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.

It has been previously reported that vitamin D deficiency is more prevalent among SLE patients than in the general population. We sought to determine the prevalence of vitamin D insufficiency and deficiency and their related factors, its relationship to SLE symptoms and disease activity on a group of supplemented and non-supplemented female SLE patients from the Mediterranean region. We performed a cross-sectional study including female SLE patients who regularly attended the outpatient Lupus Unit at Parc de Salut Mar-IMAS in Barcelona, from January 2012 to May 2014. Collected data were sociodemographics, vitamin D supplementation, fatigue degree visual analog scale, pharmacological treatment, main SLE serological markers, indexes, scales and plasma levels of 25-hydroxyvitamin D. One hundred and two consecutive female SLE patients were included. Vitamin D overall insufficiency and deficiency were exhibited by 46 and 22.5 % of patients, respectively. Vitamin D insufficiency was found in 50 % of supplemented and 60 % of non-supplemented patients. Among non-supplemented female SLE patients, it was found that patients with vitamin D insufficiency showed more fatigue (p = 0.009) and received more oral corticosteroids (p = 0.02) than those with normal levels. Patients with vitamin D insufficiency (supplemented and non-supplemented) received more oral corticosteroids than those without insufficiency (p = 0.008). Vitamin D insufficiency is highly prevalent among female SLE patients, even in southern regions. Non-supplemented female SLE patients showed more fatigue and received more oral corticosteroids than those with normal levels of vitamin D. These data were not found in supplemented patients although having a high prevalence of vitamin D insufficiency (up to 50 %). Further studies with longer follow-up and larger population are needed to confirm our observations.

Objective To describe long-term clinical and serological outcome in all systemic lupus erythematosus (SLE) domains in SLE patients with hand arthralgia (HA) and joint ultrasound (JUS) inflammatory abnormalities, and to compare them with asymptomatic SLE patients with normal JUS. Methods SLE patients with HA who presented JUS inflammatory abnormalities ('cases') and SLE patients without HA who did not exhibit JUS abnormalities at baseline ('controls') were included. All SLE clinical and serological domain involvement data were collected. End follow-up clinical activity and damage scores (systemic lupus erythematosus disease activity index (SLEDAI), Systemic Lupus International Collaborating Clinics/American College of Rheumatology (SLICC/ACR)) were recorded. JUS inflammatory abnormalities were defined based on the Proceedings of the Seventh International Consensus Conference on Outcome Measures in Rheumatology Clinical Trials (OMERACT-7) definitions. Statistical analyses were carried out to compare 'cases' and 'controls'. Results A total of 35 patients were recruited. The 'cases', n = 18/35, had a higher incidence of musculoskeletal involvement (arthralgia and/or arthritis) through the follow-up period (38.9% vs 0%, p = 0.008) and received more hydroxychloroquine (61.1% vs 25.0%, p = 0.034) and methotrexate (27.8% vs 0%, p = 0.046) compared to 'controls', n = 17/35. Other comparisons did not reveal any statistical differences. Conclusions We found SLE patients with arthralgia who presented JUS inflammatory abnormalities received more hydroxychloroquine and methotrexate, mainly due to persistent musculoskeletal involvement over time. JUS appears to be a useful technique for predicting worse musculoskeletal outcome in SLE patients.

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