https://www.selleckchem.com/products/Aloxistatin.html The exact mechanism by which inflammation decreases HDL levels is not defined, but decreases in apoA-I production and lecithin cholesterol acyltransferase (LCAT) activity, as well as increased serum amyloid A (SAA), endothelial lipase and secretory phospholipase A2 activity (PLA2) could all contribute. In addition, during inflammation multiple changes in HDL structure occur, leading to alterations in HDL function which may be implicated in the CVD complications of SLE. Therefore, this review will aim to identify the mechanisms implicated in HDL dysfunction which occurs in SLE patients.Objective To estimate the economic burden of systematic lupus erythematous (SLE), stratified by disease severity, in commercially- and Medicaid-insured US populations. Methods Adults (≥18 years) with SLE treated with antimalarials, selected biologics, immunosuppressants, and systemic glucocorticoids (2010-2014) were identified within the commercial and Medicaid insurance IBM MarketScan® databases (index date = first SLE medication claim). Both cohorts were stratified into mild (receiving antimalarial or glucocorticoid monotherapy ≤5 mg/day) versus moderate/severe SLE (receiving glucocorticoids >5 mg/day, biologic, immunosuppressant, or combination therapy) during a 6-month exposure period. All-cause healthcare utilization and costs were evaluated during the 12 months following the exposure period. Results Among 8231 commercially-insured patients, 32.6% had mild and 67.4% had moderate/severe SLE by our definition. Among 802 Medicaid-insured patients, 25.2% had mild and 74.8% had moderate/severe SLE. Adjusted mean total healthcare costs, excluding pharmacy, for moderate/severe SLE patients were higher than for mild SLE patients in the commercially-insured ($39,021 versus $23,519; p less then 0.0001) and Medicaid-insured populations ($56,050 versus $44,932; p = 0.06). In both SLE severity populations total unadjusted costs were signifi