Synopsis
Recognise protein-losing enteropathy as a syndrome, confirm gastrointestinal protein loss only after excluding common alternatives, and direct treatment towards its mucosal, lymphatic or cardiovascular cause.
- Protein-losing enteropathy describes excessive loss of plasma proteins into the gastrointestinal tract; it is a mechanism requiring an underlying diagnosis, not a final disease label.
- Before attributing hypoalbuminaemia to the gut, assess hepatic synthesis, urinary protein loss, inflammation, malnutrition, burns and dilution because these are commoner explanations.
- Mechanisms include erosive mucosal disease, non-erosive mucosal permeability and obstructed or high-pressure intestinal lymphatic drainage; several can coexist.
Key red flags
Hypotension, acute kidney injury, oliguria or severe electrolyte disturbance in an oedematous patient suggests reduced effective circulating volume and needs urgent monitored management.
Investigation priorities
Confirm severity and follow the biochemical trajectory.
Management branches
Persistent hypoalbuminaemia, oedema or effusions lack a sufficient hepatic, renal or nutritional explanation.
- Confirm the trend and review inflammation, liver synthetic function, quantified urine protein, diet, fluid state, burns and medication or infusion history.
- Request faecal alpha-1-antitrypsin testing through the local referral laboratory, following its sampling and paired-serum requirements exactly.
Key medicines
Dietary protein and energy supportIndividualised dietitian-led intake targets adjusted for ongoing losses and tolerance.
Human albumin solutionReserved specialist intravenous replacement linked to clinical indication and haemodynamic review.