Clinical use: Amyloid A blood testing can be used to monitor treatment of inflammation in amyloidosis.
Background: The term amyloidosis describes a group of disorders caused by abnormal folding, aggregation and accumulation of certain proteins in the tissues, in an abnormal form known as amyloid deposits. These deposits are composed of abnormal protein fibres, the so-called amyloid fibrils that accumulate more quickly than they are cleared away, and which progressively interfere with the structure and function of affected organs throughout the body. Normal healthy proteins are cleared away at about the same rate that they are produced, but proteins that have formed amyloid are broken down only very slowly.

Inflammatory diseases are accompanied by changes in the chemistry of the blood. The concentration of one particular blood protein called serum amyloid A protein (SAA) can increase from healthy levels of less than 3 mg per litre to more than 1000 mg per litre in the presence of inflammation, and it can remain elevated for as long as the inflammatory disease remains active. For unknown reasons, in a small proportion of such patients, SAA can at some point begin to be converted into AA amyloid fibrils, and become lodged in various tissues throughout the body. The average duration of inflammatory disease before AA amyloidosis occurs is around 20 years, but it can occur after just a few years in some cases. AA amyloid deposits tend to be greatest in the spleen, which does not usually cause any symptoms, and the kidneys where it most often does cause clinical problems. Damaged kidneys may lead to loss of healthy blood proteins in the urine and severe fluid retention (proteinuria and nephrotic syndrome), and can ultimately lead to complete kidney failure, requiring dialysis. AA amyloid can build up in the liver and gut at a later stage, though rarely in the heart.

Reference ranges: 82% population: 96% population:


SAA < 10 mg/L: amyloid deposits stable or gradually regress in virtually all patients-no increase in anti-inflammatory treatment is required.
SAA 10 – 25 mg/L: amyloid deposits stable in most patients- further monitoring without changes in therapy may be appropriate.
SAA >50 mg/L: amyloid deposits accumulate in most patients, and more intensive or alternative treatment should be considered.

Associated diseases:
Patient preparation: None required
Specimen requirements: Serum – Red top tube or SST.
Turnaround time: 4 weeks
Additional information: Note that serum amyloid A is not the most common origin of amyloid deposits. Free light chain amyloidosis is more common.
Referred test: Referred test
Location: Centre for Amyloidosis & Acute Phase Proteins