Gastroenterol Res
Gastroenterology Research, ISSN 1918-2805 print, 1918-2813 online, Open Access
Article copyright, the authors; Journal compilation copyright, Gastroenterol Res and Elmer Press Inc
Journal website

Original Article

Volume 8, Number 2, April 2015, pages 171-177

Gastroduodenal Changes Two Years After Eradication of Helicobacter pylori in a Population-Based Cohort

Stefan Redeena, Fredrik Peterssonb, Stergios Kechagiasa, Jens Rehfeldc, Kurt Borcha, d

aDepartment of Surgery and Department of Clinical and Experimental Medicine, Linkoping University, 58185 Linkoping, Sweden
bDepartment of Pathology, National University Health System, 119074 Singapore, Singapore
cDepartment of Clinical Biochemistry, Rigshospitalet, University of Copenhagen, Denmark
dCorresponding Author: Kurt Borch, Department of Clinical and Experimental Medicine, Faculty of Health Sciences, University of Linkoping, S-581 85 Linkoping, Sweden

Manuscript accepted for publication April 09, 2015
Short title: Effects of H. pylori Eradication


Background: The main cause of chronic gastritis is Helicobacter pylori (H. pylori) infection. Some individuals with H. pylori-related chronic gastritis develop atrophy of the gastric mucosa, a risk factor for gastric neoplasia. When H. pylori-associated gastritis is encountered, it is important to be aware of its natural history and reversibility of associated histopathological and hormonal changes.

Methods: A sample of 501 volunteers from the general population in the municipality of Linkoping, Sweden, was examined with esophago-gastro-duodenoscopy (EGD) with biopsy. Blood samples were collected in the fasting state and the subjects answered a questionnaire concerning lifestyle factors, medications and disease history. At a primary follow-up examination, after 8 years, 314 participants were re-examined and those infected with H. pylori received eradication. Two years after successful eradication therapy, 82 participants attended re-examination with EGD and blood sampling, as in the previous examinations.

Results: In this prospective cohort study of a sample of volunteers from the general population, all of the 82 participants had chronic gastritis with at least one positive H. pylori test before eradication therapy. During follow-up, non-steroid-inflammatory-drug (NSAID) use had decreased significantly (P = 0.007, McNemar). The H. pylori serology was still positive in 79/82 subjects (P = 0.007, McNemar). The basal gastrin and cholecystokinin (CCK) concentrations both had decreased (P < 0.001 for both, Wilcoxon), whereas the P-somatostatin had increased (P < 0.001, Wilcoxon). Symptoms included in the self-administered symptom questionnaire concerned the last 3 months showed no big difference at all. The inflammation had decreased in both antrum (before 2/38/42/0 and after 60/22/0/0, P < 0.0001) and corpus (before 3/54/22/3 and after 58/23/1/0, P < 0.0001). Changes in the inflammatory activity had decreased significantly in both the antrum (P < 0.001) and the corpus (P < 0.001). Intestinal metaplasia was without changes. Regarding the duodenal bulb, the inflammation decreased.

Conclusions: Being aware of the natural history of chronic gastritis, even beyond eradication of H. pylori, is important because of the associations to gastric neoplasia and ulcer disease. The blood mirror of gastroduodenal parameters showed decreased values, except for somatostatin that increased and a symptomatology with no significant changes although, morphologically determined, both inflammation and atrophy had decreased.

Keywords: Duodenitis; Follow-up; Gastrin; Gastritis; Helicobacter pylori; Metaplasia; Somatostatin; Symptoms


More than half of the world’s population are colonized with Helicobacter pylori (H. pylori) in the upper gastrointestinal tract, mainly the gastric mucosa. Most of these persons have no symptoms of the infection, and only a few (15%) will develop H. pylori-related chronic gastritis, although there is a subclinical cascade of changes due to the infection [1].

In 2005, Warren and Marshall were awarded the Nobel Prize for discovery of the spirochete H. pylori and its role in gastritis and ulcer disease [2, 3]. The common opinion today is that the infection usually is acquired in early childhood and that it, initially, may be associated with symptomatic acute gastritis and even ulcer in young people [4]. Transmission of H. pylori is thought to be mainly from person to person via faecal-oral or oral-oral routes. It may also be transmitted by contaminated water supply. In approximately 80% of H. pylori-infected subjects, chronic gastritis will occur. At present, the prevalence of H. pylori is decreasing in the Western World [5] but not in developing countries. People on regular treatment with NSAIDs, including, aspirin, are at risk of developing chronic gastritis [6].

Natural history of chronic gastritis

It is well documented that the majority of H. pylori-infected will develop chronic gastritis [7, 8]. It is important to understand the subclinical natural history of chronic gastritis, including the post eradication changes. Of particular importance is to understand the development and dynamics of atrophic gastritis, because it is a major risk for gastric neoplasia [9-11]. Having a young patient with uncomplicated atrophic gastritis raises the question whether regular screening with gastroscopy is indicated [10]. Awareness of a probable increase of the incidence of pancreatic neoplasia in atrophic gastritis associated with pernicious anaemia is also important [12].

The prevalence of atrophic gastritis in the general population has been assessed by screening gastric function. Specifically, screening involves analysis of S-pepsinogen I (PGI) or the S-pepsinogen I/S-pepsinogen II ratio (PGI/PGII), with subnormal levels indicating atrophy of the gastric corpus mucosa [13]. Screening with these surrogate markers shows an overall prevalence of atrophy of the corpus mucosa among adults in Europe and New Zealand of 3-6% increasing with age [14-16]. Using histology, however the prevalence of atrophy of the corpus mucosa ranges 10-37% in the general population in northern Europe [1, 17-20].

Several studies have documented the natural history of chronic gastritis in patient series [21-24], but there are few population-based studies [23, 25, 26]. The progression of H. pylori-associated chronic non-atrophic gastritis to atrophic gastritis is slow, and long-term observation is needed to obtain reliable data [27-29]. However, the longer the observation intervals are, the fewer the number of subjects available for follow-up. This is of particular concern amongst the elderly, who have the highest incidence of mucosal atrophy.

Post H. pylori eradication

There is little knowledge about post eradication functional and morphological changes. This study investigates a population, previous examined with gastroscopy including biopsy, histological examination and a standardized symptom questionnaire 2 years post eradication regarding gastric function, symptomatology, and morphology.

The aim of this study was to evaluate symptomatology, morphology and gastroduodenal function in a previously studied subpopulation from the general population, 2 years after H. pylori eradication.

Material and Methods▴Top 


The study was performed in accordance with the Helsinki Declaration and was approved by the Local Ethics Committee. Informed written consent was obtained from all participants. The approval was for baseline investigation and follow-up in the study. Ethical issues included the discomfort of performing gastroscopy of healthy volunteers and how to handle the findings at gastroscopy.

Study population

At the initiation of the study, 2,000 persons (20 men and 20 women for each year of the ages 35 - 85 years) randomly selected from the population register of the municipality of Linkoping, Sweden, were invited; 501 accepted and underwent oesophago-gastro-duodenoscopy (EGD) with biopsy and filled in a questionnaire about lifestyle, medications and disease history.

At the first follow-up examination, 314 participants were examined, and at this finally examination, 2 years after successful H. pylori eradication therapy was given 82 participants were possible to investigate in. Regarding the present study, inclusion criteria were presence of chronic gastritis, and occurrence of at least one positive H. pylori test (serology, histology, urea breath test (UBT), urease test on fresh biopsy). Successful eradication therapy was verified with UBT (13CO2-UBT (ref. limit < 3.5 per mille)). Table 1 presents the population in this study.

Table 1.
Click to view
Table 1. Background Variables

Eradication therapy consisted of esomeprazol 20 mg, two amoxicillin 500 mg and one clarithromycin 500 mg twice a day in a week. All participants were examined in a standardized way previously described with gastroscopy including biopsy for morphological examination, blood tests and a questionnaire about symptoms during last 3 months at the primary and the follow-up investigations. UBT was done in all participants 1 month after eradication therapy to confirm a successful eradication therapy. The questionnaire included question about lifestyle and medication, i.e. non-steroid-inflammatory-drug (NSAID). Five of the 82 participants experienced diarrhea during treatment. None of these required treatment.


The volunteers fasted for at least 6 h before the examination. Blood samples were drawn and EGD was carried out after pharyngeal anesthesia with lidocaine spray (Xylocaine, Astra, Sodertalje, Sweden). High resolution endoscopy was not used. The Olympus GIF-100 gastroscope was used and biopsies were taken with the same forceps design in all subjects at baseline and at follow-up examinations. Sedation with 2 - 3 mg intravenous flunitrazepam intravenously (dormicum, Roche AB, Stockholm, Sweden) was given on demand. Three biopsy specimens for histological examination were routinely collected from gastric body (major, anterior, and posterior aspect) and the antrum (within 3 cm of the pylorus). One additional biopsy specimen from each location was analyzed for H. pylori by urease test (CLO-test, Delta West Pty Ltd, Bentley, Australia), which was considered to indicate the presence of H. pylori if positive within (3 h paper I) 20 min, 1 h, 3 h and 12 h at follow-up. A further biopsy specimen from each of the corpus and antrum was collected for culture of H. pylori.

Histological examination and H. pylori status

An experienced pathologist blinded to other data from the study performed the microscopic examination at baseline and at follow-up after H. pylori eradication therapy in the same standardized manner.

After orientation, fixation in neutral formaldehyde, and routine processing of the biopsies (three biopsies from the corpus, antrum and second part of the duodenum), sections cut (5 μm thick) perpendicular to the surface the biopsies were stained with hematoxylin-eosin (inflammation), Alcian blue-periodic acid-Schiff (mucus), and Giemsa stain (H. pylori).

The density of H. pylori, chronic inflammatory (lympho-plasmocytic) infiltrate, inflammatory activity (polymorphonuclear cells), glandular atrophy and intestinal metaplasia were scored (0: none, 1: mild, 2: moderate, or 3: severe) according to the Sydney system. When inflammation or atrophy was present in both the antrum and corpus, gastritis was classified as antrum- or corpus-predominant if there was a two-grade or greater difference between the scores for inflammation (or atrophy), and as pan-gastritis when there was less than a two-grade difference. Gastritis limited strictly to the antrum or corpus was classified accordingly as antrum- or corpus-predominant. The severity scores for gastritis are equal to the highest score for inflammation (or atrophy) in the antral or corpus mucosa.

Results from the first examination in this study also included the glandular atrophy of the gastric corpus mucosa, moderate to severe atrophy. Atrophy of the duodenal mucosa was histologically classified according to Alexander, and in the present study it was defined as grade III or grade IV.

Blood analyses

At baseline and at first follow-up fasting blood samples were collected immediately preceding EGD. The samples were stored at -80 °C pending analysis. Pepsinogens in serum were measured with a sandwich enzyme immunoassay (ELISA) utilizing a pepsinogen I (PGI) and pepsinogen II (PGII) specific capture antibody, respectively, and a horseradish peroxidase (HRP) detection antibody (from GastroPanel®, Biohit Diagnostics, Helsinki, Finland). There is no cross-reactivity between the two assays. The reference interval is 30.0 - 120.0 µg/L for PGI, 3.0 - 10.0 µg/L for PGII and 3.0 - 20.0 for the ratio PGI/PGII. Values of PGI/PGII lower than 3.0 were considered as indicative of significant atrophy of the gastric corpus mucosa.

Serum IgG antibodies to H. pylori were analyzed by ELISA as described previously and reported as relative OD, that is, as a percent of positive standards (normal upper limit, 5%).

For measurement of α-amidated gastrins we used antiserum no. 2604 which is directed against the C-terminal sequence of the bioactive gastrins. The antiserum binds gastrin-71, -34 and -17 with equimolar potency, and negligible reactivity with cholecystokinins (CCKs) [30].

The CCK specific antiserum no. 92128 was used for the measurement of α-amidated and O-sulfated CCK peptides. The assay measures CCK-58, -33, -22 and -8 with equimolar potency [31]. For measurement of somatostatin we used antiserum no. R37 which binds somatostatin-14 and -28 with equimolar affinity [32].

The detection limit for all the immunoassay measurements is 0.5 pmol/L or less. P-gastrin, P-CCK and P-somatostatin are presented in picomol/L.


13CO2-UBT was performed as in clinical routine in a VG ISOCHROM-µG mass spectrometer (Fisons, UK). Breath samples were taken before and 15, 30, 45 and 60 min after ingestion of 50 mg 13C urea. The result used is from the cumulative curve at 30 min (delta over baseline 30) with an upper limit of 3.5 per mille. The participants were instructed to avoid proton pump inhibitors (PPIs) 2 weeks before the examination. Those in need of PPI, e.g. for gastro-oesophageal reflux disease, were prescribed low dose H2-blockers during the 2 weeks preceding UBT. UBT was used 2 years after eradication. UBT was done after eradication therapy was given, and the results were successful in all included patients in this study.

Statistical analyses

The MacNemar test for the significance of changes was used for categorical data and differences regarding continuous data were tested with the Mann-Whitney U test. A P-value of less than 0.05 was considered as significant.


In the present study from the general population, all of the 82 participants had chronic gastritis with at least one positive H. pylori test from the primary examination. At the follow-up examination, successful H. pylori eradication therapy was given. The UBT results were negative for all participants 2 years after eradication therapy. At the time of treatment, the median age was 68.9 (41.0 - 86.8) years and the median follow-up time after treatment was 29.8 (23.6 - 145.2) months (269.6 person years). Seventeen persons had a history of ulcer disease.

Demographic data are given in Table 1. All hormonal values from baseline and at follow-up are given in Table 2. The NSAID consumption decreased significant (P = 0.007, McNemar). The H. pylori serology was still positive in 79/82 subjects (P = 0.007, McNemar). The PGI/PGII ratio decreased significantly (P = 0.001, McNemar). The P-total gastrin decreased significantly (P < 0.001 for both, Wilcoxon), whereas the P-somatostatin and P-CCK had increased significantly (P < 0.001 for both, Wilcoxon).

Table 2.
Click to view
Table 2. Hormonal Changes Observed at Baseline and at Follow-Up After H. pylori Eradication

All symptoms are presented in Table 3 from the standardized and previously used questionnaire. Symptoms included in the self-administered symptom questionnaire concerned the last 3 months, preceeding EGD at baseline before eradication therapy and at follow-up 2 years after eradication therapy. The frequency of symptoms was graded into: none (0), not every month (1), every month (2), every week (3), and every day (4). The frequency of epigastric pain had decreased significantly (P = 0.028, McNemar), but there was no significant change in the frequency of other symptoms such as food intolerance, vomiting, acid regurgitation, heart burn, dysphagia, nausea, diarrhea, constipation, bloating and disturbing abdominal gas. None had severe problems or died. The only result regarding symptoms with some significance was epigastric pain, although in few participants. Five participants had relatively mild diarrhea after eradication therapy was given, one needed treatment, and everybody was healthy again.

Table 3.
Click to view
Table 3. Abdominal Symptoms at Baseline and Follow-Up

The morphologies both in antrum and corpus are presented in Table 4. The inflammation had decreased in both antrum (before 2/38/42/0 and after 60/22/0/0, P < 0.0001) and corpus (before 3/54/22/3 and after 58/23/1/0, P < 0.0001) after eradication of H. pylori. Changes in the inflammatory activity had decreased significantly in both the antrum (P < 0.001) and the corpus (P < 0.001). Regarding intestinal metaplasia there were no significant changes. Chronic inflammation had decreased significantly in both the antrum (before 2/38/42/0 and after 60/22/0/0, P < 0.0001) and the corpus (3/54/22/3 and after 58/23/1/0, P < 0.0001) 2 years after eradication treatment. Atrophy had decreased significantly in the antrum, but was unchanged in the corpus. Inflammatory activity had decreased significantly in both the antrum (P < 0.001) and corpus (P < 0.001).

Table 4.
Click to view
Table 4. Morphology

Table 5 shows the results presented from the duodenal bulb: 66 of 77 subjects had score 0 for inflammation before eradication therapy. At the 2-year follow-up examination, the corresponding frequency was 74 of 77 (P = 0.013, McNemar). Bulbitis was decreased after eradication. Regarding gastric metaplasia, there were no significant changes after eradication therapy.

Table 5.
Click to view
Table 5. Duodenal Inflammation and Gastric Metaplasia at First (2) and Second (3) Follow-Up

Chronic gastritis is common worldwide. If there are benefits with eradicating the H. pylori infection and related risk conditions regarding morbidity and mortality, the general population should be offered this.

In this study, we focused on gastric function, symptomatology and morphology after successful eradication therapy. It is well known that the H. pylori prevalence has decreased in the Western world. The distribution in developing countries is mainly unknown.

The follow-up period, for other studies, could include more patients and even from different countries during a longer study period. We had almost 270 person years in total as a basis for follow-up our study population.

We found changes regarding NSAID consumption which had decreased at follow-up, and the reason to decreased NSAID consumption is beyond this study. Maybe awareness of complications related to NSAID use now is common and other drugs are used instead. Plasma CCK and gastrin concentrations decreased in the follow-up period, whereas somatostatin concentrations increased. These changes can all be related to decreased inflammation of the gastric mucosa. Considering symptoms, there were no major differences.

Villako et al found interesting dynamic effects in an Urban Estonian society with gastritis affecting the body increased significantly with age and gastritis in antrum decreased [14]. The reason behind this is not obvious from this study, but shows that development exists and is important to understand.

Further from the Maastricht III consensus report with management of H. pylori infection one comment is that the burden of gastric cancer is considerable but varies geographically [6]. Weather eradication therapy should be given in asymptomatic H. pylori infection is still a matter of debate.

Follow-up studies like this with symptoms, hormonal and morphological aspects are uncommon. Houghton et al conclude from the background that gastric cancer remains a leading cause of death worldwide that in the name of preventable disease it is important with effective eradication. Still the general population are not the target for eradication.

Of course it is important to decrease inflammation and activity of inflammation, and the clinical manifestations over time needs to be investigated in the future.

From other studies we know that somatostatin increases after eradication therapy indicating possible recovery of the mucosa [33].

The bulbitis was decreased after eradication therapy of H. pylori.

In conclusion, this study shows that gastric inflammation and activity in the inflammation decrease after eradication of H. pylori. Hormonal changes occur but there are no specific major changes in symptomatology.

  1. Borch K, Jonsson KA, Petersson F, Redeen S, Mardh S, Franzen LE. Prevalence of gastroduodenitis and Helicobacter pylori infection in a general population sample: relations to symptomatology and life-style. Dig Dis Sci. 2000;45(7):1322-1329.
    doi pubmed
  2. Houghton J, Wang TC. Helicobacter pylori and gastric cancer: a new paradigm for inflammation-associated epithelial cancers. Gastroenterology. 2005;128(6):1567-1578.
    doi pubmed
  3. Unidentified curved bacilli on gastric epithelium in active chronic gastritis. Lancet. 1983;1(8336):1273-1275.
  4. Huang SC, Sheu BS, Lee SC, Yang HB, Yang YJ. Etiology and treatment of childhood peptic ulcer disease in Taiwan: a single center 9-year experience. J Formos Med Assoc. 2010;109(1):75-81.
  5. Fischbach W, Malfertheiner P, Hoffmann JC, Bolten W, Kist M, Koletzko S. Helicobacter pylori and gastroduodenal ulcer disease. Dtsch Arztebl Int. 2009;106(49):801-808.
  6. Dixon MF, Genta RM, Yardley JH, Correa P. Classification and grading of gastritis. The updated Sydney System. International Workshop on the Histopathology of Gastritis, Houston 1994. Am J Surg Pathol. 1996;20(10):1161-1181.
    doi pubmed
  7. Malfertheiner P, Megraud F, O'Morain C, Bazzoli F, El-Omar E, Graham D, Hunt R, et al. Current concepts in the management of Helicobacter pylori infection: the Maastricht III Consensus Report. Gut. 2007;56(6):772-781.
    doi pubmed
  8. Redeen S, Petersson F, Kechagias S, Mardh E, Borch K. Natural history of chronic gastritis in a population-based cohort. Scand J Gastroenterol. 2010;45(5):540-549.
    doi pubmed
  9. Borch K, Renvall H, Liedberg G. Gastric endocrine cell hyperplasia and carcinoid tumors in pernicious anemia. Gastroenterology. 1985;88(3):638-648.
  10. Borch K. Epidemiologic, clinicopathologic, and economic aspects of gastroscopic screening of patients with pernicious anemia. Scand J Gastroenterol. 1986;21(1):21-30.
    doi pubmed
  11. Borch K, Kullman E, Hallhagen S, Ledin T, Ihse I. Increased incidence of pancreatic neoplasia in pernicious anemia. World J Surg. 1988;12(6):866-870.
    doi pubmed
  12. Borch K, Jansson L, Sjodahl R, Anderberg B. Haemorrhagic gastritis. Incidence, etiological factors, and prognosis. Acta Chir Scand. 1988;154(3):211-214.
  13. Dinis-Ribeiro M, Yamaki G, Miki K, Costa-Pereira A, Matsukawa M, Kurihara M. Meta-analysis on the validity of pepsinogen test for gastric carcinoma, dysplasia or chronic atrophic gastritis screening. J Med Screen. 2004;11(3):141-147.
    doi pubmed
  14. Sipponen P, Laxen F, Huotari K, Harkonen M. Prevalence of low vitamin B12 and high homocysteine in serum in an elderly male population: association with atrophic gastritis and Helicobacter pylori infection. Scand J Gastroenterol. 2003;38(12):1209-1216.
    doi pubmed
  15. Green TJ, Venn BJ, Skeaff CM, Williams SM. Serum vitamin B12 concentrations and atrophic gastritis in older New Zealanders. Eur J Clin Nutr. 2005;59(2):205-210.
    doi pubmed
  16. Weck MN, Stegmaier C, Rothenbacher D, Brenner H. Epidemiology of chronic atrophic gastritis: population-based study among 9444 older adults from Germany. Aliment Pharmacol Ther. 2007;26(6):879-887.
    doi pubmed
  17. Siurala M, Isokoski M, Varis K, Kekki M. Prevalence of gastritis in a rural population. Bioptic study of subjects selected at random. Scand J Gastroenterol. 1968;3(2):211-223.
    doi pubmed
  18. Villako K, Tamm A, Savisaar E, Ruttas M. Prevalence of antral and fundic gastritis in a randomly selected group of an Estonian rural population. Scand J Gastroenterol. 1976;11(8):817-822.
  19. Ihamaki T, Varis K, Siurala M. Morphological, functional and immunological state of the gastric mucosa in gastric carcinoma families. Comparison with a computer-matched family sample. Scand J Gastroenterol. 1979;14(7):801-812.
    doi pubmed
  20. Villako K, Kekki M, Tamm A, Tammur R, Savisaar E, Viirsalu V, Sipponen P. Epidemiology and dynamics of gastritis in a representative sample of an Estonin urban population. Scand J Gastroenterol. 1982;17(5):601-607.
    doi pubmed
  21. Valle J, Kekki M, Sipponen P, Ihamaki T, Siurala M. Long-term course and consequences of Helicobacter pylori gastritis. Results of a 32-year follow-up study. Scand J Gastroenterol. 1996;31(6):546-550.
    doi pubmed
  22. Ormiston MC, Gear MW, Codling BW. Five year follow-up study of gastritis. J Clin Pathol. 1982;35(7):757-760.
    doi pubmed
  23. Villako K, Kekki M, Maaroos HI, Sipponen P, Tammur R, Tamm A, Keevallik R. A 12-year follow-up study of chronic gastritis and Helicobacter pylori in a population-based random sample. Scand J Gastroenterol. 1995;30(10):964-967.
    doi pubmed
  24. Sipponen P, Kimura K. Intestinal metaplasia, atrophic gastritis and stomach cancer: trends over time. Eur J Gastroenterol Hepatol. 1994;6(Suppl 1):S79-83.
  25. Siurala M, Sipponen P, Kekki M. Chronic gastritis: dynamic and clinical aspects. Scand J Gastroenterol Suppl. 1985;109:69-76.
    doi pubmed
  26. Maaroos HI, Vorobjova T, Sipponen P, Tammur R, Uibo R, Wadstrom T, Keevallik R, et al. An 18-year follow-up study of chronic gastritis and Helicobacter pylori association of CagA positivity with development of atrophy and activity of gastritis. Scand J Gastroenterol. 1999;34(9):864-869.
    doi pubmed
  27. Kandulski A, Selgrad M, Malfertheiner P. Helicobacter pylori infection: a clinical overview. Dig Liver Dis. 2008;40(8):619-626.
    doi pubmed
  28. de Vries AC, Meijer GA, Looman CW, Casparie MK, Hansen BE, van Grieken NC, Kuipers EJ. Epidemiological trends of pre-malignant gastric lesions: a long-term nationwide study in the Netherlands. Gut. 2007;56(12):1665-1670.
    doi pubmed
  29. Correa P, Houghton J. Carcinogenesis of Helicobacter pylori. Gastroenterology. 2007;133(2):659-672.
    doi pubmed
  30. Stadil F, Rehfeld JF. Determination of gastrin in serum. An evaluation of the reliability of a radioimmunoassay. Scand J Gastroenterol. 1973;8(2):101-112.
  31. Rehfeld JF. Accurate measurement of cholecystokinin in plasma. Clin Chem. 1998;44(5):991-1001.
  32. Rehfeld JF. Sequence-specific radioimmunoassays for cholecystokinin, gastrin and somatostatin. Biomedical Research 1. 1980;(Suppl 1):73-78.
  33. Milutinovich M, Koshland DE. Molecular biology. SMC complexes--wrapped up in controversy. Science. 2003;300(5622):1101-1102.
    doi pubmed

This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Gastroenterology Research is published by Elmer Press Inc.


Browse  Journals  


Journal of Clinical Medicine Research

Journal of Endocrinology and Metabolism

Journal of Clinical Gynecology and Obstetrics


World Journal of Oncology

Gastroenterology Research

Journal of Hematology


Journal of Medical Cases

Journal of Current Surgery

Clinical Infection and Immunity


Cardiology Research

World Journal of Nephrology and Urology

Cellular and Molecular Medicine Research


Journal of Neurology Research

International Journal of Clinical Pediatrics



Gastroenterology Research, bimonthly, ISSN 1918-2805 (print), 1918-2813 (online), published by Elmer Press Inc.                     
The content of this site is intended for health care professionals.

This is an open-access journal distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 International License, which permits unrestricted
non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
Creative Commons Attribution license (Attribution-NonCommercial 4.0 International CC-BY-NC 4.0)

This journal follows the International Committee of Medical Journal Editors (ICMJE) recommendations for manuscripts submitted to biomedical journals,
the Committee on Publication Ethics (COPE) guidelines, and the Principles of Transparency and Best Practice in Scholarly Publishing.

website:   editorial contact:
Address: 9225 Leslie Street, Suite 201, Richmond Hill, Ontario, L4B 3H6, Canada

© Elmer Press Inc. All Rights Reserved.

Disclaimer: The views and opinions expressed in the published articles are those of the authors and do not necessarily reflect the views or opinions of the editors and Elmer Press Inc. This website is provided for medical research and informational purposes only and does not constitute any medical advice or professional services. The information provided in this journal should not be used for diagnosis and treatment, those seeking medical advice should always consult with a licensed physician.