Glucocorticoid-induced osteoporosis—from molecular mechanism to clinical practice
Chueh Hsuan Hsu, Chueh Lin Hsu, A. Langley, Caroline Wojcik, Elysee Iraganje, Bogna Grygiel‐Górniak
Abstract
Glucocorticoids (GCs) are essential and effective medications commonly prescribed to patients with autoimmune disorders and inflammatory diseases. However, they often adversely affect bone health, including a rapid bone mineral density reduction and an increased bone fracture rate. An estimated 30% of long-term GC users develop secondary osteoporosis [glucocorticoid-induced osteoporosis (GIO)], whereas the measurement and prevention for GC-treated patients are sometimes clinically overlooked in clinical practice. Fortunately, many guidelines for GIO-related fracture risk assessment have been established, and several new drugs that benefit primary osteoporosis patients may also serve as potential GIO therapeutic options. Because of the broad application of GCs in clinical practice and the growing prevalence of GIO, increasing with the dose and time of GC administration, awareness of GIO development is crucial for implementing preventive therapy promptly and effectively. In this paper, we discuss the pathomechanisms of GIO and bone health problems depending on the method and route of GC administration in various groups of patients. Various treatment regimens are broadly analyzed, highlighting the most crucial aspects and new therapeutic options.