👤 Fatma B A Mokhtar

Lipoprotein(a) [Lp(a)] is a genetically determined, independent risk factor for atherosclerotic cardiovascular disease (ASCVD), unaffected by conventional lipid-lowering therapy. This study assessed the prevalence of elevated Lp(a) in a large, multiethnic cohort in Dubai, United Arab Emirates (UAE), analyzed its distribution across ethnicities, and evaluated its independence from low-density lipoprotein cholesterol (LDL-C). In a single-center multiethnic cohort study, 746 consecutive patients from Mediclinic Parkview Hospital, Dubai, were included. Serum Lp(a) was measured using a standardized immunoturbidometric assay. Positive Lp(a) was defined as ≥75 nmol/L. Levels were stratified by ethnic subgroups and categorized based on ESC/EAS quartiles and risk thresholds (≥105 nmol/L for high risk; >190 nmol/L for very high risk). The correlation between Lp(a) and directly measured LDL-C was assessed using Spearman's rank correlation in both patients receiving optimal lipid-lowering therapy and in those not receiving therapy. The prevalence of positive Lp(a) levels (≥75 nmol/L) was 30.2 %. At higher thresholds, 13.4 % had high-risk levels (≥105 nmol/L) and 9.9 % had very high-risk levels (>190 nmol/L). Ethnic variations were notable: South Asians (32.4 %) and White/Europeans (32.1 %) had the highest prevalence, while East Asians had the lowest (21.6 %) but the highest median level (200.5 nmol/L). Crucially, there was no correlation between Lp(a) and treated LDL-C in patients on optimal lipid-lowering therapy (Spearman's rho = 0.07, p = 0.38). We identified a high prevalence of elevated Lp(a) in a multiethnic cohort in Dubai, with nearly a quarter at high or severe risk. This risk is entirely independent of LDL-C, revealing a significant hidden burden not captured by standard lipid panels. These findings support integrating Lp(a) screening into regional cardiovascular prevention protocols. Show less

Intestinal cholesterol absorption varies widely between individuals, which may translate into differences in responsiveness to cholesterol-lowering drugs or diets. Therefore, understanding the importance of genetic variation on cholesterol absorption rates and the complex intestinal cholesterol network is important. Based on a systematic review, genetic variants in seven genes (ABCG5, ABCG8, ABO, APOE, MTTP, NPC1L1, and LDLR) were identified that were associated with intestinal cholesterol absorption. No clear associations were found for variants in APOA4, APOB, CETP, CYP7A1, HMGCR, SCARB1, SLCO1B1, and SREBF1. The seven genes were used to construct an intestinal cholesterol absorption network. Finally, a network with fifteen additional genes (APOA1, APOA4, APOB, APOC2, APOC3, CETP, HSPG2, LCAT, LDLRAP1, LIPC, LRP1, OLR1, P4HB, SAR1B, and SDC1) was generated. The constructed network shows that cholesterol absorption is complex. Further studies are needed to validate and improve this network, which may ultimately lead to a better understanding of the wide inter-individual variability in intestinal cholesterol absorption and the development of personalized interventions. Show less