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Solitary extramedullary plasmacytoma

Solitary extramedullary plasmacytoma
Literature review current through: Jan 2024.
This topic last updated: Jan 31, 2024.

INTRODUCTION — Plasma cell neoplasms (plasma cell dyscrasias) are a group of entities characterized by the neoplastic proliferation of clonal plasma cells, typically producing a monoclonal immunoglobulin. Plasma cell neoplasms can present as a single lesion (solitary plasmacytoma) or as multiple lesions (multiple myeloma). Solitary plasmacytomas most frequently occur in bone (plasmacytoma of bone), but can also be found outside bone in soft tissues (extramedullary plasmacytoma) [1-4]. Why some patients develop multiple myeloma and others a single plasmacytoma is not understood, but it might be related to differences in cellular adhesion molecules or chemokine receptor expression profiles of the malignant plasma cells [5].

Solitary extramedullary plasmacytomas (SEP; solitary extraosseous plasmacytoma) are plasma cell tumors that arise outside of the bone marrow. They are solitary lesions and are most often located in the head and neck region, mainly in the upper aerodigestive tract, but may also occur in the gastrointestinal (GI) tract, urinary bladder, central nervous system, thyroid, breast, testes, parotid gland, lymph nodes, and skin.

SEP refers to a solitary non-osseus plasma cell neoplasm in the absence of any other sign of multiple myeloma. Note that extramedullary plasmacytomas can arise in patients with multiple myeloma at any time during the course of the disease and should not be confused with SEP. The diagnosis and management of SEP will be discussed here. The diagnosis and treatment of other plasma cell disorders (eg, solitary plasmacytoma of bone, multiple myeloma, primary AL amyloidosis, monoclonal gammopathy of undetermined significance) are discussed separately.

(See "Solitary plasmacytoma of bone".)

(See "Multiple myeloma: Clinical features, laboratory manifestations, and diagnosis".)

(See "Clinical presentation, laboratory manifestations, and diagnosis of immunoglobulin light chain (AL) amyloidosis".)

(See "Diagnosis of monoclonal gammopathy of undetermined significance".)

EPIDEMIOLOGY — SEPs account for approximately 3 percent of plasma cell malignancies [6,7]. In one large population-based study from the US Surveillance, Epidemiology and End Results (SEER) program, the incidence for SEP was 0.10 per 100,000 persons per year [6]. The median age at diagnosis is 55 to 60 years, and approximately two-thirds of patients are male.

CLINICAL PRESENTATION — Most patients present with symptoms related to the location of the mass. Approximately 45 to 80 percent involve the upper respiratory tract (ie, oronasopharynx and paranasal sinuses), producing epistaxis, nasal discharge (rhinorrhea), or nasal obstruction [8-13]. Less common sites of involvement include connective/soft tissue [13], the gastrointestinal tract [14], liver [15], lymph nodes [16,17], testes [18], skin, breast [19], and central nervous system [20]. Primary plasmacytoma of the lung often presents as a pulmonary nodule or hilar mass with or without hemoptysis [21]. Regional lymph nodes may be involved.

By definition, patients with SEP do not have any myeloma-defining events including:

No end-organ damage attributable to the underlying plasma cell disorder – End-organ damage can manifest as anemia (ie, hemoglobin <10 g/dL or 2 g/dL below normal), hypercalcemia (ie, serum calcium >11.5 mg/dL [2.875 mmol/liter]), kidney impairment (ie, serum creatinine >2 mg/dL [176.8 micromol/liter]), and/or additional bone or extramedullary lesions.

No biomarkers of malignancy – Biomarkers of multiple myeloma include clonal bone marrow plasma cell ≥60 percent; involved:uninvolved serum free light chain ratio ≥100; and/or >1 focal lesions on magnetic resonance imaging (MRI) studies.

Myeloma-defining events are discussed in more detail separately. (See "Multiple myeloma: Clinical features, laboratory manifestations, and diagnosis", section on 'Diagnostic criteria'.)

EVALUATION — The evaluation of a patient with a suspected SEP should include the following studies in addition to a complete history and physical examination:

A biopsy of the suspected lesion.

A complete blood count and differential with examination of the peripheral blood smear.

A chemistry screen that includes measurements of serum calcium, creatinine, albumin, lactate dehydrogenase, beta-2 microglobulin, C-reactive protein, and serum free light chains (FLC) and FLC ratio. (See "Multiple myeloma: Staging and prognostic studies".)

A serum protein electrophoresis (SPEP) with immunofixation and quantitation of immunoglobulins. (See "Laboratory methods for analyzing monoclonal proteins".)

A routine urinalysis, a 24-hour urine collection for electrophoresis (UPEP) and immunofixation, and a serum FLC assay. The FLC assay cannot replace the 24-hour urine collection with SPEP and immunofixation in patients with a confirmed plasma cell proliferative disorder. (See "Laboratory methods for analyzing monoclonal proteins".)

A unilateral bone marrow aspiration and biopsy with fluorescent in situ hybridization (FISH) for myeloma-related chromosomal abnormalities.

Cross sectional imaging with whole body combined fluorine-18-labeled fluorodeoxyglucose positron emission tomography (PET)/computed tomography (CT) (18F-FDG PET/CT) scan [22]. If PET/CT is not available, whole body MRI is an acceptable alternative [23].

Spinal cord compression from an extramedullary plasmacytoma should be suspected in patients with severe back pain, weakness, or paresthesias of the lower extremities; bladder incontinence; or bowel dysfunction. MRI or CT myelography of the entire spine must be performed immediately if this complication is suspected. On MRI, extramedullary plasmacytoma is usually hypointense or isointense on T1-weighted images and isointense or hyperintense on T2-weighted images [24]. (See "Clinical features and diagnosis of neoplastic epidural spinal cord compression".)

DIAGNOSIS — The diagnosis of an SEP requires the following (table 1) [25]:

Biopsy-proven extramedullary tumor with evidence of clonal plasma cells (picture 1 and picture 2). (See "Multiple myeloma: Clinical features, laboratory manifestations, and diagnosis", section on 'Morphology and immunophenotype'.)

18F-FDG PET/CT must show no other lytic or extramedullary lesions (except for the primary solitary lesion). A skeletal survey is insufficient to rule out other areas of involvement, which would upstage the patient to multiple myeloma.

Bone marrow aspirate and biopsy may demonstrate no clonal plasma cells (SEP) or clonal plasma cells in the bone marrow at a level <10 percent (SEP with minimal marrow involvement).

There is no anemia, hypercalcemia, or kidney impairment that could be attributed to a clonal plasma cell proliferative disorder. (See 'Clinical presentation' above.)

Some patients may have a small monoclonal protein, usually IgA, in the serum or urine, which often disappears following treatment. The involved:uninvolved serum free light chain (FLC) ratio must be <100.

Some patients with a solitary extramedullary lesion may demonstrate up to 10 percent clonal plasma cells and are considered as having SEP with minimal marrow involvement [25]. These patients are treated in a similar fashion to SEP but have a higher risk of progression to symptomatic myeloma. If patients suspected to have SEP demonstrate 10 percent or more clonal plasma cells in the bone marrow, they should be considered to have multiple myeloma rather than SEP. These patients are also often treated in a similar fashion to SEP but may require additional systemic therapy. (See "Multiple myeloma: Clinical features, laboratory manifestations, and diagnosis", section on 'Diagnosis'.)

DIFFERENTIAL DIAGNOSIS — It is important to distinguish SEPs from other plasma cell dyscrasias for the purposes of prognosis and treatment. The main condition to consider in the differential diagnosis is multiple myeloma, but other hematologic and non-hematologic neoplasms must also be considered.

Solitary plasmacytoma can be distinguished from most neoplasms based on the morphologic appearance of plasma cells and on the clonal nature of the plasma cells, which can be established by immunostaining for kappa and lambda light chains or by flow cytometry. Typically, plasma cells in solitary plasmacytoma will be positive for CD138, CD38, and show light chain restriction (ie, stain positive for either kappa or lambda but not both). Distinction between solitary plasmacytoma and multiple myeloma or other closely related plasma cell tumors (eg, Waldenström macroglobulinemia) requires additional studies as noted below.

Multiple myeloma — SEP is composed of plasma cells that are histologically and immunophenotypically identical to those seen in multiple myeloma; however, the treatment of these two entities differs significantly, necessitating a careful review of the diagnosis. A distinction between these two conditions is made based on the exclusion of additional lesions in patients with SEP. (See "Multiple myeloma: Clinical features, laboratory manifestations, and diagnosis".)

As mentioned above, the diagnosis of SEP requires the exclusion of features of multiple myeloma as evidenced by the following:

Normal bone marrow with no evidence of clonal plasma cells. Patients with an apparent SEP who have clonal involvement of the marrow <10 percent are considered to have SEP with minimal marrow involvement. Patients with an apparent SEP and 10 percent or more clonal plasma cells detected in the bone marrow aspirate or biopsy and/or involved:uninvolved serum free light chain (FLC) ratio ≥100 meet the criteria for multiple myeloma [25].

18F-FDG PET/CT is negative for evidence of multiple myeloma (except for the primary solitary lesion).

Absence of lytic lesions, anemia, hypercalcemia, and kidney impairment, unless these are due to a cause other than a plasma cell dyscrasia.

Waldenström macroglobulinemia — Waldenström macroglobulinemia (WM) is a distinct clinicopathologic entity demonstrating lymphoplasmacytic lymphoma (LPL) in the bone marrow and/or lymphatic tissue with an IgM monoclonal gammopathy in the blood. Patients may present with symptoms related to the infiltration of the hematopoietic tissues or the effects of monoclonal IgM in the blood. In comparison, patients with SEP will have no clonal lymphoplasmacytic cells on bone marrow biopsy and only rarely have an unrelated IgM monoclonal gammopathy. (See "Epidemiology, pathogenesis, clinical manifestations, and diagnosis of Waldenström macroglobulinemia".)

TREATMENT — The treatment of choice for SEP is radiation therapy (RT) given with curative intent at a dose of 40 to 50 Gy over a four week period [13,26-28]. If a complete surgical resection was performed as part of the diagnosis, the role of adjuvant RT is less clear. Small lesions may be cured with surgery alone, and no adjuvant RT is indicated unless there is suspicion of residual local disease. Adjuvant chemotherapy does not appear to improve relapse rate or increase disease-free survival [6]. Osteoclast inhibitors (eg, bisphosphonates) are not recommended for patients with SEP, except in the setting of underlying osteopenia. (See "Multiple myeloma: The use of osteoclast inhibitors", section on 'Indications'.)

For patients with incompletely resected SEP, we recommend the use of local RT rather than further surgery, chemotherapy, or observation. For patients with completely resected SEP after diagnostic biopsy, we suggest observation rather than adjuvant RT or chemotherapy, although other experts may reasonably offer adjuvant RT in this setting. This approach is based on retrospective analyses [13,26,29,30]. As examples:

A retrospective single institution analysis of 18 consecutive patients who received RT (median dose 50 Gy) for SEP of the head and neck reported no recurrences in the radiation field [26]. There was a marginal recurrence that was treated successfully with another course of RT. At a median follow-up of 6.8 years, six patients experienced disease progression to multiple myeloma (two patients) or developed plasmacytoma at another site (four patients).

A second retrospective single institution analysis of 25 consecutive patients who received RT (median dose 45 Gy) for SEP reported local recurrence in five patients (one marginal and four in-field) [29]. At a median follow-up of 64 months, the five-year probability of progression to myeloma was 30 percent and the five-year overall survival rate was 85 percent.

In a retrospective analysis of 5056 patients with solitary plasmacytoma, including 1528 patients with SEP, treatment with both radiation and surgery resulted in superior overall survival than use of either modality alone [13]. In addition, those treated with a radiation dose <40 Gy had worse overall survival on multivariable analysis. Since treatment differed significantly by site of involvement, it is not known whether these survival differences are due to treatment given, site involved, or a combination of the two.

The ideal dose of radiation in this setting is unknown. Retrospective analyses have suggested that radiation doses of 40 Gy or greater are associated with improved local control (eg, local failure rates of 9 versus 23 percent) [7,13,26].

There are limited data regarding the preferred radiation volume for SEP. A retrospective study of patients with SEP of the head and neck suggested an increased risk of recurrence when RT was administered to the gross tumor plus a 2 cm margin when compared with those who received RT to the entire nasal cavity or paranasal sinuses [26]. However, with improved imaging, recurrence rates without nodal radiation are very low (approximately 5 percent), and elective lymph node coverage is not recommended for SEP [28].

As mentioned above, the role of RT after a complete surgical resection is less clear with some series suggesting improved median survival rates when adjuvant RT is used [8] and others suggesting no difference in outcomes [9]. Given the lack of proven benefit and potential for RT-associated complications, including radiation-induced second malignancies, we reserve adjuvant RT for patients with suspected local residual disease.

RESPONSE ASSESSMENT AND FOLLOW-UP — Following the completion of therapy, patients are seen at periodic intervals to monitor for treatment complications and assess for possible relapse. The frequency and extent of these visits depend on the comfort of both the patient and physician. If the SEP was measurable by an imaging modality prior to therapy, the same modality (eg, 18F-FDG PET/CT) should be repeated three to four months after completing therapy, and periodically thereafter.

In general, we see patients every three months for the first two years, then every six months for an additional three years, then yearly or every other year after five years. At these visits we perform a history and physical examination, urine and serum protein electrophoresis with immunofixation, free light chain (FLC) assay, complete blood count, serum creatinine, and serum calcium. For patients with head and neck involvement, we also perform a fiberoptic endoscopy every 6 to 12 months for the first five years after treatment. All patients undergo 18F-FDG PET/CT or MRI (whichever imaging modality was used for the initial evaluation) every 6 to 12 months for the first five years after therapy. Other follow-up imaging depends on the original tumor site.

There are no guidelines for the assessment of treatment response in SEP, and practice varies. We agree with an approach proposed by a European expert panel, which combines response evaluation criteria in solid tumors (RECIST) with the International Myeloma Working Group (IMWG) response criteria for multiple myeloma (MM) (table 2) [23,31,32]. RECIST is used to evaluate the extramedullary tumor while the IMWG response criteria are used to evaluate the monoclonal protein.

When present, the serum monoclonal protein can remain stable for several months before declining. If serum monoclonal protein levels increase or if the patient develops signs of myeloma-associated end-organ damage, obtain a new bone marrow sample and perform other diagnostic testing (eg, imaging) to determine if the patient has experienced progression to myeloma.

It is preferable to use the same imaging technique for diagnosis and treatment response assessment [23,31]. PET/CT is usually preferred over MRI given its superior sensitivity [33].A persistent high uptake on 18F-FDG PET/CT indicates the presence of residual disease.

RELAPSED OR REFRACTORY DISEASE — There is no consensus about the treatment of relapsed or refractory SEP because of the high cure rates following surgery or radiation therapy (RT) and limited data to guide management. At the time of relapse, a full repeat diagnostic evaluation (with a new biopsy of the lesion) is required to confirm the clonal plasma cell infiltration and exclude other plasma cell disorders. (See 'Evaluation' above.)

If the evaluation at relapse reveals a myeloma-defining event (eg, end-organ damage or a biomarker for myeloma), SEP has evolved to multiple myeloma (MM) and systemic therapy for MM is appropriate. (See "Multiple myeloma: Initial treatment".)

If there are no myeloma-defining events, management of local relapse is individualized based on the prior therapy with the following considerations (see 'Treatment' above):

A lesion that recurs in the same location following surgery alone can be treated with RT.

A lesion that recurs in the same location following RT may be amenable to surgical resection or additional RT.

A decision regarding retreatment with either surgery or RT is influenced by the patient's symptoms, prior RT dose, tumor location, and timing of relapse.

If relapse occurs at a different location, there should be a high suspicion for systemic disease (ie, multiple myeloma). Following a careful evaluation to rule out systemic disease, management is highly individualized and may include RT, surgical resection, and/or systemic therapy.

PROGNOSIS — Less than 7 percent of patients with SEP will develop a local recurrence after tumoricidal radiation [27,34]. Approximately 10 to 15 percent of patients will ultimately develop multiple myeloma [35,36]. The progression rate is higher (20 percent) in patients with SEP with minimal marrow involvement.

Reported five-year overall survival rates for patients with SEP have ranged from 40 to 85 percent [9,37-40]. It is unknown if tumor location affects outcome. Initial reports suggest that involvement of the head and neck may portend a better prognosis, while connective/soft tissue lesions may portend a worse prognosis. However, it is unclear whether differences in management can account for these different outcomes. In a retrospective analysis that included 1528 patients with SEP, the median overall survival was 11 years the population overall, 6.8 years for the 295 patients with connective/soft tissue involvement, and not reached for the 681 patients with head and neck involvement [13]. In another series of 18 patients with SEP of the head and neck treated at the Mayo Clinic, the median overall survival was 12.5 years with five- and 10-year survival rates of 88 and 55 percent, respectively [26]. Six patients developed multiple myeloma or plasmacytoma at a distant site. In addition, an analysis of the Surveillance, Epidemiology, and End Results (SEER) database that included 1185 patients with extramedullary plasmacytoma reported superior median survival among patients with involvement of the head and neck when compared with patients with other sites of extramedullary plasmacytoma (13 versus 4 years) [12]. Patients with involvement of the head and neck were less likely to be treated with surgery alone and more likely to have combined modality treatment with surgery and radiation therapy.

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Multiple myeloma" and "Society guideline links: Solitary plasmacytoma".)

SUMMARY AND RECOMMENDATIONS

Clinical presentation – Solitary extramedullary plasmacytomas (SEP) are plasma cell tumors that arise outside of the bone marrow. Most patients present with symptoms related to the location of the mass, which are most frequently located in the head and neck region. (See 'Epidemiology' above and 'Clinical presentation' above.)

Diagnostic evaluation – The evaluation of a patient with a suspected SEP should include a biopsy of the suspected lesion, a unilateral bone marrow aspirate and biopsy, and laboratory studies. Imaging should include a fluorine-18-labeled fluorodeoxyglucose positron emission tomography/computed tomography (18F-FDG PET/CT) scan. (See 'Evaluation' above.)

The diagnosis of an SEP requires the following (table 1) (see 'Diagnosis' above):

Biopsy-proven extramedullary tumor with evidence of clonal plasma cells.

18F-FDG PET/CT must show no lytic or extramedullary lesions (except for the primary solitary lesion).

Bone marrow aspirate and biopsy demonstrates <10 percent clonal plasma cells.

There is no anemia, hypercalcemia, or kidney impairment that could be attributed to a clonal plasma cell proliferative disorder.

The presence of clonal plasma cells (<10 percent) in the bone marrow is considered solitary plasmacytoma with minimal marrow involvement. Presence of ≥10 percent clonal bone marrow plasma cells in a patient with SEP will automatically meet required criteria for multiple myeloma.

Management – The treatment of SEP depends primarily on whether the diagnostic biopsy was a complete or incomplete resection of the tumor:

For patients with an incompletely resected SEP after diagnostic biopsy, we recommend the use of local radiation therapy rather than further surgery, chemotherapy, or observation (Grade 1C). (See 'Treatment' above.)

For patients with completely resected SEP after diagnostic biopsy, we suggest observation rather than adjuvant radiation therapy or chemotherapy (Grade 2C). Other experts may reasonably offer adjuvant radiation therapy. (See 'Treatment' above.)

Limited role for osteoclast inhibitors – Osteoclast inhibitors (eg, bisphosphonates) are not routinely used for patients with SEP, except in the setting of underlying osteopenia. (See "Multiple myeloma: The use of osteoclast inhibitors", section on 'Indications'.)

ACKNOWLEDGMENT — The UpToDate editorial staff acknowledges the extensive contributions of Robert A Kyle, MD to earlier versions of this topic review.

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