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PE23.12 | Malabsorption — SDL Guide (Part 2)
Management
Management of malabsorption is cause-specific: accurate diagnosis is a prerequisite for effective treatment, because there is no universal 'anti-malabsorption' therapy — the intervention must address the pathogenic mechanism.
Coeliac disease — gluten-free diet (GFD):
The only proven treatment for coeliac disease is strict, lifelong gluten-free diet — complete elimination of wheat (including atta, maida, sooji), rye, and barley from the diet. Rice, maize (corn), jowar (sorghum), bajra (pearl millet), and quinoa are safe alternatives. Oats are safe for most coeliac patients but must be certified gluten-free (contamination risk). Compliance with GFD is the primary determinant of outcome: within weeks to months of strict GFD, symptoms resolve, anti-tTG IgA titres normalise, and duodenal histology improves. Failure to respond to GFD should prompt a review of inadvertent gluten exposure (hidden gluten in sauces, spice mixes, fried snacks) before considering refractory coeliac disease. Nutritional deficiencies identified at diagnosis (iron, Vitamin D, calcium, folate) should be supplemented and monitored. Follow-up includes serial anti-tTG IgA (should decline and normalise within 1–2 years on strict GFD) and anthropometric monitoring.
Cystic fibrosis — pancreatic enzyme replacement therapy (PERT) and nutritional support:
Pancreatic enzyme replacement therapy (PERT) is given with every meal and snack: commercially available lipase/protease/amylase capsules (e.g., Creon) are taken at the start of each meal. The dose is titrated by symptom response (stool normalisation) and growth velocity. PERT normalises fat digestion and resolves steatorrhoea. High-calorie, high-fat diet is recommended — children with CF have increased caloric requirements (up to 150% of normal) due to the combined effects of malabsorption and recurrent pulmonary infections increasing metabolic demand. Fat-soluble vitamin supplementation (A, D, E, K) is given routinely because fat malabsorption predisposes to deficiency. Salt supplementation is important in hot climates or during febrile illness (CF patients lose excess salt in sweat). Respiratory management (airway clearance physiotherapy, antibiotics for pulmonary exacerbations) is beyond the scope of this GI module. CFTR modulators (ivacaftor for specific mutations; elexacaftor-tezacaftor-ivacaftor for F508del) are transformative new therapies that improve CFTR function — access in India is limited but increasing.
Post-infectious enteropathy:
Management is primarily nutritional rehabilitation and correction of the triggering infection. Temporarily reduce lactose intake if secondary lactase deficiency is confirmed (reduced-lactose or lactose-free formula in infants). Zinc supplementation (20 mg/day for 10–14 days) promotes mucosal recovery. Resume normal diet as the mucosa heals (typically weeks). Empiric albendazole for Giardia if stool microscopy is not available and response to standard treatment is poor.
Monitoring and long-term follow-up:
Growth velocity (weight, height, head circumference) is the primary outcome measure — catch-up growth after initiating appropriate treatment confirms the diagnosis and the adequacy of management. Nutritional deficiency states (anaemia, rickets, coagulopathy) require specific supplementation and monitoring.
SELF-CHECK
A 7-year-old boy with confirmed coeliac disease by positive anti-tTG IgA and duodenal biopsy (Marsh 3b) is started on a gluten-free diet. Six months later his symptoms have not improved and his anti-tTG IgA remains elevated. What is the most likely explanation?
A. Coeliac disease is progressive and will not respond to diet alone — steroid therapy is needed
B. Inadvertent or intentional gluten ingestion (dietary non-compliance or hidden gluten in foods)
C. The Marsh 3b biopsy means surgery is required to restore villous architecture
D. Anti-tTG IgA always remains elevated in coeliac disease regardless of treatment
Reveal Answer
Answer: B. Inadvertent or intentional gluten ingestion (dietary non-compliance or hidden gluten in foods)
The most common cause of failure to respond to a gluten-free diet in coeliac disease is ongoing gluten exposure — either inadvertent (hidden gluten in processed foods, spice mixes, medications) or from dietary non-compliance. Anti-tTG IgA is a reliable biomarker of continued gluten exposure; it should decline progressively and normalise within 12–24 months on strict GFD. If it remains elevated, a detailed dietary history looking for hidden gluten sources must be conducted. Steroids are not first-line; true refractory coeliac disease is rare and a diagnosis of exclusion. Surgery has no role in uncomplicated coeliac disease.
Self-Assessment
This self-assessment section consolidates the key diagnostic and management reasoning for malabsorption in children. Work through the questions below before reviewing the answers, focusing on your ability to reason from the clinical scenario to the correct investigation and management decision — not just recall facts in isolation. The two highest-yield clinical distinctions in this module are: (1) coeliac disease is diagnosed by anti-tTG IgA plus total IgA plus duodenal biopsy (Marsh classification); (2) cystic fibrosis is diagnosed by sweat chloride >60 mmol/L plus CFTR genetics. Both require lifelong, cause-specific management.
The diagnostic workup for malabsorption follows a consistent clinical logic: pattern-recognition (which features point to coeliac vs CF vs post-infectious), test selection (targeted serology and confirmatory biopsy or sweat chloride), and treatment verification (growth catch-up + serological normalisation). Before reviewing the answers, ask yourself which investigation you would order FIRST in each scenario, and why — this decision-making process is what distinguishes a clinically-competent graduate from one who simply memorised a list of tests.
Key recall questions:
1. What is the first-line blood test for coeliac disease, and which additional test must always accompany it?
2. What sweat chloride value is diagnostic for cystic fibrosis, and what is the borderline range?
3. Name the Marsh classification stages and what each represents histologically.
4. What is the treatment for coeliac disease and which grains are safe on a gluten-free diet?
5. A child with CF has persistently loose stools despite antibiotics. What specific treatment is missing?
Answers: 1. Anti-tTG IgA — and total serum IgA must also be measured (IgA deficiency causes false-negative anti-tTG IgA). 2. >60 mmol/L = diagnostic; 30–59 = borderline; <30 = normal. 3. Marsh 0=normal; 1=increased IELs only; 2=crypt hyperplasia + increased IELs, normal villi; 3a/b/c=partial/subtotal/total villous atrophy; 4=hypoplastic atrophy. 4. Strict lifelong gluten-free diet; safe grains: rice, maize, jowar, bajra, quinoa. 5. Pancreatic enzyme replacement therapy (PERT) — given with every meal and snack.
SELF-CHECK
A 5-year-old with cystic fibrosis has a sweat chloride of 72 mmol/L and CFTR mutation confirmed as homozygous F508del. His stools are bulky and greasy. He weighs less than the 3rd centile. What is the most appropriate nutritional intervention?
A. Strict gluten-free diet to resolve the steatorrhoea
B. Low-fat diet to reduce steatorrhoea in cystic fibrosis
C. Pancreatic enzyme replacement therapy with every meal and high-calorie diet
D. IV immunoglobulin to correct the underlying immune deficiency
Reveal Answer
Answer: C. Pancreatic enzyme replacement therapy with every meal and high-calorie diet
The steatorrhoea in cystic fibrosis is caused by pancreatic exocrine insufficiency — insufficient lipase, protease, and amylase secretion because thick mucus obstructs pancreatic ducts. The treatment is pancreatic enzyme replacement therapy (PERT — e.g., Creon) given with every meal and snack to provide the enzymes that the pancreas cannot secrete. A high-calorie, high-fat diet is recommended (not a low-fat diet) because children with CF have high energy requirements. Gluten-free diet is for coeliac disease, not CF. IV immunoglobulin is for immunodeficiency, not CF.