IBD treatment, coeliac disease and IBS

Medical and Surgical Treatment Algorithm

AMC Surgical Pearl: When medical therapy fails in ASUC, the emergency procedure of choice is a subtotal colectomy with end ileostomy and preservation of the rectal stump (Hartmann's pouch). Proctectomy and pelvic dissection (ileal pouch reconstruction) are strictly avoided in acute sepsis, malnutrition, and high-dose corticosteroid exposure.

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Coeliac Disease & Malabsorption

Coeliac disease is a systemic immune-mediated enteropathy triggered by the ingestion of dietary gluten (prolamins found in wheat, rye, and barley) in genetically susceptible individuals expressing HLA-DQ2 ($> 90-95\%$) or HLA-DQ8 ($5-10\%$).

Clinical Presentation

• Classical Presentation: Chronic diarrhoea, steatorrhoea, abdominal distension, flatulence, weight loss, and severe nutrient malabsorption.
• Non-Classical / Adult Presentation (More Common): Lethargy, chronic fatigue, unexplained iron deficiency anaemia (microcytic, resistant to oral iron supplementation), early-onset osteopenia/osteoporosis, recurrent aphthous stomatitis, elevated transaminases, and recurrent miscarriages.
• Dermatitis Herpetiformis: Cutaneous manifestation of coeliac disease presenting with intensely pruritic, symmetrical polymorphic vesicles, papules, and urticarial plaques over the extensor surfaces of the elbows, knees, buttocks, and scalp. Granular IgA deposition is noted in dermal papillae on direct immunofluorescence. Diagnosis confirms coeliac disease without mandatory bowel biopsy.

Diagnostic Algorithm & Serology Rules

1. Active Gluten Consumption Mandatory: All serological and histological testing must be performed while the patient is on a gluten-containing diet (consuming at least 2 slices of wheat bread daily for at least 6 weeks). Commencing a gluten-free diet before testing causes rapid serological normalization and mucosal healing, producing false-negative results.
2. First-Line Serological Screen:
   • Anti-Tissue Transglutaminase IgA (anti-tTG IgA)
   • Simultaneous Total Serum IgA Measurement: Selective IgA deficiency occurs in $2-3\%$ of coeliac patients (a 10- to 15-fold higher incidence than in the general population). In total IgA deficiency, anti-tTG IgA is falsely negative. When total IgA is low ($< 0.07\text{ g/L}$), clinicians must order IgG-based serology: anti-deamidated gliadin peptide IgG (anti-DGP IgG) or anti-tTG IgG.
3. Confirmatory Gold Standard (Adults):
   • Gastroscopy with Duodenal Biopsies: Multiple biopsies must be obtained (at least 1-2 from the duodenal bulb and at least 4 from the second/third parts of the duodenum) to account for patchy involvement.
   • Marsh Histopathological Classification:
     • Marsh 1 (Infiltrative): Increased intraepithelial lymphocytes ($> 25\text{ lymphocytes per } 100\text{ enterocytes}$).
     • Marsh 2 (Hyperplastic): Intraepithelial lymphocytosis plus crypt hyperplasia.
     • Marsh 3 (Destructive): Crypt hyperplasia plus villous blunting/atrophy (3a partial, 3b subtotal, 3c total villous atrophy).
4. HLA-DQ2 / HLA-DQ8 Genotyping: Possesses a negative predictive value $> 99\%$. A negative result effectively excludes coeliac disease. Indicated when serology and histology are discordant or when a patient has already commenced a gluten-free diet and refuses a gluten challenge.

Long-Term Management

• Oats in coeliac disease: Australian gluten-free labelling excludes oats. Some patients react to avenin; contamination is another concern. Any introduction requires specialist dietitian guidance and follow-up, not a blanket statement that pure oats are non-immunogenic.
• Nutritional correction: Oral or parenteral supplementation of iron, folate, calcium, vitamin D, and vitamin B12.
• DEXA Bone Mineral Density Scan: Recommended at diagnosis due to secondary hyperparathyroidism and malabsorption of calcium and vitamin D.
• Pneumococcal Vaccination: Due to functional hyposplenism secondary to splenic atrophy seen in chronic coeliac disease.

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Irritable Bowel Syndrome (IBS)

Irritable bowel syndrome (IBS) is a chronic functional disorder of brain-gut interaction characterized by recurrent abdominal pain associated with altered bowel habits, in the complete absence of detectable organic structural pathology.

Rome IV Diagnostic Criteria

Recurrent abdominal pain on average at least 1 day per week in the last 3 months, associated with two or more of the following criteria:

1. Related to defecation (either improved or worsened by bowel movement)
2. Associated with a change in stool frequency
3. Associated with a change in stool form (appearance)

Symptoms must have started at least 6 months prior to diagnosis and be currently active during the past 3 months.

Subtypes (Bristol Stool Form Scale)

• IBS-D (Diarrhoea-predominant): $> 25\%$ loose/watery stools (Bristol 6-7), $< 25\%$ hard stools.
• IBS-C (Constipation-predominant): $> 25\%$ hard/lumpy stools (Bristol 1-2), $< 25\%$ loose stools.
• IBS-M (Mixed bowel habits): $> 25\%$ hard stools and $> 25\%$ loose stools.
• IBS-U (Unclassified): Insufficient stool abnormality to meet above criteria.

Alarm Features ('Red Flags')

The presence of any of the following features excludes uncomplicated IBS and warrants urgent specialist referral and organic evaluation (colonoscopy and CT imaging):

• Age of onset $> 50\text{ years}$
• Unexplained, involuntary weight loss
• Rectal bleeding or melaena (in the absence of documented bleeding haemorrhoids/fissures)
• Nocturnal diarrhoea awakening the patient from sleep
• Persistent, progressive, severe symptoms or unexplained fever
• Unexplained iron deficiency anaemia or elevated inflammatory markers (CRP/ESR)
• Family history of colorectal cancer, IBD, or coeliac disease in a first-degree relative
• Palpable abdominal or rectal mass, or lymphadenopathy

Diagnostic Workup in the Absence of Red Flags

In young patients meeting Rome IV criteria without red flags, extensive invasive investigations are unnecessary. Baseline non-invasive tests include:

• Full Blood Count (FBC) & Ferritin (rules out anaemia)
• C-Reactive Protein (CRP) (rules out active systemic inflammation)
• Coeliac Serology (anti-tTG IgA + total serum IgA)
• Faecal calprotectin: A low result makes significant intestinal inflammation less likely in the right setting, but does not provide a universal exclusion. Alarm features, persistent symptoms and pre-test probability still guide investigation.

Evidence-Based Management Strategies

• Doctor-Patient Relationship: Validate symptoms, explain the gut-brain axis, visceral hypersensitivity, and the benign prognosis.
• Dietary Approaches: Structured trial of a Low-FODMAP diet (fermentable oligosaccharides, disaccharides, monosaccharides, and polyols) supervised by a specialized dietitian. Trial of soluble fibre (ispaghula / psyllium husk) for IBS-C; avoid insoluble fibre (wheat bran), which exacerbates bloating.
• Pharmacological Interventions:
  • Antispasmodics: Mebeverine, hyoscine butylbromide, or peppermint oil capsules taken prior to meals for postprandial cramping.
  • IBS-D: Loperamide as needed for loose stools; low-dose tricyclic antidepressants (TCAs) (e.g. amitriptyline $10-25\text{ mg}$ nocte) to modulate visceral hypersensitivity and slow gut transit.
  • IBS-C: Osmotic laxatives (macrogol / polyethylene glycol); avoid stimulant laxatives long term; selective serotonin reuptake inhibitors (SSRIs) if comorbid anxiety or depression.
• Psychological Interventions: Gut-directed hypnotherapy and cognitive behavioural therapy (CBT) for refractory symptoms.

Primary references (checked 7 October 2026): Coeliac Australia oats guidance.

Coeliac Australia gluten challenge explains preparation for testing.