In this study, we investigated the blood lipid profile in the patients with COVID-19 and explored the underlying factors in its development and their predictive value for the severity of COVID-19. This study was performed on patients who have not yet received treatment for Covid-19 disease. Previous studies suggested dyslipidemia in viral infections [12, 13] and COVID-19 as well [14, 15]. Various studies have been performed on the role of cholesterol in pulmonary function. In this regard, the mechanism by which LDL-C is linked to the cholesterol of surfactant in the lungs of hamsters was investigated. LDL-C and HDL-C of the bloodstream were taken by the lungs through specific receptors, thereby inhibiting the local biosynthesis of pulmonary cholesterol [16]. Other observational studies on animal models have shown that HDL-C acts as the primary source of antioxidant vitamin E for alveolar epithelial cells of type II [17], causing surfactant production by type II cells and the growth of lung fibroblasts [18]. It was shown that, although cholesterol is essential for the function of type II alveolar cells, the pulmonary surfactant and pulmonary phospholipid in a high-cholesterol (2%) diet impair surfactant function. Indeed, increased cholesterol in the diet has been shown to alter the synthesis, composition, and function of surfactants [19].
According to previous findings, dyslipidemia is common in Covid-19 patients. We found that blood levels of HDL-C and LDL-C in the severe and less severe forms of Covid-19 disease have different faces, so that the level of HDL-C, unlike LDL-C, is lower in the less severe form of the disease than in the severe form. However, only the LDL-C variable was recognized as a risk factor. Clinical data show that HDL-C concentration decreases immediately after infection and there is a significant relationship between decreased levels and poor prognosis in infectious diseases [20–22]. It is possible that due to passing the early course of the disease, in this study there was no decrease in HDL-C level in the severe form of the disease. About dyslipidemia in Covid-19 patients, some studies have reported a decrease in lipid profiles as the disease progresses [23, 24]. Contrary to our study, in studies by Li et al. and Wang et al., a decrease in HDL-C levels was observed in severe cases of the disease, and this factor was reported as a risk factor for disease severity [23, 25]. However, some studies are consistent with our results and have reported decreased LDL-C levels as a risk factor for disease severity [26].
We also examined the relationship between comorbidities in the study population and disease severity. Among the factors such as diabetes, hypertension, history of hypercholesterolemia, cancer, autoimmune diseases, and DVT, which were recorded in the patients' clinical file, only the frequency of two variables of diabetes and hypertension in severe and less severe Covid-19 had significant differences but were not considered as a risk factor for disease severity. Recent studies on the risk factors associated with disease severity and poor prognosis support the belief that diabetes [27, 28] and hypertension [29, 30] are the most important risk factors for rapid progression and poor prognosis of Covid-19.
In our study, only 6.1% of the total population had a history of hyperlipidemia and taking statins (including lovastatin, atorvastatin, rosuvastatin, and simvastatin). However, these people, along with those with no previous history of hyperlipidemia, developed dyslipidemia following Covid-19. Following the outbreak of Covid-19, research has also been done on the effect of existing drugs on the virus, and articles have been published on the role of statins in relieving the symptoms of Covid-19 and other viral infections [31–33]. However, there is a dilemma as to what stage of the disease and in which group of COVID-19, statin therapy is beneficial, and what type and the dose of statin to be given [34]. Our study population with a history of hyperlipidemia and taking the Statins are not comparable to recent studies due to its small sample size. Therefore, to prove the role of statins in the Covid-19 disease, more detailed clinical trials with larger sample sizes are needed.
This study was performed in two medical centers dedicated to the admission of patients with Covid-19, and the study population was those who had not yet received treatment for their disease, so what was concluded from the effect of the disease on the lipid profile was without therapeutic intervention. In our clinical centers among Covid-19 patients, request the lipid profile test was not routine; on the other hand, due to the inclusion criteria, the sample size of the study was affected, and this was the limitation of our study.