Saudi Journal of Gastroenterology

ORIGINAL ARTICLE
Year
: 2006  |  Volume : 12  |  Issue : 1  |  Page : 21--26

Helicobacter pylori seropositivity in children with chronic disease in Jeddah, Saudi Arabia


Soad M Jaber 
 Consultant Pediatrition, King Abdulaziz University Hospital, P.O. box 17818, Jeddah 21494, Saudi Arabia

Correspondence Address:
Soad M Jaber
Consultant Pediatrition, King Abdulaziz University Hospital, P.O. box 17818, Jeddah 21494
Saudi Arabia

Abstract

Background : Helicobacter pylori (H. pylori) is an important pathogen in gastrointestinal disorders. Seroprevalence among asymptomatic and chronically diseased children in Jeddah, Saudi Arabia was determined to gain insight into its prevalence. Methods : Serum samples obtained from 1432 children; 543 asymptomatic and 889 chronically diseased children (diabetes, chronic asthma, chronic hemolytic anemia, neurological impairment and Down«SQ»s syndrome); were tested by ELIZA for H. pylori IgG antibodies. Demographic data obtained including nationality, gender, age and disease status. Results : One hundred and twenty eight (23.6%) of 543 asympatomatic children were seropositive with no significant difference in seroprevalence of infection between Saudi and non-Saudi (p<0.09) and between boys and girls (p<0.67), but significant rise was notice with increasing age (p<0.001). An increase in risk of H. pylori among chronically diseased children was observed (diabetes: 34.4%, chronic asthma 20.4%, chronic hemolytic anemia: 31.7%, neurological impairment: 32.1%, and Down«SQ»s syndrome: 29.2%) which increased significantly in chronic anemia and neurological impairment (p<0.01 and p<0.05) compared to controls. The prevalence did not differ according to nationality and gender but significantly increased with age in chronic asthma, chronic anemia and neurological impairment (p<0.01 for all) and also increased significantly with duration of illness, number of blood transfusions, number of hospital admission and mode of feeding. Conclusion : Infection with H. pylori seems to occur early in life and its prevalence increased with age in Jeddah, Saudi Arabia. The risk of H. pylori infection was significantly increased within children suffering from chronic hemolytic anemia; neurological impairment compared to controls and was significantly related to severity of the chronic disease.



How to cite this article:
Jaber SM. Helicobacter pylori seropositivity in children with chronic disease in Jeddah, Saudi Arabia.Saudi J Gastroenterol 2006;12:21-26


How to cite this URL:
Jaber SM. Helicobacter pylori seropositivity in children with chronic disease in Jeddah, Saudi Arabia. Saudi J Gastroenterol [serial online] 2006 [cited 2019 Aug 17 ];12:21-26
Available from: http://www.saudijgastro.com/text.asp?2006/12/1/21/27740


Full Text

Since the discovery of Helicobacter pylori (H. pylori) by Warren and Marshall [1] two decades ago, evidence has been accumulating to indicate that it plays a significant role in the development of chronic gastritis, peptic ulcer diseases, mucosa-associated lymphoid tissue lymphoma, and gastric cancer. [2] Factors such as age, socio-economic level and living conditions, especially during childhood, have been postulated as important determinants in the acquisition of the microorganism. [3] Seroepidemiologic investigations have indicated that infection with H. pylori is very common throughout the world [4] and most infections are acquired during childhood. [5] The prevalence of H. pylori infection in children in developing countries is higher, and begins at a younger age, than in developed countries. [6]

It is well known that H. pylori colonization of the gastric mucosa stimulates the release of various proinflammatory substances, such as cytokines, eicosanoids and proteins of the acute phase. [7] Moreover, a cross mimicry between bacteria and antigens exists in H. pylori infected patients. [8] Therefore, a pathogenetic link between H. pylori infection and diseases characterized by activation of inflammatory mediators and/or induction of autoimmunity might exist. [9] The association between H. pylori infection and some of the chronic diseases such as diabetes, allergy, anemia, neurological impairment, and Down's syndrome in children had previously been reported. [10],[11],[12]

Seroanthropological investigations have been useful adjuncts in improving our understanding of the co-evolution of humans and infecting microorganisms. Microbiological and histological methods, as well as polymerase chain reaction and urea breath test, have been used to assess H. pylori infection; however, it has been stressed that, in children, the specific immunoglobulin G (IgG) test may provide a useful tool in the diagnostic work-up of H. pylori infection. [13]

The aim of the current study was to determine the prevalence of H. pylori infection in Jeddah, Saudi Arabia, with a well-established ELIZA technique among asymptomatic children as well as in chronically diseased children (diabetes, chronic asthma, chronic anemia, neurological impairment and Down's syndrome). The seroprevalence of H. pylori was evaluated according to nationality, age, sex and severity of the disease.

 Patients and Methods



Serum samples were collected over a 2-year period between October 2001 and October 2003 from a total of 1432 children attending outpatient clinics at King Abdulaziz University and Maternity & Children's Hospitals, Jeddah Saudi Arabia.

The participants comprised 543 asymptomatic children who served as controls, and 889 children suffering form chronic disease [diabetes (n=61); chronic asthma (n=220); chronic hemolytic anemia (n=347); neurological impairment (n=237); Down's syndrome (n=24)]. Study participation was voluntary, and written informed consent was obtained from parents and from the older children. The Medical Ethics Committee of King Abdulaziz University approved the study. Non of the participating patients complained of any specific symptoms that might be attributable to infection with H. pylori, such as gastrointestinal bleeding and abdominal pain.

Children taking antimicrobial drugs during the 2 months prior to the study, those taking immunosuppressive or chemotherapeutic drugs, and those with primary or secondary immunodeficiency diseases were excluded from the study.

Serum samples were stored at -20C until use. The sera were tested for H. pylori IgG with a commercially available enzyme linked immunosorbent assay kit (HM-CAP; Enteric Products Incorporation, Westbury, NY). Using control sera, specimens were tested in duplicate according to the manufacturer's specifications, [14] which categorize results as negative, indeterminate, or positive if absorbance values (for sera diluted 1:100 at 450 nm) are 2.2 units, respectively. Consistent results (both positive and negative) were classified accordingly; discordant or indeterminate results were repeated and if they remained indeterminate, the patients were excluded from additional analyses. The sensitivity and specificity of the kits were 98% and 94%, respectively. [15]

 Statistical analysis



Data were recorded and analyzed by the author using Epi Info (version, 6.04; CDC). [16] Odds ratio was used to determine the strength of association between the study outcome (H. pylori infection) and any factor believed to influence its risk. Further, the 95% confidence bounds were determined to test whether the strength of association is statistically significant. Mantel-Haenszel Chi-squared tests were used for statistical analysis. and values of P [6] This cross-sectional population-based serosurvey demonstrates that the prevalence of H. pylori infection among asympatomatic children in Jeddah, Saudi Arabia was 23.6%. It was not related to nationality or gender. In consistency with others [17],[18],[19] a significant increase in the seroprevalence of H. pylori infection among asympatomatic children by age was found. It has been reported that the difference in seroprevalence of H. pylori for each age group increased by approximately 1% per year. [20] A previous study in Riyadh, Saudi Arabia reported rapid increase in the prevalence of H. pylori infection with age from 40% at 5-10 years old to 70% at 20 years old [17].

Metabolic derangements that occur in diabetes may impair a number of host defenses in both humoral and cellular immunity. [21] It has been speculated that alterations in the glucose metabolism may promote H. pylori colonization, [22] which could be due to reduced gastric motility [23] or by chemical changes in gastric mucosa due to non-enzymatic glycosylation of mucins or increased sialic acid [24] which may be involved as a receptor for H. pylori on the cell surface [25] by promoting adhesion of H. pylori to gastric mucosa cells.

The current study revealed increased risk of H. pylori infection among type I diabetic children compared to controls, but the difference did not reach the significant level. The increased risk was not related to nationality, gender and age; on the other hand it was associated significantly with increase in the duration of illness. In this context, some investigators did not find any association between H. pylori infection and diabetes mellitus, [26] meanwhile others showed a lower seroprevalence of H. pylori in type I diabetic patients compares with controls. [27],[ 28] Some authors have suggested an increasing prevalence of H. pylori among diabetic patients. [29] However, the validity of those findings has been severely criticized. [30] The great heterogeneity of results reported in the different studies could be due to methodological differences. Many studies have not reported the method used for selecting cases and control subjects, or used a small sample size. It had been reported that, children with type I diabetes and H. pylori infection had an increased daily insulin requirement compared with the requirement of their uninfected peers and eradication of H. pylori infection was associated with better control of glycemia. [31] In consistence with some authors [32],[9] and in contrast with others, [33] the result of this study did not reveal increased risk of H. pylori infection in chronic asthmatic patients compared to asymptomatic children. A significant association between seroprevalence of H. pylori and increasing age was reported. On the other hand, it was not related to nationality, gender, duration of illness, number of hospital admission and number of ER visits.

Novel epidemiological data from a cross-sectional survey showed that in active H. pylori infection patients, the prevalence of asthma, eczema, and allergic rhinitis is lower than in H. pylori-negative subjects. (12)

H. pylori infection is usually associated with chronic diseases; one of them is chronic anemia. In consistence with others, [34],[35],[11] the results of the present study showed a significant increase in the prevalence of H. pylori infection in chronic anemic patients compared to asymptomatic children.

This study reported significant association between prevalence of H. pylori in studied chronic hemolytic anemic children with increase age, duration of illness and number of blood transfusions, meanwhile no association with nationality and gender was reported. Association between H. pylori infection and recurrent abdominal pain in school-age children with sickle cell anemia [36],[37] and iron deficiency anemia [10] had been reported.

Those participants who suffered from neurological impairment as reported in other studies, [38],[39] showed a significant increased in the prevalence of H. pylori seropositivity compared to asymptomatic children. The prevalence of infection was significantly related to increase in age, duration of illness, number of hospital admissions and mode of feeding, suggesting that H. pylori seropositivity frequently develops at our institution. An increased prevalence of H. pylori seropositivity in institutionalized patients with neurological impairment had been suggested by other authors. [39],[40],[41] The factors responsible for a higher prevalence of H. pylori seropositivity in institutionalized patients with neurological impairment have not been elucidated but may include domestic crowding and other conditions, such as length of stay and age of the residents. [40] In agreement with other reports, [39] this study shows that H. pylori seropositivity in institutionalized patients with neurological impairment is not associated with specific symptoms.

Mentally disabled children may be at higher risk of infections because of different feeding abilities, toileting needs, and living and sanitary arrangements. No significant difference was reported in this study between risks of H. pylori infection within children suffering from Down's syndrome compared to asymptomatic children. The prevalence also was not related to nationality and gender. On the other hand, It had been reported by Bohmer et al. [38] that intellectually disabled persons and employees with close physical contact to them for a considerable period are at high risk of developing H. pylori infection.

In conclusion, the serosurvey described here found a high prevalence of H. pylori-specific IgG among asympatomatic and with chronically diseased children in Jeddah, Saudi Arabia.

The prevalence of H. pylori seropositivity in children suffering from chronic disease (chronic anemia, neurological impairment) have higher risk of infection than asymptomatic children. The rate of seropositivity went up with increasing age in asympatomatic children and those suffering from chronic asthma, chronic anemia and neurological impairment children. Also, there was an association between the prevalence of H. pylori seropositivity and duration of illness, number of hospital admissions, number of blood transfusions and mode of feeding in the chronically diseased children studied.

References

1Warren J, Marshall B. Unidentified curved bacilli on gastric epithelium in active chronic gastritis. Lancet 1983; 1:1311-1315.
2Parsonnet J, Hansen S, Rodriguez L, Gelb A, Warnke R, Jellum E, Orentreich N, Vogelman J, Friedman G. Helicobacter pylori infection and gastric lymphoma. N Engl J Med 1994; 330:267-271.
3Mendall M, Goggin P, Molineaux N, Levy J, Toosy T, Strachan D, Northfield T. Childhood living conditions and Helicobacter pylori seropositivity in adult life. Lancet 1992; 339: 896 -897.
4Pounder R, Ng D. The prevalence of Helicobacter pylori infection in different
5Jones NL, Sherman PM. Helicobacter pylori infection in children. Curr Opin Pediatr 1998; 10:19-23.
6Bujanover Y, Reif S, Yahav J. Helicobacter pylori and peptic disease in the pediatric patient. Pediatr. Clin. North Am.1996; 43: 213 -234.
7Crabtree J. Role of cytokines in pathogenesis of Helicobacter pylori induced mucosal damage. Dig Dis Sci 1998; 43 (9): 46-55.
8Negrini R, Savio A, Poiesi C, Appelmelk BJ, Buffoli F, Paterlini A, Cesari P, Graffeo M, Vaira D, Franzin G. Antigenic mimicry between H. pylori and gastric mucosa in the pathogenesis of body atrophic gastritis. Gastroenterology 1996; 111: 655-665
9Roussos A, Philippou N, Gourgoulianis K. Helicobacter pylori infection and respiratory diseases: a review. World J Gastroenterol 2003; 15:9(1): 5-8.
10Ashorn M, Ruuska T, and Makipernaa A. Helicobacter pylori and iron deficiency anemia in children. Scand. J. Gastroenterol. 2001; 36(7):701-705.
11Sykora J, Cerna Z, Hejda V, Varvarovska J, and Stozicky F. Hypergastrinemia associated with Helicobacter pylori infection and sideropenic anemia in a 15-years-old girl. Cas Lek Cesk. 2002; 141(23): 739-741.
12Cremonini F, Gasbarrini A. Atopy, Helicobacter pylori and the hygiene hypothesis. Eur J Gastroenterol Hepatol. 2003; 15(6): 635-636.
13Fujisawa T, Kumagai T, Akamatsu T and Kiyosawa K. Changes in seroepidemiological pattern of Helicobacter pylori and hepatitis A virus over the last 20 years in Japan. Am. J. Gastroenterol. 1999; 94:2094-9.
14Chong S, Lou Q, Asnicar M. Helicobacter pylori infection in recurrent abdominal pain in childhood: comparison of diagnostic tests and therapy. Pediatrics. 1995; 96:211-215.
15Marchildon P, Ciota L, Zamaniyan F, Peacock J, Graham D. Evaluation of three commercial immunoassays compared with the 13C urea breath for detection of Helicobacter pylori infection. J Clin Microbiol. 1996; 34:1147-1152.
16Dean A, Dean J, Coulombier D, et al. Epi Info: a word-processing, database and statistics program for epidemiology on microcomputers. Version 6. Atlanta: Centers for Disease Control and Prevention, 1994.
17Al-Moagel M, Dolores D, Abdulghani M, Adam E, Evan D, Malaty H, and Graham D. Prevalence of Helicobacter pylori infection in Saudi Arabia, and comparison of those with and without upper gastrointestinal symptoms. Am. J. Gastroenterol. 1990; 85:944-948.
18Staat, M, Maron D, McQuillan G, and Kaslow R. A population-based serologic survey of Helicobacter pylori infection in children and adolescent in the United States. J. Infect. Dis. 1996; 174:1120-1123.
19Yamashita, Y, Fujisawa T, Kimura A, and Kato H. Epidemiology of Helicobacter pylori infection in children: A serologic study of the Kyushu region in Japan. Pediatric International 2001; 43:4-8.
20Mitchell H, Li Y, Hu P, Liu Q, Chen M, Du G, Wang Z, Lee A, Hazell S. Epidemiology of Helicobacter pylori in southern China: Identification of early childhood as the critical period for acquisition. J.Infect.Dis.1992; 166: 149-153.
21Rayfield E, Ault M, Keusch G, Brothers M, Nechemias C, Smith H. Infection and diabetes: the case for glucose control. Am J Med 1982; 72:439-450.
22Perdichizzi G, Bottari M, Pallio S, Fera M, Carbone M, Barresi G. Gastric infection by Helicobacter pylori and antral gastritis in hyperglycemic obese and diabetic subjects. Microbiol 1996; 19:149-154.
23Bergstrom B, Lilja B, Osterlin S, Sundkvist G. Autonomic neuropathy in non-insulin dependent (type II) diabetes mellitus. Possible influence of obesity. J Intern Med 1990; 227(1): 57-63.
24Pickup J, Day C, Bailey C, Samuel A, Chusney G, Garland H, Hamilton K, Balment R. Plasma sialic acid in animal models of diabetes mellitus: evidence for modulation of sialic acid concentrations by insulin deficiency. Life Sci 1995; 7:1383-1391.
25Valkonen K, Ringner M, Ljungh A, Wadstrom T. High-affinity binding of laminin by Helicobacter pylori: evidence for a lectin-like interaction. FEMS Immunol Med Microbiol 1993; 7:29-37.
26Anastasios R, Goritsas C, Papamiha C, Trigidou R, Garzonis P, Ferti A. Helicobacter pylori infection in diabetic patients prevalence and endoscopic findings. Eur. J. Int. Med. 2002; 13:376-379.
27Dore M, Bilotta M, Malaty H, Pacifico A, Maioli M, Graham D, and Realdi G. Diabetes mellitus and Helicobacter pylori infection. Nutrition 2000; 16(6): 407-410.
28Zelenkova J, Souckova A, Kvapil M, Soucek A, Vejvalka J, and Segethova J. Helicobacter pylori and diabetes mellitus. Cas. Lek. Cesk. 2002; 141(18): 575-577.
29Oldenburg B, Diepersloot R, Hoekstra J. High seroprevalence of Helicobacter pylori in diabetes mellitus patients. Dig Dis Sci 1996; 41 (3): 458-461.
30Danesh J. H. pylori and diabetes. Dig Dis Sci 1997; 42:2576 Letter.
31Begue R, Mirza A, Compton T, Gomez R, Vargas A. Helicobacter pylori Infection and Insulin Requirement Among Children With Type 1 Diabetes Mellitus. Pediatrics 1999; 103 (6): e83.
32Tsang K, Lam W, Chan K, Hu W, Wu A, Kwok E, Zheng L, Wong B, Lam S. Helicobacter pylori seroprevalence in asthma. Respiratory medicine 2000; 94: 756-759.
33Corrado G, Luzzi I, Pacchiarotti C, Lucarelli S, Frediani T, Cavaliere M, Rea P, and Cardi E. Helicobacter pylori seropositivity in children with atopic dermatitis as sole manifestation of food allergy. Pediatr Allergy Immunol. 2000; 11(2): 101-105
34Milman N, Rosenstock S, Andersen L, Jorgensen T, and Bonnevie O. Serum ferritin, hemoglobin, and Helicobacter pylori infection: A seroepidemiologic survey comprising 2794 Danish adults. Gastroenterology 1998; 115: 268-274.
35Berg G, Bode G, Blettner M, Boeing H, and Brenner H. Helicobacter pylori infection and serum ferritin: A population-based study among 1806 adults in Germany. Am. J. Gastroenterol. 2001; 96: 1014-1018.
36Kennedy L, Mahoney D, Redel C. Helicobacter pylori gastritis in a child with sickle cell anemia and recurrent abdominal pain. J Pediatr Hematol Oncol. 1997; 19(2): 163-164.
37Woods K, Onuoha A, Schade R, Kutlar A. Helicobacter pylori infection in sickle cell disease. J Natl Med Assoc. 2000; 92(7): 361-365.
38Bohmer C, Klinkenberg-Knol E, Kuipers E, Neizen-de Boer M, Schreuder H, Schuckink-Kool F, and Meuwissen S. The prevalence of Helicobacter pylori infection among inhabitants and healthy employees of institutes for the intellectually disabled. Am. J. Gastroenterol. 1997; 92:1000-1004.
39Kimura A, Matsubasa T, Kinoshita H, Kuriya N, Amashita Y, Fujisawa T, Terakura H, Shinohara M. Helicobacter pylori seropositivity in patients with severe neurologic impairment. Brain & Development 1999; 21: 113-117.
40Berkowicz J, Lee A. Person-to-person transmission of Campylobacter pylori. Lancet 1987; 19(8560): 680-1.
41Harris A, Douds A, Meurisse V, Dennis M, Chambers S, Gould S. Seroprevalence of Helicobacter pylori in residents of a hospital for people with severe learning difficulties. Eur J Gastroenterol Hepatol 1995; 7(1): 21-23