Abstract
Systemic vasculitides are a range of conditions characterized by inflammation of blood vessels which may manifest as single organ or life-threatening multisystem disease. The treatment of systemic vasculitis varies depending on the specific disease but historically has involved initial treatment with high dose glucocorticoids alone or in conjunction with other immunosuppressive agents. Prolonged glucocorticoid treatment is frequently required as maintenance treatment. Patients with small and large vessel vasculitis are at increased risk of fracture. Osteoporosis may occur due to intrinsic factors such as chronic inflammation, impaired renal function and to a large extent due to pharmacological therapy with high dose glucocorticoid or combination treatments. This review will outline the known mechanism of bone loss in vasculitis and will summarize factors attributing to fracture risk in different types of vasculitis. Osteoporosis treatment with specific consideration for patients with vasculitis will be discussed. The use of glucocorticoid sparing immunosuppressive agents in the treatment of systemic vasculitis is a significant area of ongoing research. Adjunctive treatments are used to reduce cumulative doses of glucocorticoids and therefore may significantly decrease the associated fracture risk in patients with vasculitis. Lastly, we will highlight the many unknowns in the relation between systemic vasculitis, its treatment and bone health and will outline key research priorities for this field.
Highlights
Systemic vasculitides frequently present as acute inflammation of various sized blood vessels which can lead to stenosis and aneurysm of the aorta and its branches in large vessel vasculitis (LVV) or necrosis of arterioles, capillaries and venules in small vessel vasculitis (SVV)
Osteoporosis and increased fracture risk are known comorbidities of prolonged and high cumulative GC doses [3, 4]. It is unclear how much the disease process and the inflammation itself contribute to accelerated bone loss or if the increased fracture risk is mainly a result of the negative impact of GC on bone health and muscle strength
Abtahi et al [71] demonstrated in a cohort of patients with rheumatoid arthritis a synergistic effect of GC and Pump Inhibitor (PPI) in increasing fracture risk. These findings may be of particular importance in patients with Giant Cell Arteritis (GCA) and LVV who at disease onset are frequently treated with a combination of high dose GC and PPI
Summary
Systemic vasculitides frequently present as acute inflammation of various sized blood vessels which can lead to stenosis and aneurysm of the aorta and its branches in large vessel vasculitis (LVV) or necrosis of arterioles, capillaries and venules in small vessel vasculitis (SVV). Abtahi et al [71] demonstrated in a cohort of patients with rheumatoid arthritis a synergistic effect of GC and PPI in increasing fracture risk These findings may be of particular importance in patients with GCA and LVV who at disease onset are frequently treated with a combination of high dose GC and PPI. Sarcopenia, measured by reduced hand grip strength, and associated with the type of vasculitis, severity and high C-reactive protein (CRP), seemed to predict increased fracture risk [90] This is in line with previous studies which have shown that change of body composition in form of muscle loss and addition of visceral fat associated with glucocorticoid use increase the risk of osteoporosis and the risk of sustaining fragility fractures [91, 92]. There is some evidence that a lower dose of 5 mg Prednisolone daily can lead to reduced BMD [119], but rates
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