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 Table of Contents  
ORIGINAL ARTICLE
Year : 2022  |  Volume : 36  |  Issue : 3  |  Page : 129-133

SARS-CoV-2 and Helicobacter pylori and some hematological parameters: A case–control study


1 Department of Medical Laboratory Technology, College of Medical Technology, The Islamic University, Najaf; Department of Microbiology, Al-Shomali General Hospital, Babylon Health Directorate, Babylon University, Babylon, Iraq
2 Department of Pharmacy, Al-Mustaqbal University College, Babylon University, Babylon, Iraq
3 Department of Medical Microbiology, College of Medicine, Babylon University, Babylon, Iraq
4 Department of Seventh Life Laboratory, Marjan Hospital, Babylon, Iraq

Date of Submission26-Jul-2022
Date of Decision27-Nov-2022
Date of Acceptance13-Dec-2022
Date of Web Publication25-Feb-2023

Correspondence Address:
Dr. Falah Hasan Obayes Al-Khikani
Department of Medical Laboratory Technology, College of Medical Technology, The Islamic University, Najaf
Iraq
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/jms.jms_55_22

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  Abstract 


Background: The SARS-CoV-2 associated with bacterial infection represents a serious public health challenge. Recently, there is a remarkable increase in the number of researches that confirms the effect of Helicobacter pylori on pulmonary diseases.
Aim: The goal of this research was to see how H. pylori affected the presentation of COVID-19 infections as a prospective risk factor.
Materials and Methods: This research was conducted in Babylon, Iraq, from January 1, 2022, to March 5, 2022. A total of 180 people were engaged in this study, with 90 patients identified with SARS-CoV-2 by polymerase chain reaction testing and 90 people serving as a control group. Antibody screening assays on blood samples were used to look for antibodies against H. pylori. The samples were processed for complete blood count and ABO blood group.
Results: COVID-19 infection was more frequent in females than in males, especially between 31 and 45 years. When compared to healthy people, COVID-19 patients had a higher white blood cell count (P = 0.0001) and a lower lymphocyte count (P = 0.0001). H. pylori and COVID-19 have been found to have a strong relationship, especially in females. When comparing patients to healthy people, blood group A is the most common.
Conclusion: People with H. pylori infections are considerably more sensitive to COVID-19 than people without H. pylori infections (P = 0.011). In combination with SARS-CoV-2, IgG for H. pylori might be a risk factor.

Keywords: ABO blood group, anti-Helicobacter pylori IgG antibody, coinfection, coronavirus, COVID-19, Helicobacter pylori, SARS-CoV-2


How to cite this article:
Al-Khikani FH, Al-Hussainy AD, Hussein AZ, Alshamary RS. SARS-CoV-2 and Helicobacter pylori and some hematological parameters: A case–control study. J Med Soc 2022;36:129-33

How to cite this URL:
Al-Khikani FH, Al-Hussainy AD, Hussein AZ, Alshamary RS. SARS-CoV-2 and Helicobacter pylori and some hematological parameters: A case–control study. J Med Soc [serial online] 2022 [cited 2023 Apr 1];36:129-33. Available from: https://www.jmedsoc.org/text.asp?2022/36/3/129/370592




  Introduction Top


According to the current research, people with preexisting medical disorders or illnesses, particularly noncommunicable diseases, are more susceptible to SARS-CoV-2 infection, as well as having a higher chance of being hospitalized and dying from severe SARS-CoV-2 infections.[1],[2],[3]

Helicobacter pylori is a Gram-negative, spiral-shaped, microaerophilic bacterium that causes gastritis and peptic ulcers, as well as being a major risk factor for stomach cancer. It infection occurs at a young age, and the illness's progress is unpredictable, relying not just on the bacteria's inherent pathogenic qualities,[4] as well as factors related to the host.[5] A faulty immune response to the bacterium and its poisons might be dangerous. The number of studies looking into the impact of H. pylori on pulmonary disorders has lately increased.[6]

Bacteria reach the lungs by toxins, aspiration of contaminated gastrointestinal (GI) contents, and inhalation of airborne particles. Increased production of inflammatory mediators and endothelial dysfunction indicators in respiratory system cells may be linked to lung injury.[7] Chronic activation against H. pylori and its toxins has been postulated to play a role in the etiology of lung and GI malignancies; nevertheless, research has failed to offer a conclusive conclusion about this involvement.[8]

The relevance of pathogenic factors, particularly the toxin VacA and CagA, was discovered in studies looking into the involvement of H. pylori in acute lung illnesses. H. pylori VacA was found in human lung tissues, causing vacuolation and the generation of Interleukin 8 (IL-8) and interleukin 6 (IL-6) by airway epithelial cells; VacA may play a role in the pathophysiology of respiratory illnesses and/or interstitial pneumonia caused by collagen vascular disease.[7]

Because the lungs and the cells that make up the digestive system have the same embryological origin, persistent H. pylori infection in the gastric epithelium may have systemic effects and lead to tissue destruction in locations other than the main infection organ, such as the lungs. H. pylori may colonize the oral cavity, according to a large body of evidence. As a result, upper respiratory system mucosa colonization has been linked to the beginning of disorders such as sinusitis, adenotonsillar hypertrophy, pharyngitis, and laryngitis. Furthermore, investigations have emphasized the involvement of stomach aspiration in H. pylori-infected patient's airway inflammation and lung illnesses.[9]

Blood groups are hereditary characteristics that differ between populations, most likely as a result of both founder effects and natural selection. H. Pylori and Plasmodium falciparum infection are two well-known instances of a relationship between blood types and infectious disease susceptibility. Antigens of the blood groups can impact disease susceptibility through a variety of processes, including acting as receptors or decoys for infectious organisms and influencing immune responses through anti-ABO antibodies.[10] The goal of this research was to see if there was a link between the presence of H. pylori IgG antibody and COVID-19 as a prospective risk factor.


  Materials and Methods Top


On January 1, 2022, this study gets permission from the Ethical Committee of the Babil Health Directorate. Moreover, the patient's verbal consent was acquired before sampling. During the sampling, precautions were taken in consideration to guarantee the safety of all the participants. This work was also performed by the Iraqi Ministry of Health's Ethics Committee and goes ahead all known national rules. This study was approved by the Faculty of Medicine, Babylon University, Iraq 1756 on December 17, 2021.

A total number of 180 persons were evolved in this work. The current research is a case–control study that included COVID-19-infected patients from Babylon's COVID-19 Isolation Center (n = 90) from January 2022 to March 2022. A control group of (90) seemingly healthy people of similar ages and sexes. COVID-19-infected patients were confirmed by polymerase chain reaction.

Venous blood samples (5 mL) were obtained from 180 persons involved in this study and then split into two portions (ethylenediaminetetraacetic acid tubes and plane tubes). The first part of each collected blood sample was subjected to a complete blood count test, and the other part was used to estimate serum anti-H. pylori antibody (anti-HP IgG antibody) test. Anti-HP IgG was diagnosed in the serum of the study groups using serum antibody detection kits (Abon Biopharm, China), the procedure was applied, and results were calculated as indicated in the manufacturer's instructions. Anticoagulated blood samples from both patients and the control group are processed through a hematology autoanalyzer to assess total counts of white blood cells (WBCs), particularly neutrophils (Minami-Ku, Kyoto, Japan).


  Results Top


COVID-19 is more frequent in females 52 (57.8%) than in males 38 (42.2%). The age of patients ranged from 16 to 87 years old with a mean of 47.11 ± 19.78. Age group of 31–45 was the most prevalent group infected with COVID-19 (37.8%) [Table 1].
Table 1: Gender and age distribution in the patient group

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H. pylori IgG antibodies were associated with 40 (44.44%) patients compared to the control group 28 (31.11%). A significant difference was observed (P = 0.011). From 90 COVID-19 patients, females are more infected with H. pylori 32 (35.5%), whereas males were just 14 (15.5%) had positive IgG antibodies in their serum significantly at (P = 0.018). Hence, females are more susceptible to both COVID-19 and H. pylori compared to males.

Compared to the healthy group at a mean of 8.19 ± 2, the patients with COVID-19 have a high rate of WBC with a mean of 11.18 ± 5.63 (P = 0.0001). As well as, the granulocyte ratio was also highly increased in patients at 73.18 ± 13.16 than the control group at 62.18 ± 9.02 (P = 0.0001). While the lymphocyte ratio was very low in patients 19.05 ± 12.31 compared to healthy persons 29.72 ± 9.11 with high significance (P = 0.0001).

The ABO blood group of 180 involved in this study has been detected from the 90 normal people displayed a percentage distribution of 27.8%, 22.2%, 6.7%, and 43.3% for blood type A, B, AB, and O, respectively, whereas the 90 patients showed an ABO distribution of 37.8%, 28.9%, 8.9%, and 24.4% for A, B, AB, and O, respectively. The predominant of blood group A in patients was significantly higher than that in normal people (P < 0.001). The proportion of blood group O in the patient's group was significantly lower than that in normal people (P < 0.001). These results refer to a significantly raised risk of blood group A for COVID-19 and decreased risk of blood group O for this disease [Figure 1].
Figure 1: Blood group distribution among patients and healthy groups

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  Discussion Top


The COVID-19 pandemic is a global health emergency, and a detailed study of its pathophysiology and relationship to other illnesses is required to fully comprehend risk factors and therapy.[11],[12] The widespread COVID-19 pandemic and the significant global incidence of chronic H. pylori infection in humans may constitute an important inflammation-prone crossroads between two infectious human illnesses that should not be overlooked.[13]

This study revealed that COVID-19 is more frequent in females 57.8% than in males 42.2%. The age of patients ranged from 16 to 87 years old with a mean of 47.11 ± 19.78. The age group of 31–45 was the most prevalent group infected with COVID-19 (37.8%). This is agreed and disagreed with some previous studies.[14],[15],[16]

H. pylori infection is a major starting and promoting step in gastric carcinogenesis because it leads to the creation of a continuous state of inflammation, which can lead to gland atrophy, intestinal metaplasia (IM), and gastric cancer. According to the timeline outlined by Correa. Due to the migration of intestine-specific cell types, including enterocytes, into the gastric lining, the increased expression of SARS-CoV-2 entry receptors angiotensin-converting enzyme-2 (ACE-2) and TMPRSS2 in the affected gastric mucosa in H. pylori-infected people is particularly interesting in this context.[17] Furthermore, gastric mucosa with IM generally occurs in conjunction with parietal cell loss, increasing intragastric juice pH. As a result, the SARS-CoV-2 virus is not inactivated by stomach acid with a low pH. Furthermore, some data shows that H. pylori infection is linked to a wide range of extragastric disorders, including neurological, dermatological, cardiovascular, metabolic, ophthalmic, allergy, renal, and respiratory diseases, all of which are essential in the context of COVID-19.[18]

The new coronavirus-2019 (COVID-19) interacts with ACE-2 receptors to enter the cell. Because these receptors are widely expressed in the colon, COVID-19 may cause GI symptoms during the illness. H. pylori is known to increase the expression of ACE-2 receptors in the GI tract.[19]

H. pylori is thought to have the potential to boost the expression of ACE-2 receptors in the gastro-tract cell, making it a vulnerable organ for SARS-CoV-2 replication. About 7% of COVID-19 hospitalized patients have Mycoplasma pneumoniae, Pseudomonas aeruginosa, and Haemophilus influenzae bacterial coinfections.[20] Bacterial and/ or fungal coinfections, such as bloodstream bacteremia and urinary tract infection, are possible in COVID-19 patients.[21],[22]

Acute pancreatitis may be present in COVID-19. Although it should be kept as a high-index clinical suspicion if abdominal pain is reported. Three confirmed cases of COVID-19, who developed acute pancreatitis without any other obvious discernible cause. One aged 48-year-old male presented with severe abdominal pain with mild symptoms of COVID-19 and was later diagnosed with acute pancreatitis. Another 40-year-old male with moderate COVID-19 developed acute pancreatitis and was treated successfully. The third 58-year-old patient with control diabetes and severe COVID-19 developed acute necrotizing pancreatitis. From these cases, COVID-19-associated GI was detected.[23]

As previously stated, there are 34 recognized human blood type systems and hundreds of different blood group antigens and alleles. Antigen expression differences across blood groups can enhance or reduce a host's susceptibility to a variety of illnesses. ABO antibodies are part of the innate immune system's defense against some bacterial pathogens and enveloped viruses, and they may have a role in the etiology and personal vulnerability to some illnesses, such as COVID-19.[24] However, there are variances between various blood type systems, blood group antigens, or alleles, which might lead to more accurate findings if the susceptibility of this novel viral infection is well understood.

The percentage of COVID-19 patients who had blood type A was much greater than the percentage of healthy persons (P = 0.001). The percentage of COVID-19 patients with blood type O was much lower than the percentage of healthy persons (P = 0.001). This supports a number of previous results[22],[23],[24],[25],[26],[27] showing the ABO blood type is a biomarker for COVID-19 susceptibility variations. To lower the risk of infection, those with blood group A may need additional physical protection, as well as more careful surveillance and active management. More research, including ABO subgroups, is needed to learn more about the relationship between COVID-19 and ABO types.

The current study revealed an increase in the percentage of WBC, and granulocytes in patients compared to the control group, whereas the lymphocyte ratio was decreased in patients significantly. This finding is agreed with some studies that confirmed these results.[27]

The main limitation of the current study is the small size of the specimens collected from both patients and controls.


  Conclusion Top


COVID-19 with positive tests for H. pylori has higher counts of total WBC, neutrophils, and lymphocytes than patients without H. pylori infection. There is a correlation between H. pylori IgG antibodies and COVID-19, suggesting that H. pylori-infected patients may be more susceptible to COVID-19 infection than other people. IgG antibodies against H. pylori may facilitate the entry of SARS-CoV-2 to the body cell by increasing cell receptor affinity to the S protein of the virus.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
The Lancet. COVID-19: A new lens for non-communicable diseases. Lancet 2020;396:649.  Back to cited text no. 1
    
2.
Al-Khikani FH. Surveillance 2019 novel coronavirus (COVID-19) spreading: Is a terrifying pandemic outbreak is soon. Biomed Biotechnol Res J 2020;4:81-2.  Back to cited text no. 2
    
3.
Al-Khikani FH. Amphotericin B as antiviral drug: Possible efficacy against COVID-19. Ann Thorac Med 2020;15:118-24.  Back to cited text no. 3
  [Full text]  
4.
Kao CY, Sheu BS, Wu JJ. Helicobacter pylori infection: An overview of bacterial virulence factors and pathogenesis. Biomed J 2016;39:14-23.  Back to cited text no. 4
    
5.
Mommersteeg MC, Yu J, Peppelenbosch MP, Fuhler GM. Genetic host factors in Helicobacter pylori-induced carcinogenesis: Emerging new paradigms. Biochim Biophys Acta Rev Cancer 2018;1869:42-52.  Back to cited text no. 5
    
6.
Muhammad JS, Sugiyama T, Zaidi SF. Gastric pathophysiological ins and outs of Helicobacter pylori: A review. J Pak Med Assoc 2013;63:1528-33.  Back to cited text no. 6
    
7.
Arismendi Sosa AC, Salinas Ibáñez AG, Pérez Chaca MV, Penissi AB, Gómez NN, Vega AE. Study of Helicobacter pylori infection on lung using an animal model. Microb Pathog 2018;123:410-8.  Back to cited text no. 7
    
8.
GonzÁlez I, Araya P, Rojas A. Helicobacter pylori infection and lung cancer: New insights and future challenges. Zhongguo Fei Ai Za Zhi 2018;21:658-62.  Back to cited text no. 8
    
9.
Dadashi A, Hosseinzadeh N. High seroprevalence of anti-Helicobacter pylori antibodies in patients with ventilator-associated pneumonia. J Res Med Sci 2018;23:79.  Back to cited text no. 9
[PUBMED]  [Full text]  
10.
Anstee DJ. The relationship between blood groups and disease. Blood 2010;115:4635-43.  Back to cited text no. 10
    
11.
AL-Khikani FH. COVID-19: Containment strategies and management options. J Nat Sci Med 2020;3:221.  Back to cited text no. 11
    
12.
Almosawey HA, AL-Khikani FH, Hameed RM, Abdullah YJ, Al-Ibraheemi MK, Al-Asadi AA. Tamoxifen from chemotherapy to antiviral drug: Possible activity against COVID-19. Biomed Biotechnol Res J (BBRJ) 2020;4:108.  Back to cited text no. 12
    
13.
Gonzalez I, Lindner C, Schneider I, Morales MA, Rojas A. Inflammation at the crossroads of Helicobacter pylori and COVID-19. Future Microbiol 2022;17:77-80.  Back to cited text no. 13
    
14.
Abate BB, Kassie AM, Kassaw MW, Aragie TG, Masresha SA. Sex difference in coronavirus disease (COVID-19): A systematic review and meta-analysis. BMJ Open 2020;10:e040129.  Back to cited text no. 14
    
15.
Kushwaha S, Khanna P, Rajagopal V, Kiran T. Biological attributes of age and gender variations in Indian COVID-19 cases: A retrospective data analysis. Clin Epidemiol Glob Health 2021;11:100788.  Back to cited text no. 15
    
16.
Al-Khikani FH. Mucormycosis “Black Fungus” new challenge associated with COVID 19. Biomed Biotechnol Res J (BBRJ) 2021;5:267.  Back to cited text no. 16
    
17.
Uno Y. Why does SARS-CoV-2 invade the gastrointestinal epithelium? Gastroenterology 2020;159:1622-3.  Back to cited text no. 17
    
18.
Price E. Could the severity of COVID-19 Be increased by low gastric acidity? Crit Care 2020;24:456.  Back to cited text no. 18
    
19.
Balamtekin N, Artuk C, Arslan M, Gülşen M. The effect of Helicobacter pylori on the presentation and clinical course of coronavirus disease 2019 Infection. J Pediatr Gastroenterol Nutr 2021;72:511-3.  Back to cited text no. 19
    
20.
Rawson TM, Moore LS, Zhu N, Ranganathan N, Skolimowska K, Gilchrist M, et al. Bacterial and fungal coinfection in individuals with coronavirus: A rapid review to support COVID-19 antimicrobial prescribing. Clin Infect Dis 2020;71:2459-68.  Back to cited text no. 20
    
21.
AL-Khikani FH. Pulmonary mycoses treated by topical amphotericin B. Biomed Biotechnol Res J (BBRJ) 2020;4:123.  Back to cited text no. 21
    
22.
Al-Khikani FH, Almosawey HA, Abdullah YJ, Al-Asadi AA, Hameed RM, Hasan NF, et al. Potential antiviral properties of antifungal drugs. J Egypt Women's Dermatol Soc 2020;17:185.  Back to cited text no. 22
    
23.
Singh J, Kumar N, Kumar K, Dinkar A. COVID-19 associated acute pancreatitis: A case series from India. Infect Disord Drug Targets 2022;21:48-52.  Back to cited text no. 23
    
24.
Cooling L. Blood groups in infection and host susceptibility. Clin Microbiol Rev 2015;28:801-70.  Back to cited text no. 24
    
25.
Al-Khikani FH. The role of blood group in COVID-19 infection: More information is needed. J Nat Sci Med 2020;3:225.  Back to cited text no. 25
    
26.
Muñiz-Diaz E, Llopis J, Parra R, Roig I, Ferrer G, Grifols J, et al. Relationship between the ABO blood group and COVID-19 susceptibility, severity and mortality in two cohorts of patients. Blood Transfus 2021;19:54-63.  Back to cited text no. 26
    
27.
Fathi N, Rezaei N. Lymphopenia in COVID-19: Therapeutic opportunities. Cell Biol Int 2020;44:1792-7.  Back to cited text no. 27
    


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