Amyloid A (serum) (SAA) – a marker of acute inflammation

General Information

Serum amyloid A was discovered in 1971 as a component of amyloid deposits (excessive accumulation of amyloid proteins in tissues) in patients with chronic inflammation. Amyloid is a representative of the family of apolipoproteins, which binds to high-density lipoproteins (HDL) in blood serum, producing several isoforms, the levels of which increase in response to various inflammatory processes.

Amyloid A is an acute phase protein, which consists of 104 amino acids and has a molecular weight of 12-14 kilodaltons. Like C-reactive protein (CRP), it is synthesized primarily in the liver in response to an infectious process, tissue damage, or stress. Extrahepatic sites of amyloid A synthesis may include macrophages, endothelial cells, epithelial cells, areas of atherosclerotic lesions, tumors, and synovial membranes. Amyloid A-1 is its main isoform.

After amyloid A is synthesized, it is released into the bloodstream and binds to high-density lipoprotein particles. Elevated serum amyloid A results in replacement of apolipoprotein-A1 and changes in high-density lipoprotein (HDL) composition. The functional change of this lipoprotein leads to the loss of atheroprotective (protecting blood vessels) properties. At high concentrations, serum amyloid A dissociates from high-density lipoprotein (HDL) and forms lipoprotein particles in the blood that contain apolipoprotein-A1 and atherogenic (bad) lipid-associated amyloid A.

These lipoproteins, synthesized by macrophages and synovial cells, accumulate in the focus of inflammation and further intensify the inflammatory processes.

Thus, circulating complexes of serum amyloid A and HDL participate in the transport and metabolism of HDL-cholesterol and are involved in such pathological processes as: atherosclerosis, rheumatoid arthritis, Alzheimer's disease and tumors.

Acute inflammatory processes lead to a rapid increase in the concentration of amyloid-A in the blood serum, so that its level may be 24 times higher than normal in 1000 hours, which is why this protein is considered a marker of inflammation.

Amyloid-A circulating in the blood attracts neutrophils, monocytes and T-lymphocytes to the site of damage and promotes the process of tissue regeneration by activating tissue protease enzymes.

The binding of amyloid A to high-density lipoproteins (HDL) provides the release of lipids at the site of damage, which is necessary for tissue repair. On the other hand, the amyloid A-HDL complex ensures the removal of excess cholesterol released from the damaged tissue.

Amyloid A-HDL complex also participates in anti-inflammatory activity by inactivating lymphocytes. Amyloid A also protects tissues from oxidative damage that typically occurs during the inflammatory process.

An increase in the concentration of amyloid A is observed in patients with both acute and chronic inflammatory processes.

In acute inflammation, amyloid A increases much faster than C-reactive protein. In addition, unlike C-reactive protein, amyloidA concentrations increase in response to both bacterial and viral inflammation (C-reactive protein increases only during bacterial inflammation).

As a result of prolonged and repeated inflammatory processes, the continuous increase of A amyloid in the serum leads to the development of a reactive, progressive disease - AA amyloidosis, with the accumulation of pathological A amyloid in the liver, kidney, spleen,

Chronic relapsing diseases such as: rheumatoid arthritis, juvenile arthritis, ankylosing spondylitis, familial Mediterranean fever, progressive systemic sclerosis, chronic infections (tuberculosis, osteomyelitis) and neoplasms (Hodgkin's disease, renal carcinoma) are conditions that lead to the development of AA amyloidosis. However, since most patients with these diagnoses do not develop amyloidosis, the risk factors for developing it are unknown (and may be the result of an interaction of genetic, environmental, and iatrogenic factors).

High levels of serum amyloid A are associated with cardiovascular disease. It is also an important marker for the early diagnostics of tissue rejection after renal transplantation. Elevation of serum amyloid A levels is also an important marker at the beginning of some malignant processes, such as lung carcinoma, esophageal, colon, endometrial, ovarian epithelial tumors, and others.

When should we do the research?

• Assessment of inflammatory processes
• Assessing the risk of secondary amyloidosis
• Detection of the risk of cardiac pathologies in the future
• Assessment-prediction of post-kidney transplant withdrawal reaction
• Monitoring of tumor processes

Preliminary preparation: no need

Material for examination: Venous blood

Referral norm - <10 mg/l

Interpretation of results

• An increase in the index in the range of 10-100 mg/l characterizes viral diseases, systemic lupus erythematosus, focal tissue inflammatory processes, brain infarction and others. Amyloid A is more common than C reactive protein in these conditions.
• An increase in the index in the range of 100-1000 mg/l characterizes bacterial and fungal infections, malignant tumors (the highest amyloid A indicator is in metastatic tumors), acute myocardial infarction, autoimmune diseases - rheumatoid arthritis and vasculitis. In rheumatoid arthritis, the level of amyloid determines the activity of the disease and the risk of developing secondary amyloidosis.
• In post-transplant evaluation, an amyloidA level > 100 mg/L indicates tissue rejection. In addition to kidney transplants, it is used to evaluate the condition after liver, bone marrow and pancreas transplants.