Tocilizumab in severe COVID-19 – A randomized, double-blind, placebo-controlled trial

Malik, Muhammad Irfan; Zafar, Sardar Al Fareed; Qayyum, Fabiha; Malik, Muna; Asghar, Muhammad Sohaib; Tahir, Muhammad Junaid; Arshad, Ammarah; Khalil, Fatima; Naz, Hafiza Shafia; Aslam, Mudassar; Saleem, Jodat; Wang, Li; Azhar, Mustafa Usman; Naqash, Muhammad; Yousaf, Zohaib

doi:10.1016/j.imj.2022.05.001

Cited by 1 publication

(1 citation statement)

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“…Moreover, they suggest that Lp(a) is unlikely as a possible therapeutic target in COVID-19. It is noteworthy that there is evidence from randomized clinical trials of better in-hospital outcomes in COVID-19 patients treated with either tocilizumab or anti-PCSK9 monoclonal antibodies [49][50][51], which are recognized pharmacological strategies with the ability to reduce Lp(a) levels by ~30% beyond their main therapeutic effects [52,53]; however, no data are available on the relationship between Lp(a) reduction by either tocilizumab or anti-PCSK9 monoclonal antibodies and the clinical outcomes of patients hospitalized for COVID-19 [49][50][51]. Thus, the available intervention studies also do not substantiate any rationale for targeting Lp(a) to improve COVID-19 prognoses.…”

Section: Discussionmentioning

confidence: 99%

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

Bianconi,

Mannarino,

Ramondino

et al. 2023

JCM

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The prothrombotic and proinflammatory properties of lipoprotein(a) (Lp(a)) have been hypothesized to play a role in the pathogenesis of severe COVID-19; however, the prognostic impact of Lp(a) on the clinical course of COVID-19 remains controversial. This study aimed to investigate whether Lp(a) may be associated with biomarkers of thrombo-inflammation and the occurrence of thrombotic events or adverse clinical outcomes in patients hospitalized for COVID-19. We consecutively enrolled a cohort of patients hospitalized for COVID-19 and collected blood samples for Lp(a) assessment at hospital admission. A prothrombotic state was evaluated through D-dimer levels, whereas a proinflammatory state was evaluated through C-reactive protein (CRP), procalcitonin, and white blood cell (WBC) levels. Thrombotic events were marked by the diagnosis of deep or superficial vein thrombosis (DVT or SVT), pulmonary embolism (PE), stroke, transient ischemic attack (TIA), acute coronary syndrome (ACS), and critical limb ischemia (CLI). The composite clinical end point of intensive care unit (ICU) admission/in-hospital death was used to evaluate adverse clinical outcomes. Among 564 patients (290 (51%) men, mean age of 74 ± 17 years) the median Lp(a) value at hospital admission was 13 (10–27) mg/dL. During hospitalization, 64 (11%) patients were diagnosed with at least one thrombotic event and 83 (15%) patients met the composite clinical end point. Lp(a), as either a continuous or categorical variable, was not associated with D-dimer, CRP, procalcitonin, and WBC levels (p > 0.05 for all correlation analyses). In addition, Lp(a) was not associated with a risk of thrombotic events (p > 0.05 for multi-adjusted odds ratios) nor with a risk of adverse clinical outcomes (p > 0.05 for multi-adjusted hazard ratios). In conclusion, Lp(a) does not influence biomarkers of plasma thrombotic activity and systemic inflammation nor has any impact on thrombotic events and adverse clinical outcomes in patients hospitalized for COVID-19.

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