Gastroenterology Today Summer 2023

Volume 33 No. 2 

Summer 2023 

Passionate about Endoscopy? 

We are clearing NHS trust waiting lists 

one weekend at a time, and 

we need your help 

18 Week Support Gastroenterology: 

Building Expert Teams

Better Resource 

Management 

for Digestive 

Disease Pathways 

Quantum Blue ® for Point of 

Care helps triage patients 

in clinic giving results in a 

rapid time frame (15 mins) 

Calprotectin Testing 

Make more informed 

clinical decisions without 

waiting for lab results. 

IBDoc ® Home Tests. Supporting 

remote patient monitoring and 

virtual clinics 

Faecal Immunochemical Testing 

Complete bespoke solutions to triage patients 

within the colorectal cancer pathway. 

New kit ordering portal for 

convenient logistics 

Customised FIT Kits delivered to patient 

‘ready to use’ – everything the patient 

requires to take their sample safely at 

home for return to a laboratory 

19 TH – 22 ND JUNE 

COME AND 

SEE US ON 

STAND B17 

Supplied by 

For more information, to discuss your requirements or organise an 

evaluation please contact: digestivedx@alphalabs.co.uk 

T: +44 (0)23 8048 3000 

E: sales@alphalabs.co.uk 

W: www.alphalabs.co.uk 

02380 483000 • sales@alphalabs.co.uk • www.alphalabs.co.uk

CONTENTS 

CONTENTS 

4 EDITORS COMMENT 

6 FEATURE Evaluation of non-gastric upper gastrointestinal 

system polyps: an epidemiological assessment 

13 FEATURE Evaluation of gut microbiota of Iranian patients 

with celiac disease, non-celiac wheat sensitivity, 

and irritable bowel syndrome: are there any 

similarities? 

29 COMPANY NEWS 

COVER STORY 

18 Week Support is the leading insourcing provider in the UK, partnering with 

trusts to address their waiting lists by optimising the utilisation of their theatres 

and clinics. Although we cover a wide range of specialties, our emphasis lies in 

Endoscopy and Gastroenterology, where we strive to ensure the highest quality 

of care for our patients. 

After Covid 19, the number of patients waiting more than 6 weeks for 

endoscopies, gastroscopies and flexible sigmoidoscopies rose dramatically, 

from 9.3% in February 2020 to 67.6% in May 2020. Since then, the NHS has 

been working tirelessly to address the influx of patients waiting for procedures, 

although this has not been easy. In March 2023, the percentage of patients 

waiting more than 6 weeks for this procedure was 37.5%; still far greater than 

the 5% aim set out by the NHS 2023/2024 Operating Plan. 

This issue edited by: 

Andrew Poullis 

c/o Media Publishing Company 

Greenoaks 

Lockhill 

Upper Sapey, Worcester, WR6 6XR 

ADVERTISING & CIRCULATION: 

Media Publishing Company 

Greenoaks, Lockhill 


Tel: 01886 853715 

E: info@mediapublishingcompany.com 

www.MediaPublishingCompany.com 

PUBLISHING DATES: 

March, June, September and December. 

COPYRIGHT: 

Media Publishing Company 

Greenoaks 

Lockhill 


PUBLISHERS STATEMENT: 

The views and opinions expressed in 

this issue are not necessarily those of 

the Publisher, the Editors or Media 

Publishing Company. 

Next Issue Autumn 2023 

Designed in the UK by me&you creative 

While progress has been made since Covid 19, recent data points to a 

potential increase in patients waiting more than 6 weeks for these procedures. 

We believe that the solution to this problem lies in maximising the use of 

existing capacity in addition to the new capacity created by the government as 

it continues to invest in community diagnostics centres. 

We need to support the NHS in transforming its model to a seven-day 

service to tackle this problem thereby making full use of the existing capacity. 

Insourcing can achieve this by providing flexible workforce models and making 

better use of the capacity already available within the NHS. 

GASTROENTEROLOGY TODAY - SUMMER 2023 

3

EDITORS COMMENT 

EDITORS COMMENT 


“Over the 

years a 

number 

of Nobel 

prize 

winners 

for 

medicine 

have 

originated 

in 

Liverpool 

or carried 

out their 

early 

works in 

this city.” 

Liverpool 2023 

Eurovision and BSG! Liverpool is having a busy 2023. Although no home grown success 

in the Eurovision this year Liverpool is a city with a long history of awards and international 

successes. Ignoring the obvious footballing awards, in the field of science and medicine 

Liverpool has a long history. 

Over the years a number of Nobel prize winners for medicine have originated in Liverpool or 

carried out their early works in this city. 

Sir Ronald Ross in 1902 was recognised for his work on transmission of malaria. 

In 1932 Sir Charles Scott Sherrington was recognised as he defined the spinal reflex and 

defined synapses. 

More pertinent to gastroenterology was Professor Rodney Porter, who started his studies in 

Liverpool, and was awarded Nobel prize in 1972 determining the chemical structure of an 

antibody - an important first step in the field of biologic drug therapies which have become 

the cornerstone of IBD management. 

The BSG conference will showcase national and international work in its annual meeting in 

Liverpool. 

Andrew Poullis 

St George’s Hospital 

4

FEATURE 

EVALUATION OF NON-GASTRIC UPPER 

GASTROINTESTINAL SYSTEM POLYPS: 

AN EPIDEMIOLOGICAL ASSESSMENT 

Çağdaş Erdoğan*, Derya Arı, Bayram Yeşil, Kenan Koşar, Orhan Coşkun, İlyas Tenlik, Hasan Tankut Köseoğlu & Mahmut Yüksel 

Department of Gastroenterology, Ankara City Hospital, University of Health Sciences, Bilkent Avenue, Çankaya, 06800 Ankara, Turkey. *email: cagdas.erdogan@saglik.gov.tr; 

cagdas_edogan@hotmail.com Scientific Reports | (2023) 13:6168 https://doi.org/10.1038/s41598-023-33451-1 

Abstract 

Non-gastric upper gastrointestinal system polyps are detected rarely 

and mostly incidentally during upper gastrointestinal endoscopy. While 

the majority of lesions are asymptomatic and benign, some lesions 

have the potential to become malignant, and may be associated with 

other malignancies. Between May 2010 and June 2022, a total of 

127,493 patients who underwent upper gastrointestinal endoscopy 

were retrospectively screened. Among these patients, those who had 

polyps in the esophagus and duodenum and biopsied were included in 

the study. A total of 248 patients with non-gastric polyps were included 

in this study. The esophageal polyp detection rate was 80.00/100,000, 

while the duodenal polyp detection rate was 114.52/100,000. In 

102 patients (41.1%) with esophageal polyps, the mean age was 

50.6 ± 15.1, and 44.1% (n = 45) were male. The most common type 

of polyps was squamous papilloma (n = 61, 59.8%), followed by 

inflammatory papilloma (n = 18, 17.6%). In 146 patients (58.9%) with 

duodenal polyps, the mean age of patients was 58.3 ± 16.5, and 69.8% 

(n = 102) were male. Brunner’s gland hyperplasia, inflammatory polyp, 

ectopic gastric mucosa, and adenomatous polyp were reported to be 

the most prevalent types of polyps in the duodenum overall (28.1%, 

27.4%, 14.4%, and 13.7%, respectively). It is crucial to identify rare nongastric 

polyps and create an effective follow-up and treatment plan in 

the era of frequently performed upper gastrointestinal endoscopies. The 

epidemiological assessment of non-gastric polyps, as well as a followup 

and treatment strategy, are presented in this study. 

some lesions can be considered as premalignant. Since glycogenic 

acanthosis, the most prevalent polypoid lesion in the esophagus, has a 

frequency of 3.5–15%, a characteristic structure, and a benign nature, 

these lesions are simple to identify and don’t need to be biopsied or 

evaluated pathologically 3-5 . With a rate between 0.01% and 0.45%, 

esophageal squamous papilloma (Fig. 1) are relatively the most prevalent 

polypoid lesions in the esophagus 6,7 . It is mostly seen in patients 

around 50 years of age, in the distal esophagus and as a single lesion 8 . 

Although most papilloma are asymptomatic, dysphagia due to large 

papilloma has been reported rarely 9 . Esophageal papillomas are followed 

in incidence by inflammatory polyps 10 , esophageal parakeratosis 11 , 

and esophageal adenomas 12-14 that develop on the basis of Barrett’s 

esophagus and carry malignant potential. 

Lymphangiomas 15 and neuroendocrine tumors that originate from the 

submucosa are other esophageal lesions that can come across. These 

lesions can, however, only be found extremely rare. Neuroendocrine 

tumors can be seen in the pancreas or tubular organs of the GI 

system and show neuroendocrine differentiation. Endoscopically, 

neuroendocrine tumors of the digestive tract can present as polypoid 

forms, nodules, masses, ulcers, or stenosis, and they can be single or 

multiple and range in size from a few millimeters to several centimeters. 

These tumors, which are rare in the esophagus (only 50 cases have 

been documented), typically form sessile polypoid structures in the 

lower third 16 . 


6 

Introduction 

Upper gastrointestinal endoscopy (esophagogastroduodenoscopy, 

EGD) includes evaluation of the oropharynx, esophagus, stomach, and 

proximal duodenum. EGD can be performed with indications such as 

dyspeptic complaints unresponsive to medical treatment, presence 

of alarm symptoms, upper gastrointestinal symptoms after the age of 

50, dysphagia, persistent vomiting, or upper gastrointestinal bleeding. 

Polyps are mostly detected incidentally during upper gastrointestinal 

endoscopy. However, management and appropriate pathological 

evaluation of polyps are very important 1,2 . 

Many benign lesions can be encountered during the endoscopic 

evaluation of the esophagus. Most lesions are rare and asymptomatic. 

Although most of these lesions do not have malignant potential, 

Duodenal polyps are generally quite rare and can be classified as nonneoplastic 

and neoplastic. Based on the respective incidence, nonneoplastic 

lesions include ectopic gastric mucosa, inflammatory polyps, 

Brunner’s gland hyperplasia, peutz-jeghers polyps, and hyperplastic 

polyps. Whereas, neoplastic lesions include adenomas, gastrointestinal 

stromal tumors, Brunner’s gland adenoma, carcinoid tumors, 

leiomyoma, lipoma, schwannoma can be counted. Duodenal adenomas 

(Figs. 2, 3) have three major types: villous adenomas, tubular adenomas, 

and Brunner’s gland adenomas. Villous adenomas carry a significant 

risk of malignancy. Since the incidence of colon adenomas increases in 

patients with duodenal polyps, colonoscopy should be performed when 

these polyps are detected 17 . 

Tubular adenomas are more common in the duodenum, are mostly 

asymptomatic and have less malignant potential. Brunner’s gland 

adenomas are rare small intestinal polyps that are more common,

FEATURE 

In this study we aimed to evaluate the epidemiological distribution of 

polyps detected during EGD and submitted to pathological assessment 

by biopsy, as well as the follow-up and treatment strategy in polyps with 

malignant potential or symptomatic. 

Patients/material and methods 

Figure 1. Esophageal squamous papilloma. 

Our study was approved by Ankara City Hospital Scientific Research 

Evaluation and Ethics Committee (Approval No: E1-22-2328). The 

procedures implemented until February 2019 were carried out at Ankara 

Turkey Yüksek İhtisas Training and Research Hospital. Since Ankara 

Turkey Yüksek İhtisas Training and Research Hospital joined the Ankara 

City Hospital after February 2019, the patients included in the study after 

this date were selected among the patients followed up and treated at 

Ankara City Hospital. 

Between May 2010 and June 2022, a total of 127,493 patients who 

underwent upper gastrointestinal endoscopy with indications such as 

dyspepsia, dysphagia, and iron deficiency anemia were retrospectively 

screened. Among these patients, those who had polyps in the 

esophagus and duodenum and biopsied were included in the study. 

Figure 2. Duodenal adenomatous polyp. 

In patients who underwent EGD, biopsy or excision was performed on 

all polyps detected in the esophagus that were solitary or larger than 

1 cm. All patients with Barrett’s esophagus discovered to have polyps 

underwent biopsies. When dysplasia clusters are observed rather 

than a single polyp formation in Barrett’s esophagus, which is where 

the majority of esophageal adenomas arise from, the vascular pattern 

was assessed with NBI endoscopy, and a biopsy was collected for 

esophageal adenoma. In addition, biopsies or excisions were performed 

on hyperemic polyps, polyps with aberrant vascular patterns on narrowband 

imaging (NBI) endoscopy, and ulcerated polyps. However, no 

biopsy was performed when multiple instances of glycogenic acanthosis 

were found. In case of detection of polyps in the duodenum, polyps 

were biopsied or excised from all patients. 

Figure 3. Duodenal adenomatous polyp magnified. 

accounting for 10.6% of duodenal tumors 18 . Ectopic gastric mucosa may 

present as polypoid lesions which are rare congenital disorders and are 

detected incidentally during upper GI endoscopy. It has been reported 

in the literature that heterotopic gastric mucosa may be associated with 

duodenal ulcers 19 . Gastrointestinal stromal tumors (GIST) are mostly 

encountered in the stomach, they can also be seen in the esophagus 

(< 1%) and duodenum (5%) 20 . Tumors originating from the upper GI may 

present with dysphagia, GI bleeding, or obstructive jaundice. 

Duodenal or ampullary NETs are extremely rare and account for 

approximately 2.6% of all NETs 21 . These tumors are of clinical 

importance as most of them are asymptomatic and potentially 

malignant. They typically occur in the I and II duodenal sections, 

preferring the peripapillary region, and under endoscopic vision, they 

show as a single, small lesion (frequently less than 1 cm in size). 

Additionally, they may exist in groups or be linked to neuroendocrine 

tumors in other organs 16 . 

Patients who had polyps but could not be biopsied due to 

antiaggregant/anticoagulant use, hemodynamic instability, and patient 

intolerance were excluded from the study. In addition, patients with 

gastric polyps were also excluded. Additionally, patients with esophageal 

polyps who underwent biopsies and who, upon pathologic inspection, 

revealed to have glycogenic acanthosis were removed from the study. 

Patients’ demographic characteristics such as age, gender, smoking, 

history of comorbid diseases and drug use were recorded. Polyp sizes, 

polyp types, number of polyps and histopathological findings were 

recorded in patients who were found to have esophageal and duodenal 

polyps and biopsied. Additionally, antrum biopsies were performed to check 

for H. pylori in patients with polyps. The pathologists stained the tissue 

samples with Giemsa and tested for the presence of H. pylori. Patients 

with helicobacter pylori positivity as a result of pathology were separately 

identified. According to the pathology results, whether the patients 

had reflux findings in their histories, whether they had a history of head 

and neck cancer, and previous endoscopic and colonoscopy findings, 

if any, were evaluated. The frequency per 100,000 of esophageal and 

duodenal polyps detected in the patients was reported. The pathological 

distributions of the polyps were also displayed as a rate per 100,000. 


7

FEATURE 

In patients undergoing colonoscopy the cleanliness of the colonoscopy 

was evaluated using the Boston Bowel Preparation Scale (BBPS). 

Following colonoscopy cleaning, patients with BBPS 0 or 1 were taken 

for another colonoscopy. Colonoscopy cleanliness scores BBPS 2 and 3 

were used to assess all study participants who had non-gastric polyps. 

Withdrawal from the colonoscopy took at least 10 min. 

Endoscopic evaluation was performed with Olympus brand GIF-Q260 

model gastroscopes. Before the procedure, patients were given 

sedo-analgesia or topical anesthetic containing 10% lidocaine to the 

oropharynx, accompanied by an anesthesiologist. The lesions were 

removed with forceps or snare. The biopsy material was fixed with 10% 

formaldehyde solution and sent for pathological evaluation. 

Statistical analysis 

All statistical analyzes were performed using SPSS software (SPSS 

for Windows, version 25.0, IBM. Corp., Armonk, NY, USA). The 

Kolmogorov–Smirnov test was used to determine the normality of the 

continuous variables. Normally distributed variables were expressed 

as mean ± standard deviation and non-normally distributed variables 

as median and interquartile range. Normally distributed variables 

were compared using the student t test and non-normally distributed 

variables using the Mann–Whitney U test. Chi-square (χ 2 ) test and 

Fisher’s Exact test were used for group comparisons (cross tables) 

of nominal variables. Two-tailed p values < 0.05 were considered 

statistically significant. 

Ethics committee approval 

This study was complied with the ethical guidelines of the 1975 Helsinki 

Declaration that was then modified in 2008. The study protocol was 

approved by Ankara City Hospital ethics committee (Approval No: E1- 

22-2328). 

Informed consent 

Informed consent was obtained from all patients participating in the 

study. 

All patients (n = 102) 

Age, years 50.6 ± 15.1 – 

Gender, male, n (%) 45 (44.1) – 

Smoking, n (%) 56 (54.9) – 

Polyp size, mm 5.0 (4.0–7.0) – 

Number of polyps 1.0 (1.0–1.0) – 

Polyp type, n (%) 

Pedunculated 65 (63.7) – 

Sessile 37 (36.3) – 

Pathology, n (%) 

Squamous papilloma 65 (63.7) 50.98 

Inflammatory polyp 21 (20.7) 16.47 

Hyperplastic polyp 3 (2.9) 2.35 

Lymphangioma 3 (2.9) 2.35 

Esophageal parakeratosis 6 (5.9) 4.70 

Esophageal adenoma 4 (3.9) 3.14 

Helicobacter pylori, n (%) 26 (25.5) – 

Reflux esophagitis, n (%) 17 (16.7) – 

Other endoscopic findings, n (%) 

Normal 8 (7.8) – 

Antral gastritis 31 (30.4) – 

Bulbitis 3 (2.9) – 

Pangastritis 49 (48.0) – 

Antral gastritis + bulbitis 9 (8.9) – 

Gastric lymphoma 2 (2.0) – 

Colonoscopy, n (%) 76 (74.5) – 

Colon polyp localization, n (%) 

Transverse + ascending + sigmoid 3 (2.9) – 

Transverse + ascending + rectum 3 (2.9) – 

Descending + transverse 4 (3.9) – 

Rectum 5 (4.9) – 

Colon polyp pathology, n (%) 

Adenomatous 15 (14.7) – 

Rate per 100,000 patients 

Table Table 1. 1. Demographic characteristics, endoscopic endoscopic and and colonoscopy colonoscopy findings, and pa 

of patients findings, with and esophageal pathological polyps, evaluations pathologic of patients findings with as esophageal rate per 100,000 patients. D 

median polyps, ± SD pathologic or median findings (IQR) or as frequency rate per 100,000 (%). SD patients. standard Data deviation. are 

expressed as median ± SD or median (IQR) or frequency (%). 

SD standard deviation. 


Results 

Vol:.(1234567890) 

A total of 248 patients who were evaluated for non-gastric polyps 

were included in this study. Total evaluation revealed a detection rate 

of 194.52 non-gastric polyps per 100,000 patients. In this context, 

the esophageal polyp detection rate was 80.00 per 100,000, while 

the duodenal polyp detection rate was 114.52 per 100,000. 

One hundred and two (41.1%) of the included patients were those 

with esophageal polyps. The mean age of patients with esophageal 

polyps was 50.6 ± 15.1, and 44.1% (n = 45) were male. The median 

size of esophageal polyps was 5.0 (4.0–7.0) mm. Pedunculated 

polyps were seen in 63.7% of cases (n = 65), while sessile polyps 

were found in 36.3% of cases (n = 37). The most common type 

of polyps was squamous papilloma (n = 65, 63.7%), followed by 

inflammatory papilloma (n = 18, 17.6%). Helicobacter pylori was 

found in 26 (25.5%) and reflux esophagitis in 21 (20.7%) patients. 

The most common endoscopic gastric finding was pangastritis 

(n = 49, %48.0) followed by antral gastritis (n = 31, %30.4). 

Adenomatous polyps were detected in 15 of 76 patients with 

esophageal polyps who underwent colonoscopy. Table 1 includes 

demographic information as well as endoscopic and colonoscopic 

findings, pathology results, and epidemiological rates of patients 

with esophageal polyps. 

When patients with duodenal polyps were evaluated (n = 146), 

polyps were observed in the duodenal bulb in 91 patients (62.3%) 

and in the second part of the duodenum (D2) in 55 patients (37.7%). 

The mean age of patients with duodenal polyps was 58.3 ± 16.5, 

and 69.8% (n = 102) were male. The median size of duodenal polyps 

was 7.0 (3.5–15.0) mm. Brunner’s gland hyperplasia, inflammatory 

polyp, ectopic gastric mucosa, and adenomatous polyp were 

reported to be the most prevalent types of polyps in the duodenum 

overall (28.1%, 27.4%, 14.4%, and 13.7%, respectively). In 

subgroup analysis Brunner’s gland hyperplasia was most common 

in bulbus (36%), while adenomatous polyp was most common in D2 

(bulbus vs. D2; 2 vs. 18; p < 0.001). All polyps with adenomatous 

pathology were detected in the second continent of the duodenum, 

whereas individuals with ectopic gastric mucosa as a result of 

pathology had polyp localization in the first continent (p0.00.1 for 

both findings). The presence of antral gastritis, bulbitis, duodenitis, 

8

FEATURE 

pangastritis, pangastritis + bulbitis, atrophic gastritis, FAP, gastric 

cancer and peutz-jeghers syndrome was at similar rates between 

both groups. In addition, colonoscopy was performed in 88 (%60.3) 

patients with polyps in the duodenum, and polyps were detected in 

the colon in 35 (%24) of them. While hyperplastic polyp was found 

in the colon in two patients with polyp in the bulbus, adenomatous 

polyp was detected in the colon in the 33 patients and in all patients 

with polyps in the second part of the duodenum. Table 2 includes 

demographic information as well as endoscopic and colonoscopic 

findings, pathology results, and epidemiological rates of patients 

with duodenal polyps. 

All patients (n = 146) 

Age, years 58.3 ± 16.5 – 

Gender, male, n (%) 102 (69.8) – 

Smoking, n (%) 81 (55.5) – 

Polyp size, mm 7.0 (3.5–15.0) – 

Number of polyps 1.0 (1.0–2.5) – 

Polyp localization, n (%) 

Duodenal bulb 91 (62.3) 71.38 

Second part of the duodenum (D2) 55 (37.7) 43.14 

Pathology, n (%) 

Brunner gland hyperplasia 41 (28.1) 32.16 

Ectopic gastric mucosa 21 (14.4) 16.47 

Inflammatory polyp 40 (27.4) 31.37 

Villous adenoma 4 (2.7) 3.14 

Neuroendocrine tumor 3 (2.1) 2.35 

Tubular adenoma 4 (2.7) 3.14 

Hyperplastic polyp 7 (4.8) 5.49 

Adenomatous polyp 20 (13.7) 15.69 

Hamartomatous polyp 6 (4.1) 4.71 

Helicobacter pylori, n (%) 14 (9.6) – 

Other endoscopic findings, n (%) 

Antral gastritis 50 (34.2) – 

Duodenal ulcer 13 (8.8) – 

Duodenitis 3 (2.1) – 

Pangastritis 64 (43.8) – 

Pangastritis + bulbitis 5 (3.4) – 

Atrophic gastritis 3 (2.1) – 

FAP 3 (2.1) – 

Gastric CA 3 (2.1) – 

Peutz-jeger 2 (1.4) – 

Colonoscopy, n (%) 88 (60.3) 

Detection of polyps in colonoscopy, n (%) 35 (24.0) – 

Colon polyp localization, n (%) 

Rectosigmoid 22 (15.1) – 

Other colonic parts 13 (8.9) – 

Polyp type, n (%) 

Rate per 100,000 patients 

In our study, esophageal adenocarcinoma was diagnosed in 6 

individuals who underwent biopsies following the discovery of an 

esophageal polypoid lesion. Two of the individuals who were found 

to have duodenal polypoid lesions had a biopsy, which revealed 

duodenal adenocarcinoma. All malignant esophageal and duodenal 

lesions were ulcero-vegetative and fragile in appearance, and they 

were all assessed separately from benign esophageal lesions. 

Discussion 

As the frequency of performing upper GI endoscopy increases in 

the world, the detection of non-gastric polyps has also increased. 

Although gastric polyps can be assessed more easily due to their 

frequency, non-gastric polyps cannot be recognized adequately 

due to their rarity. These polyps may be benign, as well as they 

may carry the risk of malignancy, and may be an indicator of an 

accompanying malignancy. In this study we sought to assess the 

prevalence of non-gastric polyps in the general population, their 

distribution by localization, their clinical significance, and follow-up 

and treatment approaches. Our research revealed that 194.52 out of 

100,000 upper GI endoscopies discovered non-gastric polyps. When 

assessed according to polyp localization, the rate of esophageal 

polyp identification was 80.00 per 100,000, whereas the rate of 

duodenal polyp detection was 114.52 per 100,000. Squamous 

papilloma, inflammatory papilloma, and esophageal parakeratosis are 

the most frequently detected esophageal polyps (50.98, 16.47, and 

4.70 per 100,000, respectively), whereas Brunner gland hyperplasia, 

inflammatory polyp, ectopic gastric mucosa, and adenomatous polyp 

are the most frequently detected duodenal polyps (32.16, 31.37, 

16.47, and 15.69 per 100,000, respectively,). 

Bulur et al. 22 evaluated 19,560 patients and found non-gastric polyps 

in 38 of them. In our study, 127,493 patients were evaluated, and 

248 non-gastric polyps were detected. Total evaluation revealed a 

detection rate of 194.52 non-gastric polyps per 100,000 patients. 

We were able to report the incidence rate in 100,000 patients as an 

epidemiological data for rare non-gastric polyps as a result of our 

study because of the large patient group we screened. 

Hyperplastic 2 (1.4) – 

Adenomatous 33 (22.6) – 

In the series of Szanto et al. 7 evaluating 35-year upper gastrointestinal 

endoscopies, nearly 60,000 upper GI endoscopy was performed, 

Table Table 2. 2. Demographic characteristics, characteristics, endoscopic endoscopic and colonoscopy and colonoscopy findings, and pathological and squamous evaluations papilloma was detected in 155 patients. None of 

of patients findings, with and duodenal pathological polyps, evaluations pathologic findings of patients as rate with per duodenal 100,000 patients. Data are expressed as 

median polyps, ± SD pathologic or median (IQR) findings or frequency as rate per (%). 100,000 SD standard patients. deviation. Data are 

expressed as median ± SD or median (IQR) or frequency (%). 

SD standard deviation. 

these have turned into malignancies. Mosca et al. 9 examined 7618 

upper GI endoscopy procedures and detected squamous papilloma 

in 9 patients. In our study, squamous papilloma was detected in 65 

of 127,493 patients evaluated over a 12-year period. Looking at the 

studies in the literature, the rate of detecting squamous papilloma 

in upper GIS endoscopy has been reported between 0.045 and 

0.26% 6,7,9 . Consistently with the literature, this rate was found 50.98 

per 100,000 patients in our study. None of the patients developed 

malignancy during their mean follow-up of 3.2 years. In a case 

presented by Kostiainen et al. 23 , the patient had the symptoms 

of dysphagia and vomiting due to large squamous papilloma. 

In our study, 63 of 65 patients with squamous papillomas were 

asymptomatic, while squamous papilloma larger then 20 mm was 

detected in two patient who had intermittent nausea and vomiting. 

Mandard et al. 24 found accompanying esophageal parakeratosis in 

approximately 40% of 400 patients, newly diagnosed with head and 

neck squamous cell carcinoma. However, no malignancy was found to 

originate from the parakeratotic area in the esophagus. In our study, 4 

Vol.:(0123456789) 

of 6 patients (66.6%) with esophageal parakeratosis had a history of 

squamous cell head and neck cancer (larynx and hypopharynx). In the 

light of these findings, it would be appropriate to screen the patients 

for possible head and neck malignancies in the case of esophageal 

parakeratosis detected incidentally in upper GI endoscopy. 


9

FEATURE 

Esophageal adenomas typically present as wide islets of dysplasia rather 

than a single polyp and typically develop in the presence of Barrett’s 

esophagus. In a case series presented by Wong et al. 13 , polypoid 

lesions developing on the ground of Barrett’s esophagus, with dysplastic 

adenomas and adenocarcinomas found in the pathology were evaluated. 

In our study, esophageal adenoma was detected in four patients and all 

four also had Barrett’s esophagus. These patients underwent surgical 

esophagectomy afterward. The risk of adenocarcinoma is quite high 

in patients with Barrett’s esophagus and accompanying adenoma in 

the esophagus, and these patients should be evaluated further, and 

the lesion should be removed endoscopically or surgically. Due to the 

presence of Barrett’s esophagus in these patients, mucosectomy or 

ablation procedures for the disease should be integrated into endoscopic 

treatment strategies in addition to polyp excision. An esophagectomy is a 

surgical option in which the patient’s polyp and esophagus segment are 

removed together, and the small intestine or stomach is anastomosed. 

Europe. In addition to being an epidemiological study with a large 

patient group to evaluate, our study also offers suggestions for the best 

examination and treatment approaches to use when non-gastric polyps 

are found. The epidemiological study we conducted is the largest on 

non-gastric polyps ever published in the world’s literature. 

In conclusion, nowadays, with the widespread utilization upper GI 

system endoscopy, it is critical to recognize, monitor, and treat common 

lesions as well as less frequent but clinically significant lesions. Our 

study is not only the broadest evaluation of non-gastric polyps, but it 

also provides clinical approach recommendations for these polyps and 

discloses the prevalence of these polyps in the general population. 

Data availability 

The datasets used and/or analyzed during the current study available 

from the corresponding author on reasonable request. 


Levine et al. 25 evaluated 27 patients with Brunner gland hyperplasia 

detected in the duodenum, and GIS bleeding was found in 10 of the 

patients, obstruction in 10, and incidentally in 7 patients. In our study, 

Brunner’s gland hyperplasia was detected in the duodenum in 41 

patients with 21 of them having GI bleeding and 9 signs of obstruction. 

It was detected incidentally in 11 of them. Although Brunner’s gland 

hyperplasia are benign lesions, they should be treated as they may have 

clinical symptoms. We treated all patients endoscopically, except for one 

patient with obstruction. In the long-term follow-up, the patients were 

observed up as stable. 

Ectopic gastric mucosa are benign lesions that can be detected incidentally 

in the duodenum. Naguchi et al. 19 found ectopic gastric mucosa in 76 (55%) 

of 137 patients with duodenal ulcer, and Helicobacter pylori was detected in 

59% (45/76) of the biopsies taken from them. In our study, duodenal ulcer 

was detected in 12 (57.1%) of 21 patients with ectopic gastric mucosa, and 

HP positivity was observed in 13 (61.9%) of them. 

Sporadic duodenal adenomas are very rare and have the potential to 

transform into adenocarcinoma by showing similar morphological and 

molecular features with colorectal adenomas. The majority of sporadic 

duodenal adenomas are flat or sessile solitary lesions with pearly villi 

surfaces that develop on the descending duodenum’s posterior or lateral 

walls 26 . Witterman et al. 17 showed that 42% of patients with duodenal 

villous adenoma had malignant cells. In addition, it was shown that the 

rate of detecting concomitant colon adenoma is increased in these 

patients. In our study, all 20 adenomas detected in the duodenum 

originated from the second part of the duodenum, and malignant cells 

were detected in 1 of 4 villous adenomas. Again, 17 (85.0%) of these 

patients had adenomatous polyps in the colon. When polyps are found 

in the duodenum, they should be removed via snare polypectomy, 

endoscopic mucosal resection (EMR), endoscopic submucosal 

dissection (ESD), or argon plasma coagulation (APC) ablation due to 

their potential for malignancy. Then again, based on these findings, it 

would be a reasonable approach to be careful in terms of malignancy 

in patients with adenomatous polyps in the duodenum and to perform 

colon screening in these patients. 

With a bed capacity of 3600 patients and more than 300 endoscopic 

procedures carried out each day, our center has the title of largest 

institution in Turkey and one of the three largest institutes in all of 

Received: 20 December 2022; Accepted: 13 April 2023 

Published online: 15 April 2023 

References 

1. Hirota, W. K. et al. ASGE guideline: The role of endoscopy in 

the surveillance of premalignant conditions of the upper GI tract. 

Gastrointest. Endosc. 63, 570 (2006). 

2. ASGE Standards of Practice Committee et al. Endoscopic mucosal 

tissue sampling. Gastrointest. Endosc. 78, 216 (2013). 

3. Vadva, M. D. & Triadafilopoulos, G. Glycogenic acanthosis of the 

esophagus and gastroesophageal reflux. J. Clin. Gastroenterol. 17, 

79 (1993). 

4. Ghahremani, G. G. & Rushovich, A. M. Glycogenic acanthosis of 

the esophagus: Radiographic and pathologic features. Gastrointest. 

Radiol. 9, 93 (1984). 

5. Stern, Z. et al. Glycogenic acanthosis of the esophagus. A benign 

but confusing endoscopic lesion. Am. J. Gastroenterol. 74, 261 

(1980). 

6. Sablich, R., Benedetti, G., Bignucolo, S. & Serraino, D. Squamous 

cell papilloma of the esophagus. Report on 35 endoscopic cases. 

Endoscopy 20, 5 (1988). 

7. Szántó, I. et al. Squamous papilloma of the esophagus. Clinical and 

pathological observations based on 172 papillomas in 155 patients. 

Orv. Hetil. 146, 547 (2005). 

8. Carr, N. J., Monihan, J. M. & Sobin, L. H. Squamous cell papilloma 

of the esophagus: A clinicopathologic and follow-up study of 25 

cases. Am. J. Gastroenterol. 89, 245 (1994). 

9. Mosca, S. et al. Squamous papilloma of the esophagus: Long-term 

follow up. J. Gastroenterol. Hepatol. 16, 857 (2001). 

10. LiVolsi, V. A. & Perzin, K. H. Inflammatory pseudotumors 

(inflammatory fibrous polyps) of the esophagus. A clinicopathologic 

study. Am. J. Dig. Dis. 20, 475 (1975). 

11. Guelrud, M., Herrera, I. & Eggenfeld, H. Compact parakeratosis of 

esophageal mucosa. Gastrointest. Endosc. 51, 329 (2000). 

12. Lee, R. G. Adenomas arising in Barrett’s esophagus. Am. J. Clin. 

Pathol. 85, 629 (1986). 

13. Wong, R. S. et al. Multiple polyposis and adenocarcinoma arising in 

Barrett’s esophagus. Ann. Thorac. Surg. 61, 216 (1996). 

14. Adoke, K. U. et al. Hyperplastic polyps of the esophagus and 

esophagogastric junction with esophageal constriction—a 

case report. Pathology 46(Supplement 2), S81. https://doi. 

org/10.1097/01.PAT.0000454378.95070.60 (2014). 

15. Saers, T., Parusel, M., Brockmann, M. & Krakamp, B. 

Lymphangioma of the esophagus. Gastrointest. Endosc. 62, 181 

(2005). 

10

FEATURE 

16. Sivero, L. et al. Endoscopic diagnosis and treatment of 

neuroendocrine tumors of the digestive system. Open Med. 11(1), 

369–373. https://doi.org/10.1515/med-2016-0067 (2016). 

17. Witteman, B. J., Janssens, A. R., Griffioen, G. & Lamers, C. B. 

Villous tumours of the duodenum. An analysis of the literature with 

emphasis on malignant transformation. Neth. J. Med. 42, 5 (1993). 

18. Levine, J. A., Burgart, L. J., Batts, K. P. & Wang, K. K. Brunner’s 

gland hamartomas: Clinical presentation and pathological features 

of 27 cases. Am. J. Gastroenterol. 90, 290–294 (1995). 

19. Noguchi, H. et al. Prevalence of Helicobacter pylori infection rate 

in heterotopic gastric mucosa in histological analysis of duodenal 

specimens from patients with duodenal ulcer. Histol. Histopathol. 

35(2), 169–176. https://doi.org/10.14670/HH-18-142 (2020) 

(Epub 2019 Jul 2). 

20. Singhal, S. et al. Anorectal gastrointestinal stromal tumor: A case 

report and literature review. Case Rep. Gastrointest. Med. 2013, 

934875 (2013). 

21. Modlin, I. M., Lye, K. D. & Kidd, M. A 5-decade analysis of 13,715 

carcinoid tumors. Cancer 97, 934–959 (2003). 

22. Bulur, A. et al. Polypoid lesions detected in the upper 

gastrointestinal endoscopy: A retrospective analysis in 19560 

patients, a single-center study of a 5-year experience in Turkey. 

N. Clin. Istanb. 8(2), 178–185. https://doi.org/10.14744/ 

nci.2020.16779 (2020). 

23. Kostiainen, S., Teppo, L. & Virkkula, L. Papilloma of the 

oesophagus. Report of a case. Scand. J. Thorac. Cardiovasc. 

Surg. 7(1), 95–97. https://doi.org/10.3109/14017437309139176 

(1973). 

24. Mandard, A. M. et al. Cancer of the esophagus and associated 

lesions: Detailed pathologic study of 100 esophagectomy 

specimens. Hum. Pathol. 15, 660 (1984). 

25. Levine, J. A., Burgart, L. J., Batts, K. P. & Wang, K. K. Brunner’s 

gland hamartomas: Clinical presentation and pathological features 

of 27 cases. Am. J. Gastroenterol. 90(2), 290–294 (1995). 

26. Ma, M. X. & Bourke, M. J. Management of duodenal polyps. Best 

Pract. Res. Clin. Gastroenterol. 31(4), 389–399 (2017). 

Author contributions 

Ç.E., M.Y.: conception, design, supervision, materials, data collection 

and processing, analysis and interpretation, literature review, writer 

and critical review. D.A., B.Y., K.K. O.C., İ.T., H.T.K.: materials, data 

collection and processing, analysis and interpretation, literature review 

and manuscript supervision. 

Competing interests 

The authors declare no competing interests. 

Additional information 

Correspondence and requests for materials should be addressed to Ç.E. 

Reprints and permissions information is available at 

www.nature.com/reprints. 

Publisher’s note Springer Nature remains neutral with regard to 

jurisdictional claims in published maps and institutional affiliations. 

Open Access This article is licensed under a Creative Commons 

Attribution 4.0 International License, which permits use, sharing, 

adaptation, distribution and reproduction in any medium or format, as 

long as you give appropriate credit to the original author(s) and the source, 

provide a link to the Creative Commons licence, and indicate if changes 

were made. The images or other third party material in this article are 

included in the article’s Creative Commons licence, unless indicated 

otherwise in a credit line to the material. If material is not included in the 

article’s Creative Commons licence and your intended use is not permitted 

by statutory regulation or exceeds the permitted use, you will need to 

obtain permission directly from the copyright holder. To view a copy of this 

licence, visit http:// creat iveco mmons. org/ licen ses/ by/4. 0/. 

© The Author(s) 2023 

WHY NOT WRITE FOR US? 

Gastroenterology Today welcomes the submission of 

clinical papers and case reports or news that 

you feel will be of interest to your colleagues. 

Material submitted will be seen by those working within all 

UK gastroenterology departments and endoscopy units. 

All submissions should be forwarded to info@mediapublishingcompany.com 

If you have any queries please contact the publisher Terry Gardner via: 

info@mediapublishingcompany.com 


11

FEATURE 

Stronger Together 

Cantel, Key Surgical and Diagmed are now part of STERIS. 

Our companies share a commitment to provide the very best 

solutions for our Customers and we are excited to bring the 

power of our teams together, and to provide a more extensive 

and innovative suite of offerings to new and existing 

Customers around the world. 

The unique strength of our collective organisation will continue 

to uphold our mission of HELPING OUR CUSTOMERS CREATE 

A HEALTHIER AND SAFER WORLD. 


Come join us 

at BSG! 

Stand A26 

The Arena 

12 

www.steris.com

FEATURE 

EVALUATION OF GUT MICROBIOTA OF IRANIAN 

PATIENTS WITH CELIAC DISEASE, NON-CELIAC WHEAT 

SENSITIVITY, AND IRRITABLE BOWEL SYNDROME: 

ARE THERE ANY SIMILARITIES? 

Kaveh Naseri 1 , Hossein Dabiri 2 , Meysam Olfatifar 3 , Mohammad Amin Shahrbaf 4 , Abbas Yadegar 5 , Mona Soheilian‐Khorzoghi 4 , 

Amir Sadeghi 4 , Saeede Saadati 4 , Mohammad Rostami‐Nejad 4* , Anil K. Verma 6 and Mohammad Reza Zali 4 

Naseri et al. BMC Gastroenterology (2023) 23:15 https://doi.org/10.1186/s12876-023-02649-y 

Abstract 

Introduction 

Background and aims 

Individuals with celiac disease (CD), non-celiac wheat sensitivity 

(NCWS), and irritable bowel syndrome (IBS), show overlapping clinical 

symptoms and experience gut dysbiosis. A limited number of studies so 

far compared the gut microbiota among these intestinal conditions. This 

study aimed to investigate the similarities in the gut microbiota among 

patients with CD, NCWS, and IBS in comparison to healthy controls 

(HC). 

Materials and methods 

In this prospective study, in total 72 adult subjects, including CD (n = 15), 

NCWS (n = 12), IBS (n = 30), and HC (n = 15) were recruited. Fecal 

samples were collected from each individual. A quantitative real-time 

PCR (qPCR) test using 16S ribosomal RNA was conducted on stool 

samples to assess the relative abundance of Firmicutes, Bacteroidetes, 

Bifidobacterium spp., and Lactobacillus spp. 

Results 

In all groups, Firmicutes and Lactobacillus spp. had the highest and 

lowest relative abundance respectively. The phylum Firmicutes had 

a higher relative abundance in CD patients than other groups. On 

the other hand, the phylum Bacteroidetes had the highest relative 

abundance among healthy subjects but the lowest in patients with 

NCWS. The relative abundance of Bifidobacterium spp. was lower in 

subjects with CD (P = 0.035) and IBS (P = 0.001) compared to the HCs. 

Also, the alteration of Firmicutes to Bacteroidetes ratio (F/B ratio) was 

statistically significant in NCWS and CD patients compared to the HCs 

(P = 0.05). 

Conclusion 

The principal coordinate analysis (PCoA), as a powerful multivariate 

analysis, suggested that the investigated gut microbial profile of patients 

with IBS and NCWS share more similarities to the HCs. In contrast, 

patients with CD had the most dissimilarity compared to the other 

groups in the context of the studied gut microbiota. 

Keywords 

Celiac disease, Irritable bowel syndrome, Non-celiac wheat sensitivity, 

Gut microbiota, Dysbiosis 

The human gastrointestinal (GI) tract harbors an incredibly complex 

and abundant ensemble of microbes referred to as gut microbiota 

[1]. Gut microbiota plays a pivotal role in human health and 

diseases [2–4] and its composition depends on various factors, 

including age [5], diet [6], geography [7], malnourishment [8], race, 

ethnicity [9], and socioeconomic status [10]. Balance in the gut 

microbiota composition and the presence or absence of critical 

species capable of causing specific responses contribute to 

ensuring homeostasis in the intestinal mucosa and other organs 

[11–14]. An imbalanced or disturbed composition and quantity 

of the gut microbiota, known as dysbiosis [15], can affect the 

bacterial function and is associated with a variety of GI disorders 

[16–20]. Celiac disease (CD), non-celiac wheat sensitivity (NCWS), 

and irritable bowel syndrome (IBS), have intestinal dysbiosis as 

a causative factor in the initiation of their symptoms [21–24]. 

CD is a chronic small intestinal inflammation, triggered by the 

consumption of gluten, resulting in villous atrophy in genetically 

susceptible individuals [25]. IBS is a functional gastrointestinal 

disorder that afflicts nearly 15% of the population worldwide, 

characterized by recurrent abdominal pain or discomfort, and 

changes in bowel habits, in the absence of any other disease to 

cause these symptoms [26, 27]. NCWS is still an unclear diagnosis, 

characterized by a combination of CD-like or IBS-like symptoms 

(e.g., diarrhea, abdominal pain, bloating), behavior disturbances, 

and systemic manifestations, related to the ingestion of gluten in 

subjects who are not affected by either CD or wheat allergy [28, 

29]. Therefore, since these three disorders are related to dysbiosis 

in gut microbiota and share similarities in their symptoms, these 

data form a hypothesis regarding the possible similarities in the 

alterations of the gut microbiota in subjects with the aforementioned 

disorders. Although the findings are inconsistent, previous 

studies mainly reported decreased levels of fecal Lactobacilli and 

Bifidobacteria, and increased ratios of Firmicutes to Bacteroidetes 

in patients with IBS when compared to healthy individuals [21, 30– 

32]. According to most studies conducted on the gut microbiota of 

CD patients, Bifidobacteria and Lactobacilli levels are decreased in 

comparison to healthy controls [22, 33, 34]. Due to NCWS being a 

relatively new diagnosis, few studies have examined gut microbiota 

in this group. 


* Correspondence: Mohammad Rostami‐Nejad 

m.rostamii@gmail.com 

© The Author(s) 2023. 

13

FEATURE 


14 

To the best of our knowledge, no previous studies have investigated 

the possible similarities in the gut microbiota profile of patients with CD, 

NCWS, and IBS compared to healthy control. Hence, we designed this 

monocentric prospective observational study to compare the relative 

abundance of Firmicutes and Bacteroidetes, as the two most dominant 

phyla [35–38], and Bifidobacterium and Lactobacillus, as two highly 

controversial genera of fecal microbial communities, among Iranian 

subjects with CD, NCWS, and IBS compared to HCs. 

Materials and methods 

Study population 

From March 2020 to November 2020, consecutive newly diagnosed 

CD, NCWS, and IBS patients were recruited from an outpatient 

gastroenterology clinic in Taleghani Hospital, Tehran, Iran. Convenience 

sampling was used for participants’ selection. Subjects who had 

recently been diagnosed with CD, NCWS, and IBS, and were not 

on therapeutic diets such as gluten-free or low-FODMAP diets or 

taking supplements such as probiotics, prebiotics, or synbiotics were 

considered as patients groups. CD diagnosis was established according 

to the “4 out of 5” rule and four of the following criteria were considered 

sufficient for disease diagnosis: typical CD related symptoms, positivity 

of CD-specific antibodies, HLA-DQ2 or 8 genotypes, intestinal damages 

at duodenal biopsy and clinical response to GFD [39]. Twelve patients 

with NCWS that fulfilled the Salerno consensus criteria [40] were 

included. All NCWS subjects demonstrated negative serology results for 

tissue-transglutaminase IgA antibodies, and the duodenal biopsy results 

were normal [41]. 

IBS diagnosis was based on fulfilling the ROME-IV criteria [27], including 

recurrent abdominal pain at least one day per week over the previous 

3 months, along with two or more of the following criteria: (a) changes 

in defecation, (b) changes in frequency, and (c) changes in the form of 

stool, with no medication to alleviate symptoms in the last 3 months. 

Anti-Tissue Trans-glutaminase (Anti-tTG) and/or endomysial antibodies 

(EMA), histological findings compatible with atrophy (according to the 

Marsh classification), and wheat-specific Immunoglobulin E (IgE) levels 

were negative in all thirty patients with IBS. Apart from these, fifteen 

healthy volunteers, with no history of digestive pathologies lacking 

CD-specific antibodies, were enrolled in the healthy control (HC) 

group. These HCs had normal bowel movements without abdominal 

symptoms, coronary artery disease, inflammatory conditions, IBS, 

NCWS, and diabetes mellitus. 

Pregnant and lactating women, individuals with any systemic 

inflammatory diseases like autoimmune conditions, gastrointestinal 

diseases (i.e. inflammatory bowel disease (IBD)) or any other acute 

or chronic diseases, gastrointestinal surgery, cancer, and those who 

were not willing to participate in the study were excluded from all 

study groups. Non-steroidal anti-inflammatory drugs (NSAIDs) usage, 

excessive alcohol consumption, systemic use of immunosuppressive 

agents, poorly controlled psychiatric diseases and the history of broadspectrum 

antibiotics and probiotics consumption were also considered 

as exclusion criteria. Participants were also asked not to take any 

antibiotics, eat spicy food, and smoke four weeks prior to sample 

collection. 

Fecal samples collection and homogenization 

Fresh early-morning fecal samples, representative of whole gut 

microbiome, were collected from each participant in sterile fecal 

specimen containers at the study’s baseline. A water ban was also 

required after midnight and before collecting the samples in the morning. 

Stool specimens were collected and handled by experienced clinicians 

and trained technicians. Homogenization of the stool samples was 

conducted through agitation by using a vortex. Afterward, stool samples 

were divided into three aliquots within 3 h of defecation. Using screwcapped 

cryovial containers, the aliquots were immediately frozen and 

stored at − 80 °C until used for DNA extraction [42]. 

DNA extraction from fecal samples 

QIAamp ® DNA Stool Mini Kit (Qiagen Retsch GmbH, Hannover, 

Germany) was used for DNA extraction [43]. DNA concentration was 

quantified by NanoDrop ND-2000 Spectrophotometer (NanoDrop 

products, Wilmington, DE, USA). In addition, Nanodrop (DeNovix 

Inc., USA) was used for assessing the concentration and purity of the 

extracted DNA. Extracted DNA samples were stored at − 20 °C until 

further analysis. 

Microbiota analysis by quantitative real-time PCR (qPCR) 

We performed qPCR assay to evaluate the relative abundance of two 

bacterial phyla, including Firmicutes and Bacteroidetes, and two genera, 

including Bifidobacterium spp. and Lactobacillus spp. The qPCR was 

conducted by SYBR Green chemistry using universal and group-specific 

primers based on the bacterial 16S rRNA sequences presented in 

Additional file 1: Table S1. All PCRs were performed in a volume of 25 

μL, comprising 12.5 μL of SYBR green PCR master mix (Ampliqon, 

Odense, Denmark), 1 μL of 10 pmol of forward, and reverse primers, 

and 100 ng of the DNA template. 

Rotor-Gene ® Q (Qiagen, Germany) real-time PCR system was used 

for the PCR amplification. The amplification reaction parameters were 

assumed as 95 °C for 10 min and 40 cycles at 95 °C for 20 and 30 s for 

each primer (Additional file 1: Table S1) and 72 °C for the 20 s. Melting 

curve analysis was conducted to assess the amplification accuracy by 

increasing temperature from 60 to 95 °C (0.5 °C increase in every 5 s). 

The relative abundance of studied taxa was evaluated based on the ratio 

of the 16S rRNA copy number of the specific bacteria to the total 16S 

rRNA copy number of all bacteria using the previously described method 

[32]. Accordingly, the average Ct value for primers was reported as the 

percentage values using the following formula: 

univ 

(Eff. Univ)Ct 

Χ = 

(Eff. Spec) 

Ct spec 

×100 

The percentage of 16S taxon-specific copy numbers was indicated by 

“X”. Furthermore, “Eff. Univ” and “Eff. Spec” represents the efficiency 

of the universal primers (2 = 100% and 1 = 0%) and the efficiency of the 

taxon-specific primers respectively. The threshold cycles registered by 

the thermocycler were indicated by “Ct univ” and “Ct spec”. 

Statistical analysis 

Analysis of collected data was performed using Statistical Package 

for the Social Sciences (SPSS) version 25.0, SPSS Inc., Chicago, IL, 

USA. Figures were drawn using GRAPHPAD Prism 8.4.0 (GraphPad 

Software, Inc, San Diego, CA). Quantitative variables were reported as

FEATURE 

Table 1 Baseline characteristics of study participants at enrollment 

Variables HC (n = 15) IBS (n = 30) NCWS (n = 12) CD (n = 15) Total (n = 72) P‐value* 

Table Age (years) 1 Baseline characteristics 32.8 ± 12.2 of study 37.8 participants ± 10.7 at enrollment 31.8 ± 6.4 40.1 ± 8.2 35.5 ± 6.4 0.76 

Variables 

Males (n%) 

HC 

7 (46.7%) 

(n = 15) IBS 

15 (50%) 

(n = 30) NCWS 

5 (41.7%) 

(n = 12) CD 

6 (50%) 

(n = 15) Total 

33 (45.8%) 

(n = 72) P‐value* 

0.83 

Females (n%) 8 (53.3%) 15 (50%) 7 (58.3%) 6 (50%) 39 (54.2%) 0.45 

Age Smoking (years) (n%) 32.8 4 (26.6%) ± 12.2 37.8 9 (30%) ± 10.7 31.8 4 (33.3%) ± 6.4 40.1 2 (13.3%) ± 8.2 35.5 19 (26.4%) ± 0.76 0.65 

Males (n%) 7 (46.7%) 15 (50%) 5 (41.7%) 6 (50%) 33 (45.8%) 0.83 

HC, healthy control; IBS, irritable bowel syndrome; NCWS, non-celiac wheat sensitivity; CD, celiac disease 

Females (n%) 8 (53.3%) 15 (50%) 7 (58.3%) 6 (50%) 39 (54.2%) 0.45 

*P-values obtained by Kruskal–Wallis test 

Smoking (n%) 4 (26.6%) 9 (30%) 4 (33.3%) 2 (13.3%) 19 (26.4%) 0.65 

HC, healthy control; IBS, irritable bowel syndrome; NCWS, non-celiac wheat sensitivity; CD, celiac disease 

*P-values obtained by Kruskal–Wallis test 

mean ± standard deviation (SD) and qualitative variables were reported statistically significant (p = 0.002). Whereas the phylum Bacteroidetes 

as numerical (%) data. ANOVA test was used for the assessment of the was significantly lower in patients with IBS (P = 0.049) and NCWS 

relative abundance differences between the two phyla. In addition, we (P = 0.006). This phylum had the lowest relative abundance in the 

used R software and Principal Coordinate Analysis (PCoA) method to NCWS group (7.3 ± 4.0%). In addition, the relative abundance of 

assess dissimilarities in this study. The PCoA was calculated based on Bifidobacterium spp. was statistically lower in subjects with CD 

the Bray Curtis dissimilarity method [44]. 

(P = 0.022) and IBS (P = 0.001); with the lowest percentage in the IBS 

group (0.5 ± 0.5). Moreover, Lactobacillus spp. was significantly lower 

Results 

in subjects with CD (P = 0.022) and IBS (P = 0.007) compared to the 

HCs. The relative abundance of this genus was also lower in subjects 

with NCWS, though not statistically significant (P = 0.12). The results 

Demographics 

Seventy-two samples from adult participants were enrolled in this 

study. Due to age-related changes in the gut microbiota, the study 

groups were adjusted according to their age so as not to have 

for the relative abundance are presented in Table 2 and Fig. 1. As 

shown in Table 2 the results obtained from the Kruskal–Wallis test also 

revealed significant inter-groups differences for all the studied bacteria 

(p

FEATURE 

Fig. 1 Box plot for the distribution of the selected bacterial taxa by the median abundance that constitutes the fecal microbiota in each group of 

the study population. Differences in each group of the patients were compared to the healthy control (HC) and were considered to be statistically 

significant when *P < 0.05, **P < 0.01, and ***P < 0.001 


16 

Discussion 

The current study examined fecal samples from adult participants 

with three GI disorders, including CD, NCWS, and IBS. Comparing 

gut dysbiosis to healthy controls, the microbiota analysis interestingly 

showed a significant difference in the relative abundance of Firmicutes, 

Bacteroidetes, Bifidobacterium spp., and Lactobacillus spp. in 

CD patients. In addition, the analysis of the relative abundance of 

Bifidobacterium spp. and Lactobacillus spp. in IBS patients and 

Bacteroidetes in NCWS revealed a statistically significant decrease 

compared to the HC group. Furthermore, Firmicutes to Bacteroidetes 

ratio (F/B ratio) assessment, as a valuable index for detecting the 

alterations in gut microbiota, was another aim of the current study. 

Changes in the F/B ratio could be particularly important. Firmicutes and 

Bacteroidetes are two predominant phyla accounting for up to 90% 

of the total gut microbiota composition [45]. The F/B ratio has been 

suggested as an important index of gut microbiota health. [46]. This 

ratio is associated with different pathological states [47]. For instance, 

the association of a high F/B ratio with several conditions including 

GI disorders has been observed repeatedly [48–50]. Particularly, it 

is associated with the production of short-chain fatty acids such as 

butyrate and propionate [51]. Short-chain fatty acids generated by 

microbiota can have a significant influence on human health. The antiinflammatory 

molecule butyrate, in particular, acts both on enterocytes 

and circulating immune cells, regulating gut barrier integrity. Additionally, 

propionate production plays a crucial role in human health since it 

promotes satiety and prevents hepatic lipogenesis, which in turn lowers 

cholesterol production [52, 53]. Moreover, the increased F/B ratio is 

associated with an increased energy harvest from colonic fermentation 

[54]. According to our analysis, the F/B ratio was significantly higher in 

the subjects with CD and NCWS than in the HCs. In contrast, it was 

not statistically significant in subjects with IBS, suggesting a higher level 

of alteration in the gut microbiota of individuals with CD and NCWS 

than in the IBS compared to the HCs. Recent studies suggested that 

the alteration of gut microbiota composition is associated with CD 

pathogenesis [55–57]. In the study of Golfetto et al., the concentration 

of Bifidobacterium spp. in CD patients was significantly lower compared 

to the HCs [58]. Another study conducted by Bodkhe et al., reported 

that Firmicutes and Bacteroidetes were the major phyla in the duodenal 

microbiota of subjects with CD [59]. Several other studies have 

demonstrated that Bifidobacterium spp. and Lactobacillus spp. protect 

the intestinal epithelial cells from gliadin damage [60,61,62]. Accordingly, 

it has been suggested that the fecal transplant which can cause an 

increment in Bifidobacterium spp. could reverse the inflammatory 

pathway in CD patients [63]. Among all the groups we studied, 

Firmicutes predominated the gut microbiota. In addition, Bacteroidetes,

FEATURE 

Bifidobacterium spp., and Lactobacillus spp. had significantly lower 

abundance in subjects with CD compared to the HCs. In terms of the 

alteration and relative abundance of the studied bacterial groups, the 

current study’s results were largely consistent with the previous reports. 

Fig. 2 Box plots showing the Firmicutes to Bacteroidetes (F/B) I each 

group of participants. This ratio was significantly (*P = 0.05) increased 

in the NCWS and CD patients but non‐significant in the IBS patients 

compared with the healthy controls (HC) 

Gut microbiota dysbiosis in individuals with IBS has been reported 

in several studies [64–66]. In fact, gastrointestinal dysbiosis in these 

patients is associated with intestinal hypersensitivity, mucosal immune 

activation, and chronic inflammation, which are the three important 

pathophysiological factors in this disease [67, 68]. A number of studies 

have reported lower amounts of Bacteroidetes and higher amounts of 

Firmicutes in subjects with IBS compared to HCs [32, 69, 70]. In the 

current study, both of these phyla had lower relative abundances than 

those of HCs, although their differences were not statistically significant. 

Furthermore, it has been suggested that IBS is associated with the 

lower relative abundance of Bifidobacterium spp. and Lactobacillus 

spp. [71, 72] which is in accordance with the current study. However, it 

is noteworthy that Maccaferri et al. observed an increase in the relative 

abundance of Bifidobacterium spp. and Lactobacillus among subjects 

with IBS [73]. It seems that further evidence is needed to confirm 

these results. As for NCWS, dysbiosis in these individuals is one of 

the important issues which can cause constipation, diarrhea, chronic 

inflammation, intestinal hypersensitivity, and immune dysfunction [74]. 

Fig. 3 Shepherd plot showing the correlation between the distance from the dissimilarity matrix and the coordination distance for NMDS analysis 


17

FEATURE 

Fig. 4 Bray–Curtis dissimilarity metric plotted in PCoA space comparing the microbial communities from different patient groups (CD, NCWS, IBS, 

and HC). Each circle representing a participant colored according to the studied group 


18 

Garcia-Mazcorro et al. reported a high relative abundance of Firmicutes 

and a low relative abundance of Bacteroidetes in the fecal microbiota 

of the individuals with NCWS [75]. According to the current study, 

the Phylum Bacteroidetes was significantly lower in NCWS patients 

compared to HCs, in agreement with the previous study. 

Analysis of the dissimilarity and PCoA in this study suggests that 

individuals with CD experience a higher level of dysbiosis compared to 

the other subjects with microbiota-related GI disorders. In fact, fewer 

similarities were observed in the studied bacterial profile of subjects 

with IBS and those with NCWS. Overall, it may explain why this 

disorder exhibits more severe symptoms when compared to the other 

GI disorders, suggesting that the recovery of gut microbiota should be 

emphasized more in the treatment of this disease. According to these 

analyses, the composition of the gut microbiota in the subjects with IBS 

and NCWS is more similar to that of the HCs’, which may suggest a 

more favorable outcome for IBS and NCWS than for CD. 

The present study had some limitations. First, the sample size is not 

large enough to extrapolate the results. Actually, the present study has 

monocentric nature that was conducted in a limited population with 

specific features. Even if this matter has been addressed with bigger 

sample sizes, the results cannot be generalized from one population 

to others. Second, based on the meta-genomic data, the human gut 

microbiome may contain more than 1000 bacterial species. Although 

the studied bacterial phyla and genera are the most dominant and 

critical taxonomical groups, there are other groups that should be taken 

into consideration. Third, alimentary habits of the included subjects, 

which can consistently modify gut microbiota, were not assessed in the 

current study. Considering the fact that, eating habits such as using fiber 

sub-types, food additives, ultra-processed foods and etc. can affect the 

gut bacteria composition, performing further similar microbiota studies 

evaluating patients’ dietary pattern is highly recommended. Moreover, 

the lack of a follow-up of patients and comparison of results before and 

after receiving treatment is another important limitation. 

To our knowledge, no previous publication has compared the gut 

microbiota profile of subjects with CD, NCWS, and IBS. In fact, 

the potential overlap between NCWS and IBS diagnosis and the 

unavailability of gluten challenge tests in many medical centers make it 

difficult to explore the gut microbiota among these groups. Thus, this 

study represents promising findings for future research. Additionally, 

investigating all components of the gut microbiota including bacteria, 

viruses, fungi, and archaea in order to identify microbial patterns,

FEATURE 

conducting multi-centric studies, and examining the fecal microbiome 

and mucosal microbiome simultaneously to have a better perspective on 

the differences between the mucosal microbiome and fecal microbiome 

would have been of great importance. 

Consent for publication 

Not applicable. 

Competing interests 

The authors declare that they have no competing interests. 

Conclusion 

Results of our study indicate that the human intestinal microbiota 

composition differs across the studied groups with different microbiotarelated 

GI disorders. Specifically, patients with CD had the highest 

level of dissimilarity compared to the other studied groups with GI 

disorders and HCs. In contrast, those with IBS had the lowest level of 

dissimilarity with HCs. This study found some microbial changes that 

were inconsistent with the previous results, possibly due to genetics, 

geographical pattern, ethnicity, or diet. 

Supplementary Information 

The online version contains supplementary material available at 

https://doi.org/10.1186/s12876-023-02649-y. 

Additional file 1: Supplementary Table 1. The taxon-specific primers 

used in this study. 

Acknowledgements 

The authors wish to thank the laboratory staffs of the Foodborne 

and Waterborne Diseases Research Center, Research Institute for 

Gastroenterology and Liver Diseases, Shahid Beheshti University of 

Medical Sciences, Tehran, Iran, specially Ms. Masoumeh Azimirad and 

Ms. Nastaran Asri for their sincere assistance. 

Author contributions 

KN, SS, and MSK collected the samples and KN performed the 

real-time PCR analysis; MRN and HD designed and supervised the 

study; KN and MO participated in data analysis; KN, and MAS wrote 

the manuscript; MRN, AY, AS, HD, AKV, and MRZ critically revised the 

manuscript. All authors approved the final version of the manuscript. 

Funding 

Gastroenterology and Liver Diseases Research Center, Research 

Institute for Gastroenterology and Liver Diseases, Shahid Beheshti 

University of Medical Sciences, Tehran, Iran, supported the study. 

Availability of data and materials 

The datasets used and/or analysed during the current study available 

from the corresponding author on reasonable request. 

Declarations 

Ethics approval and consent to participate 

The study protocol was submitted for evaluation and approval to the Ethical 

Review Committee of the Research Institute for Gastroenterology and Liver 

Diseases, Shahid Beheshti University of Medical Sciences to ensure that it 

meets ethical standards and guidelines. The present study was approved 

by mentioned Ethical Review Committee under the number IR.SBMU. 

RIGLD. REC.1396.154. The study was performed according to the revised 

Declaration of Helsinki 2013 [39] and informed consent was obtained from 

all subjects and/or their legal guardians prior to sample collection. 

Author details 

1 

School of Health and Biomedical Sciences, RMIT University, Melbourne, 

VIC, Australia. 2 Department of Microbiology, School of Medicine, Shahid 

Beheshti University of Medical Sciences, Tehran, Iran. 3 Gastroenterology 

and Hepatology Diseases Research Center, Qom University of Medical 

Sciences, Qom, Iran. 4 Celiac Disease Department, Gastroenterology and 

Liver Diseases Research Center, Research Institute for Gastroenterology 

and Liver Diseases, Shahid Beheshti University of Medical Sciences, 

Tehran, Iran. 5 Foodborne and Waterborne Diseases Research Center, 

Research Institute for Gastroenterology and Liver Diseases, Shahid 

Beheshti University of Medical Sciences, Tehran, Iran. 6 Celiac Disease 

Research Laboratory, Department of Pediatrics, Università Politecnica 

Delle Marche, 60123 Ancona, Italy. 

Received: 2 June 2022 Accepted: 11 January 2023 

Published online: 16 January 2023 

References 

1. Hooper LV, Wong MH, Thelin A, et al. Molecular analysis of 

commensal host-microbial relationships in the intestine. Science. 

2001;291(5505):881–4. 

2. Altveş S, Yildiz HK, Vural HC. Interaction of the microbiota with the 

human body in health and diseases. Biosci Microbiota Food Health. 

2019;39:19–023. 

3. Clemente JC, Ursell LK, Parfrey LW, et al. The impact of the 

gut microbiota on human health: an integrative view. Cell. 

2012;148(6):1258–70. 

4. Ogunrinola GA, Oyewale JO, Oshamika OO, et al. The human 

microbiome and its impacts on health. Int J Microbiol. 2020;2020. 

5. Teng F, Felix KM, Bradley CP, et al. The impact of age and gut 

microbiota on Th17 and Tfh cells in K/BxN autoimmune arthritis. 

Arthritis Res Ther. 2017;19(1):1–13. 

6. David LA, Maurice CF, Carmody RN, et al. Diet rapidly and 

reproducibly alters the human gut microbiome. Nature. 

2014;505(7484):559–63. 

7. Prideaux L, Kang S, Wagner J, et al. Impact of ethnicity, geography, 

and disease on the microbiota in health and inflammatory bowel 

disease. Inflamm Bowel Dis. 2013;19(13):2906–18. 

8. Million M, Diallo A, Raoult D. Gut microbiota and malnutrition. 

Microb Pathog. 2017;106:127–38. 

9. Renson A, Herd P, Dowd JB. Sick individuals and sick (microbial) 

populations: challenges in epidemiology and the microbiome. Annu 

Rev Public Health. 2020;2(41):63–80. 

10. Chong CW, Ahmad AF, Lim YAL, et al. Effect of ethnicity and 

socioeconomic variation to the gut microbiota composition among 

pre-adolescent in Malaysia. Sci Rep. 2015;5(1):1–12. 


19

FEATURE 


20 

11. Lin L, Zhang J. Role of intestinal microbiota and metabolites on gut 

homeostasis and human diseases. BMC Immunol. 2017;18(1):1– 

25. 

12. Takiishi T, Fenero CIM, Câmara NOS. Intestinal barrier and gut 

microbiota: shaping our immune responses throughout life. Tissue 

barriers. 2017;5(4): e1373208. 

13. Thursby E, Juge N. Introduction to the human gut microbiota. 

Biochem J. 2017;474(11):1823–36. 

14. Wu H-J, Wu E. The role of gut microbiota in immune homeostasis 

and autoimmunity. Gut Microb. 2012;3(1):4–14. 

15. Belizário JE, Faintuch J. Microbiome and gut dysbiosis. Metabolic 

interaction in infection. Springer; 2018. p. 459–76. 

16. Chang C, Lin H. Dysbiosis in gastrointestinal disorders. Best Pract 

Res Clin Gastroenterol. 2016;30(1):3–15. 

17. Fukui H, Xu X, Miwa H. Role of gut microbiota-gut hormone axis 

in the pathophysiology of functional gastrointestinal disorders. J 

Neurogastroenterol Motil. 2018;24(3):367. 

18. Lopetuso LR, Petito V, Graziani C, et al. Gut microbiota in health, 

diverticular disease, irritable bowel syndrome, and inflammatory 

bowel diseases: time for microbial marker of gastrointestinal 

disorders. Dig Dis. 2018;36(1):56–65. 

19. Malikowski T, Khanna S, Pardi DS. Fecal microbiota transplantation 

for gastrointestinal disorders. Curr Opin Gastroenterol. 

2017;33(1):8–13. 

20. Ostadmohammadi S, Azimirad M, Houri H, et al. Characterization 

of the gut microbiota in patients with primary sclerosing cholangitis 

compared to inflammatory bowel disease and healthy controls. Mol 

Biol Rep. 2021;48(7):5519–29. 

21. Bhattarai Y, Muniz Pedrogo DA, Kashyap PC. Irritable bowel 

syndrome: a gut microbiota-related disorder? Am J Physiol 

Gastrointestinal Liver Physiol. 2017;312(1):52–62. 

22. Marasco G, Di Biase AR, Schiumerini R, et al. Gut microbiota and 

celiac disease. Dig Dis Sci. 2016;61(6):1461–72. 

23. Igbinedion SO, Ansari J, Vasikaran A, et al. Non-celiac gluten 

sensitivity: all wheat attack is not celiac. World J Gastroenterol. 

2017;23(40):7201. 

24. Leccioli V, Oliveri M, Romeo M, et al. A new proposal for the 

pathogenic mechanism of non-coeliac/non-allergic gluten/wheat 

sensitivity: piecing together the puzzle of recent scientific evidence. 

Nutrients. 2017;9(11):1203. 

25. Shannahan S, Leffler DA. Diagnosis and updates in celiac disease. 

Gastrointestinal Endosc Clin. 2017;27(1):79–92. 

26. Buono JL, Carson RT, Flores NM. Health-related quality of life, work 

productivity, and indirect costs among patients with irritable bowel 

syndrome with diarrhea. Health Qual Life Outcomes. 2017;15(1):1–8. 

27. Lacy BE, Patel NK. Rome criteria and a diagnostic approach to 

irritable bowel syndrome. J Clin Med. 2017;6(11):99. 

28. Barbaro MR, Cremon C, Stanghellini V, et al. Recent advances 

in understanding non-celiac gluten sensitivity. F1000Research. 

2018;7. 

29. Catassi C, Bai JC, Bonaz B, et al. Non-celiac gluten sensitivity: 

the new frontier of gluten related disorders. Nutrients. 

2013;5(10):3839–53. 

30. Hills RD Jr, Pontefract BA, Mishcon HR, et al. Gut Microbiome: 

profound implications for diet and disease. Nutrients. 

2019;11(7):1613. 

31. Salem AE, Singh R, Ayoub YK, et al. The gut microbiome and 

irritable bowel syndrome: state of art review. Arab J Gastroenterol. 

2018;19(3):136–41. 

32. Naseri K, Dabiri H, Rostami-Nejad M, et al. Influence of low 

FODMAP-gluten free diet on gut microbiota alterations and 

symptom severity in Iranian patients with irritable bowel syndrome. 

BMC Gastroenterol. 2021;21(1):1–14. 

33. Chander AM, Yadav H, Jain S, et al. Cross-talk between gluten, 

intestinal microbiota and intestinal mucosa in celiac disease: recent 

advances and basis of autoimmunity. Front Microbiol. 2018;9:2597. 

34. Losurdo G, Principi M, Iannone A, et al. The interaction between 

celiac disease and intestinal microbiota. J Clin Gastroenterol. 

2016;50:S145–7. 

35. Khanna S, Tosh PK. A clinician’s primer on the role of the 

microbiome in human health and disease. Mayo Clin Proc. 

2014;89(1):107–14. 

36. Johnson EL, Heaver SL, Walters WA, et al. Microbiome and 

metabolic disease: revisiting the bacterial phylum Bacteroidetes. J 

Mol Med. 2017;95(1):1–8. 

37. Kumar H, Lund R, Laiho A, et al. Gut microbiota as an epigenetic 

regulator: pilot study based on whole-genome methylation analysis. 

MBio. 2014;5(6):e02113-e2114. 

38. Mahowald MA, Rey FE, Seedorf H, et al. Characterizing a model 

human gut microbiota composed of members of its two dominant 

bacterial phyla. Proc Natl Acad Sci. 2009;106(14):5859–64. 

39. Raiteri A, Granito A, Giamperoli A, et al. Current guidelines for 

the management of celiac disease: a systematic review with 

comparative analysis. World J Gastroenterol. 2022;28(1):154–75. 

40. Catassi C, Elli L, Bonaz B, et al. Diagnosis of non-celiac gluten 

sensitivity (NCGS): the Salerno experts’ criteria. Nutrients. 

2015;7(6):4966–77. 

41. Taraghikhah N, Ashtari S, Asri N, et al. An updated overview 

of spectrum of gluten-related disorders: clinical and diagnostic 

aspects. BMC Gastroenterol. 2020;20(1):258. 

42. Soheilian-Khorzoghi M, Rezasoltani S, Moheb-Alian A, Yadegar A, 

Rostami-Nejad M, Azizmohammad-Looha M, Verma AK, Haddadi 

A, Dabiri H. Impact of nutritional profile on gut microbiota diversity 

in patients with celiac disease. Curr Microbiol. 2022;79(5):129. 

https://doi.org/10.1007/s00284-022-02820-w. 

43. Mirsepasi H, Persson S, Struve C, et al. Microbial diversity in fecal 

samples depends on DNA extraction method: easyMag DNA 

extraction compared to QIAamp DNA stool mini kit extraction. BMC 

Res Notes. 2014;21(7):50. 

44. Bray JR, Curtis JT. An ordination of the upland forest communities 

of southern Wisconsin. Ecol Monogr. 1957;27(4):326–49.

Distal 

ulcerative colitis: 

Together we know more. 

Together we do more. 

FEATURE 

Real 

challenges 

When you’ve just been diagnosed with ulcerative colitis, 

rectal therapy isn’t always the most welcome prospect 

Real 

solution 

Salofalk Granules are a simple oral treatment providing the 

once-daily dosing that patients prefer, along with the efficacy 

that patients need – even for those with distal disease 1-3 

Salofalk Granules have a clever delivery mechanism providing prolonged 

release throughout the colon, shown using gamma-scintigraphy 1,4 

4 h 6 h 8 h 10 h 12 h 

Mesalazine, the Dr Falk way 

Prescribing Information (refer to full SPC before prescribing): 

Presentation: Salofalk 250mg gastro-resistant tablets: gastro-resistant tablet 

Prescribing containing 250mg Information mesalazine. (refer Salofalk to full 500mg SPC and before 1g gastro-resistant prescribing): tablet (UK 

Salofalk ONLY) containing gastro-resistant 500mg prolonged-release and 1g mesalazine granules respectively. Salofalk 

Presentation: 500mg/1000mg/1500mg/3000mg Stick-formed or prolonged-release round, greyish granules: white prolonged-release 

gastro-resistant 

granules containing 500mg,1000mg, 1500mg or 3000mg mesalazine per sachet. 

prolonged-release granules in sachets containing 500mg, 1000mg, 

Indications: Salofalk 250mg tablets (UK): treatment and maintenance of remission 

1.5g of mild/moderate or 3g mesalazine ulcerative per colitis. sachet. Salofalk Indications: 250mg tablets Treatment (Ireland): as of an acute antiinflammatory 

and in the management maintenance of ulcerative of remission colitis and of in ulcerative the treatment colitis. of 

episodes 

Dosage: Crohn’s disease. Adults: Salofalk Once daily 500mg 1 tablets sachet (UK): of 3g treatment granules, and 1 or maintenance 2 sachets of of 

1.5g remission granules of ulcerative or 3 sachets colitis. Salofalk 1000mg 1g tablets or 500mg (UK): treatment granules of (equivalent acute episodes to 

of mild/moderate ulcerative colitis. Salofalk granules: treatment of acute episodes 

1.5 – 3.0g mesalazine daily) preferably taken in the morning, according 

and the maintenance of remission of mild to moderate ulcerative colitis. Dosage: 

to Salofalk individual 250mg clinical tablets - requirement. Adults and elderly: May acute be treatment taken in 6 three -12 tablets divided daily doses in 3 

(1 divided sachet doses. of 500mg Maintenance granules treatment three 6 tablets times daily in or 3 divided 1 sachet doses. of 1000mg Salofalk 

granules 500mg tablets three (UK times only): 1 daily) or 2 tablets if more 3 times convenient. daily. Maintenance: Maintenance: 1 tablet 3 times 0.5g 

mesalazine daily. Salofalk 1g three tablets times (UK only): daily 1 tablet (morning, three times midday daily. Salofalk and granules evening) – 

corresponding 

adults: acute treatment 

to a 

– 

total 

once 

dose 

daily 1 

of 

sachet 

1.5g 

of 

mesalazine 

3g granules, 1 

per 

or 2 

day. 

sachets 

For 

of 

patients 

Salofalk 

1.5g granules, 3 sachets of 500mg granules or 3 sachets of 1000mg granules 

known (equivalent to be to at 1.5 increased – 3.0g mesalazine risk for relapse daily), preferably for medical taken reasons in the or morning. due to 

difficulties Alternatively, the to dose adhere can to be taken three divided daily doses, in three doses. give 3.0g Maintenance mesalazine treatment as a 

single – 1 sachet daily of 500mg dose, granules preferably 3 times in daily the (1.5g morning. mesalazine Children: daily). Where There needed, is only 

limited 3.0g per day documentation in a single morning for dose an may effect be taken. in children Method of administration: (age 6-18 years). oral. 

Children 

Tablets - taken 

6 years 

whole without 

of age 

chewing, 

and older: 

with 

Active 

liquid, one 

disease: 

hour before 

To be 

meals. 

determined 

Granules 

- taken on the tongue and swallowed, without chewing, with plenty of liquid. 

individually, Duration of treatment starting is with usually 30-50mg/kg/day 8 weeks. To be determined once daily by physician. preferably Children in the 

morning (all formulations): in divided there is only doses. limited Maximum documentation dose: for 75mg/kg/day. an effect in children The (age total 

dose 6-18 years). should Children not 6 exceed years and the older: maximum active disease adult – on individual dose. Maintenance 

basis starting 

treatment: with 30-50mg/kg/day To be determined either once daily individually, (granules) starting or divided with doses 15-30mg/kg/day (tablets and 

in granules). divided Maximum doses. The 75mg/kg/day. total dose Total should dose not should exceed not exceed the recommended 

adult dose. Maintenance - on individual basis starting with 15-30mg/kg/day in 

adult 

divided 

dose. 

doses. 

It 

Total 

is generally 

dose should 

recommended 

not exceed recommended 

that half the 

adult 

adult 

dose. 

dose 

Generally 

may 

be recommended given to children that half the up adult to a body dose may weight be given of 40kg; to children and up the to normal a body weight adult 

dose of 40kg to and those the above normal 40kg. adult dose Method to those of administration: above 40kg. Contra-indications: 

Taken the 

tongue Hypersensitivity and swallowed, to salicylates without or any of chewing, the excipients. with Severe plenty impairment of liquid. of Contraindications: 

hepatic function. Hypersensitivity Warnings/Precautions: to salicylates Blood tests and or any urinary of status the excipients. (dip sticks) 

renal or 

should be determined prior to and during treatment. Caution is recommended in 

Severe impairment of renal or hepatic function. Warnings/Precautions: 

patients with impaired hepatic function. Should not be used in patients with 

Blood impaired tests renal and function. urinary Mesalazine-induced status (dip sticks) renal should toxicity should be determined be considered prior if 

to renal and function during deteriorates treatment. during Caution treatment is - recommended stop treatment immediately in patients in such with 

impaired cases. Cases hepatic of nephrolithiasis function. reported; Should ensure not good be used hydration. in patients Serious blood with 

impaired dyscrasias renal have been function. reported Mesalazine-induced very rarely with mesalazine. renal toxicity Hematological should be 

investigations should be performed if patients suffer from unexplained 

considered if renal function deteriorates during treatment. Cases of 

haemorrhages, bruises, purpura, anaemia, fever or pharyngolaryngeal pain. Salofalk 

should be discontinued in case of suspected or confirmed blood dyscrasia. Cardiac 

hypersensitivity reactions (myocarditis, and pericarditis) induced by mesalazine 

nephrolithiasis have been rarely reported. reported; Salofalk ensure should good then be hydration. discontinued Patients immediately. with 

pulmonary Patients with disease, pulmonary in disease, particular in particular asthma, asthma, should should be be carefully 

monitored. Severe Patients cutaneous with adverse a history reactions of (SCARs), adverse including drug reactions drug reaction to 

with eosinophilia and systemic symptoms (DRESS), Stevens-Johnson syndrome 

preparations 

(SJS) and toxic 

containing 

epidermal necrolysis 

sulphasalazine 

(TEN), have 

should 

been 

be 

reported. 

kept under 

Discontinue 

close 

medical treatment surveillance. at the first appearance If acute of signs intolerance and symptoms reactions of severe e.g., skin abdominal reactions, 

cramps, such as skin acute rash, abdominal mucosal lesions, pain, or fever, any severe other sign headache of hypersensitivity. and rash, Patients occur, 

stop with a treatment history of adverse immediately. drug reactions Severe to preparations cutaneous containing adverse sulphasalazine reactions 

(SCARs), should be kept including under close Stevens-Johnson medical surveillance. syndrome If acute intolerance (SJS) reactions and toxic e.g., 

abdominal cramps, acute abdominal pain, fever, severe headache and rash occur, 

epidermal 

stop treatment 

necrolysis 

immediately. 

(TEN), 

Tablets may 

have 

be excreted 

been 

undissolved 

reported. 

in 

Discontinue 

patients with 

treatment the ileocecal at valve the first removed. appearance Salofalk of granules: signs and contain symptoms aspartame, of severe a source skin of 

reactions, phenylalanine. such May as be skin harmful rash, to patients mucosal with lesions, phenylketonuria. or any other Granules sign also of 

hypersensitivity. contain sucrose: 0.04mg, Salofalk 0.08mg, granules 0.12mg, contain 0.24mg aspartame, (500mg/1g/1.5g a source and 3g of 

phenylalanine granules respectively). that Salofalk may be tablets: harmful For patients for patients on a sodium-controlled with phenylketonuria. diet: the 

250mg and 500mg tablets contain 48mg and 49mg of sodium, equivalent to 2.4% 

Salofalk granules contain sucrose: 0.02mg, 0.04mg, 0.06mg and 

and 2.5% of the recommended maximum daily intake for sodium. Urine may be 

0.12mg discoloured (500mg/1g/1.5g red-brown after and contact 3g with granules sodium respectively). hypochlorite bleach Interactions: used in 

Specific toilets. Interactions: interaction Specific studies interaction have not studies been have performed. not been performed. Lactulose With or 

similar concomitant preparations treatment with that azathioprine, lower stool 6-mercaptopurine pH: possible or reduction thioguanine, of 

mesalazine consider a possible release increase from granules in their myelosuppressive due to decreased effects. pH There caused is weak by 

bacterial 

evidence that 

metabolism 

mesalazine 

of 

might 

lactulose. 

decrease 

With 

the 

concomitant 

anticoagulant effect 

treatment 

of warfarin. 

with 

Salofalk granules (additionally): lactulose, or similar preparations which lower stool 

azathioprine, pH: possible reduction 6-mercaptopurine of mesalazine release or thioguanine from granules consider due to decreased a possible pH 

increase caused by in bacterial their myelosuppressive metabolism of lactulose. effects. Use in There pregnancy is weak and lactation: evidence do that not 

mesalazine use Salofalk during might pregnancy decrease unless the anticoagulant the potential benefit effect outweighs of warfarin. the possible Use in 

pregnancy risks. Limited and experience lactation: in the lactation There are period. no Salofalk adequate should data. only be Do used not during use 

during 

breast-feeding 

pregnancy 

if the potential 

unless 

benefit 

the potential 

outweighs 

benefit 

the possible 

outweighs 

risks; if 

the breast-fed 

possible 

infant develops diarrhoea, breast-feeding should be discontinued. Undesirable 

risks. effects: Limited altered blood experience counts in (aplastic the lactation anaemia, period. agranulocytosis, Use during pancytopenia, breastfeeding 

neutropenia, only leukopenia, if the potential thrombocytopenia), benefit outweighs hypersensitivity the possible reactions risks; such if the as 

infant allergic develops exanthema, diarrhoea, drug fever, breast-feeding lupus erythematosus should syndrome, be discontinued. pancolitis, 

Undesirable headache, dizziness, effects: peripheral Headache, neuropathy, dizziness, peri- and peri- myo-carditis, and myocarditis, allergic and 

abdominal fibrotic lung pain, reactions diarrhoea, (including dyspepsia, dyspnoea, cough, flatulence, bronchospasm, nausea, vomiting, alveolitis, 

pulmonary eosinophilia, lung infiltration, pneumonitis), abdominal pain, diarrhoea, 

aplastic 

dyspepsia, flatulence, 

anaemia, 

nausea, 

agranulocytosis, 

vomiting, acute 

pancytopenia, 

pancreatitis, cholestatic 

neutropenia, 

hepatitis, 

leukopenia, hepatitis, rash, thrombocytopenia, pruritus, photosensitivity peripheral – especially neuropathy, with pre-existing allergic skin and 

fibrotic conditions, lung alopecia, reactions severe (including cutaneous adverse dyspnoea, reactions cough, (SCARs) bronchospasm, 

including drug 

alveolitis, reaction with pulmonary eosinophilia eosinophilia, and systemic symptoms lung infiltration, (DRESS), Stevens-Johnson 

pneumonitis), 

acute syndrome pancreatitis, (SJS), toxic epidermal impairment necrolysis of renal (TEN), function arthralgia, including myalgia, impairment acute and 

of renal function including acute and chronic interstitial nephritis and renal 

chronic interstitial nephritis and renal insufficiency, nephrolithiasis, 

insufficiency, nephrolithiasis, asthenia, fatigue, oligospermia (reversible), changes 

in hepatic function parameters, changes in pancreatic enzymes, eosinophil count 

increased. Legal category: POM. Cost (UK - basic NHS price; Ireland - PtW): Salofalk 

photosensitivity 250mg tablets (100s) especially £16.19; with €13.48. pre-existing Salofalk 500mg skin conditions, tablets (100s) alopecia, £32.38. 

Stevens-Johnson Salofalk 1g tablets (90s) syndrome £58.50. (SJS), Salofalk toxic 500mg epidermal granules (100 necrolysis sachets) (TEN), £28.74; 

myalgia, 

€27.93. Salofalk 

arthralgia, 

1000mg granules 

hypersensitivity 

(50 sachets) 

reactions 

£28.74; €32.87. 

such 

Salofalk 

as allergic 

1500mg 

granules (60 sachets) £48.85; €49.66. Salofalk 3g granules (60 sachets) £97.70; 

exanthema, 

€101.64. Product 

drug 

licence 

fever, lupus 

number: 

erythematosus 

Salofalk 250mg 

syndrome, 

tablets: PL10341/0004; 

pancolitis, 

changes PA573/4/3. in hepatic Salofalk function 500mg parameters, tablets: PL08637/0019. hepatitis, cholestatic Salofalk 1g hepatitis tablets: 

and PL08637/0027. oligospermia Salofalk (reversible), 500mg granules: asthenia, PL08637/0007; fatigue, changes PA573/3/1. in pancreatic Salofalk 

enzymes, 1000mg granules: eosinophil PL08637/0008; count increased. PA573/3/2. Legal Salofalk category: 1500mg POM. granules: Basic 

cost: PL08637/0016; Salofalk 500mg PA573/3/7. granules, Salofalk pack 3g size granules: 100 sachets PL08637/0025; - £28.74; PA573/3/6. €30.39. 

Product licence holder: Salofalk 250mg tablets in the UK: Dr Falk Pharma UK Ltd, 

Salofalk 

Bourne End 

1000mg 

Business 

granules, 

Park, Cores 

pack 

End Road, 

size 

Bourne 

50 sachets 

End, SL8 

– 

5AS. 

£28.74; 

Salofalk 

32.87€. 

500mg 

Salofalk and 1g tablets 1.5g Granules, and all granules: pack Dr size Falk 60 Pharma sachets GmbH, - £48.85; Leinenweberstr.5, €50.02. Salofalk D-79108 

3g Freiburg, Granules Germany. pack Date size of 60 preparation: sachets - January £97.70; 2023 €102.62 (UK- NHS price; IE 

- PtW). Product licence number: Salofalk 500mg granules – 

Further information is available on request. 

PL08637/0007; PA573/3/1. Salofalk 1000mg granules – PL08637/0008; 

PA573/3/2. Salofalk 1.5g granules PL08637/0016; PA573/3/7. Salofalk 

Adverse events should be reported. In the UK: Reporting forms 

3g 

and 

granules 

information 

PL08637/0025; 

can be 

PA573/3/6.Product 

found at https://yellowcard.mhra.gov. 

licence holder: Dr Falk 

Pharma uk/ In GmbH, Ireland: Leinenweberstr.5, Reporting forms D-79108 and information Freiburg, Germany. can be found Date of 

preparation: at https://www.hpra.ie/homepage/about-us/report-an-issue/ 

January 2022. 

Further human-adverse-reaction-form information is available on Adverse request. events should also be 

reported to Dr Falk Pharma UK Ltd at PV@drfalkpharma.co.uk. 


Adverse events should be reported. Reporting forms and information 

References: 

can be found at https://yellowcard.mhra.gov.uk/ (UK residents) or in 

1. Ireland Salofalk at Granules. https://www.hpra.ie/homepage/about-us/report-anissue/human-adverse-reaction-form 

Kruis W et al. Gut 2009; 58(2): Adverse 233-40. events should also be 

Summary of Product Characteristics. 

2. 

3. 

reported 

Leifeld 

to 

L 

Dr 

et 

Falk 

al. Aliment 

Pharma 

Pharmacol 

UK Ltd at PV@drfalkpharma.co.uk 

Ther 2011; 34(9): 1115-22. 

4. Data on file, Dr Falk Pharma. 

References: UC: ulcerative colitis 

1. Salofalk Granules. Summary of Product Characteristics. 

2. Date Kruis of W preparation: et al. Gut 2009; March 58(2): 2023 233-40. 

3. UI--2300071 

Leifeld L et al. Aliment Pharmacol Ther 2011; 34(9): 1115-22. 

4. Data on file, Dr Falk Pharma. 

Date of preparation: To March find out 2022more about Salofalk Granules 

UI--2200080 watch this 60s animation 

21

FEATURE 


45. Consortium HMP. Structure, function and diversity of the healthy 

human microbiome. Nature. 2012;486(7402):207. 

46. Li W, Ma ZS. FBA ecological guild: trio of firmicutesbacteroidetes 

alliance against actinobacteria in human oral 

microbiome. Sci Rep. 2020;10(1):1–11. 

47. Liang D, Leung RKK, Guan W, et al. Involvement of gut 

microbiome in human health and disease: brief overview, 

knowledge gaps and research opportunities. Gut Pathogens. 

2018;10(1):1–9. 

48. Rowin J, Xia Y, Jung B, et al. Gut inflammation and dysbiosis in 

human motor neuron disease. Physiol Rep. 2017;5(18): e13443. 

49. Stojanov S, Berlec A, Štrukelj B. The influence of probiotics on 

the firmicutes/bacteroidetes ratio in the treatment of obesity and 

inflammatory bowel disease. Microorganisms. 2020;8(11):1715. 

50. Woting A, Blaut M. The intestinal microbiota in metabolic 

disease. Nutrients. 2016;8(4):202. 

51. Fernandes J, Su W, Rahat-Rozenbloom S, et al. Adiposity, gut 

microbiota and faecal short chain fatty acids are linked in adult 

humans. Nutr Diabetes. 2014;4(6):e121–e121. 

52. Bifari F, Ruocco C, Decimo I, et al. Amino acid supplements 

and metabolic health: a potential interplay between intestinal 

microbiota and systems control. Genes Nutr. 2017;12(1):1–12. 

53. Chambers ES, Preston T, Frost G, et al. Role of gut 

microbiota-generated short-chain fatty acids in metabolic and 

cardiovascular health. Curr Nutr Rep. 2018;7(4):198–206. 

54. Turnbaugh PJ, Ley RE, Mahowald MA, et al. An obesityassociated 

gut microbiome with increased capacity for energy 

harvest. Nature. 2006;444(7122):1027–31. 

55. Akobeng AK, Singh P, Kumar M, et al. Role of the gut microbiota 

in the pathogenesis of coeliac disease and potential therapeutic 

implications. Eur J Nutr. 2020;59:1–22. 

56. Caio G, Lungaro L, Segata N, et al. Effect of gluten-free diet on 

gut microbiota composition in patients with celiac disease and 

non-celiac gluten/wheat sensitivity. Nutrients. 2020;12(6):1832. 

57. Schiepatti A, Bacchi S, Biagi F, et al. Relationship between 

duodenal microbiota composition, clinical features at diagnosis, 

and persistent symptoms in adult Coeliac disease. Dig Liver Dis. 

2021;53:972–9. 

58. Golfetto L, de Senna FD, Hermes J, et al. Lower bifidobacteria 

counts in adult patients with celiac disease on a gluten-free diet. 

Arq Gastroenterol. 2014;51(2):139–43. 

59. Bodkhe R, Shetty SA, Dhotre DP, et al. Comparison of small 

gut and whole gut microbiota of first-degree relatives with 

adult celiac disease patients and controls. Front Microbiol. 

2019;10:164–164. 

60. de Sousa Moraes LF, Grzeskowiak LM, de Sales Teixeira TF, et 

al. Intestinal microbiota and probiotics in celiac disease. Clin 

Microbiol Rev. 2014;27(3):482–9. 

61. Ghodsi A, Sarabi M, Ranjbar G, et al. The gut microbiota and 

probiotics in celiac disease. J Nutr Fast Health. 2021;9(2):105–12. 

62. Norouzbeigi S, Vahid-Dastjerdi L, Yekta R, et al. Celiac therapy 

by administration of probiotics in food products: a review. Curr 

Opin Food Sci. 2020;32:58–66. 

63. Medina M, De Palma G, Ribes-Koninckx C, et al. 

Bifidobacterium strains suppress in vitro the pro-inflammatory 

milieu triggered by the large intestinal microbiota of coeliac 

patients. J Inflamm. 2008;5(1):1–13. 

64. Javanmard A, Ashtari S, Sabet B, et al. Probiotics and their 

role in gastrointestinal cancers prevention and treatment; an 

overview. Gastroenterol Hepatol Bed Bench. 2018;11(4):284. 

65. Chey WD, Kurlander J, Eswaran S. Irritable bowel syndrome: a 

clinical review. JAMA. 2015;313(9):949–58. 

66. Wang Z, Xu C-M, Liu Y-X, et al. Characteristic dysbiosis of 

gut microbiota of Chinese patients with diarrhea-predominant 

irritable bowel syndrome by an insight into the pan-microbiome. 

Chin Med J. 2019;132(8):889. 

67. Wang L, Alammar N, Singh R, et al. Gut microbial dysbiosis 

in the irritable bowel syndrome: a systematic review and 

meta-analysis of case-control studies. J Acad Nutr Diet. 

2020;120(4):565–86. 

68. Chong PP, Chin VK, Looi CY, et al. The microbiome and irritable 

bowel syndrome—a review on the pathophysiology, current 

research and future therapy. Front Microbiol. 2019;10:1136. 

69. Labus JS, Hollister EB, Jacobs J, et al. Differences in gut 

microbial composition correlate with regional brain volumes in 

irritable bowel syndrome. Microbiome. 2017;5(1):49. 

70. Duan R, Zhu S, Wang B, et al. Alterations of gut microbiota 

in patients with irritable bowel syndrome based on 16S 

rRNA-targeted sequencing: a systematic review. Clin Transl 

Gastroenterol. 2019;10:2. 

71. Lee BJ, Bak Y-T. Irritable bowel syndrome, gut microbiota and 

probiotics. J Neurogastroenterol Motil. 2011;17(3):252. 

72. Bellini M, Gambaccini D, Stasi C, et al. Irritable bowel syndrome: 

a disease still searching for pathogenesis, diagnosis and 

therapy. World J Gastroenterol. 2014;20(27):8807. 

73. Maccaferri S, Candela M, Turroni S, et al. IBS-associated 

phylogenetic unbalances of the intestinal microbiota are 

not reverted by probiotic supplementation. Gut Microb. 

2012;3(5):406–13. 

74. Daulatzai MA. Non-celiac gluten sensitivity triggers gut 

dysbiosis, neuroinflammation, gut-brain axis dysfunction, and 

vulnerability for dementia. CNS Neurol Disord Drug Targets. 

2015;14(1):110–31. 

75. Garcia-Mazcorro JF, Rivera-Gutierrez X, Cobos-Quevedo OJ, 

et al. First insights into the gut microbiota of Mexican patients 

with celiac disease and non-celiac gluten sensitivity. Nutrients. 

2018;10(11):1641. 

Publisher’s Note 

Springer Nature remains neutral with regard to jurisdictional claims in 

published maps and institutional affiliations. 

22

We get the gut 

JOIN OUR BSG LIVE ‘23 

SYMPOSIUM 

FEATURE 

Manipulation of the gut microbiome 

in gastrointestinal health 

WEDNESDAY 21ST JUNE 

13.00-13.40pm 

Stay on tract. 

Go further. 

A healthy microbiome is vital for a balanced 

digestive system. 

Delivering 450 billion bacteria across 8 diverse strains, 

VSL#3 is one of the most powerful polybiotics available 

to help enrich your patients’ gut microbiome. 1 Proven 

to survive the harsh stomach conditions 2 , VSL#3 

contributes to the diversity of good gut bacteria. 3 

Help to enrich your patient’s gut microbiome; 

Help them stay on track, with VSL # 3 ® . 

For information and samples, visit www.vsl3.co.uk 

Sign up to our NEW healthcare 

professional newsletter for the 

latest updates and research on 

gut health and probiotics. 


VSL-23-001. Date of Preparation: April 2023. 

1. Cancello R, et al. Nutrients 2019, 11, 3011. 

2. Vecchione A, et al. Front Med. 2018;5(59). doi: 10.3389/fmed.2018.00059. 

3. Singh G, et al. 2021 Clinical Nutrition ESPEN 47 (2022) 70-77. 

23

FEATURE 

TRIAGE GASTROSCOPY 

REFERRALS WITH 

A first-line test for the stomach 

BIOHIT HealthCare’s GastroPanel® is a simple 

and effective non-invasive test to diagnose 

advanced atrophic gastritis and Helicobacter 

pylori (H. pylori) in patients presenting with 

dyspepsia and upper abdominal symptoms. 

Where endoscopy resources and capacity are stretched, 

GastroPanel helps select cases for gastroscopy. 

GastroPanel measures three stomach-specific biomarkers, 

enabling a thorough and objective investigation of the whole 

gastric mucosa, non-invasively, and offers clinicians more 

confidence in their diagnoses or referrals. 

Atrophic gastritis – a chronic condition of the gastric mucosa, 

is considered to be the greatest independent risk factor for 

developing gastric cancer and current guidance recommends 

that individuals with extensive gastric atrophy undergo 

regular endoscopic surveillance to closely monitor their 

disease progression. Early detection of those individuals 

with a significant risk of developing gastric cancer is the 

key to effective patient management, helping to reduce 

unnecessary referrals, and improving survival rates through 

earlier diagnoses. 

Figure 1. 

GastroPanel measures 

plasma concentrations of 

Pepsinogen I, Pepsinogen II, 

Gastrin-17 and H. pylori IgG. 


GastroPanel is a simple, effective and low cost blood test This patient-friendly blood test can help transform the 

that, through extensive validation, has consistently proven referral pathway for upper GI investigations by identifying 

to be effective in the determination of chronic atrophic 

those who need enhanced endoscopy with biopsies. 

gastritis, acid output disorders, and other diseases of 

Implementing GastroPanel could help to relieve the 

the gastric mucosa resulting from a H. pylori infection. 

burden on overstretched gastroscopy services, streamline 

When GastroPanel is positive, it helps direct appropriate and referrals for higher-risk patients, and effectively rule-out 

effective treatment plans, including, eradication therapy, 

atrophic gastritis for others. 

surveillance gastroscopy, and antacid prescription. 

Scan to find out more or visit www.biohithealthcare.co.uk 

24 

BIOHIT HealthCare Ltd 

Pioneer House, Pioneer Business Park, North Road, 

Ellesmere Port, Cheshire, United Kingdom CH65 1AD 

Tel. +44 151 550 4 550 

info@biohithealthcare.co.uk 

www.biohithealthcare.co.uk

ADVERTORIAL FEATURE 

THE NEXT, BRUSHLESS STEP IN 

ENDOSCOPE REPROCESSING 

Endoscopy continues to witness a number of important innovations that 

contribute to even better clinical outcomes. At the same time, there are still 

significant opportunities for further improving patient safety and infection 

prevention in the field. Given the constantly changing environment of medical 

device reprocessing, which is marked by a heightened consciousness of the 

overall environmental impact of healthcare and endoscopy, coupled with a 

shortage of hospital staff following Covid-19, improving the decontamination 

of endoscopes has become increasingly critical. Market feedback shows 

that there is a need for an automated and standardized process to clean 

endoscopes to ensure all steps are carried out in a uniform manner. 

Paul Caesar, Head of Hygiene, Infection Control and Reprocessing at 

PENTAX Medical EMEA, explains: “PENTAX Medical is launching the 

AquaTYPHOON to do just that. It is a new brushless solution for the 

automated pre-cleaning of endoscopes. The device was developed in 

association with PlasmaBiotics and offers an alternative to the manual 

pre-cleaning step in endoscope reprocessing without the need for brushes 

or detergent, addressing hygiene and sustainability challenges faced by 

healthcare providers in daily clinical practice.” 

Daniel Vinteler CEO of PlasmaBiotics, explains: “Thanks to its patented 

technology, the AquaTYPHOON disperses millions of water droplets in the 

endoscope channels through a compressed air flow at up to 200 kilometres 

per hour. Such high velocity creates a high shear stress which eliminates the 

residues from the endoscope channels walls.” 

Vinteler pursues: “Moreover, as this new technology replaces the mechanical 

brushing of the endoscope channels, wrist injuries are prevented. The 

reprocessing staff can work more comfortably with the height-adjustable 

AquaBOX which prevents splashing of the operator and the surrounding 

environment or uncomfortable positions.” 

Caesar continues: “The AquaTYPHOON offers a completely standardized, 

controlled and validated process, thus optimizing the pre-cleaning phase. 

No steps can be skipped any more so the results are more constant. I truly 

believe this new cutting-edge solution offers more balance between patient 

safety and staff productivity along with their well-being as the process is 

automated, lowering the risk of contamination.” 

PENTAX Medical AquaTYPHOON system with the AquaBOX 

The automated solution has built-in validation and safety features that help 

preventing human errors. The automated routine, unlike manual pre-cleaning, 

is always fully in line with the protocol and the full pre-cleaning procedure is 

documented. The system also offers full traceability and can be connected to 

hospital networks. 

Reprocessing staff member using the PENTAX Medical AquaTYPHOON 

Enhancing hygiene with automated pre-cleaning 

As an alternative to the manual pre-cleaning phase, the AquaTYPHOON 

improves hygiene and patient safety by further enhancing reprocessing 

of reusable endoscopes, through developing new ways of pre-cleaning 

to reduce the risk of infection. It automatically cleans all endoscope 

channels, including the non-brushable ones, removing organic residues 

very effectively, supporting the automated endoscope reprocessing (AER) 

process following the pre-cleaning. 

Supporting reprocessing staff for increased 

efficiency and ergonomics 

Focusing on efficiency, the AquaTYPHOON was designed to offer a 

solution to limits faced by staff, such as time constraints, heavy workloads, 

and ergonomic issues. It requires between two and five times less labour 

time , which reduces the daily workload for staff and increases productivity. 

Depending on the endoscope type being used, the device reduces channel 

pre-cleaning time to just 2-7 minutes. 

Balancing patient safety, productivity and sustainability 

As the AquaTYPHOON combines only water and air, waste generation 

due to consumables and/or chemicals is avoided. This solution reduces 

significantly water consumption, using this natural resource between six 

and ten times less than manual pre-cleaning . By optimizing efficiency but 

also reducing waste generation, it not only yields cost benefits but also has 

a positive environmental impact - making it an ideal solution for endoscopy 

departments looking to minimize their environmental footprint. 

By offering a reliable solution which enhances the reprocessing of reusable 

and semi-reusables endoscopes like the AquaTYPHOON, PENTAX Medical 

removes setbacks physicians might have when considering these devices, 

allowing them the highest possible freedom to pick the right equipment for 

their procedure. Paul Caesar concludes: “In the reprocessing process of 

endoscopes, stringent endoscope pre-cleaning is vital. However, it is much 

more than just a flush and a brush. As the industry seeks ways to optimize 

endoscope reprocessing, PENTAX Medical is turning to automated precleaning 

devices with this cutting-edge solution. Not only does it improve 

patient safety, but it also addresses the productivity challenges faced by staff 

along with hospitals’ sustainability and costs concerns.” 

Join our Digital 

Hygiene Event 

to learn more about 

sustainability in endoscopy. 

1 

Depending on the local guidelines, AquaTYPHOON requires between 2 and 5 times less labour time compared with today’s manual pre-cleaning solutions. 

2 

Depending on the endoscope type, AquaTYPHOON requires between 6 and 10 times less water compared with today’s manual pre-cleaning solutions. 


25


FAECAL CALPROTECTIN 

ASK TWICE 

Dr Peter Rimmer, The Queen Elizabeth Hospital, Birmingham and Amanda Appleton, Senior Product Manager, Alpha Laboratories Ltd. 

We are all very familiar with the use of faecal calprotectin testing to help 

distinguish inflammatory bowel disease (IBD) from functional disorders, 

and it has become a staple tool to support the clinical teams in their 

diagnosis and management of patients. If a negative faecal calprotectin 

result is obtained the cause of a patient’s symptoms is unlikely to be 

IBD, however, calprotectin is a non-specific marker for inflammation, and 

so a high result may be due to something other than IBD. 

There was a significant difference in the median initial calprotectin which 

was 949µg/g for patients who were subsequently diagnosed with IBD 

compared to 353µg/g for those who didn’t have IBD. If two results were 

available, then the difference was even more pronounced with 749µg/g 

for those with IBD compared to 34µg/g for those without. This data is 

presented in the graphs below: 

The literature highlights numerous other situations that can cause 

(usually transient) increases in the calprotectin concentration found in 

stool samples, for example: 

• Use of certain medication e.g. NSAIDs, proton pump inhibitors 

• Diverticulitis 

• Infections e.g. Salmonella, Campylobacter 

• Stomach/duodenal ulcers 

• Excessive alcohol 

• Cancer 

Basically, anything that causes an irritation/ inflammatory response in the 

digestive system (mouth to anus) can cause an increase in calprotectin 

concentrations. Whereas a negative calprotectin is a good rule out for 

IBD, a positive calprotectin result isn’t necessarily a cause for instant 

referral to secondary care. 

The Queen Elizabeth Hospital in Birmingham introduced a rapid 

access ‘Inception IBD’ clinic based on symptoms and a raised faecal 

calprotectin test, Dr Peter Rimmer presented their findings and some 

proposed changes to the pathway at the European Crohn’s and Colitis 

Organisation (ECCO) conference in Copenhagen earlier this year (P126 

Ask Twice: The importance of a repeated faecal calprotectin testing prior 

to diagnostic colonoscopy in an adult inception cohort). 

The importance of repeated testing prior to diagnostic colonoscopy in 

an adult inception cohort - Comparison of first and second testing 

Supplementary graphs not presented on the poster show that 88.6% 

of calprotectin results fell between the first and second result in patients 

that subsequently had IBD excluded: 


26 

“During the triaging process (for the Rapid Access clinic) it became 

apparent that the majority of patients only had one result at the point 

of referral, so patients were sent a sample pot in the post and asked to 

bring the sample back with them to their first outpatient appointment. The 

median time between the GP referral and this second result was 34 days. 

During this project, we did not reject referrals due to the lack of a 

second test, but we did delay the request for a colonoscopy until the 

second test was available in those with a borderline initial result or the 

clinical history was not strongly suggestive of IBD. This was only a few 

days as most brought the sample along to the appointment.” 

The data presented in the ECCO poster showed that there were 425 patients 

with a single calprotectin result and 185 patients who had two calprotectin 

results (using BÜHLMANN fCAL turbo on Abbott Alinity analysers) and a 

final diagnosis between January 2021 and November 2022.


It also demonstrates that 83% of patients with an increase 

between their first and second calprotectin test were subsequently 

found to have IBD.Although the overall statistics are compelling, 

interpretation is not always straightforward as Dr Rimmer explains: 

The poster concluded that the data, in general, supports repeat 

FCP testing to avoid unnecessary investigations adding to post 

COVID endoscopy backlogs. A cut-off of two values >200µg/g 

had the best overall performance but can miss a small number of 

IBD cases, particularly those with isolated ileitis or more indolent 

disease course. This cut-off should not be used in those with a 

marked increase between the 1st and 2nd result, where IBD is 

likely. 

Modifications to the local referral pathway are currently being 

determined, taking into account the data generated in the study. 

This will hopefully enable better use of over stretched resources 

which should in turn result in quicker access to those with most 

need. 

For more information on Faecal Calprotectin Testing visit: 

www.calprotectin.co.uk 

“We certainly feel that the faecal calprotectin (FCAL) is a highly 

accurate test, but there are some inconsistencies and pitfalls, which 

to an extent the graph represents: 

• The FCAL is just a snapshot from a single time point. In acute 

infection it will be high but if symptoms improve and FCAL 

normalises then investigation isn’t needed – post infective IBS is 

common in this patient group. 

• However, IBD is also characterised by periods of relapse and 

remission and FCAL will fluctuate alongside this, occasionally 

by the time we come to investigate they may have entered a 

milder phase of the disease. The clinical history and duration of 

symptoms in these patients is important, particularly with Crohn’s 

disease where the symptoms can be more insidious. 

We also had a handful of patients with mild proctitis in our 

cohort would not have been picked up with FCAL alone as 

their inflammation had largely resolved by the time we saw 

them. 

• FCAL will on rare occasions fail to correlate with disease severity, 

in the majority of our patients that was in ileal Crohn’s disease. 

Again, careful attention to the clinical history is necessary and 

investigation required regardless of the FCAL result in those with 

progressive symptoms or concerning features such as weight 

loss.” 

A variety of cut-off values were assessed on the poster, and two 

results of >200µg/g gave the best performance overall with a 85.7 

PPV% , 86.2 NPV% and a specificity of 89.5% but the sensitivity 

was lower than other cut-off values at 81.5%. 

SCOPE EVENTS FOR 2023-24 

Scope Health UK 

Best Health Care Training & Education Courses Provider 2022 

from Northern Enterprise Awards 2022 

THERAPEUTIC ENDOSCOPY COURSE FOR ENDOSCOPY 

NURSE ASSISTANTS AND NURSE CONSULTANTS 

28th TECNA COURSE 17th JUNE SAT 2023 MANCHESTER 

29th TECNA COURSE 4th NOV SAT 2023 BRISTOL 

GASTROENTEROLOGY COURSE FOR GENERAL PRACTITIONERS 

1st GCGP COURSE 9th Sept 2023 MANCHESTER 

ENDOSCOPIC LESION RECOGNITION & IMAGING COURSE 

1st ELRIC COURSE 9th March 2024 MANCHESTER 

REGISTER AS EXHIBITORS/SPONSORS FOR 2023/2024 

https://scopehealthuk.com/ 

SCOPE HEALTH UK is Registered in England and Wales. Registration No 8170455 

TECNA : “A COURSE WITH VISION & MISSION TO EDUCATE” 

We look forward to meeting you at the course. 


27

NEWS 


28

COMPANY NEWS 

TAILOR-MADE INSOURCING/OUTSOURCING 

GASTROENTEROLOGY AND ENDOSCOPY CLINICAL SERVICES 

From delivering a full patient pathway, to building services based 

on individual requirements, ID Medical’s gastroenterology and 

endoscopy clinical services significantly reduce wait times, improve 

patient access, and increase outpatients and diagnostic capacity. 

ID Medical Clinical Services is a CQC-registered provider already helping 

many NHS trusts manage their patients’ healthcare pathways and 

improve patient outcomes. All while delivering millions of pounds worth 

of savings against NHS Tariffs. 

Our Gastroenterology Clinical Services are delivered by experienced NHS 

Consultants and nursing healthcare professionals. They work alongside our 

Senior Operations team, Gastroenterology Clinical Lead and Medical Director. 

We appreciate how important it is to comply with local service protocols, 

policies and processes which is why, whether insourcing or outsourcing 

is chosen, we are able to seamlessly integrate within existing services, 

working in full partnership with hospitals/trusts as an extension of the 

gastroenterology department. 

The service can be up and running in as little as two weeks and set up 

to meet exacting requirements: a 24/7 elective care service, weekends, 

during the week and/or evenings. 

More key benefits of IDM Clinical Services include: 

• National coverage 

• Insourcing/outsourcing options: fixed premises or mobile units to suit 

your requirements 

• No extra work for staff – from queries to admin, we take care of 

everything 

• Capacity to flex up or down based on demand 

• All Major Framework(s) approved, providing simple contractual 

engagement 

For further information, please visit id-medical.com/clinical-services, 

email clinicalservices@id-medical.com or call 01908 525 756. 

CONSTIPATION AFFECTS 14% OF OTHERWISE 

HEALTHY PEOPLE 

For the 1 in 7 people in the UK struggling with constipation, 1 

VSL# Fibre offers a unique combination of fibre, poly-biotics and 

hibiscus extract, to help maintain a healthy bowel and facilitate 

intestinal transit. These natural ingredients are designed to gently 

relieve symptoms of constipation, replenish the gut microbiota, and 

naturally restore a healthy toilet routine. 

Relieve: Psyllium Husk is recommended by NICE for the selfmanagement 

of constipation, as it’s over three times more effective than 

wheat bran at increasing stool output 2 . Psyllium Husk swells to form a 

gel-like substance when in contact with water, helping to ease bowel 

movements. It has also been associated with significant changes in gut 

microbiota in both healthy adults and people with constipation 3 . 

Replenish: Osmotic laxative use has been shown to destroy the 

gastrointestinal mucous barrier and alter gut microbial composition, with 

long-lasting effect 4 . VSL# Fibre contains the same 8 strains of bacteria 

found in VSL#3, offering 30 Billion CFU per serving. These strains 

have been proven to survive the harsh conditions of the stomach 5 and 

contribute to the diversity of good gut bacteria 6 . 

Restore: Alongside lifestyle management, VSL# Fibre could help 

restore a healthy toilet routine, facilitating intestinal transit and helping 

to maintain a healthy bowel. It can easily slot into your patients’ daily 

routine, by mixing it with 200ml water for a delicious fruity drink. 

VSL# Fibre is available to order through AAH, or can be purchased by 

patients directly from www.vsl3.co.uk 

1. Guts UK Charity. https://gutscharity.org.uk/advice-and-information/ 

symptoms/constipation/ 

2. NICE Clinical Knowledge Summary: Constipation in Adults. https:// 

cks.nice.org.uk/ topics/constipation/management/adults/#initial-selfmanagement 

3. Jalanka et al. Int. J. Mol. Sci 2019, 20(2) 433 

4. Tropini et al. Cell. 2018 June 14; 173(7): 1742–1754 

5. Vecchione et al. Front Med. 2018;5(59) 

6. Kubacher et al Gut. 2006: 55(6): 833-841 


29

COMPANY NEWS 

MICROBIOME CHARACTERISATION ENSURES SUCCESS 

IN FAECAL MICROBIOTA TRANSPLANTATION 

Graham Johnson, Managing Director, BIOHIT Healthcare 


Faecal microbiota transplantation (FMT) is becoming a more widespread 

treatment for dysbiosis-associated conditions, in particular, for 

gastrointestinal disorders, and its use was further endorsed recently 

when, in 2022, the National Institute for Health and Care Excellence 

(NICE) approved it for treating recurrent Clostridium difficile infections. 

[1] However, several randomized controlled trials investigating FMT in 

irritable bowel syndrome (IBS) patients have revealed huge variability in 

treatment response.[2] These contradictory findings may be attributable 

to a lack of standardisation in various aspects of the trial protocol 

design, one of which is donor selection criteria.[3] At the same time, 

there has been a rising tendency to recruit ‘super-donors’ – favourable 

both in terms of their microbial diversity and stool composition – with 

the aim of ensuring positive outcomes for recipient patients.[4, 5] The 

gut microbiota of these donors is currently not always characterised, 

but some advocates of FMT are beginning to suggest that this may be 

more valuable than simple clinical screening when it comes to matching 

recipients to donors, especially with the innovative diagnostic tools 

that are now available.[6] Microbial profiling undoubtedly provides key 

information, such as the abundance and diversity of bacteria in the 

gut – as well as a measure of dysbiosis in patients – and applying this 

approach across the board as a measure of standardisation could help 

to refine therapeutic FMT strategies and lead to more consistent study 

results with favourable patient outcomes.[7] 

Purposeful protocol design 

This is certainly the strategy chosen by Magdy El-Salhy, Professor of 

Gastroenterology and Hepatology at the University of Bergen, whose 

research team recently conducted a clinical trial to determine the efficacy 

of FMT for IBS patients.[8] The study found that FMT is an effective 

therapy for IBS, with up to 89.1 % of patients responding to treatment, 

and around half of all patients experiencing clinical improvements in 

abdominal symptoms, fatigue and quality of life. However, Magdy is 

convinced that protocol design was key to ensuring the validity of the 

study results. There were five important factors: the super-donors 

were screened against set criteria; there was frequent faecal analysis 

of the donor to monitor microbiome stability; the fresh donor faeces 

were immediately frozen; the sample was mixed manually prior to 

administration; and the donor material was administered by gastroscope 

directly into the recipient’s duodenum. 

The right tool for the job 

On top of this, the GA-map ® Dysbiosis Test (GA-map ® Test) – a gut 

microbiota DNA-based platform that identifies and characterises 

dysbiosis – was used throughout the trial, as Magdy explained: “The 

GA map ® Test was fundamental to the analytical element of our trial; 

we used it to profile the faecal samples from the donor and to evaluate 

the intestinal bacterial profiles of patients following transplantation.” 

GA-map ® Test assigns each sample with an index that ranges from 1 

for ‘normobiosis’ to any score greater than 2 to represent an increasing 

degree of dysbiosis. Samples are then cross-indexed with an additional 

value that represents the abundance of present species compared to 

the reference population. Indexing in this manner refines the definition of 

dysbiosis and multiple FMT studies have correlated the GA-map ® Test 

index with effectiveness of therapeutic intervention.[9-12] 

Standardisation for success 

The trial protocol included faecal analysis of the super-donor at the 

start of the study to ensure that they had normal gut microbiota, and 

then at three monthly intervals throughout the year to confirm stability 

of their microbiome. Christina Casèn, Senior Vice President, Clinical 

and Medical Affairs at Genetic Analysis AS, said: “A standardised and 

validated test that could be conducted in situ was vital for this study as it 

involved repeated sampling and measurements of the donor. Performing 

analyses with the GA-map ® Test allowed the trial clinicians to compare 

results from different time periods instantaneously and evaluate FMT 

efficacy on site.” 

Characterisation to further understanding 

The study conducted by Magdy and his team confirmed that the 

outcome of FMT in IBS patients is donor dependent, and demonstrated 

that standardisation of key aspects of the trial protocol is critical. A 

donor needs to be well defined with both a normal dysbiosis index and 

a favourable specific microbial signature, and using dysbiosis testing 

platforms for characterisation can reduce variability in clinical response 

and ultimately ensure success of the FMT method. When clinicians are 

able to perform DNA-based faecal analysis themselves during trials – 

without needing to send samples to an external sequencing laboratory 

– they benefit from instantaneous information that guides FMT as an 

effective therapeutic intervention. 

References 

[1] NICE recommends transplant with good bacteria taken from poo to resolve recurrent Clostridium 

difficile infections | News | News | NICE, https://www.nice.org.uk/news/nice-recommends-faecalmicrobiota-transplant-for-recurrent-clostridioides-difficile-infection 

(accessed 16 January 2023). 

[2] Cammarota G, Ianiro G, Tilg H, et al. European consensus conference on faecal microbiota 

transplantation in clinical practice. Gut 2017; 66: 569–580. 

[3] El-Salhy M, Hausken T, Hatlebakk JG. Current status of fecal microbiota transplantation for 

irritable bowel syndrome. Neurogastroenterology and Motility; 33. Epub ahead of print 1 

November 2021. DOI: 10.1111/NMO.14157. 

[4] Koren O, Fiorucci S, O’sullivan JM, et al. The Super-Donor Phenomenon in Fecal Microbiota 

Transplantation. Frontiers in Cellular and Infection Microbiology | www.frontiersin.org; 1. Epub 

ahead of print 2019. DOI: 10.3389/fcimb.2019.00002. 

[5] Moayyedi P, Surette MG, Kim PT, et al. Fecal Microbiota Transplantation Induces Remission in 

Patients With Active Ulcerative Colitis in a Randomized Controlled Trial. Gastroenterology 2015; 

149: 102-109.e6. 

[6] Allegretti JR, Mullish BH, Kelly C, et al. The evolution of the use of faecal microbiota 

transplantation and emerging therapeutic indications. The Lancet 2019; 394: 420–431. 

[7] Ianiro G, Punčochář M, Karcher N, et al. Variability of strain engraftment and predictability of 

microbiome composition after fecal microbiota transplantation across different diseases. Nature 

Medicine 2022 28:9 2022; 28: 1913–1923. 

[8] El-Salhy M, Gunnar Hatlebakk J, Kristoffersen AB, et al. Gut microbiota Efficacy of faecal 

microbiota transplantation for patients with irritable bowel syndrome in a randomised, doubleblind, 

placebo-controlled study. Gut 2020; 69: 859–867. 

[9] Wei S, Bahl MI, Dahl Baunwall SM, et al. Determining Gut Microbial Dysbiosis: a Review of Applied 

Indexes for Assessment of Intestinal Microbiota Imbalances. Epub ahead of print 2021. DOI: 

10.1128/AEM.00395-21. 

[10] El-Salhy M, Hausken T, Hatlebakk JG. Increasing the Dose and/or Repeating Faecal Microbiota 

Transplantation (FMT) Increases the Response in Patients with Irritable Bowel Syndrome (IBS). 

DOI: 10.3390/nu11061415. 

[11] Mazzawi T, Lied GA, Sangnes DA, et al. The kinetics of gut microbial community composition in 

patients with irritable bowel syndrome following fecal microbiota transplantation. PLoS One 2018; 

13: e0194904. 

[12] El-Salhy M, Hatlebakk JG, Gilja OH, et al. Efficacy of faecal microbiota transplantation for patients 

with irritable bowel syndrome in a randomised, double-blind, placebo-controlled study. Gut 2020; 

69: 859–867. 

30

COMPANY NEWS 

PENTAX MEDICAL’S NEW PREMIUM VIDEO PROCESSOR 

AND ENDOSCOPE SERIES NOW LAUNCHED 

See the future of endoscopy with the PENTAX Medical INSPIRA video processor (EPK-i8020c) and i20c endoscope series 

HAMBURG, 19 April 2023 – PENTAX Medical, a division of HOYA 

Group, has launched its two newest innovations: the PENTAX 

Medical INSPIRA premium video processor, and the i20c video 

endoscope series. The video processor acts as the bridge for 

legacy endoscopes 1 , bringing them to next level image quality, 

whilst the i20c video endoscope series supports procedures with 

superior vision and ergonomics. 

Improved clinical outcomes 

Boosting diagnostic and therapeutic capabilities is a core consideration 

in the development of all PENTAX Medical products. The new 

PENTAX Medical INSPIRA video processor aims to improve clinical 

outcomes by providing optimum image quality for all PENTAX Medical 

endoscopes, including legacy endoscopes 1 . When this processor is 

combined with the new i20c endoscope series, visualization is further 

enhanced by providing highly detailed images to show vessels and 

structures in the best possible clarity. Its ergonomic control body and 

steering wheels allow for improved maneuverability. The new platform is 

designed to support healthcare professionals in detection, diagnosis and 

therapy better than ever. 

Maximized value 

The PENTAX Medical INSPIRA video processor and i20c video 

endoscope series are designed to maximize the value of the endoscopy 

suite. The new video processor upgrades legacy endoscope portfolios 

to the latest imaging standards 1 , allowing current endoscope 

generations to meet high-class clinical needs for an extended duration 

of time. By providing an LED light source and smart image processing 

to a wide range of compatible endoscopes, it extends the lifecycle of 

each endoscope for greater sustainability. The processor’s dual port 

is compatible with two connection types, which makes this solution 

a gateway to the future of endoscopes. This i20c endoscope series 

consists of a unique control body and lightweight connector to enhance 

the user experience. 

Rainer Burkard, Global President at PENTAX Medical, comments: 

“At PENTAX Medical we care about providing the best possible 

support for health care professionals. We are very excited about our 

new premium platform INSPIRA setting new standards in endoscopy: 

the INSPIRA video processor allows physicians to upgrade legacy 

endoscopes, whilst being future-proof for the next generation, like 

the new i20c video endoscopes. Physicians benefit from optimized 

endoscopic workflows, improved imaging, and visualization, while 

extending lifecycles and experiencing superior ergonomics.” 

Enhanced experience and satisfaction 

PENTAX Medical is committed to continuously developing innovative 

products in accordance with physicians’ needs, as they spend countless 

hours working with these instruments. The unique 7-inch touchscreen 

with intuitive plug-and-play features of the new video processor, 

alongside the customizable graphical user interface, means that they 

can truly focus on their patient. 

Dr. Marc Giovannini, Chief of the Department of Medico-surgical 

Digestive Oncology, Institut Paoli-Calmettes, France, shares: “This 

new processor improves dramatically the quality of the endoscopic 

image, especially with the 4K screen.” The i20c endoscope series 

features improved ergonomics and adjustable stiffness, significantly 

improving the user experience for all physicians. This new generation of 

endoscopes offers richly detailed imaging, and the Auto-HDR feature 

provides true colors and high contrasts. Healthcare professionals can 

enjoy outstanding maneuverability, angulation and handling, combined 

with further improved vision. 

After receiving CE marks in January, these solutions are commercially 

available from April 19th, 2023. Launch dates may vary between global 

regions, please contact your local PENTAX Medical sales representative 

for further information. 

Join PENTAX Medical at the ESGE Days 2023, in Dublin, for the official 

launch event. A team of experts will be there to showcase how these 

new innovations help any department meet its goals for patient safety, 

productivity, and sustainability. If you are interested in attending this 

event in-person or online, or in an interview with an executive, please 

contact Charlotte Hérault (charlotte.herault@omnicomprgroup.com). 

1 

90i, i10, J10, 90K and i10c series endoscopes. Not all models are 

compatible. For details, contact your local PENTAX Medical service 

facility. 


PENTAX Medical INSPIRA video processor (EPK-i8020c) and i20c endoscope series 

31

Helicobacter Test INFAI ® 

One of the most used 

13 

C-urea breath tests for the diagnosis 

of Hp-infections worldwide 

• New line of INFAI packaging and serialization according the EU’s Falsified Medicines Directive 

• More than 7.0 million Helicobacter Test INFAI performed worldwide 

• Registered in more than 40 countries worldwide 

• First approved Hp test for children from the ages of 3 to 11 

• Modified Hp test for patients taking PPIs (REFEX) 

• Modified Hp test for patients with atrophic gastritis 

• Cost-effective CliniPac Basic for hospital and GPs use 

INFAI UK Ltd 

Innovation Centre, York Science Park 

University Road, Heslington 

York YO10 5DG UK 

Phone: +44 1904 435 228 

Fax: +44 1904 435 229 

E-Mail: mail@infai.co.uk 

Web: www.infai1.com

Gastroenterology Today Summer 2023

Create successful ePaper yourself

Delete template?

Save as template?