👤 Saeed Aslani

Elevated levels of lipoprotein(a) [Lp(a)] are increasingly recognized as an independent risk factor for cardiovascular diseases (CVDs). This systematic review and meta-analysis aimed to evaluate the impact of lipid apheresis therapy on serum Lp(a) levels in a wide array of disorders, particularly CVDs. Following PRISMA guidelines, we searched PubMed, Scopus, and Web of Science databases up to May 2025. Studies reporting pre- and post-treatment Lp(a) levels in participants undergoing lipid apheresis were included. A random-effects model was used when heterogeneity was significant. Subgroup and meta-regression analyses were conducted to explore potential sources of heterogeneity. A total of 43 publications comprising 67 studies with 2466 participants were analysed. Lipid apheresis significantly reduced serum Lp(a) levels (SMD = -1.52; 95% CI = -1.76 to -1.29; P < 0.001). Subgroup analyses confirmed significant reductions across various methods of Lp(a) detection, disease backgrounds, and initial Lp(a) levels. One-session lipid apheresis studies (n = 6) also demonstrated a significant reduction (SMD = -1.51; 95% CI = -1.72 to -1.29; P < 0.001). Meta-regression suggested that publication year and disease background contributed to heterogeneity. Lipid apheresis is effective in significantly lowering serum Lp(a) concentrations across a range of patient groups and treatment modalities. These findings support the therapeutic role of lipid apheresis in managing elevated Lp(a). Show less

Ankylosing spondylitis (AS) is a common complex inflammatory disease; however, up to now distinct genes with monogenic pattern have not been reported for this disease. In the present study, we report a large Iranian family with several affected members with AS. DNAs of the three affected and two healthy cases were chosen for performing whole-exome sequencing (WES). After several filtering steps, candidate variants in the following genes were detected: RELN, DNMT1, TAF4β, MUC16, DLG2, and FAM208. However, segregation analysis confirmed the association of only one variant, c.7456A>G; p.(Ser2486Gly) in the RELN gene with AS in this family. In addition, in silico predictions supported the probable pathogenicity of this variant. In this study, for the first time, we report a novel variant in the RELN gene, c.7456A>G; p.(Ser2486Gly), which completely co-segregates with AS. This association suggests potential insights into the pathophysiological bases of AS and it could broaden horizons toward new therapeutic strategies. Show less

The footprint of cytokines is evident in almost every biological process, such as development, as well as the pathogenesis of the different diseases, immune responses to pathogens, etc. These small proteins are categorized into different functional classes; for instance, they can play a pro-inflammatory or anti-inflammatory role in different situations, or they can confer a polarization to the immune system. Interleukin (IL)-27 is a member of the IL-12 family. Antigen-presenting cells are the primary source of IL-27 production, which exerts its effects by bindings to the IL-27 receptor expressed on the surface of target cells. Interaction of IL-27 and IL-27 receptor leads to activation of the JAK-STAT and p38 MAPK signaling pathways. Most studies focused on the inflammatory effects of this cytokine, but gradually anti-inflammatory effects were also revealed for this cytokine, which changed the traditional perception of the function of this cytokine. The functionality of IL-27 in the pathogenesis of rheumatic diseases has been attributed to a double-blade sword. Hence, novel therapeutic approaches have been devised targeting IL-12 family that has been accompanied with promising results. In this review, we focused on the inflammatory and anti-inflammatory properties of IL-27 in different autoimmune rheumatologic diseases and its plausible therapeutic potentials. Show less