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Lipoprotein(a) [Lp(a)] consists of a low-density lipoprotein-like molecule and an apolipoprotein(a) [apo(a)] particle. Lp(a) has been suggested to be an independent risk factor of atherosclerotic cardiovascular disease (ASCVD). Lp(a) plasma levels are considered to be 70–90% genetically determined through the codominant expression of the LPA gene. Therefore, Lp(a) levels are almost stable during an individual's lifetime. This lifelong stability, together with the difficulties in measuring Lp(a) levels in a standardized manner, may account for the scarcity of available drugs targeting Lp(a). In this review, we synopsize the latest data regarding the structure, metabolism, and factors affecting circulating levels of Lp(a), as well as the laboratory determination measurement of Lp(a), its role in the pathogenesis of ASCVD and thrombosis, and the potential use of various therapeutic agents targeting Lp(a). In particular, we discuss novel agents, such as antisense oligonucleotides (ASOs) and small interfering RNAs (siRNAs) that are currently being developed and target Lp(a). The promising role of muvalaplin, an oral inhibitor of Lp(a) formation, is then further analyzed. [ABSTRACT FROM AUTHOR]

ApoB is the main protein of triglyceride-rich lipoproteins and is further divided into ApoB48 in the intestine and ApoB100 in the liver. Very low-density lipoprotein (VLDL) is produced by the liver, contains ApoB100, and is metabolized into its remnants, intermediate-density lipoprotein (IDL) and low-density lipoprotein (LDL). ApoB100 has been suggested to play a crucial role in the formation of the atherogenic plaque. Apart from being a biomarker of atherosclerosis, ApoB100 seems to be implicated in the inflammatory process of atherosclerosis per se. In this review, we will focus on the structure, the metabolism, and the function of ApoB100, as well as its role as a predictor biomarker of cardiovascular risk. Moreover, we will elaborate upon the molecular mechanisms regarding the pathophysiology of atherosclerosis, and we will discuss the disorders associated with the APOB gene mutations, and the potential role of various drugs as therapeutic targets. [ABSTRACT FROM AUTHOR]

Background The incidence of postoperative complications (POC) in patients with Crohn's disease (CD) who undergo intestinal resection is high. The literature provides conflicting data about the risk factors for POC, especially regarding preoperative immunosuppressive medications. The purpose of this study was to evaluate the impact of anti-tumor necrosis factor (TNF) agents on the postoperative course and identify other predictors for POC after ileocolic resection (ICR). Methods This was a single-center retrospective study that included 153 CD patients who underwent elective ICR in a Greek tertiary center between January 2010 and December 2018. Risk factors for overall POC and intra-abdominal septic complications (IASC) were assessed with univariate and multivariate analyses. Results Overall POC and IASC occurred in 35 (22.9%) and 19 (12.4%) patients, respectively. In multivariate analysis, anti-TNF agents (n=61), as either monotherapy or combination treatment, were not associated with an increased risk for overall POC (21.3% vs. 23.9%, P=0.71) or IASC (13.1% vs. 12.0%, P=0.83). Similarly, no combined immunosuppressive regimen significantly correlated with POC. Patients with perianal disease, disease duration >10 years, or previous intestinal resections had significantly higher rates of both overall POC and IASC. In multivariate analysis, previous resection was the only independent risk factor for overall POC (odds ratio [OR] 3.90, 95% confidence interval [CI] 1.38-11.06; P=0.010) and IASC (OR 4.56, 95%CI 1.51-13.77; P=0.007). Conclusions Preoperative administration of anti-TNF agents or other immunosuppressive regimens was not a risk factor for total POC or IASC. A history of previous resection independently correlated with both overall POC and IASC. [ABSTRACT FROM AUTHOR]