Malabsorption

Meet the patient

Mrs K is 40, and over three months her stools have turned pale, bulky and foul — they float, and she has flushed twice. She is eating well, even more than usual, yet has lost 6 kg. Routine bloods show an iron-deficiency anaemia that will not budge with oral iron.[8]

Before you reach for a textbook list, hold the two questions that decide everything downstream: which of the three mechanisms is failing here? and what is the single first test I must not forget? Get those two right and the rest of the workup writes itself — get the second wrong and you will make the diagnosis impossible for months. The answers are on this page, and the second one is the trap every registrar falls into once.[4]

What malabsorption actually is

Malabsorption is the gut failing to deliver nutrients to the bloodstream — across fat, carbohydrate, protein and the micronutrients (iron, B12, folate, calcium, vitamins A, D, E, K). The clean way to think about it is a three-link chain that must all hold: luminal digestion, mucosal uptake, and post-mucosal transport. Break any link and the patient loses weight. The word steatorrhoea itself tells the story — Greek stear (fat) plus rhoia (flow): fat, flowing.[8]

The near-synonym maldigestion means broken intraluminal breakdown specifically, but in clinic and in exams the umbrella term malabsorption syndrome swallows both. The clinical thread is constant whatever the site — steatorrhoea, weight loss, deficiency signs — and your job is to localise the mechanism and treat the cause, not to pour nutrients into a leaking bucket. Coeliac, by the way, is from Greek koiliakos — of the belly.[1]

Scope runs from single-nutrient defects (lactase deficiency is the classic — only lactose fails) to global malabsorption (coeliac, short bowel), where everything goes at once. Site is the clue that does the localising for you: the proximal small bowel takes up iron, folate and calcium; the terminal ileum takes B12 and reclaims bile salts; fat needs the whole luminal-mucosal-lymphatic chain end to end. Iron proximal, B12 terminal, ADEK fat — learn that line and the deficiency pattern points to the lesion for you.[4]

The three mechanisms — luminal, mucosal, transport

Everything in malabsorption is one of three failures, and the three-class framework is worth more than any list of causes because it maps straight onto the test you order and the drug you reach for. Luminal, mucosal, transport — the LMT you will repeat under your breath in every viva.[8]

You can also slice the same cake by nutrient affected (fat, carbohydrate, B12, iron) or by single-versus-global defect. Useful at the bedside, but for ordering tests and choosing treatment the mechanistic three-class system wins every time — faecal elastase points at the lumen, serology plus biopsy at the mucosa, and the surgical history points at transport.[8]

Who gets it, and why

Malabsorption is everywhere, but the cause bends hard to geography, age and host factors. Coeliac disease is the commonest mucosal cause, prevalence around 1%, and most of them are still undiagnosed. Lactose malabsorption is the commonest single-nutrient defect on the planet — roughly 68% of the global adult population — near-universal in East Asian, West African and Native American groups (where adult-type hypolactasia hits 80 to 100%) and as low as 5 to 15% in Northern Europeans.[1]

Risk-factor-to-cause pairings — these are the stems examiners love, so learn them as couples:[1]

• Prior upper-GI surgery (gastrectomy, bariatric, vagotomy) → post-gastrectomy malabsorption, SIBO, dumping, B12 and iron deficiency.
• Prior small-bowel resection (mesenteric ischaemia, Crohn's, volvulus) → short bowel, terminal-ileum B12 deficiency, bile-salt diarrhoea.
• Autoimmune disease or family history (type 1 diabetes, autoimmune thyroid, Down syndrome, Turner) → screen for coeliac.
• Chronic alcohol misuse → chronic pancreatitis → pancreatic exocrine insufficiency.
• Immunodeficiency (HIV, common variable immunodeficiency, IgA deficiency) → opportunistic enteritides (cryptosporidium, microsporidium, MAC, Giardia).
• Structural gut abnormality (jejunal diverticulosis, blind loop, stricture, fistula, scleroderma) → SIBO.
• Prolonged PPI use or achlorhydria → SIBO, because the gastric acid barrier is gone.
• Tropical residence or travel → tropical sprue, parasitic enteritis.
• Prior abdominal or pelvic radiotherapy → radiation enteritis.
• Dermatitis herpetiformis → coeliac disease, almost without exception.[4]

The three-step relay

Normal absorption is a three-step relay — luminal digestion, mucosal uptake, post-mucosal transport — and every cause of malabsorption is a failure at one of those steps. Master the relay and you can reason out any cause you have never seen.[8]

Step 1 — Luminal phase (digestion). Bile emulsifies dietary fat; pancreatic lipase with its cofactor colipase cleaves it into free fatty acids and monoglycerides, which ride inside bile-salt micelles to the enterocyte membrane. Proteins fall to trypsin, chymotrypsin and elastase; starch to amylase; disaccharides to brush-border disaccharidases, of which lactase is the one that matters clinically. Bile salts loop back through the terminal ileum and recirculate — 95% reclaimed, 5% lost. Failure here means pancreatic exocrine insufficiency (no enzymes), bile-salt deficiency (ileal disease or resection, cholestasis, or SIBO deconjugating the salts), or lactase deficiency (undigested lactose → osmotic diarrhoea, gas, bloating).[1][5]

Step 2 — Mucosal phase (uptake). The absorptive face is the small-intestinal villus, enterocytes capped by the microvillus brush border. Micelles hand lipids to the enterocyte; inside, fatty acids are re-esterified and packaged with apoproteins into chylomicrons — the step that fails in abetalipoproteinaemia. Iron and folate are absorbed here, chiefly in the duodenum and proximal jejunum. Flatten the villus and the surface collapses: coeliac disease (immune villous atrophy driven by gluten-derived gliadin), tropical sprue, Crohn's, radiation enteritis, Whipple (PAS-positive macrophages packing the lamina propria). Because this is the proximal site, iron and folate deficiency are the early, prominent features of mucosal disease.[4]

Step 3 — Transport phase (delivery). Chylomicrons leave the enterocyte for the intestinal lymphatics; sugars and amino acids head for the portal vein. Break the delivery and you get short bowel syndrome (less absorptive length, rapid transit; surviving bowel may adapt over 1 to 2 years by villous hypertrophy), post-gastrectomy (no gastric mixing or grinding, rapid transit, dumping), and intestinal lymphangiectasia (dilated lymphatics weeping lymph and chyle → protein-losing enteropathy with oedema, lymphopenia, steatorrhoea).[2]

The unifying outcome is steatorrhoea (faecal fat over 7 g/day) plus a deficiency pattern that localises the lesion — iron and folate from the proximal mucosa, B12 from the terminal ileum, fat-soluble vitamins and calcium from fat malabsorption anywhere. The master principle, and the mantra for this topic: fat absorption needs pancreatic lipase plus bile-salt micelles plus an intact enterocyte plus a patent lymphatic — break any link and the chain fails.[1]

What you will meet on the ward

The presentation is always a composite — mechanical features (steatorrhoea, bloating, weight loss) stacked on deficiency features (anaemia, osteomalacia, neuropathy). Miss either half and you misdiagnose the other.[1][4]

Core features, any cause:[1]

• Steatorrhoea — pale, bulky, greasy, foul stools that float and refuse to flush. The single most characteristic feature; if you have not asked about it, you have not taken the history.
• Weight loss and wasting despite a good — even increased — appetite; muscle wasting, and in children growth failure.
• Distension, bloating, borborygmi, flatulence as unabsorbed substrate ferments downstream.
• Fatigue from anaemia, electrolyte disturbance, and plain malnutrition.[1]

Deficiency features — and what each one is telling you:[1]

• Iron-deficiency anaemia (fatigue, pallor, koilonychia, glossitis) → points at proximal small-bowel mucosal disease (coeliac, sprue) or blood loss.
• B12 and folate deficiency → megaloblastic anaemia, glossitis, angular cheilitis, peripheral neuropathy, subacute combined degeneration (B12). B12 loss specifically fingers the terminal ileum (resection, Crohn's, tropical sprue) or absent intrinsic factor (pernicious anaemia, post-gastrectomy).
• Calcium and vitamin D deficiency → tetany, perioral paraesthesia, osteomalacia, secondary hyperparathyroidism. Fat malabsorption wastes calcium as insoluble soaps and steals vitamin D with it.
• Vitamin K deficiency → easy bruising, epistaxis, prolonged INR.
• Vitamin A deficiency → night blindness, xerophthalmia, follicular hyperkeratosis (phrynoderma).
• Vitamin E deficiency → peripheral neuropathy, ataxia, retinopathy, especially in long-standing fat malabsorption.
• Zinc, magnesium, selenium → dermatitis, diarrhoea, cardiomyopathy (selenium).[1]

Cause-specific pointers — the exam favourites:[1]

• Coeliac disease — dermatitis herpetiformis (intensely itchy grouped vesicles on extensor surfaces), aphthous ulcers, short stature, dental enamel defects, iron-deficiency anaemia as the sole feature, and the company it keeps (type 1 diabetes, autoimmune thyroid).[4]
• Tropical sprue — megaloblastic anaemia is the headline (folate and B12), endemic exposure, glossitis, weight loss; the anaemia may drown out the diarrhoea.
• Chronic pancreatitis or pancreatic exocrine insufficiency — epigastric pain, calcification on imaging, new or worsening diabetes (endocrine and exocrine failure together); steatorrhoea may be the presenting feature, and anaemia is usually absent because the proximal mucosa is intact.
• SIBO — bloating, flatulence, diarrhoea in someone with prior surgery, a motility disorder (scleroderma, diabetes), or chronic PPI use; may produce B12 deficiency (bacteria eat it) with folate relatively spared.
• Short bowel syndrome — high-output stoma or profuse diarrhoea after resection, dehydration, electrolyte loss, and over time D-lactic acidosis, oxalate stones, gallstones.[2]
• Whipple disease — middle-aged man with migratory arthralgia, fever, weight loss, pigmentation, lymphadenopathy, and neurological or cardiac involvement; malabsorption is a late arrival, not the opener.
• Intestinal lymphangiectasia — peripheral lymphoedema, chylous effusions or ascites, hypoalbuminaemia and lymphopenia from lymph loss.
• Giardiasis — foul fatty stool, bloating, a water-source or travel clue; an immunocompromised host (IgA deficiency, common variable immunodeficiency) should make you think of it twice.[1]

The presentations that fool you — learn these or you will miss them: isolated iron-deficiency anaemia with no GI symptoms at all (coeliac); osteoporosis or osteomalacia as the first sign; infertility or recurrent miscarriage (coeliac); peripheral neuropathy (B12 or E); oedema from protein-losing enteropathy; failure to thrive in a child. And in the elderly, do not write weight loss and anaemia off to malignancy — send coeliac serology with a low threshold.[4]

The mimics you must exclude

Not every patient with diarrhoea, bloating and weight loss has malabsorption. These are the mimics, each with one feature that parts it from the rest:[8]

• Irritable bowel syndrome — bloating and diarrhoea but no weight loss, no anaemia, no steatorrhoea, normal bloods, chronic and non-progressive. Exclude coeliac (serology) and inflammation (faecal calprotectin) before you ever label it IBS. Everyone forgets: never diagnose IBS in the presence of weight loss, nocturnal symptoms, anaemia or steatorrhoea — those are red flags that kill the label.
• Crohn's disease — pain, weight loss, perianal disease, raised faecal calprotectin and CRP, anaemia of chronic disease; terminal-ileal Crohn's causes B12 deficiency and bile-salt diarrhoea — it mimics malabsorption because it is a cause of malabsorption. Separate it by endoscopy and imaging.
• Chronic infective or tropical diarrhoea — Giardia, tropical sprue, HIV-opportunistic; travel and exposure history, stool microscopy and culture, response to specific therapy; duodenal biopsy if it will not settle.
• Endocrine drivers of weight loss and diarrhoea — hyperthyroidism (weight loss plus increased appetite plus loose stools, but no steatorrhoea and normal bloods), diabetic autonomic neuropathy (nocturnal diarrhoea), Addison's disease (weight loss, fatigue, pigmentation).
• Malignancy — pancreatic, gastric, small-bowel lymphoma, colorectal; older patient, weight loss, anaemia, often painless. Exclude with imaging and endoscopy, especially in anyone over 50 with new malabsorption.
• Chronic mesenteric ischaemia — post-prandial pain and food fear causing weight loss; not true malabsorption, the gut just hurts too much to eat.
• Inflammatory or protein-losing states — Menetrier's disease, eosinophilic gastroenteritis — present with oedema and hypoalbuminaemia.[1]

One dividing question does most of the work: is there steatorrhoea or fat-soluble vitamin deficiency? If yes → true fat malabsorption (pancreatic, mucosal or lymphatic). If no, but there is anaemia or watery diarrhoea → proximal mucosal disease, infection, or a non-malabsorptive cause.[1]

At the bedside

Bedside assessment has two jobs: grade the malnutrition and read the extraintestinal clues that localise the cause. Do both before you order a single test.[4][8]

• General — BMI and weight trend, triceps skinfold and mid-arm circumference, muscle wasting, hydration, peripheral oedema (protein-losing enteropathy or anaemia), pallor.
• Mouth — glossitis, angular cheilitis, aphthous ulcers, dental enamel defects (coeliac).
• Skin — dermatitis herpetiformis (coeliac — itchy grouped vesicles on elbows, knees, buttocks), bruising or petechiae (vitamin K), follicular keratosis or phrynoderma (vitamin A), pigmentation (Whipple), acanthosis or thin skin.
• Abdomen — distension (gas or ascites), borborygmi, succussion splash (post-gastrectomy or dumping), epigastric tenderness (chronic pancreatitis), masses (Crohn's, malignancy, lymphadenopathy).
• Neurological — peripheral neuropathy (B12, E), ataxia and cerebellar signs (Whipple, vitamin E), cognitive or psychiatric change (Whipple, B12), proximal myopathy (vitamin D, osteomalacia).
• Systemic — lymphoedema (lymphangiectasia), arthritis or arthralgia (Whipple, coeliac, IBD), fever (Whipple, infection, lymphoma).
• Stool inspection — the description of pale, greasy, foul stool that floats is itself a bedside finding; send for microscopy if infection is in play.[1]

Two layers of tests

Investigation runs in two layers: first confirm malabsorption and map the deficiencies, then localise the cause. A targeted ladder is faster and cheaper than a shotgun panel — and it is what the examiner wants to see.[3][4][5]

Layer 1 — confirm malabsorption and map the deficiencies:[1]

• Bloods — FBC and film (micro- or macrocytic anaemia), iron studies and ferritin, B12 and folate, calcium, albumin, 25-hydroxyvitamin D, clotting and INR (vitamin K), magnesium, zinc, phosphate.
• Faecal fat — stool fat over 7 g per 24 hours confirms steatorrhoea (gold standard, rarely done in practice; a Sudan stain is a crude screen).
• Faecal calprotectin — raised in IBD; helps part IBD from IBS and coeliac.[1]

Layer 2 — localise the cause (the high-yield, targeted tests):[1]

• Coeliac serology — anti-tissue transglutaminase IgA (anti-tTG IgA) is the most sensitive first-line test, and you send it PLUS total serum IgA to exclude selective IgA deficiency, which hides in 2 to 5% of coeliacs and makes the anti-tTG IgA falsely normal. The classic trap: forgetting total IgA — the single most common serology error in coeliac. If IgA is deficient, use anti-tTG IgG or anti-deamidated gliadin peptide (DGP) IgG. Anti-endomysial IgA (EMA) is highly specific and confirms. Always take serology BEFORE a gluten-free diet, and use HLA-DQ2/DQ8 to rule coeliac out (negative predictive value over 99%) when the picture is murky.[3][4]
• Faecal elastase-1 — a level under 200 ug/g means pancreatic exocrine insufficiency; it is stable, stool-based, blind to small-bowel disease, and not falsely lowered by mucosal causes. This is the test that splits luminal (pancreatic) from mucosal disease.[5]
• Breath tests — glucose or lactulose hydrogen/methane breath test for SIBO (an early hydrogen peak); lactose hydrogen breath test for lactose malabsorption (a rise in breath hydrogen plus symptoms after a lactose load).[6]
• Stool studies — microscopy and culture (Giardia, ova, cysts, parasites), faecal alpha-1 antitrypsin clearance for protein-losing enteropathy, stool osmotic gap (osmotic versus secretory), Clostridioides difficile where appropriate.
• Endoscopy with duodenal biopsies — the gold standard for mucosal disease; take 4 to 6 biopsies from the distal duodenum and 1 to 2 from the bulb (bulbar disease is patchy in coeliac). Histology is graded by the Marsh classification below. Capsule and balloon-assisted enteroscopy reach lesions beyond the standard scope; colonoscopy with terminal-ileal biopsy assesses terminal-ileum disease (B12, Crohn's).
• Imaging — CT or MR enterography (Crohn's, strictures, tumours, short bowel, lymphadenopathy); MRCP or CT pancreas (atrophy, calcification, duct dilation in chronic pancreatitis); barium follow-through (strictures, diverticula, blind loops).
• Special tests — D-xylose (historical; proximal mucosal uptake), Schilling (historical; B12 localisation), capsule motility, sweat chloride (cystic fibrosis in the young), HIV test.

Marsh classification of coeliac histology — learn it verbatim:[4]

• Marsh I — intraepithelial lymphocytosis (over 30 IELs per 100 enterocytes); villi normal.
• Marsh II — IELs plus crypt hyperplasia; villi still normal.
• Marsh III — villous atrophy plus crypt hyperplasia and IELs: IIIa partial, IIIb subtotal, IIIc total.
• Marsh IV — total villous atrophy with hypoplastic (atrophic) mucosa (rare, severe).[4]

Resuscitation — and do not forget refeeding

Malabsorption is usually chronic, and the emergency is rare. Resuscitation earns its keep in three settings: severe dehydration or electrolyte depletion (a high-output short-bowel stoma, severe secretory diarrhoea), severe malnutrition (the refeeding danger), and symptomatic anaemia or hypocalcaemia.[2]

• ABCDE first; secure IV access. Correct volume with balanced crystalloid; replace potassium, magnesium, calcium, phosphate guided by bloods.
• Refeeding syndrome prevention in severe malnutrition (BMI under 16, unintentional weight loss over 15%, minimal intake for over 10 days): start nutrition at 5 to 10 kcal/kg/day, raise it slowly over a week, give thiamine before and during feeding, and watch phosphate, potassium and magnesium daily — they will fall as cells flip into anabolism. Miss this and you can kill a patient with a sandwich.
• Severe symptomatic anaemia — transfuse only if haemodynamically compromised; otherwise replace iron, B12, folate by the route that works (oral if absorbed, intravenous iron if oral fails, intramuscular hydroxocobalamin for B12).
• Symptomatic hypocalcaemia — IV calcium gluconate; correct magnesium first or the calcium will not normalise. Replete vitamin D.
• Treat any acute precipitant — decompensated chronic pancreatitis, line sepsis in a PN-dependent short bowel.[1]

Treat the cause — the only management that matters

The governing principle, and the mantra of this whole topic: three mechanisms — luminal, mucosal, transport; treat the cause first, then replete. Replacing nutrients while the disease runs on is the cardinal error. Say it out loud until the viva examiner stops you.[1][2][3][4][5]

Cause-specific definitive treatment — drug, dose, route, rationale:[1]

• Coeliac disease — lifelong strict gluten-free diet (exclude wheat, barley, rye; pure uncontaminated oats are tolerated by most). Replete iron, folate, B12, calcium and vitamin D; arrange DEXA at diagnosis (osteoporosis is common); pneumococcal vaccination where hyposplenism is present. Refractory coeliac disease — persistent symptoms and villous atrophy despite a strict gluten-free diet for over 12 months, after you have excluded inadvertent gluten and everything else — needs specialist input and may need oral steroids (prednisolone, budesonide) or immunosuppression; these patients carry a real risk of enteropathy-associated T-cell lymphoma (EATL).[3][4]
• Pancreatic exocrine insufficiency — pancreatic enzyme replacement therapy (PERT): enteric-coated porcine pancreatin (e.g. Creon 25,000 to 40,000 PhU lipase units) with every meal and every snack, titrated to symptoms. The enzymes digest fat and protein in the lumen — that is the whole point. Add a PPI or H2-blocker to protect the enzymes from gastric acid. Replace the fat-soluble vitamins A, D, E, K. Treat the underlying pancreatitis — alcohol abstinence, analgesia, endoscopic or surgical drainage of duct obstruction.[5]
• SIBO — rifaximin 550 mg PO three times daily for 14 days is first-line; alternatives are metronidazole, ciprofloxacin or tetracycline in rotating courses, because relapse is common. Add a prokinetic (low-dose erythromycin, prucalopride) if the driver is motility; correct anaemia and deficiencies; fix the structural cause (surgery for strictures, diverticula, blind loops) where you can.[6]
• Lactose malabsorption — reduce dietary lactose (milk, ice cream, soft cheese); use lactase enzyme replacement (e.g. Lactaid) with dairy meals; keep calcium and vitamin D up. Hard cheese and live yoghurt are often tolerated — low in lactose, or carrying lactase-producing bacteria.[1]
• Short bowel syndrome — staged: (1) control output with anti-diarrhoeals (loperamide, codeine phosphate) and a PPI (gastric-acid hypersecretion is fierce early after resection); (2) PERT if the colon is in continuity or pancreatic function is impaired; (3) oral rehydration solution and fluid-electrolyte monitoring; (4) octreotide to cut secretions and output; (5) teduglutide (a GLP-2 analogue) 0.05 mg/kg subcutaneously once daily — the only drug proven to drive intestinal adaptation and reduce PN dependence; (6) parenteral nutrition (PN) if remaining small bowel is under about 100 cm without colon, or if oral and enteral routes cannot hold hydration and nutrition. Long-term PN demands central-line care and surveillance for line sepsis, PN-associated liver disease and metabolic bone disease.[2]
• Tropical sprue — folic acid 5 mg daily plus vitamin B12 (e.g. hydroxocobalamin 1 mg IM daily for a week, then maintenance), plus a prolonged tetracycline — tetracycline 250 mg four times daily (or doxycycline) for 3 to 6 months. The combination cures most patients.
• Whipple disease — induction with ceftriaxone 2 g IV daily for 2 weeks (or penicillin G plus streptomycin), then oral co-trimoxazole (TMP-SMX) for at least 1 year. Relapse and CNS recurrence are the price of undertreatment.
• Intestinal lymphangiectasia — low-fat diet with medium-chain triglycerides (MCT), because MCTs absorb straight into the portal vein and bypass the lymphatics; octreotide; surgical resection if the lesion is localised.
• Bile-salt diarrhoea (terminal ileal resection or disease) — bile-acid sequestrant cholestyramine 4 g with meals, plus fat-soluble vitamin replacement. The classic trap: cholestyramine works only after a modest ileal resection (under about 100 cm); after an extensive resection there is a true bile-salt deficiency, no excess bile acid reaches the colon, and cholestyramine worsens the fat malabsorption.[2]

Universal nutritional support, any cause:[1]

• Dietitian-led assessment and a tailored diet (energy, protein, micronutrient targets).
• Oral nutritional supplements (high-energy, high-protein sip feeds) if intake is inadequate.
• Enteral tube feeding (nasogastric or PEG) if oral intake is insufficient but the gut works.
• Parenteral nutrition only when the gut is unusable or too short — "if the gut works, use it." Never reach for PN when enteral feeding is possible.
• Replace every deficiency you found — iron (oral ferrous sulfate or fumarate, or IV ferric carboxymaltose if oral fails), B12 (IM hydroxocobalamin), folate (oral folic acid 5 mg daily), calcium 1000 to 1200 mg/day and vitamin D (colecalciferol, loading then maintenance; calcitriol if CKD), plus vitamin K, A, E, zinc and magnesium as needed.[1][2]

Escalation triggers: weight loss despite cause-specific therapy and supplementation; refractory coeliac; suspected EATL or small-bowel lymphoma (new weight loss, abdominal pain, refractory disease after a strict gluten-free diet); high-output stoma unresponsive to medical therapy; short bowel with PN dependence and complications (line sepsis, PN-liver disease) — refer to an intestinal-failure centre for autologous gastrointestinal reconstruction or intestinal or multivisceral transplant assessment.[1]

Named subtypes and scenarios

• Coeliac disease — the prototype mucosal malabsorption, with its own topic. Anti-tTG IgA plus total IgA, duodenal biopsy (Marsh), lifelong gluten-free diet; screen first-degree relatives; DEXA at diagnosis. The single commonest cause of chronic malabsorption across much of the world.[4]
• Tropical sprue — endemic in South and SE Asia, the Caribbean, Central and South America; hits residents and long-term travellers, rarely short-term tourists. Cause presumed infective, no single organism. Histology mimics coeliac (villous atrophy, IELs) but megaloblastic anaemia from folate and B12 deficiency is prominent and the lesion spans the whole small bowel, not just the proximal part. Treat with folate plus B12 plus prolonged tetracycline.[8]
• Whipple disease — rare infection by Tropheryma whipplei; middle-aged men; the classic triad is migratory arthralgia, weight loss and diarrhoea, with fever, lymphadenopathy, hyperpigmentation, and cardiac and neurological involvement (oculomasticatory myorhythmia is pathognomonic if present). Diagnosis: PAS-positive foamy macrophages on duodenal biopsy, confirmed by PCR. Treat with prolonged antibiotics — ceftriaxone, then co-trimoxazole for at least a year.[8]
• Short bowel syndrome — follows massive resection (mesenteric ischaemia, Crohn's, volvulus, trauma); outcome turns on remaining bowel length and whether the colon is in continuity (the colon salvages fluid and energy from short-chain fatty acids). Three phases — early (high output, fluid and electrolyte chaos), adaptation (1 to 2 years, villous hypertrophy raises absorption), maintenance. Complications: D-lactic acidosis (colonic bacterial fermentation), calcium-oxalate kidney stones (more colonic oxalate absorption), cholelithiasis (a shrunken bile-acid pool), and PN-related line sepsis and liver disease.[2]
• Intestinal lymphangiectasia — dilated intestinal lymphatics weeping protein- and lipid-rich lymph; primary (congenital) or secondary to lymphatic obstruction (lymphoma, tuberculosis, retroperitoneal fibrosis, right-heart failure). Presents with oedema, hypoalbuminaemia, lymphopenia and chylous effusions. Treat with low-fat plus MCT diet, octreotide, surgery if localised.[8]
• Protein-losing enteropathy — a cross-cutting subtype (lymphangiectasia, Menetrier's, IBD, coeliac, eosinophilic gastroenteritis): hypoalbuminaemia and oedema with normal liver and kidney. Diagnose with faecal alpha-1 antitrypsin clearance; treat the underlying cause.
• Abetalipoproteinaemia — rare autosomal recessive defect in microsomal triglyceride transfer protein; fat malabsorption from birth, acanthocytes on the blood film, retinitis pigmentosa, ataxia. Treat with low-fat diet plus fat-soluble vitamin replacement, especially vitamin E.
• Post-bariatric surgery malabsorption — increasingly common; iron, B12, folate, calcium, thiamine and protein deficiencies plus dumping syndrome. Lifelong micronutrient supplementation is mandatory.[1]

Complications and the classic traps

Complications of malabsorption itself:[1]

• Malnutrition, sarcopenia, growth failure (children, delayed puberty).
• Deficiency syndromes — iron, B12 and folate anaemia; osteomalacia and osteoporosis (vitamin D and calcium); bleeding (vitamin K); night blindness (vitamin A); peripheral neuropathy and ataxia (B12 and E); cardiomyopathy (selenium).
• Electrolyte and metabolic disturbance — hypokalaemia, hypocalcaemia, hypomagnesaemia, dehydration, especially in the short-bowel high-output patient.
• Refeeding syndrome if you feed a malnourished patient too fast.[2]

Cause-specific complications:[1]

• Short bowel — D-lactic acidosis (confusion, ataxia, high anion gap after a carbohydrate load), calcium-oxalate nephrolithiasis, cholelithiasis, central-line sepsis and PN-associated liver disease in long-term PN patients.[2]
• Untreated coeliac — iron-deficiency anaemia, osteoporosis, infertility, hyposplenism, and malignancy (enteropathy-associated T-cell lymphoma, small-bowel adenocarcinoma, oesophageal and oropharyngeal cancer); refractory coeliac disease, types I and II, the latter a precursor of EATL.[4]
• Crohn's — strictures, fistulae, fistula-related bypass causing malabsorption, colorectal and small-bowel cancer.
• Whipple — untreated: cardiac (endocarditis), CNS disease, malnutrition, death; treated: relapse if the antibiotic course is too short.

Classic traps — the recurring errors:[1]

• Diagnosing IBS in someone with weight loss, anaemia or steatorrhoea — these are red flags that exclude IBS outright.
• Starting a gluten-free diet before coeliac serology and biopsy — it normalises both and makes the diagnosis impossible for months. Everyone reaches for the diet sheet. That is how you lose the diagnosis.
• Replacing nutrients without treating the cause — the cardinal error of the whole topic.
• Forgetting total IgA with anti-tTG IgA — a coeliac with selective IgA deficiency has a falsely normal serology.
• Confusing fat malabsorption with osmotic diarrhoea — the stool and the deficiency pattern tell them apart.
• Missing refeeding syndrome in a severely malnourished patient.
• Overtreating with PN when enteral nutrition would work — if the gut works, use it.[2]

Prognosis and disposition

Prognosis turns on the cause and whether it is reversible:[1][2][4]

• Coeliac disease — excellent on a strict gluten-free diet: serology and histology recover, symptoms resolve, and the lymphoma risk falls towards baseline. Non-adherence drives relapse and malignancy.
• Lactose intolerance — benign; well controlled with dietary adjustment and lactase.
• Pancreatic exocrine insufficiency — manageable with lifelong PERT and fat-soluble vitamins; prognosis follows the underlying pancreatitis.
• Tropical sprue — curable with folate plus B12 plus prolonged tetracycline.
• Whipple disease — curable if treated early and fully with prolonged antibiotics; fatal if untreated, or if the CNS is involved and undertreated.
• Short bowel syndrome — a chronic, lifelong burden; some reach PN independence over 1 to 2 years of adaptation (more often with teduglutide and an intact colon), others stay PN-dependent with significant morbidity. Intestinal transplant is the last resort for PN failure.[2][7]
• Crohn's-related malabsorption — a chronic relapsing course governed by disease activity and cumulative resections.

Disposition — most malabsorption is managed outpatient with a dietitian and gastroenterology. Admit for severe dehydration or electrolyte disturbance, refeeding-risk malnutrition needing supervised nutrition, acute severe anaemia, or complications (line sepsis, suspected lymphoma, refractory disease). Patients on PN need structured intestinal-failure service follow-up.[2]

Special populations

• Children — focus on growth and puberty; failure to thrive is a key coeliac presentation. Cystic fibrosis is the dominant cause of pancreatic exocrine insufficiency in children. Congenital enteropathies (abetalipoproteinaemia, tufting enteropathy, microvillus inclusion disease, congenital sucrase-isomaltase deficiency) present with lifelong malabsorption from infancy. Weight-based dosing for every supplement and enzyme.
• Pregnancy — untreated coeliac disease is linked to recurrent miscarriage, intrauterine growth restriction, preterm birth and anaemia; screen at-risk women with serology and hold a strict gluten-free diet; ensure adequate folate, iron and vitamin D. Malabsorption in pregnancy demands prompt investigation (avoid radiation) and aggressive deficiency correction.
• Elderly — weight loss and anaemia may be wrongly written off to malignancy; keep a low threshold for coeliac serology. Beware refeeding syndrome and polypharmacy (metformin, cholestyramine and orlistat can all cause or worsen malabsorption).
• Immunocompromised (HIV or AIDS, CVID, post-transplant) — opportunistic enteritides (cryptosporidium, microsporidium, Mycobacterium avium complex, CMV) cause malabsorption; treat the organism and support nutrition; Giardia is common and easily missed in IgA deficiency.
• Post-bariatric surgery population — rapid nutrient malabsorption (iron, B12, folate, calcium, thiamine, protein) and dumping syndrome; lifelong micronutrient supplementation is mandatory, with annual bloods.
• Tropical-region residents — keep a high index for tropical sprue and parasitic causes; empirical deworming (albendazole or mebendazole) is reasonable where helminthiasis is endemic; Giardia is common in contaminated water sources.[1]

Evidence, guidelines and regional deltas

Diagnostic shift in coeliac disease: the "no-biopsy" pathway now allows an adult coeliac diagnosis on serology alone when anti-tTG IgA is over 10x the upper limit of normal, EMA is positive on a separate sample, and HLA-DQ2/DQ8 is positive — endorsed by BSG, ACG and (in children) ESPGHAN. It lightens the diagnostic burden, but the duodenal biopsy remains the gold standard in equivocal cases and across most of the world.[3][4]

Key evidence:[1]

• Faecal elastase under 100 ug/g carries high sensitivity and specificity for pancreatic exocrine insufficiency and is now the first-line pancreatic test.[5]
• Rifaximin is established as first-line therapy for SIBO, with a high initial response but frequent relapse that may need rotating antibiotics.[6]
• Teduglutide (a GLP-2 analogue) is the only pharmacotherapy proven — in phase-3 trials — to drive intestinal adaptation and reduce parenteral nutrition dependence in short bowel syndrome with intestinal failure; roughly half of treated patients achieve a clinically meaningful PN reduction.[7]
• The ESsCD coeliac guideline codifies the gluten-free diet as the only proven treatment and stresses annual serological and biochemical surveillance.[3]

Regional deltas — high-yield:[1]

• Lactose intolerance prevalence varies by ethnicity — high in East Asian, African and South Asian populations (where adult-type hypolactasia is near-universal) and low in Northern Europeans. In India the prevalence is high and dietary lactose reduction is the norm; secondary lactase deficiency from mucosal disease (coeliac, gastroenteritis) is common everywhere.
• Tropical sprue is endemic in South and SE Asia, the Caribbean and parts of South America; managed empirically with folate plus B12 plus prolonged tetracycline in resource-limited settings without a full workup. Notably absent in Africa — a geographic clue in itself.[8]
• Coeliac disease — long thought rare in South Asia, now increasingly recognised as serology becomes available; HLA-DQ2/DQ8 frequency is lower than in European populations, but the disease is real and under-diagnosed.
• Pancreatic exocrine insufficiency — in India the dominant cause is alcoholic chronic pancreatitis (and tropical calcific pancreatitis, a distinctive entity of South India and other tropical regions); in the West, alcohol and cystic fibrosis dominate.[5]
• The WGO (World Gastroenterology Organisation) offers a practical, resource-stratified malabsorption guideline suited to tropical and resource-limited settings.[8]

Ward-round test

Stem 1. A 40-year-old presents with pale, foul, floating stools, 6 kg weight loss despite a good appetite, and an iron-deficiency anaemia that has not responded to oral iron. Which mechanism is failing, and what is the single first test you must not forget?[4]

Stem 2. A patient three months after a 60 cm terminal-ileum resection has watery diarrhoea that responds to cholestyramine. Why does the same drug harm the patient next door, who lost 200 cm of ileum?[2]

Stem 3. A long-term PN-dependent short-bowel patient asks if anything might reduce their line-days. What do you offer, and what is the dose?[7]

Stem 4. A middle-aged man returns from rural South Asia with diarrhoea, glossitis and a macrocytic anaemia far out of proportion to the stool change. Name the diagnosis and the treatment bundle.[8]

Exam Pearls

• Three mechanisms: luminal (pancreatic, bile-salt, SIBO, lactase), mucosal (coeliac, sprue, Crohn's, Whipple), transport or surgical (short bowel, lymphangiectasia).
• Steatorrhoea = pale, bulky, greasy, foul, difficult-to-flush stool; faecal fat over 7 g/day.
• Coeliac: anti-tTG IgA (most sensitive) plus anti-endomysial IgA (most specific); always check total IgA — selective IgA deficiency hides in roughly 5%. Biopsy = Marsh (intraepithelial lymphocytes, crypt hyperplasia, villous atrophy).[3]
• Faecal elastase for pancreatic insufficiency (under 200 ug/g); breath tests for SIBO and lactose.
• Iron-deficiency anaemia with no obvious cause = screen for coeliac (and colonoscopy if over 50).
• Fat-soluble vitamins A D E K deficiency = fat malabsorption.
• Tropical sprue: megaloblastic anaemia prominent, endemic area; treat with folate plus B12 plus tetracycline.
• Whipple disease: PAS-positive macrophages, Troheryma whipplei; arthralgia plus pigmentation plus CNS signs; prolonged antibiotics.
• Short bowel: teduglutide (GLP-2) reduces PN dependence; complications are D-lactic acidosis, oxalate stones, gallstones, line sepsis.[2][7]
• Treat the cause first, then replete — never replace nutrients blindly.
• No gluten-free diet before coeliac serology and biopsy.
• Cholestyramine for bile-salt diarrhoea after terminal-ileum resection — only if the resection is modest.
• Rifaximin 550 mg TDS for 14 days for SIBO; think blind loops, diverticula, scleroderma, chronic PPI.[6]

Exam application bank (NEET-PG / INICET)

One-line answer

Malabsorption is impaired absorption of nutrients across the gut, divided into three mechanistic classes: luminal (defective digestion — pancreatic exocrine insufficiency, bile-salt deficiency, small-intestinal bacterial overgrowth, lactase deficiency), mucosal (defective uptake — coeliac disease, tropical sprue, Crohn's disease, radiation enteritis, Whipple disease) and transport/post-mucosal (short bowel syndrome, post-gastrectomy, intestinal lymphangiectasia). The hallmark is steatorrhoea (pale, bulky, greasy, foul-smelling, difficult-to-flush stool) with weight loss, bloating and deficiency signs (iron, B12, folate, calcium, and the fat-soluble vitamins A, D, E, K). Diagnosis combines blood deficiency screens, coeliac serology (anti-tTG IgA plus total IgA), faecal elastase, breath tests and duodenal biopsy (Marsh). Management is to treat the underlying cause — gluten-free diet for coeliac, pancreatic enzymes for insufficiency, rifaximin for SIBO, teduglutide and PN for short bowel, folate plus B12 plus tetracycline for tropical sprue, prolonged antibiotics for Whipple — and then replace every deficiency.[1]

Worked stems (answer without another resource)

Stem 1 — Classic presentation. Map the symptoms to a mechanism; name the first investigation and the first treatment step, with dose and route if drug therapy is standard.[1]

Stem 2 — Unstable or complicated. List the red flags that force immediate resuscitation, theatre, ICU, an antidote or reperfusion — and what you do in the first 15 minutes.[1]

Stem 3 — Atypical group. Elderly, pregnant, a child, or immunocompromised: how the presentation and the thresholds change.[1]

Stem 4 — Differential trap. Name the three closest mimics and one discriminator for each.[1]

Stem 5 — Disposition. Who goes home with safety-netting, who is admitted, who needs HDU, ICU or theatre, and what follow-up is mandatory.[1]

Rapid viva checklist

1. Definition plus classification
2. Pathophysiology chain
3. Bedside signs and criteria
4. Score with exact components, if any
5. Emergency bundle
6. Definitive therapy with doses
7. Complications of disease and of treatment
8. Special populations
9. Guideline or trial name if classic
10. Three exam traps[1]

Coverage self-check

If you cannot answer any stem above from this page alone, re-read the matching section — the page is built to be self-sufficient for final-prof and NEET-PG or INICET questions on Malabsorption.[1]