key: cord-319851-mhnp42xo
authors: Cao, Xiaoling; Wang, Hui; Tan, Wenbin
title: Authors’ response to letter by Fogacci, Borghi and Cicero, “Misinterpreting data in lipidology in the era of COVID-19”
date: 2020-07-09
journal: J Clin Lipidol
DOI: 10.1016/j.jacl.2020.07.005
sha: 
doc_id: 319851
cord_uid: mhnp42xo

nan

While we appreciate the comments from Drs. Fogacci, Borghi and Cicero on our publication "Hypolipidemia is associated with the severity of COVID-19", 1 we disagree on their opinions. Our data has been properly interpreted and our conclusions are supported by much emerging evidence from other studies. [2] [3] [4] [5] Those in our cohort of 597 COVID-19 inpatients were diagnosed and had lipid profiles taken at the time of admission. Patients were categorized according to stage of disease course based on symptomatic severity. Therefore, the lipid profiles taken at the same time represented the corresponding disease courses. Furthermore, in a longitudinal study at another hospital in Wuhan, we examined lipid profiles from inpatients (n=21) before viral infection, on admission, and during the course of their illness. 2 Levels of LDL-c, HDL-c and TC decreased at the time the patients were hospitalized, remained low during the disease progression, and returned to baseline in patients who were discharged, but decreased continuously in patients who did not survive. 2 In addition, a parallel study (n=71) carried out in Wenzhou, China, found similar patterns with LDL-c, HDL-c and TC levels in patients. 5 They also monitored lipid profiles daily for one ICU patient for 16 days 5 and obtained data consistent with our study. 2 Collectively, this evidence demonstrates that decreases in LDL-c levels are associated with severity of COVID-19 and reflect the disease course.

Either genetic or acquired factors (e.g., viral infections) can cause hypolipidemia. Currently, there is no consensus of clear threshold to define hypolipidemia. Therefore, we followed the guidelines in the literature and set the median value of TC (174 mg/dL) of normal control subjects in Wuhan to define hypolipidemia for this cohort; this was a reasonable assessment. The concept of "hypolipidemia" was appropriately expanded and adapted in our report to describe the decreased cholesterol levels in COVID-19 patients.

We are well aware of the concerns raised by Drs. Fogacci, Borghi and Cicero about the potential effects of lipid-lowing medications being given routinely to those patients with cardiovascular disorders (CVD) or diabetes on their LDL-c levels on admission. In U.S., Italy and other nations, as many as half or more of patients with CVD or diabetes would be taking statins prior to onset of COVID-19 and many of them would continue until the time of hospital admission. However, prevalent use of lipid-lowering medications such as statins in China has been very low, even in people with CVD or diabetes, about 1.0~1.5%. 6, 7 Inpatients of this cohort were not given statins by physicians during their COVID-19 treatments in our hospital. We performed an oral survey of our frontline colleagues (n=12) in other hospitals in Wuhan; none of them prescribed statins for their COVID-19 inpatients, not even for patients with CVD, hypertension or diabetes. We also conducted a follow-up phone inquiry with patients (or their families) in our small cohort study. 2 We confirmed that only three out of 21 patients (14%) routinely self-administered a lipid-lowering medication prior to onset of COVID-19; a similar or lower percentage is expected to apply to the cohort of 597 patients. Furthermore, under the standard care, the patients showed decreased LDL-c levels on admission and elevated LDL-c levels after they recovered. 2 Therefore, the contribution of self-administered lipid-lowering drugs was very minimal, if there was any, to the hypolipidemia in this cohort. We do acknowledge that a follow-up lipid test on patients will be needed to further confirm their lipid dynamics. More importantly, emerging evidence has shown that SARS-CoV-2 has direct impacts on the downregulation of lipid metabolism related proteins and pathways, leading to dyslipidemia. 3, 4 Therefore, hypolipidemia in COVID-19 patients most likely results from SARS-CoV-2 infection and associated hyper-inflammation, not lipid-lowering medications.

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