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| ORIGINAL ARTICLE |
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| Year : 2022 | Volume
: 8
| Issue : 1 | Page : 51-55 |
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Serum Lipids in COVID-19: A Case–Control Comparative Study from a Tertiary Care Center, New Delhi, India
Anita Rani1, Omkar K. Choudhari1, Rohit Kumar2, Paarth Bhatia3
1 Department of Biochemistry, Vardhman Mahavir Medical College and Safdarjung Hospital, New Delhi, India
2 Department of Respiratory Medicine, Vardhman Mahavir Medical College and Safdarjung Hospital, New Delhi, India
3 Himalayan Institute of Medical Sciences, Dehradun, India
| Date of Submission | 24-Jul-2021 |
| Date of Decision | 08-Sep-2021 |
| Date of Acceptance | 09-Feb-2022 |
| Date of Web Publication | 29-Apr-2022 |
Correspondence Address:
Dr. Anita Rani
Director Professor and Unit Head Clinical Biochemistry, Department of Biochemistry, Vardhman Mahavir Medical College and Safdarjung Hospital, New Delhi-110029
India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/mamcjms.mamcjms_84_21
Background: The coronavirus disease 2019 (COVID-19) pandemic still remains as an evolving condition. The available literature suggested that the level of various biochemical parameters was found to be associated with severity of the infection and can be used as markers of severity in patients with COVID-19. However, speculation for association of hypolipidemia with COVID-19 severity was also postulated. Hence, present study is conducted to find association of lipid profile with the severity of the disease. Materials and methods: A case–control study was carried out in the months of August to October 2020 in Vardhman Mahavir Medical College and Safdarjung Hospital, New Delhi, India. Cases included 103 severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) real-time polymerase chain reaction (RT-PCR)-positive admitted patients (52 with moderate disease and 51 with severe disease), whereas control included 100 SARS-CoV-2 RT-PCR-negative patients visiting outpatient clinic of Department of Respiratory Medicine of the hospital. Total cholesterol, triglycerides, high-density lipoprotein cholesterol (HDL-C), and low-density lipoprotein cholesterol (LDL-C) values of participants were evaluated and compared among severe COVID-19 cases and controls as well as in moderate and severe COVID-19 diseased. Results: Among 103 patients, 52 patients had moderate disease and 51 had severe COVID-19 on admission. The mean serum total cholesterol level in cases was 145 ± 64.21 and 161.43 ± 43.48 mg/dL in controls (P = 0.035). Mean serum triglyceride level was 167.22 ± 99.04 mg/dL in COVID-19 cases and 141.73 ± 71.76 mg/dL in control (P = 0.037). Mean serum LDL-C level was 93.77 ± 38.68 mg/dL in cases and 110.74 ± 43.11 mg/dL in control (P = 0.004). Mean serum HDL-C level was 29.61 ± 11.71 mg/dL in cases and 42.35 ± 13.87 mg/dL in control population (P < 0.001). Conclusion: Hypolipidemia was found to be significantly associated with COVID-19 infection in the current study. There was no statistically significant difference found in patients with moderate and severe COVID-19 in this small group study.
Keywords: Biochemical, cholesterol, COVID-19, HDL-C, LDL-C
How to cite this article:
Rani A, Choudhari O, Kumar R, Bhatia P. Serum Lipids in COVID-19: A Case–Control Comparative Study from a Tertiary Care Center, New Delhi, India. MAMC J Med Sci 2022;8:51-5 |
How to cite this URL:
Rani A, Choudhari O, Kumar R, Bhatia P. Serum Lipids in COVID-19: A Case–Control Comparative Study from a Tertiary Care Center, New Delhi, India. MAMC J Med Sci [serial online] 2022 [cited 2023 Jun 5];8:51-5. Available from: https://www.mamcjms.in/text.asp?2022/8/1/51/344353 |
| Introduction | |  |
World health organization (WHO) in March 2020 declared coronavirus disease 2019 (COVID-19) as a pandemic.[1] It has reached all over the world claiming many lives. Until the writing of this manuscript, more than a million people have reportedly died and this pandemic still has maintained its presence around the world.[2] COVID-19 has made a significant impact on our already overstretched health-care infrastructure. Hence, classifying patients according to the severity is necessary for the allocation of requisite resources. Various prognostic markers are speculated in the COVID-19, segregating the disease into mild, moderate, and severe types apart from triage on the basis of clinical presentation. Many times, disease clinical manifestation lags behind the biochemical changes and hence it is imperative to look after these early changes from the baseline and predict disease severity for timely triage of the patients and treatment modification which would not only decrease mortality and also shorten the hospital stay.
The presentation of the disease may be with fever, dry cough, diarrhea, and anosmia, whereas substantial patients remain asymptomatic.[3] Many patients present without any significant hypoxic symptoms with low oxygen saturation (SpO2) on pulseoximetry denoted as “happy hypoxia” and clinical deterioration is followed by a long latency period.[4] These cases if segregated early on the basis of biochemical parameters would certainly help in timely management.
As the origin of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), every measure was carried out to curb the infection and optimize the use of available resources in an already overwhelmed health-care system. The morbidity and mortality among different ethnicities are different; however, as per the biochemical parameters are concerned, available literature showed changes in these parameters in different population across the continents and their levels corresponded to the severity of infection.[5],[6] Additionally, hypolipidemia was observed associated with the severity of the infection in Chinese studies.[7] Hypolipidemia was also reported in the patients requiring intensive care unit admission in a European study.[8] Keeping in view, the present study was carried out to explore the role of lipids in Indian COVID-19 patients and their association with the severity of the disease if any.
| Materials and Methods | | |
Study design and participants
A single-centered, observational case–control study was carried out in the months of August to October 2020. A total of 103 patients with SARS-CoV-2 real-time polymerase chain reaction (RT-PCR) positive, moderate to severe COVID-19, admitted to Safdarjung Hospital, New Delhi, India, were taken into the study. All the enrolled patients were SARS-CoV-2 RT-PCR positive from nasopharyngeal swab/oropharyngeal swab. Demographic information, clinical characteristics including previous comorbidities and treatment were obtained from each patient. Moderate COVID-19 was defined in an adult as clinical signs of pneumonia with SpO2 ≥ 90% on ambient air with no concomitant features of severe pneumonia, whereas severe COVID-19 was defined as clinical signs of pneumonia such as fever, cough with expectoration, chest pain, loss of appetite with respiratory distress along with respiratory rate of ≥30/minute and SpO2 <90% according to WHO classification.[9] The participants were divided into moderate and severe disease according to the above-mentioned criteria on admission. Inclusion criteria include patient admitted in hospital with RT-PCR positive from nasopharyngeal swab/oropharyngeal swab and giving consent. Demographic characteristics along with clinical presentation are summarized in [Table 1]. Patients not giving consent were excluded from the study. Controls were age-matched SARS-CoV-2 RT-PCR-negative patients visiting outpatient clinic of Department of Respiratory Medicine of the hospital and with no history of intake any lipid-lowering drugs. Demographic profile including their clinical characteristic on presentation is summarized in [Table 2]. | Table 1 Baseline, clinical profile with laboratory findings of 103 participants with coronavirus disease 2019
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 | Table 2 Baseline, clinical profile with laboratory findings of 100 controls
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Data collection
About 2 mL of the blood sample was taken from participants on admission/outpatient clinic visit. Lipid profile [total cholesterol, triglycerides (TGs), high-density lipoprotein cholesterol (HDL-C), and low-density lipoprotein cholesterol (LDL-C)] along with other biochemical tests was performed and data were collected. The samples were analyzed with AU-680 automatic analyzer along with maintaining requisite quality control. Lipid profile of participants was compared among cases and controls along with moderate and severe COVID-19 diseased participants.
Statistical analysis
Values of total cholesterol, TG, HDL-C, and LDL-C were obtained at admission and compared with control and in patient with moderate and severe COVID-19 with Mann–Whitney U test. Nonparametric data were represented as median and interquartile range, and categorical data were presented as a percentage. Demographic and clinical parameters among median and severe disease patients were statistically compared with Fisher exact test. P-value of less than 0.05 was considered significant. All data were analyzed by SPSS version 21.0 (IBM Corp., USA).
| Results | | |
The analysis included 103 patients with 52 having moderate COVID-19 disease and 51 participants had severe disease. The mean age of the moderate group was 41.68 ± 6.80 years. The mean age of the severe group was 58.28 ± 9.58 years. The baseline characteristic of participants is summarized in [Table 1]. Fisher exact test was used to get the relationship between the values obtained in moderate and severe diseased patients. The participants’ age group in moderate and severe disease did not differ significantly (P > 0.05). Diabetes mellitus (DM) was the most common morbidity among participants followed by hypertension (HTN) and coronary artery disease (CAD) in moderately diseased participants, whereas HTN was the most common comorbidity in severe disease followed by DM and CAD. These comorbidities when compared among the moderate and severe groups were found statistically insignificant (HTN: P = 0.42; DM: P = 0.05; CAD: P = 1.0). Malaise was the most common symptom on presentation in patients of both the groups (moderate and severe disease) followed by fever, cough, and expectoration and sore throat, whereas anosmia was the least common symptom in the participants. Overall, no significant difference (P > 0.05) was observed in presenting symptoms among cases of moderate and severe disease patients.
Lipid profile in severe COVID-19 cases and controls
The mean age group for control was 49.13 ± 16.40 years. A T test was used to compare lipid profile of COVID-19 with the control group. There was significant difference in lipid levels among the severe COVID-19 case and control groups. The mean serum total cholesterol level in cases was 145 ± 64.21 mg/dL and 161.43 ± 43.48 mg/dL in controls (P = 0.035). Mean serum TG level was 167.22 ± 99.04 mg/dL in COVID-19 cases, whereas 141.73 ± 71.76 mg/dL in control (P = 0.037). Mean serum LDL-C level was 93.77 ± 38.68 mg/dL in cases, whereas 110.74 ± 43.11 mg/dL in control (P = 0.004). Mean serum HDL-C level was 29.61 ± 11.71 mg/dL in cases, whereas 42.35 ± 13.87 mg/dL in control population (P < 0.001), suggesting association of hypolipidemia with COVID-19 patients [Table 3]. | Table 3 Comparison of serum lipid profile among patients with severe COVID-19 and controls
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Lipid profile in moderate and severe disease
A T test was used to compare the serum lipid profile in patients with moderate and severe COVID-19 which did not show any significant difference. Mean serum total cholesterol level in moderate disease patients when compared with severe disease patients was 147.33 ± 74.41 mg/dL versus 142.75 ± 52.46 mg/dL, respectively (P = 0.719). Mean serum TG level was 167.67 ± 87.43 mg/dL in COVID-19 moderate cases, whereas 166.76 ± 110.51 mg/dL in severe cases (P = 0.963). Mean serum LDL-C level was 94.46 ± 42.64 mg/dL in moderate cases, whereas 93.06 ± 34.61 mg/dL in severe subjects (P = 0.855). Mean serum HDL-C level was 28.63 ± 11.20 mg/dL in moderate cases, whereas 30.61 ± 11.15 mg/dL in severe cases (P = 0.373) [Table 4], suggesting the serum lipid profile (all the parameters) levels do not correspond to severity of the disease in this small group study group. | Table 4 Serum lipid profile of patients with moderate and severe coronavirus disease 2019
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| Discussion | | |
In our study, the comparison of the lipid profile of patients with COVID-19 and controls revealed a statistically significant lower value in the cases for serum total cholesterol, serum LDC-C, serum HDL-C; however, no significant difference was observed among the moderate and severe groups. Previous studies have also observed a low level of total cholesterol, HDL-C, and LDL-C in patients with COVID-19, when compared with normal controls. Some studies have also reported a correlation between inflammatory markers and the lipid profile parameters.[7],[8],[10]
The COVID-19-induced coagulopathy is one of the important factors associated with prolonged hospital stay and mortality. Endothelial dysfunction is associated with coagulopathy.[11] The role of dyslipidemia in endothelial dysfunction has been known for a long time along with the role of HDL-C acting as a protective barrier.[12],[13] In our study, we did not find any significant association between HDL-C in assigned groups (moderate and severe) but when values were compared with control, the significantly low value was observed in cases (P < 0.001). Our findings are similar to the study, on the role of HDL-C in the coagulopathy, probably contributing to the coagulopathy by activating the coagulation cascade, decrease in clot lysis along with the decreased release of nitric oxide, increasing platelet activation and subsequent thrombosis.[14],[15] The COVID-19 coagulopathy, however, involves cascades of events in the formation of thrombus/embolism and is due to multifactorial causation, including cytokine storm-mediated endothelial dysfunction and not limited to dyslipidemia.[16]
A meta-analysis involving seven studies with 6922 patients also concluded dyslipidemia as a risk factor for causing severe COVID-19 disease; however, many of the included studies documented very few events of dyslipidemia.[17] A study from New York, also included in this meta-analysis, taking into account 5279 COVID-19-positive patients with 1714 patients of dyslipidemia showed a protective role of hyperlipidemia for hospital admission.[18] This study, however, included those patients as well who had mild disease. In our study, only moderate and severe disease individuals were included along with the normal controls, where the comparison between lipid parameters among assigned groups showed hypolipidemia in cases.
The role of cytokine storm leading to severe COVID-19 has been observed in studies. The systemic inflammation brings remodeling of HDL-C, apart from decreasing levels of apolipoprotein A1.[19] Further, low level of HDL-C causes increased oxidative stress further accelerating inflammatory cascade. HDL has antiatherogenic, antithrombotic, and immune-modulatory function.[20] In our study, HDL-C levels found not to be associated with the disease severity; however, lipid studies pertaining to COVID-19 are limited, and our sample size was smaller; hence, probably results are contrary to other mentioned studies. Large sample size should be taken to understand possible role of lipoproteins in COVID-19 inflammation.
Viral diseases cause low lipid profile, due to the involvement of liver per se infecting hepatocytes, causing liver parameter abnormalities.[21] Secondly, the role of interleukin-1β (IL-1β), tumor necrosis factor-α, and IL-6 inflammatory markers in the dyslipidemia is also known and may contribute to our findings.[22]
Our study has some limitations. Serum lipid levels were performed at once on admission only in patients admitting with moderate or severe disease. Their role in case of transformation of moderate disease to severe form was not studied. Patient’s baseline lipid profile was not known and few patients in case groups were on statins and β-blockers, attributing to bias in our study.
| Conclusion | | |
Hypolipidemia found to be significantly associated with COVID-19 infection. There was no statistically significant difference found in patients with moderate and severe COVID-19 in this small group study.
Acknowledgment
The authors thank Dr Charanjeet Kaur, Head of Department Biochemistry, Vardhman Mahavir Medical College and Safdarjung Hospital, New Delhi for her guidance during the project work.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
| References | | |
| 1. | |
| 2. | WHO Coronavirus Disease (COVID-19) Dashboard [Internet]. Covid19.who.int. 2020. Available at https://covid19.who.int/. Accessed September 3, 2020.  |
| 3. | |
| 4. | González-Duarte A, Norcliffe-Kaufmann L. Is ’happy hypoxia’ in COVID-19 a disorder of autonomic interoception? A hypothesis. Clin Auton Res 2020;30:331-3. |
| 5. | Wang D, Li R, Wang J et al. Correlation analysis between disease severity and clinical and biochemical characteristics of 143 cases of COVID-19 in Wuhan, China: a descriptive study. BMC Infect Dis 2020;20:519. https://doi.org/10.1186/s12879-020-05242-w |
| 6. | Cai Q, Huang D, Yu H et al. COVID-19: abnormal liver function tests. J Hepatol 2020;73:566-74. |
| 7. | Wei X, Zeng W, Su J et al. Hypolipidemia is associated with the severity of COVID-19. J Clin Lipidol 2020;14:297-304. |
| 8. | Tanaka S, De Tymowski C, Assadi M et al. Lipoprotein concentrations over time in the intensive care unit COVID-19 patients: results from the ApoCOVID study. PLoS One 2020;15:e0239573. |
| 9. | |
| 10. | Hu X, Chen D, Wu L, He G, Ye W. Declined serum high density lipoprotein cholesterol is associated with the severity of COVID-19 infection. Clin Chim Acta 2020;510:105-10. |
| 11. | Walborn A, Rondina M, Mosier M, Fareed J, Hoppensteadt D. Endothelial dysfunction is associated with mortality and severity of coagulopathy in patients with sepsis and disseminated intravascular coagulation. Clin Appl Thromb Hemost 2019;25:1076029619852163. |
| 12. | Merkovska L, Jedlickova L, Jackova L et al. Lipid lowering therapy and endothelial function in patients with metabolic syndrome. Interdiscip J Microinflammation 2015;1:128. |
| 13. | Kim JA, Montagnani M, Chandrasekran S, Quon MJ. Role of lipotoxicity in endothelial dysfunction. Heart Fail Clin 2012;8:589-607. |
| 14. | Van der Stoep M, Korporaal SJ, Van Eck M. High-density lipoprotein as a modulator of platelet and coagulation responses. Cardiovasc Res 2014;103:362-71. |
| 15. | Brodde M, Korporaal S, Herminghaus G et al. Native high-density lipoproteins inhibit platelet activation via scavenger receptor BI. Atherosclerosis 2011;215:374-82. |
| 16. | Jose RJ, Manuel A. COVID-19 cytokine storm: the interplay between inflammation and coagulation. Lancet Respir Med 2020;8:e46-7. |
| 17. | Hariyanto TI, Kurniawan A. Dyslipidemia is associated with severe coronavirus disease 2019 (COVID-19) infection. Diabetes Metab Syndr 2020;14:1463-65. |
| 18. | Petrilli CM, Jones SA, Yang J et al. Factors associated with hospital admission and critical illness among 5279 people with coronavirus disease 2019 in New York City: prospective cohort study. BMJ 2020;369:m1966. |
| 19. | Jahangiri A. High-density lipoprotein and the acute phase response. Curr Opin Endocrinol Diabetes Obes 2010;17:156-60. |
| 20. | Tabet F, Rye KA. High-density lipoproteins, inflammation and oxidative stress. Clin Sci (Lond) 2009;116:87-98. |
| 21. | Quaye O, Amuzu BG, Adadey SM, Tagoe EA. Effect of hepatitis B virus (HBV) infection on lipid profile in Ghanaian patients. Virology (Auckl) 2019;10:1178122-19827606. |
| 22. | Sorokin A, Karathanasis S, Yang Z, Freeman L, Kotani K, Remaley A. COVID-19 Associated dyslipidemia: implications for mechanism of impaired resolution and novel therapeutic approaches. FASEB J 2020;34:9843-5. |
[Table 1], [Table 2], [Table 3], [Table 4]
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