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Research Article | Volume 2 Issue 1 (Jan-June, 2021) | Pages 1 - 6
The Effects of COVID-19 on Some Liver Enzymes Patients at Al Furat General Hospital in Baghdad
 ,
 ,
 ,
 ,
1
Director of Baghdad Al-Karkh Health Department
2
MSc biochemistry, PhD clinical biochemistry
3
BSc.chemistry MSc students in biochemistry
4
BSc biology MSc Molecular Biology
5
BMT, MSc immunology, PhD student virology
Under a Creative Commons license
Open Access
Received
Jan. 3, 2021
Revised
Feb. 9, 2021
Accepted
March 19, 2021
Published
April 30, 2021
Abstract

Coronavirus has been recognized in October, 2019, but the first infection with the virus in Iraq was identified in the province of Najaf, about 160 km south of Baghdad, on February 24, 2020 and aim of the research Knowing the extent of coronavirus effect on liver function, especially liver enzymes, which play a vital role in the vital processes in the human body 60 samples were collected at Al-Furat General Hospital from patients with COVID-19, of which 38 samples were for men, and 22 samples were for women; the blood was separated to extract serum by the centrifuge, then the results were obtained by an Automatic Biochemistry Analyzer device with Accent-200 and (GPT, ALP, TSB, GOT enzymes) were identified for comparisons between control and patients Through taking a section, analyses were performed for 60 patients, average age was 46, and ages were between 23-75 years. The values of the statistical analyses were clarified when compared to healthy people: the nature of the relationship where it was shown that there is a negative relationship in the amounts of GOT, GPT, ALP Proven by sig, which is higher than 0.05 and research shows that Coronavirus has actual effects on liver function, and the majority of patients have high GOT, GPT ALP due to a clear impact of COVID-19 on the liver enzymes.

Keywords
INTRODUCTION

Quality of Coronavirus was recognized in 2019, and the first case was discovered in China in the Wuhan region. When reading the direct impact of these viruses, a significant impact on the work of the liver was found [1]. The occurrence of functional difference and not only this but there was an effect on the clinical characteristics of patients with COVID -19 [2]. This clinical effect was not recognized to this day, and dealing with it has become something vague and not clear-cut and through multiple studies [3] and then proving that liver disease is present in abundance in people with the disease. If we examine it further, we'll find that SARS-Cov2 is similar in the genetic chain to SARS-Cov. Studies related to this subject published in 2004 show that 60% of people with the disease face a risk of liver damage [4].The symptoms of COVID19 were not limited only to the liver, but the effects included all parts of the body COVID-19 patients, including the lungs, heart, and kidneys [5]. So that it can damage the intestine and formation Infections in the heart, and this was evidenced by analyzing the urine [6]. This indicates that there was an early presence of kidney damage. Liger said that initial data also shows that 14 to 30% of ICU patients lose kidney function and need dialysis or continuous treatment [7]. The disease can also harm the heart, as doctors in China and New York reported inflammation Heart muscle and arrhythmias, which can lead to cardiac arrest in patients with COVID-19 .Its effect extends to the digestive system, causing disruption in liver function and an increase in its enzymes. It also poses a high risk to liver patients to join the list of groups most vulnerable to severe complications from the virus [3]. As for cirrhosis, which occurs, or its impact on people who already or previously have liver diseases, including functional disorders caused by the disease [8].

 

Clear evidence of attacking it directly on the part, or it may consist of these functional disorders or infections in the liver as a result of the use of medications such as antagonists Vitality and increase the risk to people who already have a chronic disease or have liver damage in this way will lead to complications depending on the type of patient the liver and as for people who suffer from a fatty liver disease where most patients suffer from heart disease and blood pressure which makes them more vulnerable to health problems when infection with the virus [9]. The symptoms of Coronavirus contribute to high levels of the liver and that 35% of patients have had a rise in the levels of liver enzymes and found the effect of coronavirus on the liver as form where the patient who suffers from high levels of enzymes and increased activity in a virus B will be attacked by Coronavirus. In this situation, it is violent for the patient due to significant weakening of the immune system [10]. As for the patients who have liver transplantation, they do not suffer from any of the many problems when infected with the virus as a result of using anti-immunosuppressive drugs [11].

MATERIALS AND METHODS

Clinical in Vitro Diagnostic Reagent kit

 

  • GPT For in vitro diagnostics use R1: 1x30mL R2: 1x8ML

  • GOT For in vitro diagnostics use R1: 1x30mL R2: 1x8ML

  • ALP For in vitro diagnostics use R1: 1x30mL R2: 1x8ML

  • TSB For in vitro diagnostics use R1: 1x24mL R2: 1x5ML

  • TSB For in vitro diagnostics use R1: 1x24mL R2: 1x5ML 

  • TSB: 10 μl serum

  • ALP: 4 μl serum GPT = 15 μl serum GOT = 10 μl serum

 

Separation

The device separates the blood components to obtain serum and shown in figure 3 device centrifuge

In these tables that are performed in the results between patients with high levels in some liver enzymes (GPT, TSB, GOT, ALP) and the control group of COVID-19 we notice that the percentage increases by 33% in patients with COVID-19 and the highest rate achieved by 108 if compare enzymes in elevated liver levels [12].

        

The results also showed that a 5% rate indicates a severe reduction in enzyme levels for patients with COVID-19 patients [13]. In general, we note that In the case of the COVID-19, enzyme levels increase by 15% to 45%, and liver infections are significantly more common among patients [14].

 

 

Figure 1: Automatic Biochemistry Analyzer / For Clinical Diagnostic / Benchtop Accent-2000

 

 

Figure 2: Syringe, pipette and Gel Tube

 

Table 1: Shown Results of Patients COVID-19

PAgeGander

Tsb (1.70-21)

Μmol/L

Gpt (5-

41) U/L

Got (8-40)U/LAlp (56-119)U/L
p164M9.232643147
p262F14.29263787
p348M12.7486845
p446M12414865
p531M10.61703380
p630M13.5593860
p742M12402766
p847M83530123
p944M12423048
p1031F9.82272860
p1135M12293437
p1234M10332886
p1335M8493273
p1425F11.27121749
p1553F6.13263573
p1625M14.8102148
p1748F7.642238141
p1823M6.11322087
p1970M14.076634128
p2048M12966858
p2160M14.1655675
p2275M6.61195099
p2342F14.3554556
p2436F6.1892047
p2552M6.67172144
p2660M9.71353870
p2775F23362759
p2851M12302766
p2935M101087.945
p3031M103337106
p3138M8.6333080
p3218F6101644
p3335M14663770
p3433M12472766
p3519F7.74152455
p3630F8.261631244
p3740M11.21039246
p3829M13.8182271
p3930M6.22533588
p4040M12132188
p4125M19.5292952
p4240M12.3603175
p4350M34.8152486
p4444M13.9362464
p4527M27352556
p4635F12.5212276
p4750F17.6132272
p4830F9.492270
p4916F4.61120114
p5054M126747113
p5129M15.3413557
p5225M10142667
p5345F7.62935124
p5439F12.9112858
p5549F11.31020111
p5633F9192365
p5729F6.11321111
p5850F22183861
p5970F19.5485749
p6034M10354174

 

Table 2: Results of Healthy People

pAGETSB (1.70-21) μmol/LGPT (5-41) U/LGOT (8-40)U/LALP (56-119) U/L
p1407.32811.173
p25510.625.29.970
p3707.940.214.788
p466123311.690
p567153721.559
p666204840110

 

Table 2: Continue 

p7451233.331.4118
p8541441.320.160
p97711.73316.467
p108310321864
p114412.1192277
p12238.53427.587.4
p131318.927.92266.9
p142817.3293159.9
p153211191160.4
p166899.81667
p17451434.222.680
p18446.7239.988.7
p1943101222.973.4
p20401121.53370.7

 

 

Figure 3: Device Centrifuge

 

 

Figure 4: Shown the Rate the Rate of Decline and Rise of GOT in Patients CO-19

 

 

Figure 5: Shown the Rate the Rate of Decline and Rise of TSB in Patients CO-19

 

 

Figure 6: shown the Rate the Rate of Decline and Rise of GPT in Patients CO-19S

 

 

Figure 7: Shown the Rate the Rate of Decline and Rise of GOT in Patients CO-19

 

 

Figure 8: Shown the Rate the Rate of Decline and Rise of GOT in Patients CO-19

 

 

Figure 9: Shows the Rate of Decline and Rise of TSB in Patients CO-19

 

 

Figure 10: Shown the Rate the Rate of Decline and Rise of GPT in Patients CO-19

 

 

Figure 11: Frequency Distribution of Liver Function Test Parameters in COVID-19 Patients

 

Table 3: Correlations between Control and COVID-19 Patients in GOT

Correlations
 

GOT

Healthy

GOT Co19

 

 

Spearman's rho

GOT healthyCorrelation1-0.216
Sig. (2-tailed) 0.406
 2020
 GOT CO-19Correlation-.2161
Sig. (2-tailed)0.406 
N2060

 

Table 4: Correlations between Control and COVID-19 Patients in GPT Enzymes

Correlations
 

GPT

healthy

GPT CO-19
GPT healthySpearman's rhoCorrelation10.184
Sig. (2-tailed) 0.436
N2020
GPT CO-19Spearman's rhoCorrelation0.1841
Sig. (2-tailed)0.436 
N2060

 

Table 5: Correlations between Control and COVID-19 Patients in ALP Enzymes

Correlations
 ALP healthyALP CO-19
ALP healthySpearman's rho Correlation1-0.096
Sig. (2-tailed) 0.689
N2020
ALP CO-19Spearman's rho Correlation-.0961
Sig. (2-tailed)0.689 
N2060

Correlation is significant at the 0.05 level (2-tailed)

DISCUSSION

In this research, values were found through TSB, GPT, GOT, ALP analyzes and evaluation of the necessary analysis to the affected person COVID-19 Patients, After that, healthy people were compared, where clinical results were demonstrated by the presence of symptoms appearing on the patient in the beginning [15-16].

 

As the current results showed that there are significant differences between persons infected with COVID 19 Patients and healthy people and that there is no direct effect to the following analyzes GPT, GOT, ALP, and TSB on the person's age according to what was shown to us in the outcome. Still, it is difficult to neglect this effect [16]. Relationship It is non-existent, but it is present, and its existence cannot be denied by TSB analysis. Most of the results were normal, and this is what corresponds to it in healthy people, but a percentage was found that represented one value for a person aged 50 years, and the rate was (31.8) [17-18].

 

Correlation for GOT between COVID - 19 Patients and Healthy People

Testing the relationship between GOT between COVID 19 Patients with healthy people noted the Correlation Coefficient is negative and this shows an inverse relationship between GOT between COVID19 Patients with healthy people and that the significance or (p-value) Sig. (2-tailed) was equal to0.406 and when compared to the level of significance (0.05) we notice that it is smaller than the level of significance and this means that no relationship.

 

Correlation for GPT between COVID - 19 Patients and Healthy People

Through statistical analysis Test the relationship between GPT healthy people with GPT CO-19 Note this Correlation coefficient is negative and this shows an inverse relationship between Test for the importance of (p-value) (Two-way) It was equal to 0.436 and when compared to the importance level (0.05) We note that it is greater than the level of significance and this means that there is not relationship between GPT healthy people with GPT CO-19 patients(Table 1-2).

 

Correlation for ALP between CO- 19and Healthy People

Statistical analysis demonstrated an inverse relationship between ALP between CO- 19and healthy People by taking 60 samples from patients and 20 from healthy, and the statistical indication of the quality of this relationship showed that it was (p- value) 0.689, i.e. it is greater than 0.05 We note that it is greater than the level of significance and this means that there is not relationship between ALP healthy people with ALP CO-19 patients ( Table 3-5).

CONCLUSION

The relationship between GOT, GPT, and ALP analysis was found between infected and healthy people As for TSB, the significant difference between the two groups was not [19] (Figure1-8).

 

The effects of GOT on infected people caused major damage to the liver and were among the main factors leading to liver damage about with COVID- 19 Patients [20-21].

 

According to the results that proved that age was not one of the main factors, but rather a contributing factor to the increase in poor health for the patient if he suffers from other diseases [19,22] (Figure 9-12).

 

If a person who suffers from COVID-19 is healthy from other diseases and contains immunity here, age does not become a contributing factor [23-24].

REFERENCE
  1. Hui, D.S. et al. “The Continuing 2019-nCoV Epidemic Threat of Novel Coronaviruses to Global Health—The Latest 2019 Novel Coronavirus Outbreak in Wuhan, China.” International Journal of Infectious Diseases, vol. 91, 2020, pp. 264–266.

  2. Gorbalenya, A.E. et al. “Severe Acute Respiratory Syndrome-Related Coronavirus: The Species and Its Viruses–A Statement of the Coronavirus Study Group.” 2020.

  3. Chen, N. et al. “Epidemiological and Clinical Characteristics of 99 Cases of 2019 Novel Coronavirus Pneumonia in Wuhan, China: A Descriptive Study.” The Lancet, vol. 395, no. 10223, 2020, pp. 507–513.

  4. Hughes, J.M. et al. “Transmission of Human Infection with Nipah Virus.” Clinical Infectious Diseases, vol. 49, no. 11, 2009, pp. 1743–1748.

  5. Wichmann, D. et al. “Autopsy Findings and Venous Thromboembolism in Patients with COVID-19: A Prospective Cohort Study.” Annals of Internal Medicine, vol. 173, no. 4, 2020, pp. 268–277.

  6. Tang, N. et al. “Abnormal Coagulation Parameters Are Associated with Poor Prognosis in Patients with Novel Coronavirus Pneumonia.” Journal of Thrombosis and Haemostasis, vol. 18, no. 4, 2020, pp. 844–847.

  7. Chen, G. et al. “Clinical and Immunological Features of Severe and Moderate Coronavirus Disease 2019.” The Journal of Clinical Investigation, vol. 130, no. 5, 2020, pp. 2620–2629.

  8. Diao, B. et al. “Reduction and Functional Exhaustion of T Cells in Patients with Coronavirus Disease 2019 (COVID-19).” Frontiers in Immunology, vol. 11, 2020, p. 827.

  9. Ianiro, G. et al. “Screening of Faecal Microbiota Transplant Donors during the COVID-19 Outbreak: Suggestions for Urgent Updates from an International Expert Panel.” The Lancet Gastroenterology & Hepatology, vol. 5, no. 5, 2020, pp. 430–432.

  10. Bermingham, A. et al. “Severe Respiratory Illness Caused by a Novel Coronavirus, in a Patient Transferred to the United Kingdom from the Middle East, September 2012.” Eurosurveillance, vol. 17, no. 40, 2012, p. 20290.

  11. Geller, C. et al. “Human Coronaviruses: Insights into Environmental Resistance and Its Influence on the Development of New Antiseptic Strategies.” Viruses, vol. 4, no. 11, 2012, pp. 3044–3068.

  12. Calderwood, A.H. et al. “ASGE Guideline for Infection Control during GI Endoscopy.” Gastrointestinal Endoscopy, vol. 87, no. 5, 2018, pp. 1167–1179.

  13. Hamming, I. et al. “Tissue Distribution of ACE2 Protein, the Functional Receptor for SARS Coronavirus: A First Step in Understanding SARS Pathogenesis.” The Journal of Pathology, vol. 203, no. 2, 2004, pp. 631–637.

  14. Xiao, F. et al. “Evidence for Gastrointestinal Infection of SARS-CoV-2.” Gastroenterology, vol. 158, no. 6, 2020, pp. 1831–1833.

  15. Chau, T.N. et al. “SARS-Associated Viral Hepatitis Caused by a Novel Coronavirus: Report of Three Cases.” Hepatology, vol. 39, no. 2, 2004, pp. 302–310.

  16. Su, L. et al. “The Different Clinical Characteristics of Coronavirus Disease Cases between Children and Their Families in China–The Character of Children with COVID-19.” Emerging Microbes & Infections, vol. 9, no. 1, 2020, pp. 707–713.

  17. Huang, C. et al. “Clinical Features of Patients Infected with 2019 Novel Coronavirus in Wuhan, China.” The Lancet, vol. 395, no. 10223, 2020, pp. 497–506.

  18. Riley, S. et al. “Transmission Dynamics of the Etiological Agent of SARS in Hong Kong: Impact of Public Health Interventions.” Science, vol. 300, no. 5627, 2003, pp. 1961–1966.

  19. Zhang, C. et al. “Liver Injury in COVID-19: Management and Challenges.” The Lancet Gastroenterology & Hepatology, vol. 5, no. 5, 2020, pp. 428–430.

  20. Yi, Y. et al. “COVID-19: What Has Been Learned and to Be Learned about the Novel Coronavirus Disease.” International Journal of Biological Sciences, vol. 16, no. 10, 2020, p. 1753.

  21. van Deursen, V.M. et al. “Co-Morbidities in Heart Failure.” Heart Failure Reviews, vol. 19, no. 2, 2014, pp. 163–172.

  22. Cowling, B.J. and G.M. Leung. “Epidemiological Research Priorities for Public Health Control of the Ongoing Global Novel Coronavirus (2019-nCoV) Outbreak.” Eurosurveillance, vol. 25, no. 6, 2020, p. 2000110.

  23. Mehta, P. et al. “COVID-19: Consider Cytokine Storm Syndromes and Immunosuppression.” Lancet, vol. 395, no. 10229, 2020, p. 1033.

  24. Monteleone, G. et al. “Preventing COVID-19-Induced Pneumonia with Anticytokine Therapy.” The Lancet Rheumatology, vol. 2, no. 5, 2020, pp. e255–e256.

     

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