A 70-year-old man with a past medical history of dyslipidemia was referred to Jeju National University Hospital with a 5-month history of recurrent vertebral compression fractures with back pain. He suddenly had back pain while changing his pants and was treated for T11 and L3 vertebral compression fractures 5 months prior. He had slipped down on the stairs, landing on his backside, and was hospitalized for treatment of L2 and L4 vertebral compression fractures 2 months prior. He had felt back pain while sneezing and had difficulty in walking 5 days prior. Eventually, he was referred to our hospital. Bone densitometry of the spine from previous hospital visits revealed osteopenia, and magnetic resonance imaging (MRI) of the lumbar spine from a previous hospital visit showed multiple compression fractures of the vertebral bodies with inconspicuous retropulsion of the cortex into the spinal canal (). X-ray images of the T-L spine () revealed degenerative changes with compression fractures at T12, and the L1 to L3 vertebral bodies and the pelvic bones () showed osteopenia. A bone scan () showed a vertebral compression fracture in the L1 spine area; post-traumatic changes in the right first and eighth to tenth ribs and the left sixth rib; and arthritic and degenerative changes in the T9 to L5 spines and both hip joint areas.\nLaboratory tests did not reveal specific results. The hemoglobin level was 11.0 g/dL, showing normocytic normochromic anemia on the peripheral blood smear. We also noted the absence of hypercalcemia (8.9 mg/dL), and a normal serum creatinine level of 0.78 mg/dL. Laboratory tests and imaging studies did not provide evidence to suspect that the recurrent compression fractures may have resulted from osteoporosis, metabolic diseases such as hyperparathyroidism, Paget disease and other metabolic processes, or obvious tumors. Therefore, serum and urine protein electrophoresis were conducted for the differential diagnosis of MM. Serum protein electrophoresis did not reveal abnormal Ig levels and the patient’s gamma globulin levels were normal. Urine protein electrophoresis showed no monoclonal protein in any significant fraction. Consequently, a presumptive diagnosis of vertebral compression fractures with osteopenia was made, and conservative management was undertaken for 2 weeks.\nHowever, the patient complained of right hip pain during his first ambulation after conservative management. Hip X-ray images () suggested several osteolytic lesions, and computed tomography detected multiple inconspicuous osteolytic lesions with greater variegation in opacity than expected in the spine, pelvic bones, both femurs, and ribs, suggesting MM or metastasis (). In addition, positron emission tomography revealed a high possibility of bone metastasis or bone-related malignancy based on a significant abnormal 18F-fluorodeoxyglucose uptake in the skull, spine, sternum, ribs, scapula, pelvic bones, and both femurs (). Moreover, a serum free light chain (SFLC) assay revealed elevated levels of kappa free light chain (12.667 mg/dL) and abnormal free light chain ratios with free lambda (1.105 mg/dL).\nTherefore, we performed a bone marrow biopsy for the definitive diagnosis of NSMM. The marrow was mildly to moderately hypercellular and infiltrated by plasmacytoid cells in clusters with some normal hematopoietic cells (). The plasmacytoid cells showed reactivity to CD138 () and kappa free light chain on immunohistochemical staining (), with no reactivity to lambda light chain (), which supports monoclonal plasma cell proliferation and favors the diagnosis of MM. Finally, the patient was diagnosed with NSMM 7 months since the onset of the first symptom and was referred to the oncology center for further management and therapy.
A 60-year-old male was referred to our clinic with 5-month history of gradual but progressive weight loss, recurrent fever, anorexia, progressive fatigue, and generalized bone pains. Two months after the onset of these symptoms, he developed inability to walk. There was no associated sphincteric dysfunction or sensory loss. There was no history of chronic cough. At the time of presentation, significant examination findings were pallor, inability to walk, and general bone tenderness. X rays of the skull, thoracolumbar spine, and pelvis showed lytic lesions (). Blood film and bone marrow aspiration were essentially normal with <5% plasma cells reported in the bone marrow. Erythrocyte sedimentation rate, C reactive protein, and serum protein electrophoresis were normal and urinary Bence Jones protein was negative. Laboratory data are summarized in .\nA bone marrow trephine biopsy was done and showed osteosclerotic changes and focal scalloping with prominent osteoclastic activity. The marrow was moderately to markedly hypercellular and was densely infiltrated by a cellular infiltrate. The cells were mostly small cells with fairly condensed chromatin. They showed a variable amount of cytoplasm and there was a fair sized subpopulation of plasmacytoid lymphocytes.\nImmunohistochemistry showed positivity of CD138 (which strongly supports the diagnosis of plasma cell myeloma) and cyclin D1 (which is associated with cases of plasma cell myeloma with lymphoplasmacytic morphology and correlates with the presence of the translocation t(11;14)(q13;q32)).