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Secondary osteoporosis is defined as a decline in bone mineral density due to any underlying etiology, which usually results in accelerated bone loss than expected for the individual's age or gender. Almost 50-80% of men diagnosed with osteoporosis have secondary osteoporosis. We present a case of a 60-year-old male with secondary osteoporosis with...
Context in source publication
Context 1
... X-ray absorptiometry (DXA) showed a T score of -3.3 and a Z score of -2.9 at the lumbar spine (L2-L4), L1 was excluded due to compression fracture (Figure 2). At the left total hip, the T score was -2.2, and the Z score was -1.8; at the left femur neck, the T score was -2.3, and the Z score was -1.3 ( Figure 3). No previous DXA scans were performed. ...
Citations
... Furthermore, previous studies have reported that TKIs affect bone and mineral homeostasis. Hypophosphatemia, secondary hyperparathyroidism [11], and osteoporosis [12] are observed following imatinib treatment because imatinib inhibits PDGFR, which promotes osteoblast differentiation and suppresses osteoclast differentiation [13]. Nilotinib also suppresses PDGFR-dependent osteoblast proliferation and osteoclastogenesis by stromal-cell-dependent mechanism in vitro [14]. ...
Given the increasing prevalence of chronic myeloid leukemia (CML) in older individuals, careful selection of tyrosine kinase inhibitors (TKIs) is required. The case of an 84-year-old woman with chronic-phase CML and chronic kidney disease undergoing osteoporosis, in whom dasatinib triggered severe hypocalcemia, is reported. She was intolerant to both imatinib and nilotinib. Initiation of low-dose dasatinib treatment led to severe hypocalcemia and long QT syndrome, compounded by vitamin D deficiency and denosumab use. We stopped dasatinib, and her hypocalcemia was improved after calcium administration. This case highlights the potential of TKIs in triggering hypocalcemia, emphasizing the need to assess mineral disorders before initiating TKI therapy.
