Prealbumin. A major constituent of vitreous amyloid

P D Gorevic1, M M Rodrigues, W H Spencer

  • 1Department of Medicine, State University of New York, Stony Brook 11794-8161.

Ophthalmology
|July 1, 1987
PubMed

Insights

Vitreous amyloid, linked to familial amyloidotic polyneuropathy, involves abnormal prealbumin protein. This study confirms prealbumin as the key component in both familial and non-familial vitreous amyloid cases.

Area of Science:

  • Ophthalmology
  • Neurology
  • Biochemistry

Background:

  • Familial amyloidotic polyneuropathy (types 1 and 2) can present with or be complicated by vitreous amyloid.
  • Research indicates abnormal prealbumin is the primary component of amyloid fibrils in these conditions, with affected individuals exhibiting low blood prealbumin levels.

Observation:

  • This study analyzed vitreous amyloid samples from two patients, one with non-familial and one with familial amyloidosis.
  • Biochemical analysis using two-dimensional gels identified the amyloid protein as prealbumin monomer in both cases.
  • Immunoelectron microscopy confirmed the presence of prealbumin fibrils using a specific antiserum.

Findings:

  • Vitreous amyloid, in both familial and non-familial forms, is composed of prealbumin.
  • The biochemical and immunohistologic characteristics of vitreous amyloid can be determined from samples obtained during vitrectomy.

Implications:

  • Vitreous amyloid deposition may indicate systemic prealbumin amyloidosis.
  • Vitrectomy samples offer a viable method for diagnosing and characterizing prealbumin amyloidosis, aiding in understanding familial amyloidotic polyneuropathy.