A 65-year-old man presented with a 2-year history of progressive hair loss involving the scalp, the eyebrows and the upper trunk, and recent onset of small papules and blisters on the dorsal hands as well as longitudinal ridging and fissuring of the fingernails. Clinical examination showed diffuse alopecia most pronounced on the androgen dependent scalp; the skin was slightly indurated on palpation []. There were focal petechiae. The lateral sides of both eyebrows and most of the hair on the chest were absent too. The axillary, pubic, and limb hair was preserved.\nTrichoscopic examination of the scalp showed prominent salmon colored halos (0.3-1 mm in diameter) surrounding the follicular ostia []. These halos were seen around empty follicles as well as around follicles containing terminal and vellus hairs, black dots, and/or broken hairs. This trichoscopic finding was present over the entire scalp.\nA 4 mm punch biopsy from the alopecic scalp was obtained and bisected in horizontal sections. There was overall preserved follicular architecture with intact sebaceous glands []. There were no terminal anagen follicles, one terminal telogen follicles, two vellus anagen follicles and 10 atrophic follicular structures reminiscent of telogen germinal units (secondary germs). All follicular structures were surrounded by amorphous eosinophilic material, which formed either a compact- or loosely- folded fibrillar cast []. The same material was deposited in all fibrous streamers, which appeared eosinophilic, homogenized and avascular. Congo red stain evaluated under polarized light highlighted the apple green stain of the amyloid [].\nSerum electrophoresis and bone marrow biopsy established the diagnosis of multiple myeloma.
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.