure: Nothing to disclose.

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