Faecal alpha1-antitrypsin (FAAT) can normally be found in low concentrations in stool. It is believed that some of the FAAT comes from liver-derived circulating AAT in a pure form or as AAT-protease complex. It has also been proposed that some FAAT are synthesized locally from gut epithelial cells. The expression of these gut derived variants differ between individuals and under different pathological states.
AAT is not reabsorbed in the gut and is resistant to luminal proteolysis. These properties render it used as a marker for Protein Losing Enteropathy (PLE). PLE can occur in diseases affecting gastrointestinal mucosa e.g. inflammatory bowel diseases, infective diarrhoea, coeliac disease or secondary to systemic burns. Conditions causing elevated lymphatic pressure e.g. intestinal lymphangietasia, intestinal lymphoma, congestive heart failure, post Fontan cardiac surgery can also cause PLE. Giant hypertrophic gastropathy (Menetrier's disease) or Zollinger-Ellison syndrome although can cause gastric protein loss but because of low gastric pH, AAT are degraded thus FAAT is not useful for these conditions. FAAT has also been used for monitoring e.g. heparin therapy in PLE.
Diarrhoea per se e.g. caused by lactulose laxative can already induce increase in FAAT. Furthermore, excessive liquid from watery diarrhoea can reduce sensitivity to pick up abnormal gut protein loss as our current FAAT method report in mg/gram wet stool. It is desirable to have non-diarrhoeal stool samples for proper FAAT testing.
Neonates less than 1 wk old have high FAAT from meconium contamination. Breast or formula fed infants have slightly higher FAAT compare with older children and adults.
It is difficult to interpret FAAT from patients with significant genetic alpha1-antitrypsin deficiency.
Specialist Biochemistry
FAAT
Frozen (preferred) 4 weeks
3 weeks
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