Molecule2 diseases
Serum Amyloid A (SAA)
Acute-phase reactant and amyloid precursor
- Expression change
- Elevated
- Evidence level
- established
- Targeted by
- Colchicine, IL-1 blockers (indirect)
Expression across diseases
| Disease | Role | Expression | Evidence |
|---|---|---|---|
| Familial Mediterranean Fever | Acute-phase reactant and amyloid precursor | Elevated | established |
| TNF Receptor-Associated Periodic Syndrome | Acute phase protein — amyloid precursor | Markedly elevated | established |
Role in pathogenesis
SAA is produced by the liver in response to IL-1beta and IL-6 during FMF attacks. Persistently elevated SAA during remission periods (subclinical inflammation) is the precursor to AA amyloidosis. Median SAA >155 mg/L confers 17.7x relative risk of death. SAA is the key biomarker for monitoring disease control.
Targeting drugs (1)
| Drug | Mechanism | Response rate | Line |
|---|---|---|---|
| Colchicine | Microtubule disruption; reduces leukocyte motility and phagocytosis | ~95% (attack prevention) | 1st |