Elevated Lp(a) and course of COVID-19: Is there a relationship?

Abstract

Background Lipoprotein (a)–Lp(a) has proinflammatory, prothrombotic and proatherogenic properties and may theoretically influence the course of COVID-19. Objectives The aim of the study was to explore whether patients hospitalized due to COVID-19 with Lp(a) ≥30mg/dl may develop a worse course of the disease, increased incidence of thromboembolic complications, intubation and ICU hospitalization or death. Patients and methods A retrospective analysis was performed of 124 patients hospitalized due to COVID-19 in the Department of Internal Diseases and Clinical Pharmacology between 29 November 2020 and 15 April 2021. The only exclusion criterion was age≥80 years. Patients were divided into two groups: 1. COVID-19 patients with Lp(a) <30mg/dl regarded as not elevated n = 80; 2. COVID-19 patients with Lp(a) ≥30 regarded as elevated n = 44. Results A total of 124 COVID-19 patients were included in the study (66 men and 58 women) with a mean age of 62.8±11 years. COVID-19 patients with elevated Lp(a) level had significantly longer hospitalization time (11 vs. 9.5 days; p = 0.0362), more extensive radiological changes in CT scan (35 vs. 30%; p = 0.0301) and higher oxygen demand on admission (8 vs. 5L/min; p = 0.0428). Elevated Lp(a) was also associated with significantly higher OR for High Flow Nasal Oxygen Therapy (HFNOT) OR = 3.5 95%CI(1.2;8.9), p = 0.0140, Intubation and ICU OR = 4.1 95%CI(1.1;15.2) p = 0.0423, Death OR = 2.8 95%CI(0.9;8.5), p = 0.0409. Conclusions Elevated Lp(a) might be one of the factors which contribute to a more severe course of COVID-19; however, further studies including larger groups of patients are needed.

Lipoprotein(a) Does Not Predict Thrombotic Events and In-Hospital Outcomes in Patients with COVID-19

“…Our observation of a non-significant association between D-dimer and Lp(a) levels is in contrast with the results of two previous studies [26,29]. Indeed, Kaltoft et al previously reported that two-fold higher D-dimer levels were associated with 14% higher Lp(a) levels among 211 patients admitted with COVID-19 [29].…”

“…The lack of an association between Lp(a) and venous thrombotic events observed in our study fits into the context of inconsistent literature data. Pawlos et al reported comparable rates of pulmonary embolism between COVID-19 patients with Lp(a) < 30 mg/dL and those with Lp(a) ≥ 30 mg/dL [26]. In contrast, Nurmohamed et al showed a three-fold higher risk of venous thromboembolism with increasing Lp(a) levels during the hospital stay [28].…”

“…Only a few studies have investigated the association between circulating Lp(a) levels and different biomarkers of systemic inflammation and plasma thrombotic activity in the context of COVID-19, showing inconsistent results [26][27][28][29]. Additionally, data on the association between Lp(a) and either COVID-19 thrombotic complications or COVID-19 in-hospital outcomes are limited and contrasting [26,[28][29][30][31].…”

The 10 essential questions regarding lipoprotein(a)

“…Of note are also the observations that Lp(a) is involved in thrombotic complications of COVID-19 patients [13 ▪ ,14 ▪ ,15].…”

Reply

“…In general, the effect of expression quantitative trait loci (eQTL) is cell-type specific and context-dependent. Previous reports and data from the ImmuNexUT immune cell gene expression database (https://www.immunexut.org) have shown that the risk allele of rs2297550 has a negative eQTL effect on the IKBKE gene in T and B cells, whereas it is associated with higher IKBKE expression in nonstimulated monocytes (3,4). Furthermore, the eQTL effect might be different in individuals with SLE than in healthy controls (5).…”