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The immunomodulatory effects of vitamin D have been extensively studied in the context of autoimmunity. Multiple studies have demonstrated a high prevalence of vitamin D deficiency in autoimmune diseases. Recently, a possible protective role of vitamin D in autoimmunity has been described; however, this function remains controversial. Few studies have investigated the role of vitamin D in patients with Sjögren syndrome (SS). In this review, we compiled the main features of SS pathogenesis, the vitamin D immunomodulatory effects and the possible interaction between both. Data suggests that vitamin D may play a role in the SS pathogenesis. In addition, vitamin D low levels have been found in SS patients, which are associated with extra-glandular manifestations, such as lymphoma or neuropathy, suggesting a possible benefit effect of vitamin D in SS.

P-glycoprotein (Pgp) is a transmembrane protein of 170 kD encoded by the multidrug resistance 1 (MDR-1) gene, localized on chromosome 7. More than 50 polymorphisms of the MDR-1 gene have been described; a subset of these has been shown to play a pathophysiological role in the development of inflammatory bowel disease, femoral head osteonecrosis induced by steroids, lung cancer and renal epithelial tumors. Polymorphisms that have a protective effect on the development of conditions such as Parkinson disease have also been identified. P-glycoprotein belongs to the adenosine triphosphate binding cassette transporter superfamily and its structure comprises a chain of approximately 1280 aminoacid residues with an N-C terminal structure, arranged as 2 homologous halves, each of which has 6 transmembrane segments, with a total of 12 segments with 2 cytoplasmic nucleotide binding domains. Many cytokines like interleukin 2 and tumor necrosis factor alpha increase Pgp expression and activity. Pgp functions as an efflux pump for a variety of toxins in order to protect particular organs and tissues as the central nervous system. Pgp transports a variety of substrates including glucocorticoids while other drugs such as tacrolimus and cyclosporine A act as modulators of this protein. The most widely used method to measure Pgp activity is flow cytometry using naturally fluorescent substrates such as anthracyclines or rhodamine 123. The study of drug resistance and its association to Pgp began with the study of resistance to chemotherapy in the treatment of cancer and antiretroviral therapy for human immunodeficiency virus; however, the role of Pgp in the treatment of systemic lupus erythematosus, rheumatoid arthritis and psoriatic arthritis has been a focus of study lately and has emerged as an important mechanism by which treatment failure occurs. The present review analyzes the role of Pgp in these autoimmune diseases.

Background: Patients with acute cutaneous lupus erythematosus (ACLE) usually have systemic manifestations and there is a strong association between ACLE and systemic lupus erythematosus (SLE) involvement. However, there is scarce information on the differences in the systemic manifestations when compared with subacute cutaneous lupus erythematosus (SCLE) and chronic cutaneous lupus erythematosus (CCLE). Objective: To analyse and compare the prevalence and characteristics of the main clinical and immunological manifestations of patients with ACLE, who were initially attending a Department of Dermatology, with respect to those with SCLE and CCLE. Methods: A total of 38 patients with ACLE were studied. The clinical and serological characteristics of all the patients were collected in a chart review. These patients were compared to 112 patients with SCLE and 158 with CCLE that were previously reported. Results: Patients with ACLE had a higher prevalence of mucous membrane ulcers (p=0.012), livedo reticularis (p=0.036), vasculitis (p=0.030), nephropathy (p=0.025) and serositis (p=0.036) compared with patients with SCLE. Patients with ACLE also had a higher frequency of livedo reticularis (P=0.001), mucous membrane ulcers (P