The higher right HIPD values in females having a value of 0.047 might not be as meaningful as the HIPV variations. the bilateral HIPV and the right HIPD. Urine protein amount was negatively correlated with the bilateral HIPV and HIPD. Hydroxychloroquine (HCQ) showed a protecting effect on right HIPV. In conclusion, we found that the early hippocampal atrophy could happen before obvious neuropsychiatric manifestations and might be associated with SLE disease activity and organ damages. Early detection and treatment of hippocampal damage might prevent the progression to NPSLE. More studies are needed to fully understand the underlying mechanisms of hippocampal atrophy in SLE. 1. Intro Systemic lupus erythematosus (SLE) is an autoimmune disease with multiorgan involvement. It is definitely characterized by SMN high titers of various serum antibodies focusing on nuclear or cytoplasmic antigens. Glucocorticoids (GC) and immunosuppressive providers (ISA) are used to help individuals reach the prospective of remission or low disease activity. Hydroxychloroquine (HCQ), cyclophosphamide (CTX), and Mycophenolate Mofetil (MMF) are widely used ISA (1). The central nervous system (CNS) is commonly involved in SLE (2, 3). Mind atrophy has been recognized in SLE individuals using several neuroimaging techniques. It is often associated with medical manifestations in SLE individuals and sometimes even in individuals without obvious CNS signs and symptoms (4, 5). The hippocampus is located in the temporal lobe of the brain and plays an important part in learning and memory space processes. Hippocampal atrophy was found in SLE individuals and was related to cognitive dysfunction, disease duration, and history of CNS manifestations (6). Magnetic resonance imaging (MRI) is one of the most commonly used techniques to evaluate mind abnormalities including mind atrophy. Many individuals with slight cognitive impairment have normal standard MRI findings because standard MRI is nonspecific or not sensitive enough for delicate constructions like hippocampus (4, 6). SLE individuals without major neuropsychiatric manifestations are usually regarded as non-NPSLE individuals. In our earlier study, we have found that the white matter volume (WMV) of the non-NPSLE patient group was significantly less than that of healthy control (HC) group and that ISA treatment might have a protecting effect on WMV (7). Furthermore, in another study, we also found that specific autoantibodies, such as anti-cardiolipin (aCL) antibodies, might contribute to the reduction of gray matter denseness (GMD) and white matter Minoxidil (U-10858) denseness (WMD) in non-NPSLE individuals. ISA treatment also showed effects in preventing the reduction of GMD and WMD (8). It has been reported that irregular hippocampal structural changes could be found in non-NPSLE individuals with normal standard mind MRI (9, 10). These results prompted our desire for exploring hippocampal structural changes in non-NPSLE individuals by using volumetric MRI. The Minoxidil (U-10858) underlying mechanisms of hippocampal involvement in SLE individuals remain unclear. Numerous autoantibodies including aCL antibodies and anti-NR2 subtype of the N-methyl-D-aspartate receptor (NMDAR) antibodies were considered to play important functions in the pathogenesis of neuropsychiatric SLE Minoxidil (U-10858) (NPSLE) (8, 11, 12). However, few studies were focused on the relationship between autoantibodies and hippocampal Minoxidil (U-10858) atrophy. Therefore, we carried out this study to explore hippocampal structural changes in non-NPSLE individuals and their possible associations with medical characteristics including specific autoantibodies, disease activity, and emotional status as well as Minoxidil (U-10858) treatment regimens. 2. Material and Methods 2.1. Subjects SLE individuals were recruited from your inpatient and outpatient facilities of Division of Rheumatology and Immunology of First Affiliated Hospital of Kunming Medical University or college, a member of the Chinese SLE Treatment and Study Group (CSTAR), from September of 2012 to September of 2014. Each participant went through a standardized protocol and was evaluated from the same investigator throughout the study. All participants experienced received total and detailed description of the study and had given written educated consent before enrollment into the study. This study protocol was authorized by the Institutional Review Table of Kunming Medical University or college, Yunnan Province, P. R. China (ClinicalTrials.gov: “type”:”clinical-trial”,”attrs”:”text”:”NCT00703742″,”term_id”:”NCT00703742″NCT00703742). The inclusion criteria included (1) individuals diagnosed as SLE according to the 1997 revised American College of Rheumatology (ACR) criteria for the classification of SLE (13), (2) subjects between the age groups of 18 and 60, and (3) subjects willing to participate in this study and give written educated consent. The exclusion criteria included (1) individuals fulfilling the ACR diagnostic criteria for rheumatoid arthritis, systemic sclerosis, Sj?gren’s syndrome (main or secondary), or other connective cells diseases and drug-induced SLE; (2) individuals with neurological disorders that would affect the brain structure (e.g., history of head stress, Parkinson’s disease, or seizures); (3) individuals with major psychiatric manifestations, such as obvious disorganized.