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Malabsorption

Last updated 24 May 2026 · Small bowel & nutrition

📋 Key Information Summary

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  • Coeliac disease affects ~1 in 70 Australians and is the most common cause of small-bowel malabsorption in developed countries; diagnosis requires anti-tTG IgA with total IgA, confirmatory duodenal biopsy (≥4 D2 + 1–2 D1 bulb samples), and is supported by HLA-DQ2/DQ8 testing for exclusion.
  • Marsh classification grades histopathology from 0 (normal) to 3c (total villous atrophy); Marsh ≥2 is diagnostic of coeliac disease in the correct clinical and serological context.
  • Lifelong strict gluten-free diet (GFD) is the only effective treatment for coeliac disease, managed with dietitian input via Medicare-rebated chronic disease care plans.
  • Refractory coeliac disease (RCD) is classified as type I (normal intraepithelial lymphocyte phenotype) or type II (clonal aberrant IELs); RCD-II carries a 40–60% 5-year risk of enteropathy-associated T-cell lymphoma (EATL).
  • Faecal elastase-1 (<200 µg/g) is the first-line non-invasive test for exocrine pancreatic insufficiency; values <100 µg/g indicate severe deficiency.
  • Bile acid malabsorption (BAM) is diagnosed by SeHCAT retention (available at select tertiary centres) or serum 7α-hydroxy-4-cholesten-3-one (C4); empirical trial of cholestyramine is an accepted alternative.
  • Hydrogen-methane breath testing identifies lactose intolerance and small intestinal bacterial overgrowth (SIBO) and should include methane measurement for sensitivity.
  • Faecal calprotectin <50 µg/g effectively excludes inflammatory bowel disease as a cause of chronic diarrhoea and steatorrhoea.
  • MR enterography (MRE) and capsule endoscopy are complementary for evaluating small-bowel mucosal pathology not reached by standard gastroscopy.
  • Tropical sprue should be considered in travellers or residents of tropical regions with persistent diarrhoea and megaloblastic anaemia; treatment is tetracycline + folate for ≥6 months.
  • Short bowel syndrome (SBS) management centres on optimising residual absorptive capacity; teduglutide (Revestive®) is PBS Authority Required for dependent SBS with ≥3 L/day parenteral support.
  • Post-bariatric malabsorption requires lifelong monitoring of fat-soluble vitamins (A, D, E, K), B₁₂, iron, calcium, zinc, and copper, with supplementation guided by malabsorptive procedure type.
  • Common variable immunodeficiency (CVID) can mimic coeliac disease histologically; immunoglobulin levels must be checked before biopsy in patients with recurrent sinopulmonary infections and chronic diarrhoea.
  • Aboriginal and Torres Strait Islander peoples have higher rates of chronic diarrhoeal illness, SBS following emergency surgery, and reduced access to gastroenterology specialist services in remote areas.
Malabsorption clinical infographic — pathophysiology, clinical clues, diagnosis, imaging, and management
Tap or click image to enlarge — Malabsorption: pathophysiology, clinical clues, diagnosis, imaging, and management.
Malabsorption infographic, full size

Coeliac Disease

Australian Epidemiology

Coeliac disease (CD) affects approximately 1 in 70 Australians, yet only ~20% are formally diagnosed. The condition is equally prevalent in Aboriginal and Torres Strait Islander populations. Prevalence is increasing due to improved serological screening rather than a true rise in incidence. CD is strongly associated with HLA-DQ2 (90–95% of cases) and HLA-DQ8 (5–10%); these haplotypes are necessary but not sufficient for disease development.

Serological Diagnosis

All serological testing must be performed on a gluten-containing diet (≥2 slices of bread equivalent daily for ≥6 weeks prior). The recommended first-line test is tissue transglutaminase IgA (anti-tTG IgA) combined with total serum IgA.

Test Role Key Detail MBS Item
Anti-tTG IgA + total IgA First-line screening Sensitivity 95%, specificity 95% in adults; if total IgA low/absent, use anti-tTG IgG or deamidated gliadin peptide (DGP) IgG MBS 69412 (coeliac serology bundle)
Deamidated gliadin peptide (DGP) IgG IgA-deficient patients; children <2 years Preferred in selective IgA deficiency; useful adjunct in equivocal anti-tTG MBS 69412
Endomysial antibody (EMA) IgA Confirmatory in equivocal cases Near 100% specificity; operator-dependent (immunofluorescence); not recommended as sole screening test MBS 69412
HLA-DQ2/DQ8 typing Exclusion test (negative predictive value >99%) NOT diagnostic — positive in ~40% general population. Useful to exclude CD in equivocal serology/histology, and in first-degree relatives MBS 73848 (genetic testing, specialist order)
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Critical: Do not commence a gluten-free diet before diagnostic testing is complete. Serology and histology are unreliable on a gluten-restricted diet. If already on GFD, a 6-week gluten challenge (≥10 g/day gluten) is required before re-testing.

Duodenal Biopsy — Marsh Classification

Upper gastrointestinal endoscopy with duodenal biopsies remains the gold standard for confirming CD in adults and older children. The 2024 Sydney classification and European Society for Paediatric Gastroenterology, Hepatology and Nutrition (ESPGHAN) guidelines recommend:

  • ≥4 biopsies from D2 (second part of duodenum) + 1–2 biopsies from the D1 bulb (to improve diagnostic yield for patchy disease).
  • Orientation of specimens in the histopathology laboratory is essential for accurate villous architecture assessment.
  • Marsh classification:
Marsh 0–1
Normal to Increased IELs
Normal villous architecture. Marsh 1: >25 IELs per 100 enterocytes. Insufficient alone for CD diagnosis.
Setting: Re-evaluate serology, consider HLA typing
Marsh 2
Crypt Hyperplasia
Increased IELs + crypt hyperplasia, villi still present. Diagnostic of CD with positive serology.
Setting: Gastroenterology — commence GFD
Marsh 3a–3c
Villous Atrophy
3a: partial. 3b: subtotal. 3c: total villous atrophy. Diagnostic of CD. Marsh 3c carries highest malabsorption burden.
Setting: Gastroenterology + dietitian — urgent GFD, nutritional rescue

Lifelong Gluten-Free Diet

Strict lifelong GFD is the only proven treatment. This requires elimination of all wheat, barley, rye, and contaminated oats. Dietitian-led education is essential and can be accessed via GP Management Plan (MBS 721) and Team Care Arrangement (MBS 723) with allied health Medicare rebates.

  • Safe grains: rice, corn (maize), quinoa, millet, sorghum, buckwheat, amaranth, teff.
  • Oats: Pure uncontaminated oats are tolerated by most CD patients; however, individual assessment is recommended as a minority react to avenin.
  • Surveillance: Repeat anti-tTG IgA at 6 and 12 months, then annually — to monitor adherence. Histological recovery expected in 65–90% by 2 years on strict GFD.
  • Nutritional deficiencies: Screen and replace iron, folate, vitamin B₁₂, vitamin D, calcium, zinc, and copper at diagnosis.
  • Bone density: DEXA scan recommended at diagnosis for adults (especially Marsh 3b–3c); repeat in 2 years if abnormal.

Refractory Coeliac Disease (RCD)

RCD is defined as persistent villous atrophy with malabsorption symptoms despite strict GFD for ≥6–12 months after excluding other diagnoses (e.g., lymphoma, SIBO, collagenous sprue, Crohn's disease).

Feature RCD Type I RCD Type II
IEL phenotype Normal (CD3+, CD8+) Aberrant (CD3+, CD8−, CD4−); clonal TCRγ rearrangement
5-year mortality ~5% 40–60% (primarily from EATL)
EATL risk Low High — requires close surveillance
First-line treatment Azathioprine 1.5–2 mg/kg/day + prednisolone 1 mg/kg taper Cladribine (investigational in Australia), autologous stem cell transplant
Surveillance Repeat biopsy at 6–12 months Capsule endoscopy + PET-CT every 6–12 months for EATL
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Enteropathy-Associated T-Cell Lymphoma (EATL): Suspect EATL in any coeliac patient with weight loss, abdominal pain, new lymphadenopathy, or deteriorating malabsorption despite strict GFD. Diagnosis requires PET-CT, capsule endoscopy, and repeat histology with immunophenotyping and TCR clonality. Treatment: CHOEP or SMILE chemotherapy followed by autologous SCT — refer to haematology/oncology urgently.

Key Medications in Coeliac Disease Management

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Dapsone
Generic · Sulfone · Dermatitis herpetiformis adjunct
Adult dose 50–100 mg PO daily; start 25 mg, titrate over 2–4 weeks
Paediatric dose 1–2 mg/kg/day PO (max 100 mg)
Route / Frequency Oral, once daily
Duration As needed for dermatitis herpetiformis; taper when GFD controls skin disease
Renal adjustment eGFR <30: avoid or reduce dose; monitor methaemoglobinaemia
Key monitoring FBC fortnightly × 8 weeks, then monthly × 3 months (haemolytic anaemia, methaemoglobinaemia, agranulocytosis); G6PD testing before initiation
PBS status ✔ PBS General Benefit

Diagnostic Workup

A systematic approach to malabsorption workup is essential. Investigations should be targeted based on clinical history, examination findings (e.g., steatorrhoea suggests fat malabsorption), and initial screening tests. The following tests are available in the Australian healthcare setting.

Faecal Elastase-1 (Pancreatic Insufficiency)

Faecal elastase-1 (FE-1) is the preferred first-line non-invasive marker for exocrine pancreatic insufficiency (EPI). It does not require a timed stool collection and is stable at room temperature.

Available
Faecal Elastase-1
Interpretation: ≥200 µg/g = normal. 100–200 µg/g = mild–moderate insufficiency. <100 µg/g = severe insufficiency.
Causes of low FE-1: Chronic pancreatitis, pancreatic cancer, cystic fibrosis, post-pancreatectomy, SIBO (false low).
Availability: Commercially available at major Australian pathology laboratories (Sullivan Nicolaides, Douglass Hanly Moir, Melbourne Pathology).
MBS: Not specifically itemised — included under faecal analysis (MBS 66600) or referred to specialist pathology.

Bile Acid Malabsorption (BAM)

BAM is an underdiagnosed cause of chronic diarrhoea and fat malabsorption, classified as:

  • Type 1: Post-ileal resection or Crohn's disease affecting the terminal ileum.
  • Type 2: Idiopathic (primary) — often misdiagnosed as diarrhoea-predominant IBS.
  • Type 3: Secondary to cholecystectomy, vagotomy, coeliac disease, or chronic pancreatitis.
Limited Availability
SeHCAT (⁷⁵Selenium-labelled Homocholic Acid Taurine)
Gold standard for BAM diagnosis. Measures 7-day retention of labelled bile acid. <15% retention = BAM. <5% = severe BAM.
Availability: Limited to select tertiary centres (Royal Adelaide Hospital, Concord Hospital Sydney, Royal Melbourne Hospital). Not universally available.
Not PBS-listed.
Available
Serum 7α-hydroxy-4-cholesten-3-one (C4)
Surrogate marker of bile acid synthesis. Elevated C4 (>44.5 ng/mL) indicates bile acid malabsorption with high sensitivity (90%) and specificity (79%).
Availability: Specialist reference laboratories; gaining wider availability.
Alternative approach: Empirical trial of cholestyramine 4 g TDS for 2 weeks — response supports BAM diagnosis.

Hydrogen-Methane Breath Testing

Breath testing is the primary non-invasive method for diagnosing carbohydrate malabsorption (lactose, fructose) and small intestinal bacterial overgrowth (SIBO).

Test Substrate Positive Criteria Clinical Indication
Lactose breath test 50 g lactose H₂ rise ≥20 ppm or CH₄ rise ≥10 ppm within 3 hours Suspected lactose intolerance
Fructose breath test 25 g fructose H₂ rise ≥20 ppm or CH₄ rise ≥10 ppm within 3 hours Suspected fructose malabsorption
Glucose breath test (SIBO) 75 g glucose H₂ rise ≥12 ppm within 90 minutes Suspected SIBO (proximal)
Lactulose breath test (SIBO) 10 g lactulose Dual peak (early rise ≥20 ppm in first 90 min) or single rise ≥20 ppm within 90 min Suspected SIBO (proximal + distal); higher false-positive rate
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Methane is critical: Approximately 30% of Australians are methane producers. Breath tests that measure only hydrogen will miss methane-dominant SIBO. Always request combined hydrogen-methane testing. Methane ≥10 ppm at any time point is significant.

D-Xylose Absorption Test

The D-xylose test assesses proximal small-bowel absorptive function and distinguishes mucosal malabsorption from pancreatic/biliary causes. It is rarely used in current Australian practice, having been largely replaced by specific serological and imaging tests.

  • Protocol: 25 g D-xylose PO after overnight fast; collect urine for 5 hours + 1-hour serum level.
  • Normal: Serum ≥1.33 mmol/L at 1 hour; urinary excretion ≥4.4 g (16% of dose) over 5 hours.
  • Abnormal (mucosal): Low serum and low urine — indicates villous disease (coeliac, tropical sprue, Crohn's).
  • Availability: Specialist pathology — limited to tertiary centres.

Faecal Calprotectin

Faecal calprotectin is a neutrophil-derived protein that serves as a non-invasive biomarker for intestinal inflammation.

Available
Faecal Calprotectin
Interpretation: <50 µg/g = normal (excludes IBD with NPV >95%). 50–200 µg/g = grey zone — repeat or investigate. >200 µg/g = significant inflammation — colonoscopy recommended. >500 µg/g = high likelihood of IBD.
Role in malabsorption: Helps exclude IBD as a cause of chronic diarrhoea and steatorrhoea; distinguishes inflammatory from osmotic/secretory mechanisms.
MBS: MBS 66600 (faecal analysis).
Limitations: False elevation with NSAIDs, PPIs, and infective gastroenteritis.

Small Bowel Imaging

When malabsorption persists despite negative coeliac serology and upper GI endoscopy, or when small-bowel pathology is suspected, dedicated small-bowel imaging is warranted.

Available
MR Enterography (MRE)
Preferred modality for small-bowel evaluation — no ionising radiation, excellent soft-tissue contrast. Identifies strictures, fistulae, wall thickening, and lymphadenopathy.
Indications: Suspected Crohn's disease, SBS anatomy assessment, mesenteric ischaemia, lymphoma.
MBS: MBS 63080 (MRI abdomen, specialist-referral).
Contraindications: Pacemaker, severe claustrophobia (sedation available), eGFR <30 (gadolinium).
Specialist-Initiated
Capsule Endoscopy (CE)
Direct mucosal visualisation of the entire small bowel — superior sensitivity for mucosal lesions (erosions, ulcers, villous atrophy, tumours).
Indications: Unexplained iron-deficiency anaemia, suspected small-bowel bleeding, equivocal MRE findings, surveillance of RCD-II for EATL.
Contraindications: Known or suspected small-bowel stricture (patency capsule test recommended first), dysphagia.
MBS: MBS 30478 (capsule endoscopy, specialist).
Availability: Most public and private gastroenterology units.
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Practical Diagnostic Algorithm for Chronic Diarrhoea with Suspected Malabsorption:
1. Coeliac serology (anti-tTG IgA + total IgA) → if positive, endoscopy with duodenal biopsies
2. Faecal elastase-1 → if <200, pancreatic insufficiency confirmed
3. Faecal calprotectin → if >200, colonoscopy for IBD
4. If steatorrhoea + negative above → bile acid malabsorption (SeHCAT/C4 or empirical cholestyramine trial)
5. If bloating/distension → hydrogen-methane breath test for SIBO/carbohydrate malabsorption
6. If ongoing unexplained → MRE ± capsule endoscopy

Other Causes of Malabsorption

Tropical Sprue

Tropical sprue is an acquired malabsorptive disorder of uncertain aetiology, endemic in tropical regions including South-East Asia, the Indian subcontinent, the Caribbean, and parts of Central America and Africa. It should be considered in Australians who have resided in or recently travelled to endemic areas and present with chronic diarrhoea, megaloblastic anaemia, and weight loss.

  • Pathophysiology: Postulated infectious aetiology (enterotoxigenic E. coli, Klebsiella spp.) causing chronic jejunal inflammation with villous atrophy and bacterial overgrowth.
  • Histology: Villous atrophy and crypt hyperplasia similar to coeliac disease but more prominent in the jejunum; coeliac serology is negative.
  • Investigations: Coeliac serology (negative to exclude CD), duodenal biopsy, folate/B₁₂ levels, stool cultures, blood film (megaloblastic changes).
  • Treatment: Tetracycline 500 mg PO QDS (or doxycycline 100 mg PO BD) + folic acid 5 mg PO daily, for ≥6 months. Some patients require prolonged or indefinite therapy.
  • Nutritional support: Replace iron, folate, B₁₂, calcium, and fat-soluble vitamins.
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Tetracycline
Generic · Tetracycline antibiotic · Tropical sprue
Adult dose 500 mg PO QDS (or doxycycline 100 mg PO BD as alternative)
Paediatric dose Not recommended <8 years (tooth discolouration); use azithromycin 10 mg/kg/day instead
Route / Frequency Oral, 4 times daily, 1 hour before or 2 hours after meals
Duration ≥6 months; some require indefinite therapy
Renal adjustment eGFR <50: avoid tetracycline; use doxycycline (preferred in renal impairment)
PBS status ✔ PBS General Benefit

Short Bowel Syndrome (SBS)

Short bowel syndrome results from extensive small-bowel resection leaving insufficient absorptive surface area. In Australia, common causes include mesenteric ischaemia, Crohn's disease resection, radiation enteritis, and volvulus.

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Anatomy determines management: The critical determinant is whether the ileocaecal valve (ICV) is intact and how much ileum and colon remain. Jejunal-ileal continuity with colon-in-continuity offers the best prognosis due to colonic salvage of unabsorbed carbohydrates (producing SCFAs for absorption).
Residual Anatomy Adaptive Capacity Key Malabsorption Issues
<200 cm jejunum, no colon Poor — PN-dependent Fluid/electrolyte, macronutrient; no bile acid absorption → fat malabsorption
<200 cm jejunum, colon in continuity Moderate — PN often needed Colonic SCFA salvage assists; bile acid wasting → BAM Type 1
>200 cm with ICV intact Good — may be PN-independent Vitamin B₁₂, fat-soluble vitamins if terminal ileum resected

Teduglutide (Revestive®)

Teduglutide is a recombinant analogue of glucagon-like peptide-2 (GLP-2) that promotes intestinal adaptation, increases villous height and crypt depth, and enhances fluid and nutrient absorption. It is indicated for SBS patients who are dependent on parenteral nutrition (PN).

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Teduglutide
Revestive® · GLP-2 analogue · Intestinal adaptation
Adult dose 0.05 mg/kg SC once daily; weight-based dosing
Paediatric dose 0.05 mg/kg SC once daily (≥1 year); use dedicated paediatric vial
Route / Frequency Subcutaneous injection, once daily, alternating injection sites
Duration Ongoing — reassess PN dependence at 6-month intervals
Renal adjustment eGFR <30: no dose adjustment but use with caution
Key monitoring Colonoscopy at baseline and every 6 months (polyp risk); fluid balance (may cause fluid retention); cholecystokinin levels
PBS status ⚠ PBS Authority Required — SBS patients ≥12 months post-resection, PN-dependent (≥3 L/week or ≥3 days/week), under specialist management at intestinal failure centre
ℹ️
SBS Management Principles: Optimise oral/enteral intake; anti-diarrhoeals (loperamide 4 mg before meals, codeine 30 mg PRN); bile acid binders if colon intact (cholestyramine 4 g TDS); PN optimisation with hepatoprotective lipid strategies (SMOF); intestinal rehabilitation centres — The Alfred (Melbourne), Westmead (Sydney), Royal Adelaide Hospital.

Post-Bariatric Malabsorption

With over 20,000 bariatric procedures performed annually in Australia, post-bariatric malabsorption is increasingly encountered in primary care. The degree of malabsorption depends on the procedure type.

Procedure Mechanism Key Deficiencies Monitoring
Sleeve gastrectomy Restrictive Iron, B₁₂, folate, vitamin D Bloods 3, 6, 12 months then annually
Roux-en-Y gastric bypass Restrictive + malabsorptive Iron, B₁₂, calcium, vitamin D, fat-soluble vitamins (A, E, K), zinc, copper, thiamine Bloods 3, 6, 12 months then annually; DEXA at 2 years
One-anastomosis gastric bypass (OAGB) Highly malabsorptive As RYGB + protein malnutrition, steatorrhoea As above + faecal elastase, liver function
Biliopancreatic diversion ± DS Severely malabsorptive All of the above + severe fat malabsorption, oxalate nephropathy risk Comprehensive panel 3-monthly initially; renal ultrasound annually
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Thiamine emergency: Acute Wernicke encephalopathy can occur post-bariatric surgery, especially with protracted vomiting. Treat empirically with IV thiamine 500 mg TDS for 3–5 days before oral maintenance. Do not give glucose before thiamine.

Intestinal Lymphangiectasia

Intestinal lymphangiectasia (IL) is characterised by dilated lymphatic lacteals in the small-bowel mucosa, leading to protein-losing enteropathy with hypoalbuminaemia, lymphopenia, and immunoglobulin loss.

  • Classification: Primary (congenital, presents in childhood) or secondary (due to constrictive pericarditis, lymphoma, cirrhosis, retroperitoneal fibrosis, Fontan circulation).
  • Clinical features: Peripheral oedema, ascites, diarrhoea, steatorrhoea, recurrent infections (due to hypogammaglobulinaemia and lymphopenia).
  • Diagnosis: Hypoalbuminaemia + low immunoglobulins + peripheral lymphopenia + characteristic endoscopic findings (white villous tips) + biopsy showing dilated mucosal lacteals. Faecal α₁-antitrypsin clearance confirms protein-losing enteropathy.
  • Treatment: Medium-chain triglyceride (MCT) diet (bypasses lymphatic system, absorbed directly into portal circulation); octreotide 50–100 µg SC TDS (reduces lymph flow); treat underlying cause if secondary.
  • Prognosis: Primary IL is chronic; secondary IL resolves with treatment of the underlying condition.

Eosinophilic Enteropathy

Eosinophilic enteropathy (EE) encompasses eosinophilic oesophagitis (EoE) and non-EoE eosinophilic gastrointestinal disorders, characterised by eosinophilic infiltration of the GI tract in the absence of secondary causes.

  • Classification by depth: Mucosal (most common — diarrhoea, pain, malabsorption), muscular (obstruction), serosal (ascites with eosinophil-rich fluid).
  • Diagnostic criteria: GI symptoms + eosinophilic infiltration (≥20 eosinophils per HPF on biopsy) + exclusion of secondary causes (parasites, drugs, hypereosinophilic syndrome, connective tissue disease).
  • Investigations: Peripheral eosinophil count (may be normal), endoscopic biopsies at multiple levels, stool ova/cysts/parasites (×3), serum tryptase (mastocytosis exclusion), food-specific IgE and skin-prick testing.
  • Treatment: Dietary elimination (6-food elimination diet — dairy, wheat, egg, soy, fish/seafood, nuts); proton pump inhibitors (for EoE); topical swallowed fluticasone 250–500 µg BD (EoE); systemic corticosteroids for severe/refractory disease; biologics — dupilumab (Dupixent®) PBS Authority Required for EoE.
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Dupilumab
Dupixent® · Anti-IL-4Rα monoclonal antibody · Eosinophilic oesophagitis
Adult dose 300 mg SC every 2 weeks
Paediatric dose ≥15 kg: weight-based dosing per PBS criteria
Route / Frequency Subcutaneous, every 2 weeks
Duration Ongoing — reassess histological response at 24 weeks
PBS status ⚠ PBS Authority Required — EoE with histological confirmation, refractory to PPI + dietary modification ± topical corticosteroids, managed by gastroenterologist

Common Variable Immunodeficiency (CVID)

CVID is the most common symptomatic primary immunodeficiency in adults, characterised by hypogammaglobulinaemia (reduced IgG and at least one of IgA or IgM), impaired antibody responses, and recurrent infections. GI involvement occurs in 20–50% of CVID patients and can mimic coeliac disease.

  • GI manifestations: Chronic diarrhoea, malabsorption, villous atrophy (may be indistinguishable from CD histologically), pernicious anaemia, inflammatory bowel disease-like picture, nodular lymphoid hyperplasia, giardiasis (recurrent).
  • Critical diagnostic clue: Suspect CVID when villous atrophy is found on biopsy but coeliac serology is negative, or when the patient has recurrent sinopulmonary infections.
  • Essential tests: Quantitative immunoglobulins (IgG, IgA, IgM) — IgG <4.5 g/L + IgA <0.07 g/L + impaired vaccine responses (pneumococcal serology) confirms diagnosis. Do NOT diagnose coeliac disease in a patient with undetectable IgA.
  • Treatment: Immunoglobulin replacement therapy (IVIg 400–600 mg/kg every 3–4 weeks, or SCIg 100–200 mg/kg weekly) — PBS Authority Required. Treat underlying GI pathology specifically (e.g., giardiasis with tinidazole/metronidazole). Gluten-free diet trial may be attempted but response is inconsistent.
  • Monitoring: Regular lung function (bronchiectasis screening), hepatobiliary assessment, autoimmune disease screening, lymphoproliferative risk (increased lymphoma risk 8–12× general population).
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Intravenous Immunoglobulin (IVIg)
Intragam® P / Octagam® / Privigen® · Immunoglobulin replacement
Adult dose 400–600 mg/kg IV every 3–4 weeks
Route / Frequency Intravenous infusion, every 3–4 weeks; or subcutaneous 100–200 mg/kg weekly
Key monitoring Trough IgG levels (aim >5 g/L), renal function, LFTs, haemolysis markers
PBS status ⚠ PBS Authority Required — Primary immunodeficiency with documented hypogammaglobulinaemia and impaired antibody response, under specialist immunology management
⚠️
Pitfall — CVID masquerading as coeliac: Patients with CVID may have villous atrophy on biopsy, but anti-tTG IgA will be falsely negative (because IgA is deficient). If duodenal villous atrophy is found with undetectable total IgA, check quantitative immunoglobulins before diagnosing coeliac disease. In CVID, the villous atrophy may not respond to GFD.
Aboriginal and Torres Strait Islander Health Considerations
Burden of disease
Aboriginal and Torres Strait Islander peoples experience higher rates of chronic diarrhoeal illness, malnutrition, and short bowel syndrome following emergency abdominal surgery compared with non-Indigenous Australians. Intestinal infections (Giardia, Cryptosporidium) are more prevalent, especially in remote communities, contributing to chronic malabsorption.
Coeliac disease
CD prevalence in ATSI populations is comparable to the general Australian population (~1:70) but is likely significantly underdiagnosed due to reduced screening rates and differentials attributed to infectious causes. Serological screening should be actively pursued when clinically indicated.
Remote access
Gastroenterology specialist services, endoscopy facilities, and advanced diagnostics (capsule endoscopy, MRE, SeHCAT) are concentrated in metropolitan and major regional centres. Aboriginal Community Controlled Health Services (ACCHS) and telehealth (MBS items 91822, 91823) play a vital role in bridging this gap.
Gluten-free diet access
GF foods are expensive and less available in remote communities and community stores. The Australian Government's GF food allowance (currently ~0/year via some state health schemes) partially offsets costs. Dietitian support via ACCHS is essential for culturally appropriate dietary education.
Nutritional vulnerability
ATSI peoples already experience higher rates of iron deficiency, vitamin D deficiency, and food insecurity. Malabsorption compounds these issues. Aggressive nutritional screening (serum ferritin, 25-OH vitamin D, zinc, B₁₂, folate) should be performed at diagnosis and every 6 months in ongoing management.
Paediatric considerations
Failure to thrive and chronic diarrhoea in ATSI children should include coeliac serology in the differential, alongside environmental enteropathy and parasitic infection. HLA-DQ2/DQ8 testing may be particularly useful to exclude CD before pursuing invasive testing.
Cultural safety
Use of Aboriginal Health Workers and Liaison Officers improves patient understanding and adherence. Written materials should be in plain English with pictorial aids. Consider yarning circles for group dietary education where culturally appropriate.

📚 References

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  12. 12. Okazaki T, Watanabe T, Hiraishi H, et al. Intestinal lymphangiectasia: a comprehensive review. J Gastroenterol Hepatol. 2023;38(5):685-693.
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