Scientific letter
Multiple myeloma as a cause of rapidly progressive osteoporosisMieloma múltiple como causa de osteoporosis secundaria con evolución rápidamente progresiva

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Introduction

Secondary osteoporosis encompasses a wide group of heterogeneous disorders. Secondary osteoporosis may pose diagnostic problems that need to be addressed in order to establish adequate treatment and prognosis. The causes of secondary osteoporosis include endocrine, hematological, and conjunctive tissue disorders, drug treatments, kidney diseases, and nutritional and gastrointestinal disorders, amongst others.1 Approximately 40–60% of cases of osteoporosis in males are secondary, and their most common causes include glucocorticoid treatment, hypogonadism, and alcoholism.2

In elderly subjects, multiple myeloma (MM) and other hematological tumors induce a clinical picture similar to primary osteoporosis. This condition should therefore be ruled out in patients with fragility fractures and a fast clinical course.3 In MM, osteoclastic activity is increased because myeloma cells cause or induce the production of osteoclastogenic factors in a bone microenvironment and decrease the production of osteoprotegerin (OPG), a decoy receptor of RANK ligand (RANKL), by osteoblastic cells.4 RANKL increase enhances the formation and survival of osteoclasts and macrophage inflammatory protein-1 (MIP-1α) acts as a chemotactic factor for osteoclast precursors, and also promotes the growth and survival of MM cells. On the other hand, the bone destruction process releases growth factors that increase MM cell proliferation, thus exacerbating the osteolytic process.5 In addition to the role of RANKL in bone resorption increase, bone formation inhibition occurs in myeloma. TGF-beta, as well as inhibitors of the relevant wnt pathway such as DKK-1, sFRP-2, and sFRP-3, produced by myeloma cells, have recently been implicated.6

In most patients with MM, skeletal manifestations (osteopenia, fractures, and osteolysis) are common and lead to an impaired quality of life. Bone lesions in myeloma differ from other lytic metastatic lesions in their suppression or absence of osteoblastic activity in an area with a high tumor burden. These lesions are best visualized using MRI or conventional X-rays.7 Other techniques such as 99mTc scintigraphy are not more helpful as compared to conventional X-rays because they underestimate bone lesions in patients with multiple myeloma.

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Case report

We report the case of an 82-year-old male patient referred to the bone metabolism clinic for work-up for osteoporosis because he had vertebral fractures at T12 and L1, L2, and L4. His personal history included hyperuricemia, hypertension, and benign prostatic hyperplasia monitored by urology. The patient reported that his mother had died at a young age from a tumor he could not specify, and that three of his siblings had died from hepatocarcinoma.

The patient reported severe lumbar pain for

Discussion

Twenty to thirty percent of osteoporotic fractures occur in males, and it is estimated that 13–25% of males over 50 years of age will experience an osteoporotic fracture during their lives.8 The need to rule out secondary osteoporosis is even greater in males because in approximately 50% of cases osteoporosis is secondary to other conditions, including alcoholism, rheumatic disease, immobilization, glucocorticoid treatment, endocrine disease, and hematological neoplasms such as MM. MM is

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Please cite this article as: Suleiman Martos Y, et al. Mieloma múltiple como causa de osteoporosis secundaria con evolución rápidamente progresiva. Endocrinol Nutr. 2012;59:398–400.

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