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 complaints of low back ache of one year duration. The pain was radiating down the right lower limb as far as the knee joint. There was no history of trauma or history suggestive of any significant medical co-morbid conditions.\nExamination revealed tenderness on the right side of the lumbosacral spine and right sacroiliac joint. There was para vertebral muscle spasm with loss of lumbar lordosis. Hip movements were normal with no major disability. There were no root stretch signs and no neurological deficit was noted.\nAn x-ray of the lumbosacral spine showed evidence of old fracture of L1 vertebra []. The Magnetic Resonance Imaging (MRI) scan showed collapse of the L2 vertebra with extrusion of the bone posteriorly into the spinal canal []. There was soft tissue infiltration seen in the sacrum. While awaiting clinic review the patient presented to the casualty with fracture clavicle on the left side following a trivial fall. The fracture of the clavicle was at the medial end (unusual site). A subsequent bone scan showed increased uptake in the medial end of the left clavicle and L2 vertebra. There were areas of increased activity in the region of the ribs [].\nLab investigations revealed hemoglobin of 12.8 g/dl, erythrocyte sedimentation rate (ESR) of 21mm/hr and hematocrit ratio of 0.357 (normal 0.370-0.470 ratio). Creatinine was 50 μmol/l (normal 50-141μmol/l) and urea of 5.9mmol/l (normal 2.5-7.5 mmol/l). The serum calcium 2.28 mmol/l (normal 2.1-2.6 mmol/l) and phosphate levels 1.13 mmol/l (normal 0.81-1.45 mmol/l) were normal. Lactic acid dehydrogenase was elevated, 1061 IU/l (normal 313-618 IU/l) and Alkaline phosphatase was normal, 125 IU/l (normal 25-150 IU/l).\nMyeloma screen which did not reveal presence of any abnormal compact bands was obtained and there was no Bence-Jones proteinuria. The levels of the immunoglobulin were Ig G 6.6 g/l (normal 5.3-16.5 g/l), Ig A 0.21 g/l (normal 0.80-4.00 g/l) and Ig M was 0.36 g/l (normal 0.50-2.00 g/l), which were lower than normal.\nIn view of the bony pain, pathological fracture of the L2 vertebra, unusual fracture of the clavicle, normal myeloma screen, normal calcium levels and bone scan findings it was decided to organize a Computerized Tomography (CT) scan of the thorax and abdomen to look for the primary with secondaries as the first working diagnosis. The CT scan merely confirmed the findings of MRI scan and there was no evidence of any primary or other secondaries []. A bone biopsy was planned.\nA percutaneous bone biopsy from the medial end of the clavicle was done because of easy accessibility which was negative for malignancy. A CT guided biopsy from the L2 vertebra was again negative for malignancy. A bone marrow aspirate and trephine biopsy were done from the iliac crest which confirmed the diagnosis of multiple myeloma. The biopsy showed a hyper cellular marrow with normal haemopoiesis replaced entirely with malignant plasma cells suggestive of myeloma. Aspirate showed plasma cells to be about 52% of the marrow with marked atypia. The patient was referred to further treatment in the form of chemotherapy and radiotherapy. The patient died one month after diagnosis while undergoing treatment. There was, however, a delay of two months between the first presentation and final diagnosis.