The deposition of an amorphic eosinophilic material is obvious. Hepatocytes are irregularly affected by the process, as some hepatocytes are still present while others have been entirely replaced.
Amyloid deposition begins in the space of Disse and progressively encroaches into the sinusoids and hepatocytes.
Massive deposition eventually leads to pressure atrophy of the hepatocytes.
This is a different patient with amyloidosis, but the deposition primarily affects the vessels, whereas the hepatocytes are preserved.
Amyloid is a pathologic protein that can be deposited in a wide range of organs and tissues. This substance progressively accumulates and causes pressure atrophy of cells. The liver can be involved in primary amyloidosis such multiple myeloma (associated with AL type fibrils) or secondary amyloidosis related to chronic inflammatory conditions (associated with AA type fibrils)(Kumar).
Microscopically, deposits of extracellular amorphous eosinophilic material is seen in the blood vessels and sinusoids. The deposits when demonstrate apple-green birefringence after Congo red staining. As amyloid accumulates, the hepatocytes become atrophic and are replaced by amyloid.
Note that in light chain deposition disease, deposits resembling amyloid are also deposited in the perisinusoidal spaces as well as portal tracts. However, the light chains (usually kappa) do not demonstrate apple-green birefringence with Congo red, but will be highlighted with an immunostain for kappa light chain (Rosai).
Cheng L, Bostwick DG, eds. Essentials of Anatomic Pathology. 2nd Ed. Totowa, NJ: Humana Press; 2006: 1404.
Kumar V, Abbas AK, Fausto N. Robbins and Cotran Pathologic Basis of Disease. 7th Ed. Philadelphia, PA: Elsevier; 2005: 258-263.
Rosai, J. Rosai and Ackerman's Surgical Pathology. 9th Ed. Philadelphia, PA: Elsevier; 2004: 964-5.