GastroenterologyTier 1Disease (DEADMAN)

Iron deficiency

Description

*Iron deficiency in an adult is a symptom, not a diagnosis - find the source*
Absolute (depleted stores) vs functional (adequate stores, unavailable - inflammation, ESA therapy)
In a gastroenterological frame, three mechanisms:
- BLOOD LOSS - GI tract until proven otherwise in men and post-menopausal women
- MALABSORPTION - duodenum/proximal jejunum
- dec INTAKE - vegan/vegetarian, poverty, elderly

Commonest nutritional deficiency worldwide; ~1 in 8 Australian women of reproductive age
GI malignancy found in ~5-15% of men and post-menopausal women investigated for IDA
- That yield is the justification for bidirectional endoscopy
Coeliac disease in ~3-5% of patients referred with IDA
Daily requirement ~1-2 mg absorbed; menstrual loss ~30-40 mL/cycle; pregnancy requires ~1000 mg extra

Absorption physiology - explains the causes

Non-haem iron (Fe3+) -> reduced to Fe2+ by duodenal cytochrome b + ascorbate -> DMT1
*Absorbed in the DUODENUM and PROXIMAL JEJUNUM* - the key anatomical fact
Exported by ferroportin, controlled by hepcidin
- Inflammation -> IL-6 -> inc hepcidin -> ferroportin internalised -> iron trapped -> anaemia of chronic disease / functional deficiency
Enhanced by: gastric acid, vitamin C, haem iron (meat)
Inhibited by: PPIs, phytates, tannins (tea), calcium, achlorhydria

Causes

Blood loss
- GI: colorectal and gastric cancer, angiodysplasia, peptic ulcer, oesophagitis, NSAIDs/aspirin/anticoagulants, IBD, haemorrhoids, hookworm, Meckel diverticulum
- Gynaecological: menorrhagia, fibroids
- Urinary, epistaxis, haemolysis (intravascular), blood donation
Malabsorption
- *Coeliac disease - characteristically causes iron deficiency, because villous atrophy is worst in the duodenum and proximal jejunum, the main site of iron absorption*
  - With more extensive small bowel involvement: calcium, folate and fat-soluble vitamin (ADEK) deficiency as well
- *Atrophic gastritis / H. pylori / pernicious anaemia* - dec acid
- Post-gastrectomy and Roux-en-Y gastric bypass - bypasses the duodenum
- Long-term PPI, small bowel Crohn, bacterial overgrowth
inc Demand - pregnancy, growth, ESA therapy

Confirm iron deficiency

Test	Deficiency	Caveat
Ferritin	<30 microg/L confirms (<15 definite)	Acute phase reactant - normal or high does NOT exclude it if CRP raised. In inflammation or CKD, use <100 (or <300 with TSAT <20%)
Transferrin saturation	<20%	Falls in inflammation too
Transferrin/TIBC	inc	dec in inflammation - helps separate IDA from ACD
Soluble transferrin receptor	inc	Unaffected by inflammation - use when ferritin is uninterpretable
Film	Microcytic, hypochromic, anisocytosis, pencil cells, inc platelets

Microcytosis differential: iron deficiency, thalassaemia, anaemia of chronic disease, sideroblastic, lead**
- Mentzer index (MCV/RBC) <13 -> thalassaemia; >13 -> iron deficiency

Then find the cause - the part that is examined

Coeliac serology (tTG-IgA + total IgA) in EVERY case
Urinalysis (haematuria)
Bidirectional endoscopy (gastroscopy + colonoscopy) in:
- All men, all post-menopausal women
- Pre-menopausal women with GI symptoms, family history of CRC, or failure to respond to iron
- Take duodenal biopsies at gastroscopy even if serology is negative - seronegative coeliac disease exists
*If both endoscopies are negative and iron deficiency persists or recurs -> CAPSULE ENDOSCOPY* for small bowel angiodysplasia, Crohn, tumour
Do NOT stop at a plausible lesion that does not explain the degree of loss (e.g. haemorrhoids) - synchronous pathology is common

1. Treat the cause

Stop or minimise NSAIDs, aspirin, anticoagulants where possible; PPI review
Gluten-free diet in coeliac disease; treat H. pylori; tranexamic acid or hormonal treatment for menorrhagia

2. Oral iron - first line

Ferrous sulfate / fumarate / gluconate, ~100-200 mg elemental iron
*ALTERNATE-DAY dosing is at least as effective as daily and much better tolerated* - a single daily dose raises hepcidin for ~24 h, blocking the next dose
Take on an empty stomach with vitamin C; avoid tea, calcium and PPIs around the dose
Response: reticulocytosis at 1 week, Hb rise ~10 g/L per 1-2 weeks
- *Failure to respond -> non-adherence, ongoing loss, malabsorption, or wrong diagnosis*
Continue 3 months AFTER Hb normalises to refill stores

3. IV iron - when oral fails or is inappropriate

Indications: intolerance, malabsorption (coeliac, IBD, bariatric surgery), ongoing loss outpacing absorption, CKD, heart failure, late pregnancy, pre-operative optimisation
Ferric carboxymaltose (single 1000 mg dose) or iron polymaltose
- *Hypophosphataemia is common and specific to ferric carboxymaltose* (FGF23-mediated) - check phosphate with repeat dosing
- Skin staining at the cannula site is permanent - warn and secure the line
- Anaphylaxis rare with modern preparations; no test dose required for ferric carboxymaltose

4. Transfusion

Only for haemodynamic instability or symptomatic severe anaemia - iron deficiency anaemia of slow onset is remarkably well tolerated; transfusion treats the number, not the deficiency

Coeliac disease - and its other deficiencies (folate, calcium, fat-soluble vitamins)
Colorectal and gastric carcinoma - the diagnosis you cannot miss
Angiodysplasia - Heyde syndrome: aortic stenosis + angiodysplasia + acquired von Willebrand type 2A
IBD - both blood loss and anaemia of chronic disease
Hereditary haemorrhagic telangiectasia
Bariatric surgery - malabsorptive procedures (Roux-en-Y, biliopancreatic diversion) >> restrictive (sleeve, band)
Chronic kidney disease, heart failure (IV iron improves symptoms with or without anaemia)
Hookworm, schistosomiasis - travel/migration history
Pica, restless legs syndrome, koilonychia, angular stomatitis, glossitis, Plummer-Vinson (post-cricoid web)

Corrects fully once the cause is removed; recurrence means the cause was not found
Fatigue, restless legs and cognitive/exercise impairment occur with iron deficiency WITHOUT anaemia - treat on ferritin
Untreated: high-output cardiac failure, poor wound healing, adverse pregnancy outcomes (low birthweight, prematurity)
The risk of the diagnosis is the missed malignancy - a completed, documented work-up matters more than the haemoglobin

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