Diagnosis of Inflammatory Bowel Disease

February 9, 2026 updated by: Sandy Sameh Naguib Fanous, Assiut University

Non-invasive Molecular Diagnostics for Inflammatory Bowel Disease : A Genetic and Biomarkers Study

  • To quantify the expression of Nuclear enriched abundant transcript 1 (NEAT1) and Anti-sense Non RNA in the INLK4 locus (ANRIL) to determine their potential role as non invasive diagnostic biomarkers in inflammatory bowel disease.
  • To evaluate the correlation between the studied biomarkers and both the clinical presentation of the patients and the inflammatory mediators like Nuclear factor κB (NF-KB) signaling pathway.

Study Overview

Status

Not yet recruiting

Conditions

Detailed Description

Inflammatory bowel disease (IBD) is a chronic inflammatory disorder affecting the gastrointestinal tract and is characterized by a progressive and unpredictable disease course. There has been a global rise in the incidence of IBD over the last few decades. Considering the chronic, progressive nature of IBD and the costliness of its treatment, the rise of IBD entails a growing socioeconomic burden. A growing body of evidence suggests that IBD may be the result of an interaction between genetic factors, environmental factors, life style factors as diet, antibiotics, intestinal barrier dysfunctions and altered microbes.

According to a large meta-analysis of population-based studies (2000-2022) The global prevalence rates of IBD was 229.7 per 100,000 persons and the incidence was 9.7 per 100,000 persons. Europe had the highest prevalence rates of IBD while the highest IBD incidence was seen in Oceania. Research in the Arab world suggests that the IBD prevalence in Arab countries increased from ~28.9 to ~34 cases per 100,000 between 2009 and 2019, with Egypt as one of the leading countries producing IBD research output. According to a recent global burden study (1990-2021), the absolute number of deaths attributed to IBD nearly doubled: from ~21,418 in 1990 to ~42,422 in 2021 - reflecting growing numbers of people living with IBD.

It is characterized by remission and exacerbation course. Bloody stools, abdominal pain, weight loss, chronic diarrhea, and the presence of immune-mediated extra-intestinal manifestations represent the disease's symptoms.

Over time, severe inflammation within the intestine can lead to serious complications, including ulcers, narrowing of the intestinal lumen, and even perforations. Notably, IBD can cause considerable damage to the digestive system, resulting in substantial tissue injury, reduced intestinal functionality, associated disability, and a state of systemic inflammation that may impact the individual's overall health. Also, Patients with inflammatory bowel disease have an increased risk of developing colorectal cancer.

Inflammatory bowel disease manifests primarily in two major forms: Crohn's disease (CD) and ulcerative colitis (UC) . Crohn's disease typically exhibits lesions in the ileum and colon, characterized by intermittent inflammatory changes of the permeable wall while Ulcerative colitis predominately develops on the mucosal surface of the rectum, displaying continuous inflammatory foci.

The causative genes responsible for IBD remain incompletely characterized, highlighting the necessity for a thorough investigation of crucial molecular signatures involved in its development, which may provide potential avenues for effective therapies. In recent years, there has been a significant expansion in the era of RNA biology, showing the sophisticated mechanisms of gene regulation that extend far beyond the conventional protein-coding genes. While messenger RNAs (mRNAs) are transcribed and translated into proteins, most of the genome is transcribed into RNA molecules known as non-coding RNAs (ncRNAs) that do not ultimately translate into proteins.

Over 70% of genetic associations in IBD occur in the noncoding regions of the genome. The major classes of ncRNAs that have gained increased research attention are long non-coding RNAs (lncRNAs), microRNAs (miRNAs), and circular RNAs (circRNAs). Long noncoding RNA are noncoding RNAs (not get translated into protein) with a length of more than 200 base pairs , and contribute to the etiology of various diseases such as respiratory diseases, inflammatory diseases and tumors. lncRNAs are major players in the inflammatory pathway as they have crucial roles in not only expression but also differentiation of cytokines and immune cells, respectively.

Nuclear enriched abundant transcript 1 (NEAT1) is long noncoding RNA that is a key component in building the ribo-riboprotein complex to regulate DNA-mediated activation of innate immune responses and has also been found to play an important role in innate immune responses. It targets numerous genomic regions in various cells, mainly involving active genes, revealing that it is a regulator for plenty of active genes and signal pathways. It is involved in the development of colitis by acting on miR-204-5p axis through activating PI3K-AKT signaling pathway and the NF-κB signaling pathway leading to increase of Interleukin-6 (IL-6) , Imterleukin-1B (IL-1B) and Tumor necrosis factor-a (TNF-a) that result in inflammation and cell apoptosis .

Anti-sense Non RNA in the INLK4 locus (ANRIL) is long non coding RNA that doesn't encode a protein; instead, it regulates gene expression at transcriptional, epigenetic, and post-transcriptional levels . It has a pro-inflammatory role in many inflammatory and immune diseases as Coronary artery disease, Chronic kidney disease and Inflammatory bowel disease. In IBD, it mediates nuclear factor κB (NF-κB) to influence inflammation through its effects on intestinal epithelial cells, besides providing future clues for clinical diagnosis. It activates NF-ΚB leading to increase of IL-6 , IL-1B and TNF-a that result in cell apoptosis . Also, Up-regulation of ANRIL could decrease the expression of miR-199a and increase the number of apoptotic cells.

Nuclear factor kappa B (NF-KB) expression is accompanied by increased production of pro-inflammatory cytokines, such as TNF-α, IL-1 and IL-6, due to the actions of NF-kB in expanding the capacity of these cells to produce inflammatory mediators. Predominantly, the NF-kB derived pro-inflammatory cytokines are responsible for two mechanisms involved in the development of IBD lesions. Firstly, the produced pro-inflammatory cytokines directly mediate mucosal tissue damage by principally up-regulation of matrix metalloproteinases production and secretion in the intestinal lumen. Secondly, NF-kB derived pro-inflammatory cytokines also mediate the stimulation, activation, and differentiation of immunological cells derived from lamina propria of the bowel mucosa, resulting in chronic inflammation and, therefore, in the perpetuation of mucosal damage.

So the investigators will measure NEAT1 and ANRIL as diagnostic biomarkers for IBD together with the Inflammatory mediator NF-KB. This can be done by non invasive blood sample instead of the invasive endoscopic biopsy.

Study Type

Observational

Enrollment (Estimated)

62

Contacts and Locations

This section provides the contact details for those conducting the study, and information on where this study is being conducted.

Study Contact

Participation Criteria

Researchers look for people who fit a certain description, called eligibility criteria. Some examples of these criteria are a person's general health condition or prior treatments.

Eligibility Criteria

Ages Eligible for Study

  • Adult

Accepts Healthy Volunteers

Yes

Sampling Method

Non-Probability Sample

Study Population

Patients with inflammatory bowel disease

Description

Inclusion Criteria:

  • Newly histopathologicaly diagnosed IBD

Exclusion Criteria:

  • Patients with serious complications as intestinal obstruction, perforation, polyps or colorectal carcinoma
  • Patients who are taking NSAIDs or Immunosuppressive drugs
  • Patients who are having other autoimmune disorders
  • Patients with Chronic infections as TB or other diseases
  • Patients with a history of allergy
  • Pregnant or Lactating women

Study Plan

This section provides details of the study plan, including how the study is designed and what the study is measuring.

How is the study designed?

Design Details

Cohorts and Interventions

Group / Cohort
Patients with inflammatory bowel disease
Healthy normal persons

What is the study measuring?

Primary Outcome Measures

Outcome Measure
Measure Description
Time Frame
To quantify the expression of NEAT1 and ANRIL to determine their potential role as non invasive diagnostic biomarkers in inflammatory bowel disease.
Time Frame: Baseline
Measure level of NEAT1 and ANRIL genes in blood samples of inflammatory bowel disease patients
Baseline

Secondary Outcome Measures

Outcome Measure
Measure Description
Time Frame
To evaluate the correlation between the studied biomarkers among the studied groups explored and both their clinical presentations and the inflammatory mediators like NF-KB signaling pathway.
Time Frame: Baseline
To find the relation between the studied biomarkers (NEAT1 and ANRIL) and the inflammatory mediators like NF-KB signaling pathway.
Baseline

Collaborators and Investigators

This is where you will find people and organizations involved with this study.

Sponsor

Assiut University

Publications and helpful links

The person responsible for entering information about the study voluntarily provides these publications. These may be about anything related to the study.

General Publications

Study record dates

These dates track the progress of study record and summary results submissions to ClinicalTrials.gov. Study records and reported results are reviewed by the National Library of Medicine (NLM) to make sure they meet specific quality control standards before being posted on the public website.

Study Major Dates

Study Start (Estimated)

April 1, 2026

Primary Completion (Estimated)

April 1, 2028

Study Completion (Estimated)

June 1, 2028

Study Registration Dates

First Submitted

February 3, 2026

First Submitted That Met QC Criteria

February 3, 2026

First Posted (Actual)

February 10, 2026

Study Record Updates

Last Update Posted (Actual)

February 11, 2026

Last Update Submitted That Met QC Criteria

February 9, 2026

Last Verified

February 1, 2026

More Information

Terms related to this study

Additional Relevant MeSH Terms

Other Study ID Numbers

  • Non-invasive diagnosis of IBD

Plan for Individual participant data (IPD)

Plan to Share Individual Participant Data (IPD)?

UNDECIDED

Drug and device information, study documents

Studies a U.S. FDA-regulated drug product

No

Studies a U.S. FDA-regulated device product

No

This information was retrieved directly from the website clinicaltrials.gov without any changes. If you have any requests to change, remove or update your study details, please contact register@clinicaltrials.gov. As soon as a change is implemented on clinicaltrials.gov, this will be updated automatically on our website as well.

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