Helicobacter pylori infection: several studies on epidemiology, eradication and gastric epithelial cell turnover Liu, W.

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1 UvA-DARE (Digital Academic Repository) Helicobacter pylori infection: several studies on epidemiology, eradication and gastric epithelial cell turnover Liu, W. Link to publication Citation for published version (APA): Liu, W. (1999). Helicobacter pylori infection: several studies on epidemiology, eradication and gastric epithelial cell turnover General rights It is not permitted to download or to forward/distribute the text or part of it without the consent of the author(s) and/or copyright holder(s), other than for strictly personal, individual use, unless the work is under an open content license (like Creative Commons). Disclaimer/Complaints regulations If you believe that digital publication of certain material infringes any of your rights or (privacy) interests, please let the Library know, stating your reasons. In case of a legitimate complaint, the Library will make the material inaccessible and/or remove it from the website. Please Ask the Library: or a letter to: Library of the University of Amsterdam, Secretariat, Singel 425, 1012 WP Amsterdam, The Netherlands. You will be contacted as soon as possible. UvA-DARE is a service provided by the library of the University of Amsterdam ( Download date: 13 Dec 2018

2 CHAPTER 2 Seroprevalence of Helicobacter Pylori Infection in Medical Staff in Shanghai Wen-Zhong Liu, Shu-Dong Xiao, Shao-Ji Jiang, Rong-Rong Li & Zhi-Jun Pang Shanghai Institute of Digestive Disease, Ren-Ji Hospital Affiliated to Shanghai Second Medical University, Shanghai, People's Republic of China Scand J Gastroenterol 1996; 31:

3 Abstract Background/Aim: The epidemiology of H. pylori is still under investigation. It is postulated that the human stomach is the natural reservoir and that spread occurs by oral-oral or fecal-oral transmission. The aim of this study was to determine whether medical staff, especially endoscopy unit personnel, are at an increased risk of acquiring H. pylori infection. Methods: An enzyme-linked immunosorbent assay technique was used to detect circulating H. pylori IgG antibodies in 1050 medical staff from 16 hospitals in Shanghai, including 125 GI endoscopists, 45 endoscopy unit nurses. 71 gastroenterologists not doing endoscopy, 105 nurses working in gastroenterology wards. 417 internists, and 287 general nurses. This group Was compared with an agematched population obtained from the same urban area of the city. Results: The overall prevalence of//, pylori infection in total medical staff was 70.0%, compared to 44.6% in general population (PO.0001). Age-adjusted comparisons between subgroups of medical staff were made. The prevalence of H. pylori in GI endoscopists was 82.4%, which is significantly higher than 66.4% in internists and 65.8% in general nurses (all, P < 0.01) but not significantly different from 77.7% in endoscopy unit nurses or from 74.2% in nurses working in gastroenterology wards (all P>0.05). Further analysis did not show any significant difference in the prevalence of H. pylori between other subgroups. The prevalence of H. pylori infection in GI endoscopists increased with the number of years of practice. Conclusions: Medical staff, especially endoscopy unit personnel, are at increased risk of infection with H. pylori.these findings strongly suggest the medical practice and endoscopy procedures are risk factors for H. pylori infection end support person-to-person transmission in this setting, probably from patients to medical staff. 34

4 Introduction H. pylori is the principal cause of chronic active antral gastritis and is strongly associated with peptic ulcer disease and gastric carcinoma (1-3). However, the epidemiology of H. pylori infection is still under investigation. Although the exact source of infection and mode of transmission have not been fully elucidated, epidemiologic studies have suggested that the most likely manner of spread of H. pylori is by direct person-to-person transmission or by exposure to a common source. The evidence in support of this hypothesis includes intrafamilial clustering of H. pylori infection (4-6) and the higher prevalence of H. pylori infection among institutionalized subjects (7). Because the H. pylori infection rate among patients undergoing endoscopy for dyspepsia in Shanghai is as high as 70% (8), and the organism can be isolated from gastric secretions and dental plaque of patients with H. pylori infection (9-10), medical staff, especially those involved in upper GI endoscopy procedures, may have an increased risk of exposure to and subsequent infection with H. pylori. Previous studies of the seroprevalence of H. pylori in endoscopy personnel have shown conflicting results. The aim of this prospective study was to assess the prevalence of H. pylori in endoscopy personnel and other medical staff, to determine whether medical staff are at an increased risk of acquiring H. pylori infection. Materials and Methods Subjects One thousand and fifty medical staff from 16 principal hospitals in Shanghai, including 125 GI endoscopists, 45 endoscopy unit nurses. 71 gastroenterologists not doing endoscopy, 105 nurses working in gastroenterology wards,417 internists, and 287 general nurses, were recruited for this study. All GI endoscopists performed 35

5 gastroscopy, and 20% did both gastroscopy and colonoscopy. Of the subjects eligible for assessment at the time sampling, about 90% of GI endoscopists and endoscopy unit nurses and 50% of gastroenterologists not doing endoscopy and nurses working in gastroenterology wards were studied. All subjects completed a questionnaire that included information relating to age, sex, present professions, duration of clinical practice, number of years working with endoscopy, previous diagnosis of peptic ulcer disease, GI symptoms, known H. pylori infection, and medications for this organism. Methods Blood specimens were obtained from each participant by a standard venipuncture technique, labeled, and immediately sent to the biochemical laboratory of Shanghai Institute of Digestive Disease for detection of serum H. pylori IgG antibodies. ELISA technique The enzyme-linked immunosorbent assay (ELISA) used in this study has been evaluated in a clinical setting and compared with reference methods of culture and smear of antral biopsy specimens (11), showing a sensitivity of 94% and a specificity of 87%. A brief outline of the method is given here. The antigen used was a pool of sonicates from eight human H. pylori isolates. The optimal dilutions of all reagents provided for this ELISA were determined by checkerboard titration. The antigen was diluted with 0.5 mol/1 carbonate buffer (ph 9.6) and coated to the wells of a polystyrene microtiter plate. Serum specimens and positive and negative controls were added to the appropriate wells on the microtiter plate after dilution and incubated for 2h at 37 C. After being washed with the washing buffer, diluted horseradish peroxidase-conjugated goat anti-human IgG was added to each well. After a further 1- h incubation and washing, the enzyme substrate reagent, o-phenylenediamine, was added to each well. The microtiter plate was incubated in the dark for 20 min, and then the reaction was terminated with stopping solution. The absorbance was read on an ELISA processor at 490nm. All samples were evaluated in duplicate. The results were 36

6 expressed as the ratio of each sample's optical density to that of a negative control, and a ratio higher than 1.8 was positive. Control group H. pylori prevalence in this group was compared with that of an age-matched group consisting of 702 'healthy' subjects other than medical staff for routine health check in same urban area of the city (12). Statistical analysis The data were analyzed with the chi-squared test and Fisher's exact test. The odds ratio was used to provide a measure of the strength of the association between suspected risk factors and outcome variables (H. pylori). Results H. pylori prevalence in medical staff and control group The percentage of H. pylori positivity in the entire experimental group, 70.0%, (735 of 1050), differed significantly from that of the control group, 44.6% (313 of 702) (P < ). Because the prevalence of H. pylori infection was not statistically significantly different between men and women (71.9%, 233 of 324 versus 69.1%, 502 of 726; P =0.366) in the experimental group, further comparisons were made only on the basis of age stratification. Table 1 shows H. pylori prevalence in the two groups stratified by age. H. pylori prevalence rates increased with age before 60 years and then decreased slightly. This age-associated trend of H. pylori prevalence existed in both groups. In each age segment H. pylori prevalence in the experimental group was always significantly higher than that of the control group. 37

7 Table 1. Comparisons of seroprevalence of H. pylori infection between medical staff and healthy controls with statistical stratification of age Ages H. pylori positive (%) (year) Medical staff Healthy controls Odds ratio 95% CI P value (245/365) 41.4(48/116) O (202/294) 46.2 (61/132) < (137/190) 47.3 (69/146) O (123/162) 50.0(521104) < (23/32) 47.3 (53/112) < (5/7) 32.6 (30/92) <0.05 Total 70.0 (735/1050) 44.6( ) O.001 Table 2. Comparisons of seroprevalence of H. pylori infection among medical staff with various professions Professions Mean age (years) No. studied H. pylori positive (%) GI endoscopists (82.4)* Endoscopy nurses (77.7) GI doctors (74.6) GI nurses (74.2) Internists (66.4) General nurses (65.8) Total (70.0) *P = 0.001, compared with groups, after adjustment for age. H. pylori prevalence in medical staff with various professions The total prevalence rate of H. pylori in this group was 70.0%; the prevalence rates in the subgroups are shown in Table 2. Because the mean ages of GI endoscopists and endoscopy nurses differed significantly from that of other subgroups, comparisons between subgroups were made after adjustment for age. The prevalence 38

8 of H. pylori in endoscopists was 82.4%, which is significantly higher than the 66.4% in internists (odds ratio, 2.24; 95% confidence interval (CI), ; PO.01) and 65.8% in general nurses (odds ratio, 2.43; 95% CI, ; P,< 0.01) but not significantly different from the 77.7% in endoscopy unit nurses or the 74.2% in nurses working in gastroenterology wards (all, P > 0.05). Further analysis did not show any significant difference in the prevalence of H. pylori between other subgroups. Table 3. Seroprevalence of H. pylori infection and the number of years working with endoscopy GI endoscopists Endoscopy nurses Years of practice <5 ^5 <5 ^5 Mean age (years) H. y/o/7-positive (%) (33/48) (70/77) (11/16) (24/29) Odds ratio* % CI # P values <0.01 >0.05 * Odds ratio adjusted for age # CI= confidence interval. H. pylori prevalence and years of practice in endoscopy The relationship between H. pylori infection and the number of years working with endoscopy in endoscopy unit personnel is shown in Table 3. Because of the limitation of practice years, we only divided endoscopy unit personnel into two subgroups, less than 5 years and 5 or more years. After adjustment for age, endoscopists who had worked 5 or more years with endoscopy had significantly higher H. Pylori seropositivity than those who had worked less than 5 years (P < 0.01), but there was no significant difference between endoscopy unit nurses who had worked 5 or more years with endoscopy and those who had worked less than 5 years (P > 0.05). 39

9 Table 4. Prevalence of peptic ulcer disease in medical staff with various professions No. studied GU DU Prevalence (%) GI endoscopists Endoscopy nurses GI doctors GI nurses Internists General nurses Total GU = gastric ulcer; DU = duodenal ulcer. Previous ulcer history and GI symptoms In this study peptic ulcer had been previously diagnosed by upper GI series and/or endoscopy. Endoscopists and nurses working with endoscopy had a higher prevalence of peptic ulcer disease than other medical doctors and nurses (Table 4). GI symptoms were noted by 187 participants (17.8%),and among them 152 were H. pv/on'-positive (81.2%),significantly higher than the 67.5rr/o (583 of 863) in those without GI symptoms( P < 0.001). Discussion Since the initial identification of H. pylori, exhaustive efforts have been made to better understand the organism's epidemiologic pattern. Evidence to support oral-oral and fecal-oral transmission from infected subjects is accumulating. H. pylori can be isolated from the gastric juice and dental plaque of infected subjects (9, 10).Transmission of H pylori as a result of endoscopic examination and study of acid secretion using ph probes has been suggested by several workers (13-15). Two recent reports of successful culture of H. pylori from fresh stool samples of infected subjects (16, 17) suggest the organism can be passed via the fecal route. Theoretically, therefore, any person in contact with such secretion or excretion is at increased risk of being 40

10 infected. Medical staff are in direct contact with patients during clinical practice, and endoscopy personnel are more commonly exposed to patients' secretion during endoscopic procedure. Previous reports of the seroprevalence of H. pylori in endoscopy staff have yielded conflicting results. Morris et al. (18) reported that the frequency of antibodies to H. pylori did not differ significantly between endoscopy staff and the normal population. Rawles et al. (19) found a higher frequency of H. pylori infection in endoscopy staff; however, this did not differ significantly from blood bank controls. Mitchell et al. (20), on the other hand, found a higher prevalence of H. pylori antibodies in gastroenterologists but not in gastroenterology nurses and general practitioners when compared with blood donor controls. Braden et al. (21) reported that the positive rate of 13 C-urea breath test for H. pylori infection differed significantly between medical staff and controls, but exposure to gastric secretion and endoscopy does not increase the risk of H. pylori infection, suggesting that medical practice rather than GI endoscopy is a risk factor for H. pylori infection. Two recent studies clearly showed an increased prevalence of H. pylori infection in gastroenterologists performing endoscopy. Lin et al. (22), in an Australian study, investigated four medical profession groups: gastroenterologists (n = 35)), general internists (n = 25), gastroenterology nurses (n - 107)and general nurses (n = 42). These subjects were compared with an age- and sex-matched population obtained by random sampling. The prevalence of H. pylori infection in gastroenterologists was 69%, significantly higher than the 40% in general internists, 17% in gastroenterology nurses, 19% in general nurses, and 32% in controls. The prevalence in gastroenterologists increased with years of practice. There was no significant difference in H. pylori prevalence between the gastroenterology nurses and controls or general nurses and controls. The study conducted in the United States by Chong et al. (23) included 111 gastroenterologists and 11 endoscopy nurses and showed a 41

11 statistically significant difference in the rate of H. pylori antibody positivity among endoscopy personnel compared with blood donor controls in all age groups. The prevalence of H. pylori infection in the experimental group was 53% (65 of 122) compared with 14% (72 of 510) in the control group, but there was no correlation with years involved in endoscopy. Our data clearly show a statistically significant difference in the seroprevalence of H. pylori between medical staff and controls in all age subgroups. The difference exists not only between endoscopy personnel and controls but also between other medical staff and controls, with the highest rate of H. pylori antibody positivity in GI endoscopists and the next highest in endoscopy unit nurses. The prevalence of H. Pylori in GI endoscopists increased with the years of practice. These findings strongly suggest that both medical practice and endoscopy procedures are risk factors for H. pylori infection. In the present studies the GI endoscopists did not routinely wear gloves during endoscopy, but the endoscopy unit nurses always wore gloves during endoscopy and cleaning of the endoscope. This may explain why GI endoscopists have a higher prevalence of H. pylori infection than endoscopy unit nurses, and the prevalence in GI endoscopists, but not in endoscopy unit nurses, increased with the years of practice. Our trial included the greatest variety of medical staff to date. The medical staff enrolled in the study were all from the Shanghai urban area. The overall prevalence rates of H. pylori infection were around 70% in patients undergoing endoscopy for dyspepsia, and 44% in the general population more than 20 years old in the urban area of this city 64% in the same age population in the city's rural area). Higher rates of peptic ulcer history were observed in the subgroups working with endoscopy than in other medical subgroups. Besides the factor of age, higher prevalence rates of H. pylori infection among these subgroups may account for the difference. 42

12 Our data indicate that the rates of H. pylori infection among medical staff in Shanghai are significantly higher than those of the control population. These findings support the person-to-person transmission of H. pylori and, in this setting, probably from patients to medical staff. Such a high infection rate may pose a serious public health problem and should call for stricter precautionary guidelines for endoscopic procedures and other medical procedures to protect medical staff and prevent iatrogenic transmission of//. pylori between endoscopy patients. References 1. Marshall BJ, McGechie DB, Rogers P, Glancy JR. Pyloric Campylobacter infection and gastro-duodenal disease. Med J Aust 1985;142: Tytgat GNJ, Rauws EAJ. Campylobacter pylori and its role in peptic ulcer disease. Gastroenterol Clin North Am 1990,19: Correa P, Fox J, Fontham E, Ruiz B, Lin Y, Zavala D,et al. H. pylori and gastric carcinoma: serum antibody prevalence in population with contrasting cancer risk. Cancer 1990;66: Malaty HM, Graham DY, Klein PD, Evans DG, Adam E, Evans DJ. Transmission of H. pylori infection. Studies in families of healthy individuals. Scand J Gastroenterol 1991;26: Oderda G, Vaira D, Holton J, Ainley C, Altare F.Bocro M,et al. H. pylori in children with peptic ulcer and their families. Dig Dis Sei 1991;36: Drumm B, Perez G, Blaser MJ, Sherman PM. Intrafamilial clustering of Helicobacter pylori infection. N Engl J Med 1990;322: Berkowicz J, Lee A. Person-to-person transmission of Campylobacter pylori.lancet 1987;2: Jiang SJ, Liu WZ, Zhang DZ,Shi Y, Xiao SD.Zhang ZH, et al. Campylobacter-like organisms in chronic gastritis, peptic ulcer, and gastric carcinoma. Scand J 43

13 Gastroenterol 1987;22: Varoli 0,Landini MP, LaPlaca M. Presence of H. pylori in gastric juice(letter). Am J Gastroenterol 1991;86: Desai HG, Gill HH, Shankaran K, Mehta PR, Prabhu SR. Dental plaque: a permanent reservoir of//, pylori? Scand J Gastroenterol 1991;26: Xiao SD, Pan ZJ, Zhang ZH, Jiang SJ. Enzyme-linked immunosorbent assay for detection of immunoglobulin G antibody against H. pylori. Chin Med J 1991;104: Pan ZJ, Xiao SD, Jiang SJ, Zhang ZH, Fang GF, Zhang SS, et al. Seroprevalence of H. pylori infection in urban and rural area of Shanghai. Chin J Dig 1992;12: Langenberg W, Rauws EA, Oudbier JH, Tytgat GN. Patient-to patient transmission of Campylobacter pylori infection by fiberoptic gastroduodenoscopy and biopsy. J Infect Dis 1990;161: Gullini S, Boccini S. Contarini D, et al. Is transmission of Campylobacter pylori by endoscopic examination possible? (letter). Endoscopy 1988;20: Gledhill T, Leicester RJ, Addis B, Lightfoot N, Barnard J, Vincy N, et al. Epidemic hypochlorhydria. Br Med J 1985;290: Thomas JE, Gibson GR, Darboe MK, Dale A,Weaver LI. Isolation of H. pylori from feces. Lancet 1992;340: Kelly SM, Pitcher MCI, Farmery SM, Gibson GR. Isolation of H. pylori from feces of patients with dyspepsia in the United Kingdom. Gastroenterology 1994;107: Morris A, Lloyd G, Nicholson G. Campylobacter pyloridis serology among gastro-endoscopy clinic staff. NZ Med J 1986;99: Rawles JW, Harris ML, Pauli G, Dick J, Yardley JH, Kafonek DR, et al. Antibody to Campylobacter pyloridis in endoscopy personnel, patients and controls 44

14 [abstract]. Gastroenterol 1987;92: Mitchell HM, Lee A, Carrick J. Increased incidence of Campylobacter pylori infection in gastroenterologists: further evidence to support person-to-person transmission of C. pylori. Scand J Gastroenterol 1989;24: Braden B, Duan LP, Lembcke B, Caspary WF. Upper Gl-endoscopy is not a risk factor for H. pylori infection, but medical practice is. Gut 1994;35 Suppl 4:A Lin SK, Lambert JR, Schembri MA, Nicholson L, Korman MG. H. pylori prevalence in endoscopy and medical staff. J Gastroenterol Hepatol 1994;9: Chong J, Marshall BJ, Barkin JS, McCallum RW, Reiner DK, Hoffman SR, et al. The occupational exposure to Helicobacter pylori for the endoscopy professional: a sera epidemiological study. Am J Gastroenterol 1994;89:

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