Bone mineral density and vitamin D status in systemic lupus erythematosus (SLE): A systematic review

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.

Introduction

Management of SLE, a systemic autoimmune disease with a wide range of clinical expressions, is often complicated. Despite recent scientific and technological advances and improved patient survival, SLE is still a dangerous disease that can cause irreversible damage to patients [1]. Osteoporosis and secondary bone fractures are two important 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 [2]. The exact degree to which inflammatory activity per se, versus vitamin D plasma levels or BMD, contributes to the presence of fractures remains an open question. Preventing these two comorbidities, insufficient vitamin D levels and reduced BMD, can facilitate clinical improvement in patients with SLE, a condition in which the preservation of numerous factors related to quality of life is of the utmost importance [3].

The immunomodulatory role of vitamin D have been described in the context of autoimmunity and multiple studies have demonstrated a high prevalence of vitamin D deficiency in other autoimmune diseases as rheumatoid arthritis [4], systemic sclerosis [5] and sjögren syndrome [6].

Osteoporosis is a condition of decreased bone mass density that increases the bone fracture risk. The continual resorption and re-deposition of bone mineral, or bone re-modeling, are intimately tied to the pathophysiology of osteoporosis. Previous studies have suggested an increase in bone loss and fracture in patients with SLE compared with general population [7]. Moreover, although there is a high prevalence of vitamin D insufficiency in the general population, previous studies have demonstrated lower vitamin D level in patients with SLE than age-matched controls [8], [9]. The origin of these two conditions is multifactorial and the objective of this systematic literature review is to describe the prevalence and predictors of these two comorbidities vis-à-vis the natural history of this disease.