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Journal of Family Medicine and Primary Care logoLink to Journal of Family Medicine and Primary Care
. 2019 Jul;8(7):2202–2206. doi: 10.4103/jfmpc.jfmpc_398_19

Prevalence and patient characteristics of Helicobacter pylori among adult in primary health care of security forces hospital Riyadh, Saudi Arabia, 2018

Rami Hamdan Alharbi 1,, Medhat Ghoraba 1
PMCID: PMC6691427  PMID: 31463230

Abstract

Aim:

To estimate the Helicobacter pylori prevalence and patients’ characteristics in primary health care in security forces hospital Riyadh, Saudi Arabia.

Methods:

A cross-sectional study, using a fecal H. pylori antigen, is including adults (14-64 years) in the duration from 18 March 2018 to 18 April 2018 on Saudi male and female visiting Primary care center in Security Forces Hospital, Riyadh, Saudi Arabia.

Results:

The study came up with H. pylori prevalence is significantly correlated with age for those below 20 years and more than 50 years (P-value = 0.022 and 0.016, respectively) but with no correlation with the patient's sex.

Conclusion:

In conclusion, overall prevalence of H. pylori is low among primary healthcare patients, which is 10.2% and it is correlated to younger age <20 years old and elderly >50 years old.

Keywords: Adult, gastrointestinal symptoms, Helicobacter pylori, prevalence, Saudi Arabia

Introduction

Helicobacter pylori, which is a gram-negative microaerophilic bacterium and causes stomach inflammation, was first isolated by Barry Marshall and Robin Warren in 1982. It is a highly prevalent infection in the developing countries with poor socio-economic status and an etiologic agent of the majority of upper gastrointestinal diseases associated with significant morbidity.[1] More than 50% of the world's population is infected with H. pylori, the leading cause of chronic gastritis. Chronic gastritis is always associated with peptic ulcer and in advanced stages with an increased risk of developing gastric adenocarcinoma.[2]

H. pylori is a gram-negative organism which invades gastric mucosa or sticks to the epithelial lining of the stomach. Most of the patients will be asymptomatic but sometimes associated with abdominal distention, epigastric burning sensation, and nausea.[3] H. pylori are the most common cause of peptic ulcer disease, and it is one of the risk factors for gastric cancer. Treating the disease resulting in ulcer healing and reduce the risk of recurrence, and avoid it is complications. Treatment involves 10-14 days multi drugs including antibiotics and anti-acid.[4] In 1983, H. pylori were discovered as a cause of peptic ulcer disease.[5] A study done in Riyadh 2007 by AlMadi et al. found that H. pylori prevalence was 35%.[6] Another study done in Czech Republic 2006 by Bures J et al. found that the prevalence was 41.9% in males and 41.4% in females.[7] Other study was done in China 2010 by Li et al. a total of 3153 persons the prevalence of Helicobacter pylori infection was 73% in the total.[8] In 2010, in Kampala, Uganda a study done by Hestvik et al. found that the prevalence of H. pylori was 44.3%.[9] In India, the incidence of H. pylori was 79% through study done in 2010 by Thankachan et al.[10] In Brazil, August 2010, there was a study done by Dattoli et al. in which a total of 1104 children aged 4-11 years using anti_H pylori IgG antibodies, and the result was positive in 28.7%.[11] Also, there was a study done in United States 2011 May 2011 in which a total of 689 African American and white participants from the Southern Community Cohort Study participated and the prevalence was 79% of H. pylori seropositive which done by Epplein et al.[12] So there is a difference in the incidence of different geographic area which is higher in India and United States 79% and lower in Brazil which is 28.7% H. pylori should be treated to avoid its complications which includes ulcers that formed by the organism that can damage the epithelial lining of the stomach and allows to create the ulcer by the acidity of the stomach. Stomach cancer: H. pylori is one of the risk factors for gastric cancer.[13] Endoscopy is considered essential in the classification of the patient's condition as organic or functional dyspepsia.[14,15,16,17,18] The regimens that recommended by National Institute of Clinical Excellence for H. pylori eradication are omeprazole, amoxicillin, and clarithromycin (OAC) for 10 days; bismuth subsalicylate, metronidazole, and tetracycline (BMT) for 14 days; and lansoprazole, amoxicillin, and clarithromycin (LAC) for 10–14 days of treatment. In many of the developing countries, facilities for UGI endoscopy are rare. As a result, the diagnosis of UGI diseases is carried out solely on clinical parameters in most cases. Incorrect/delayed diagnoses, and subsequent ineffective management results in increased morbidity, economic loss to the client, and even death especially in patients with malignancy.[17] Therefore, the goal of this study is to try to find out the prevalence of H. pylori and patient's characteristics among SFH visitors, to compare it with the currently available studies.

Materials and Methods

Study population

Saudi male and female adults aged 14-64 years visiting Primary care center in Security Forces Hospital during the year 2018.

Inclusion criteria

Saudi male and female

Adult 14-64 years

Patients who are complaining of gastrointestinal symptoms.

The patient did not receive treatment for H. pylori or received the therapy more than 12 months.

Exclusion criteria

Patients who could not effectively communicate in Arabic

Less than 14 years

Older than 65 years

Received treatment within 12 months.

Sample size and technique

Using the expected prevalence of H. pylori was reported 35% as given in the literature for calculating our sample size. Under the convenient sampling with a margin of error at 5% and the confidence level at 95%, we will need a sample of size 350. Allowing for 15% non-response rate the final required sample size is 411.

We use the following formula

n = (Z2 P (1 P))/e2

where n = sample size, the z = z statistic for the level of confidence, P = expected prevalence and d = allowable error. This formula assumes that “P” and “d” are decimal values.

Study area

Primary Care Center, Security Forces Hospital, Riyadh Saudi Arabia

Study duration

18 March 2018-18 April 2018.

Study design

A cross-sectional study, using a stool H. pylori antigen as a diagnostic test Included Adults (14-64 years) in 2018.

Results

Of 411 participants there was 143 (34.8%) aged 21-30 years, 96 (23.4%) aged 31-40 years, 72 (17.5%) aged >50 years. Most of them were females 281 (53%). Most of them were H. pylori negative 369 (89.8%) [Table 1].

Table 1.

Descriptive statistics

Description (n=411)
Age
 Range 14 - 64
 Mean±SD 35.3±12.8
 Median (IQR) 32 (25-47)
Age (years)
 ≤20 38 (9.2)
 21-30 143 (34.8)
 31-40 96 (23.4)
 41-50 62 (15.1)
 >50 72 (17.5)
Sex
 Male 193 (47)
 Female 218 (53)
H. pylori
 +VE 42 (10.2)
 −VE 369 (89.8)

This study showed that H. pylori prevalence is significantly correlated with age <20 and >50 years old (P-value = 0.022 and 0.016, respectively) but there was no correlation between H. pylori prevalence and sex [Table 2].

Table 2.

Demographic determinants of H. pylori infections

H. pylori P

+VE (n=42) −VE (n=369)
Age
 Range 22-64 14-64
 Mean±SD 41.9±12.1 34.5±12.7 <0.001@
 Median (IQR) 43 (32-52) 31 (24-45)
Age (years)
 ≤20 0 (0) 38 (10.3) 0.022*
 21-30 9 (21.4) 134 (36.3) 0.055*
 31-40 11 (26.2) 85 (23) 0.647*
 41-50 9 (21.4) 53 (14.4) 0.225*
 > 50 13 (31) 59 (16) 0.016*
Sex
 Male 17 (40.5) 176 (47.7) 0.374*
 Female 25 (59.5) 193 (52.3)

*Chi-square test, @t-test

Discussion

H. pylori infection has been recorded to be hyper-endemic in Saudi Arabia. Some studies on H. pylori in the Kingdom of Saudi Arabia have observed a high prevalence in various age populations, including individuals with non-ulcer dyspepsia.[19] More reviews on H. pylori infection among Saudi children had shown high infection prevalence among Saudi children in the cities of Riyadh and Jeddah.[20] The World Health Organization considers H. pylori as a carcinogen.[21] It has been reported that prevalence of infection with H. pylori accounts for 75% of non-cardia gastric malignancy worldwide.[22] The H. pylori-induced gastritis may lead to atrophic gastritis. Atrophic gastritis may progress to intestinal metaplasia, dysplasia and neoplasia, gastric adenocarcinoma and mucosa-associated lymphoid tissue lymphoma.[23] Although there are many types of research on H. pylori prevalence conducted in different regions of Saudi Arabia.[24,25,26,27,28]

The present study shows that the H. pylori prevalence was significantly higher in the older-age-group >50 years (13, P = 0.016) while there was no infection in young age <20 years (0, P = 0.002). This observation agrees with a large British study that examined patients tested with the urea breath test. The patients in this British study were randomly drawn from general practice registers, and some were not included because of dyspeptic symptoms. The study also found that H. pylori infection in primary care patients was strongly related to age.[29]

Akeel et al. (2018) carried out a prospective cross-sectional study, a total of 404 gastric biopsies were endoscopically carried out on 404 patients with dyspepsia from September 2014 to April 2016 (Jazan Province, Saudi Arabia). The study indicated that there is a high prevalence of H. pylori among Saudi patients with dyspepsia. Prevalence of H. pylori was high in ages <55 years. Chronic active gastritis was significantly related to H. pylori infection.[30]

Another study by Telmesani (2009) found that the prevalence of H. pylori among the school children in Makkah, Saudi Arabia, is relatively low compared with developing countries. The prevalence was found to be higher among the younger age group. Further, there was a significant relation between H. pylori infection and chronic recurrent abdominal pain among the school students.[31]

Previous studies reported that the prevalence of infection in younger patients was ranged between 10% and 20%,[32,33] it is anticipated that the incidence of H. pylori infection will decline as sanitary conditions improve and\ it is also considered a reflection of widespread use of antibiotics.[34] H. pylori infection has been frequently reported by several studies to be high in developing countries and associated with low levels of education and social, economic status, and poor sanitation.[17,35] Impact on endoscopic findings while the presence of H. pylori, smoking and alcohol consumption are all associated with an increased risk level of developing chronic gastritis.[35]

The overall prevalence of H. pylori-associated gastritis may be an underestimate since the majority of the participants had been on prior treatment with antibiotics. However, this value is almost similar to one found by Wabinga et al.[36] in his retrospective study in 2002.

In contrast, studies in 2012 in neighboring Kenya[37] reported a 52% prevalence of H. pylori in adults.[38] In Nigeria, a 41% prevalence was also published in Lagos state in 2008.[35] Notably, all the above researches were carried out in an urban setting where there is congestion, perhaps sub-optimal sanitary conditions but easy access to antibiotics compared to rural settings. In the East Cape region of South Africa in 2008, 66.1% H. pylori prevalence was reported.[39] The East Cape region is one of the most deprived areas of South Africa. Clinicians have to be always aware that dyspepsia in the young could be cancer.[40]

In a systematic review carried on 4,018 patients, the use of alarm symptoms to select dyspeptic patients for endoscopy caused participants with early curable cancers to be overlooked.[41] The most familiar macroscopic finding was gastritis similar to the following studies, Wabinga et al. in Uganda,[36] Sang Thomas et al.[31] and Kimang et al.[38] In Kenya, Sang Thomas et al. found about 4% normal findings at endoscopy and Kimangi et al. found that 100% of the study patients with dyspepsia had abnormal results at endoscopy. In the Eastern Cape region S.A, 33.6% of the patients had functional dyspepsia.[38] Similarly, Abioudun et al. in Nigeria stated that gastritis was the most frequent finding, but also found a high prevalence of H. pylori in endoscopically typical study participants.[42] In contrast, in Italy, a case-control study by Zagari et al. of 1033 study participants found that — were normal endoscopically. In his research, about 93.4% of PUD patients had H. pylori at histology.[43]

One weakness in our study is the fact that patient selection is somewhat inhomogeneous, and at the discretion of the GP, therefore, there are no firm inclusion and exclusion criteria. However, the study aimed to illustrate how test-and-treat could be applied successfully in the clinical setting of primary care. In both the women and men who were <20 years of age, we found a significant decline in H. pylori prevalence over the years of the study. This corresponds with recent studies that reported a general decrease in H. pylori infection in developed countries.[44,45]

Conclusion

In conclusion, H. pylori prevalence is low among the primary healthcare of Security Forces Hospital, Riyadh Saudi Arabia and highly correlated to old age and elderly >50 years old.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

References

  • 1.Warren JR, Marshall B. Un-identified curved bacilli on the gastric epithelium in active chronic gastritis. Lancet. 1983;1:1273–5. [PubMed] [Google Scholar]
  • 2.Kandulski A, Malfertheiner P. H. pylori infection: A clinical overview. Dig Liver Dis. 2008;40:619–26. doi: 10.1016/j.dld.2008.02.026. [DOI] [PubMed] [Google Scholar]
  • 3.Schubert TT, Schubert AB, Ma CK. Symptoms, gastritis and Helicobacter pylori in patients referred for endoscopy. Gastrointest Endosc. 1992;38:357–60. doi: 10.1016/s0016-5107(92)70432-5. [DOI] [PubMed] [Google Scholar]
  • 4. Available from: https://www.aafp.org/afp/2002/0401/p1327.html#afp20020401p1327-b1 .
  • 5. Available from: https://www.sciencedirect.com/science/article/pii/S0140673684918166 .
  • 6.Almadi MA, Aljebreen AM, Tounesi FA, Abdo AA. Helicobacter pylori prevalence among medical students in a high endemic area. Saudi Med J. 2007;28:896–8. [PubMed] [Google Scholar]
  • 7.Bures J, Kopácová M, Koupil I, Vorísek V, Rejchrt S, Beránek M, et al. Epidemiology of Helicobacter pylori infection in the Czech Republic. Eur Soc Primary Care Gastroenterol. 2006;11:56–65. doi: 10.1111/j.0083-8703.2006.00369.x. [DOI] [PubMed] [Google Scholar]
  • 8.Li Z, Zou D, Ma X, Chen J, Shi X, Gong Y, et al. Epidemiology of peptic ulcer disease: Endoscopic results of the systematic investigation of gastrointestinal disease in China. Am J Gastroenterol. 2010;105:2570–7. doi: 10.1038/ajg.2010.324. [DOI] [PubMed] [Google Scholar]
  • 9.Hestvik E, Tylleskar T, Kaddu-Mulindwa DH, Ndeezi G, Grahnquist L, Olafsdottir E, et al. Helicobacter pylori in the healthy children aged 0-12 years in urban Kampala, Uganda: A community-based cross-sectional survey. BMC Gastroenterol. 2010;10:62. doi: 10.1186/1471-230X-10-62. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 10.Thankachan P, Muthayya S, Sierksma A, Eilander A, Thomas T, Duchateau GS, et al. Helicobacter pylori infection doesn’t influence the efficacy of iron and vitamin B (12) fortification in marginally nourished Indian children. Eur J Clin Nutr. 2010;64:1101–7. doi: 10.1038/ejcn.2010.126. [DOI] [PubMed] [Google Scholar]
  • 11.Dattoli VC, Veiga RV, da Cunha SS, Pontes-de-Carvalho LC, Barreto ML, Alcântara-Neves NM. Seroprevalence and potential risk factors for Helicobacter pylori infection in Brazilian children. Helicobacter. 2010;15:273–8. doi: 10.1111/j.1523-5378.2010.00766.x. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 12.Epplein M, Signorello LB, Zheng W, Peek RM, Jr, Michel A, Williams SM, et al. Race, African ancestry, and Helicobacter pylori infection in a low-income United States population. Cancer Epidemiol Biomarkers Prev. 2011;20:826–34. doi: 10.1158/1055-9965.EPI-10-1258. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 13. Available from: https://www.mayoclinic.org/diseases-conditions/h-pylori/symptoms-causes/syc-20356171 .
  • 14.Truter I. Approach to dyspepsia for the pharmacist. S Afr Pharm J. 2012;79:9–16. [Google Scholar]
  • 15.Oustamanolakis P, Tack J. Dyspepsia: Organic vs functional. J Clin Gastroenterol. 2012;46:175–90. doi: 10.1097/MCG.0b013e318241b335. [DOI] [PubMed] [Google Scholar]
  • 16.NICE. Dyspepsia guidelines: Managing adults in the primary care, NICE guidelines CG184 September 2014. London, England: 2004. pp. 1–43. [Google Scholar]
  • 17.Agbakwuru EA, Fatusi AO, Ndububa D. Pattern and validity of the clinical diagnosis of upper gastrointestinal diseases in south-west Nigeria. Afr Health Sci. 2006;6:98–103. doi: 10.5555/afhs.2006.6.2.98. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 18.Tack J, Talley NJ, Camilleri M. The Functional gastroduodenal disorders. Gastroenterology. 2006;130:1466–79. doi: 10.1053/j.gastro.2005.11.059. [DOI] [PubMed] [Google Scholar]
  • 19.Al-Akwaa AM. Prevalence of Helicobacter pylori infection in a group of morbidly obese Saudi patients undergoing bariatric surgery: A preliminary report. Saudi J Gastroenterol. 2010;16:264. doi: 10.4103/1319-3767.70610. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 20.Hasosah M, Satti M, Shehzad A, Alsahafi A, Sukkar G, Alzaben A, et al. Prevalence and risk factors of h elicobacter pylori infection in Saudi Children: A three-year prospective controlled study. Helicobacter. 2015;20:56–63. doi: 10.1111/hel.12172. [DOI] [PubMed] [Google Scholar]
  • 21.De Martel C, Ferlay J, Franceschi S, Vignat J, Bray F, Forman D, et al. Global burden of cancers attributable to infections in 2008: A review and synthetic analysis. Lancet Oncol. 2012;13:607–15. doi: 10.1016/S1470-2045(12)70137-7. [DOI] [PubMed] [Google Scholar]
  • 22.Mobley HL, Mendz GL, Hazell SL. ASM Press; 2001. Restriction and Modification Systems--Helicobacter pylori: Physiology and Genetics. [PubMed] [Google Scholar]
  • 23.Wang HC, Cheng FC, Wu MS, Shu HY, Sun HS, Wang YC, et al. Genome sequences of three Helicobacter pylori strains from patients with gastric mucosa-associated lymphoid tissue lymphoma. Genome Announc. 2015;3:e00229–15. doi: 10.1128/genomeA.00229-15. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 24.Al-Moagel MA, Evans DG, Abdulghani ME, Adam E, Evans DJ, Jr, Malaty HM, et al. Prevalence of Helicobacter (formerly Campylobacter) pylori infection in Saudia Arabia, and comparison of those with and without upper gastrointestinal symptoms. Am J Gastroenterol. 1990;85:944–8. [PubMed] [Google Scholar]
  • 25.Marie MA. Alimentary tract: Seroprevalence of Helicobacter pylori infection in large series of patients in an urban area of Saudi Arabia. Korean J Gastroenterol. 2008;52:226–9. [PubMed] [Google Scholar]
  • 26.Iman N, Khan H, Iqbal S, Rehman S. Frequency of H. pylori in patients with upper GI symptoms. J Med Sci. 2008;16:1–3. [Google Scholar]
  • 27.Ayoola AE, Ageely HM, Gadour MO, Pathak VP. Prevalence of Helicobacter pylori infection among patients with dyspepsia in South-Western Saudi Arabia. Saudi Med J. 2004;25:1433–8. [PubMed] [Google Scholar]
  • 28.Momenah AM, Tayeb MT. Helicobacter pylori cagA and iceA genotypes status and risk of peptic ulcer in Saudi patients. Saudi Med J. 2007;28:382–5. [PubMed] [Google Scholar]
  • 29.Lane JA, Harvey RF, Murray LJ, Harvey IM, Donovan JL, Nair P, et al. A placebo-controlled randomized trial of eradication of H.pylori in the general population: Study design and response rates of the Bristol Helicobacter Project. Control Clin Trials. 2002;23:321–32. doi: 10.1016/s0197-2456(01)00208-2. [DOI] [PubMed] [Google Scholar]
  • 30.Akeel M, Elmakki E, Shehata A, Elhafey A, Aboshouk T, Ageely H, et al. Prevalence and factors associated with H.pylori infection in Saudi patients with dyspepsia. Electron Physician. 2018;10:7279–86. doi: 10.19082/7279. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 31.Telmesani AM. Helicobacter pylori: Prevalence and relationship with abdominal pain in school children in Makkah City, western Saudi Arabia. Saudi J Gastroenterol. 2009;15:100–3. doi: 10.4103/1319-3767.45359. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 32.Talley NJ, Vakil NB, Moayyedi P. American gastroenterological association technical review on the evaluation of dyspepsia. Gastroenterology. 2005;129:1756–80. doi: 10.1053/j.gastro.2005.09.020. [DOI] [PubMed] [Google Scholar]
  • 33.Talley NJ, Vakil N. Guidelines for the management of dyspepsia. Am J Gastroenterol. 2005;100:2324–37. doi: 10.1111/j.1572-0241.2005.00225.x. [DOI] [PubMed] [Google Scholar]
  • 34.Malaty HM, Paykov V, Bykova O, Ross AJ, Graham D, Anneger JF, et al. Helicobacter pylori and socioeconomic factors in Russia. Helicobacter. 1996;1:82–7. doi: 10.1111/j.1523-5378.1996.tb00015.x. [DOI] [PubMed] [Google Scholar]
  • 35.Hameed L, Onyekwere AC, Otegbayo J, Abdulkareem FB. A clinicopathological study of dyspeptic subjects in Lagos, Nigeria. Gastroenterol Insights. 2012;4:e11. [Google Scholar]
  • 36. Available from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4477594/
  • 37.KAP Conference; 2012. Moi STM. Prevalence of H. pylori infection and endoscopic findings in patients with dyspepsia at MoiTeaching and Referral Hospital. [Google Scholar]
  • 38.Kimang’a AN. H.pylori: Prevalence and antibiotic susceptibility among Kenyans. S Afr Med J. 2010;100:53–7. [PubMed] [Google Scholar]
  • 39.Tanih NF, Okeleye BI, Ndip R. Helicobacter pylori prevalence in dyspeptic patients in the Eastern Cape province—Race and disease status. Afr Med J. 2010;100:734–7. doi: 10.7196/samj.4041. [DOI] [PubMed] [Google Scholar]
  • 40.Olokoba AB, Obateru OA, Bojuwoye MO, Ibrahim OK, Olokoba LB. That dyspepsia in the young could be cancer. Niger Med J. 2013;54:143–5. doi: 10.4103/0300-1652.110053. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 41.Bowrey DJ, Griffin SM, Raimes S. Use of alarm symptoms to select dyspeptics for endoscopy causes patients with the curable esophagogastric cancer to be overlooked. Surg Endosc Other Interv Tech. 2006;20:1724–8. doi: 10.1007/s00464-005-0679-3. [DOI] [PubMed] [Google Scholar]
  • 42.Jemilohun AC, Otegbayo JA, Ola SO, Oluwasola OA, Akere A. Prevalence of Helicobacter pylori among Nigerian patients with dyspepsia in Ibadan. Pan Africa Med J. 2010;6:18. [PMC free article] [PubMed] [Google Scholar]
  • 43.Zagari RM, et al. Dyspeptic symptoms and endoscopic findings in the community: The Loiano–Monghidoro study. Am J Gastroenterol. 2010;105:565. doi: 10.1038/ajg.2009.706. [DOI] [PubMed] [Google Scholar]
  • 44.Miendje Deyi VY, Vanderpas J, Bontems P, Van den Borre C, De Koster E, Cadranel S, et al. Marching cohort of Helicobacter pylori infection over two decades (1988–2007): Combined effects of secular trend and population migration. Epidemiol Infect. 2011;139:572–80. doi: 10.1017/S095026881000110X. [DOI] [PubMed] [Google Scholar]
  • 45.Asfeldt AM, Straume B, Steigen SE, Lochen ML, Florholmen J, Bernersen B, et al. Changes in the prevalence of dyspepsia and H.pylori infection after 17 years: The Sorreisa gastrointestinal disorder study. Eur J Epidemiol. 2008;23:625–33. doi: 10.1007/s10654-008-9275-x. [DOI] [PubMed] [Google Scholar]

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