Abstract:
:Despite the improvement in the quality of life of patients with SLE due to scientific and technological advances, SLE remains a disease that over the years may produce irreversible damage to patients. Osteoporosis and secondary bone fractures are two of the major causes of irreparable injury in patients with SLE. Vitamin D insufficiency may play a vital role both in reduced bone mineral density (BMD) and in the appearance of fractures, although its mechanisms of action are still unclear. We performed a systematic review of the literature in order to determine the prevalence and predictors of reduced vitamin D plasma levels, bone loss and the presence of fractures in SLE patients. Our review encompassed all English-language publications using Medline and EMBase electronic databases from their inception (1966 and 1980, respectively) to December 2016. We included all intervention studies and observational studies in which vitamin D plasma levels, BMD and bone loss were measured and applied to patients with SLE. Previous studies suggested an increase in bone loss and fracture in patients with SLE compared with general population and although there is a high prevalence of vitamin D insufficiency in the general population, previous studies had demonstrated lower vitamin D levels in patients with SLE compared to age-matched controls. The etiology of reduced bone mass and reduced vitamin D plasma levels in SLE is multifactorial and includes a variety of intrinsic factors related to the disease itself and treatment side effects. SLE patients are at risk for developing these two comorbidities (reduced vitamin D plasma levels and low BMD) and it is therefore essential to study, monitor, prevent and treat bone metabolism disorders in SLE patients.
journal_name
Autoimmun Revjournal_title
Autoimmunity reviewsauthors
Salman-Monte TC,Torrente-Segarra V,Vega-Vidal AL,Corzo P,Castro-Dominguez F,Ojeda F,Carbonell-Abelló Jdoi
10.1016/j.autrev.2017.09.011subject
Has Abstractpub_date
2017-11-01 00:00:00pages
1155-1159issue
11eissn
1568-9972issn
1873-0183pii
S1568-9972(17)30235-5journal_volume
16pub_type
杂志文章,评审abstract::As autoantibodies bind to target tissues, Fc-region dependent inflammation can induce pain via mediators exciting nociceptors. But recently another possibility has emerged, where autoantibody binding to nociceptors can directly cause pain, without inflammation. This is thought to occur as a result of Fab-region mediat...
journal_title:Autoimmunity reviews
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journal_title:Autoimmunity reviews
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journal_title:Autoimmunity reviews
pub_type: 杂志文章,评审
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journal_title:Autoimmunity reviews
pub_type: 杂志文章,评审
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journal_title:Autoimmunity reviews
pub_type: 杂志文章,评审
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pub_type: 杂志文章,评审
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journal_title:Autoimmunity reviews
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doi:10.1016/j.autrev.2019.05.005
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