Secondary (AA) amyloidosis most commonly complicates chronic inflammatory diseases. The precursor serum protein that forms AA fibrils is:
- A Serum amyloid A (SAA), an acute-phase reactant ✓
- B Immunoglobulin light chain (kappa or lambda)
- C Transthyretin (TTR)
- D Beta-2 microglobulin
Explanation
AA amyloidosis results from chronic elevation of serum amyloid A (SAA), an acute-phase protein produced by the liver in response to IL-1, IL-6, and TNF during chronic inflammatory conditions (RA, osteomyelitis, bronchiectasis, FMF). AA fibrils deposit primarily in the spleen, liver, and kidneys. AL amyloidosis uses immunoglobulin light chains; transthyretin forms ATTR amyloid (cardiac/hereditary); beta-2 microglobulin accumulates in dialysis-related amyloidosis.
Reference: Robbins & Cotran Pathologic Basis of Disease, 10th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.