Inflammatory bowel disease

What is IBD?

Inflammatory bowel disease (IBD) is a group of chronic conditions that cause ongoing inflammation of the digestive tract. It mainly includes Crohn’s disease and ulcerative colitis. Both Crohn’s disease and ulcerative colitis cause long-term inflammation in the intestines, but they affect different areas and layers of the gut:

• Crohn's disease: can affect any part of the digestive tract from mouth to anus, most commonly the terminal ileum and colon. It involves all layers of the bowel wall and can cause strictures, fistulae, and abscesses. Disease is typically patchy rather than continuous.

• Ulcerative colitis (UC): confined to the colon and rectum, affecting only the inner mucosal lining in a continuous pattern. Severity ranges from proctitis (rectum only) to pancolitis (entire colon).

This chronic inflammation can lead to periods of flare-ups and remission. Understanding early warning signs and tracking inflammation markers can help you manage them more effectively.

Common symptoms of IBD

IBD symptoms vary by disease type, location, and severity. Common signs across both Crohn's and UC include:

• Persistent or recurrent abdominal pain and cramping

• Diarrhoea — often with blood or mucus, particularly in UC

• Urgent or frequent need to defecate

• Unexplained fatigue — often from anaemia, malabsorption, or chronic inflammation

• Unintentional weight loss and reduced appetite

• Bloating and nausea

Extraintestinal manifestations, affecting areas outside the bowel, occur in up to 40% of IBD patients:

• Joint pain or swelling (peripheral arthropathy or axial arthritis)

• Eye inflammation (uveitis, episcleritis)

• Skin conditions (erythema nodosum, pyoderma gangrenosum)

• Liver involvement — particularly primary sclerosing cholangitis (PSC), strongly associated with UC

What causes IBD?

IBD results from an abnormal immune response to the intestinal microbiome in genetically susceptible individuals. Contributing factors include:

• Immune dysregulation: the immune system attacks the intestinal lining in response to normal gut bacteria

• Genetic predisposition: over 200 genetic loci are associated with IBD; having a first-degree relative with IBD significantly raises risk

• Gut microbiome disruption: reduced microbial diversity and imbalance in gut bacteria composition

• Environmental triggers: westernised diet, antibiotic use, smoking (worsens Crohn's, paradoxically may be protective in UC), and psychological stress

• Infections: certain intestinal infections can trigger or precipitate IBD onset in susceptible individuals

While these factors can’t always be controlled, early awareness and regular testing can help you manage them effectively.

How is IBD detected?

Detection combines abdominal imaging, which directly visualises the bowel and identifies structural changes, with blood tests that assess inflammation and nutritional consequences.

Abdominal MRI: MRI enterography is the radiation-free gold standard for assessing the small bowel. It identifies active inflammation, wall thickening, strictures, and fistulae. Elfcare’s full body MRI captures these structural changes, providing critical diagnostic information that blood tests alone cannot detect.

Blood tests: Blood tests assess the inflammatory activity and nutritional consequences of IBD. Relevant markers in Elfcare's panel include:

• CRP: measures systemic inflammation and correlates with disease severity.

• Haemoglobin and ferritin: identifies iron deficiency anaemia caused by blood loss or poor absorption.

• Vitamin B12: specifically detects impaired absorption in the lower small intestine.

• Vitamin D: monitors levels essential for intestinal immune regulation.

• Albumin: reflects both nutritional status and the severity of active disease.

• tTG-IgA: rules out coeliac disease, which often mimics IBD symptoms.

• ALP and GGT: screens for liver complications specifically associated with ulcerative colitis.

Long-term complications

Untreated or poorly managed IBD carries significant risks that can impact your entire body:

• Colorectal cancer: risk increases significantly with long-standing colonic inflammation.

• Strictures and fistulae: chronic inflammation can cause bowel obstructions or abnormal organ connections.

• Primary sclerosing cholangitis: a progressive bile duct condition often associated with ulcerative colitis.

• Osteoporosis: bone loss resulting from chronic malabsorption and vitamin D deficiency.

• Nutritional deficiencies: Depletion of iron, B12, and zinc due to impaired intestinal absorption.

Why early detection matters

IBD progresses through fluctuating phases of activity and remission, often causing cumulative bowel damage with every untreated flare. Early detection is vital to identify inflammation before strictures, fistulae, or permanent nutritional depletion occur. By diagnosing IBD early, often missing the typical 2-to-3-year delay, you can implement a management plan that preserves bowel function and significantly reduces the long-term risks of surgery and colorectal cancer.

Early insight allows you to:

• Identify triggers: pinpoint dietary, stress, or medication factors that spark flares.

• Prevent deficiencies: support nutrient levels before malabsorption impacts your energy.

• Maintain remission: work on a proactive plan to keep the gut calm and functional.

• Protect long term health: reduce the risk of complications and maintain overall well-being.

How Elfcare can help

Elfcare's abdominal MRI can identify bowel wall changes, mesenteric lymphadenopathy, and structural complications consistent with IBD, particularly relevant for Crohn's disease involving the small bowel, which is inaccessible to colonoscopy.

Our blood panel covers CRP, a full nutritional profile (iron, ferritin, B12, vitamin D, albumin), tTG-IgA, and liver markers, providing a comprehensive picture of inflammatory activity, nutritional status, and hepatic complications.

If our MRI or blood tests identify a suspicious finding, we take care of further diagnostics or refer you to the appropriate specialist.