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GIANT‐CELL ARTERITIS Histological, Immunohistochemical and Electronmicroscopic Studies.
Author(s) -
CHEMNITZ JOHN,
CHRISTENSEN BENT COLLATZ,
CHRISTOFFERSEN P.,
GARBARSCH CHARLY,
HANSEN TROELS MØRK,
LORENZEN IB
Publication year - 1987
Publication title -
acta pathologica microbiologica scandinavica series a :pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.909
H-Index - 88
eISSN - 1600-0463
pISSN - 0108-0164
DOI - 10.1111/j.1699-0463.1987.tb00039_95a.x
Subject(s) - giant cell arteritis , arteritis , pathology , polymyalgia rheumatica , giant cell , medicine , fibrin , vasculitis , immunology , disease
Biopsies from the temporal artery of 32 patients suspected of giant‐cell arteritis were evaluated retrospectively by light microscopy, histochemical, and immunohistochemical methods, as well as by transmission electron microscopy (TEM). At the clinical follow‐up the 32 patients included four clinical groups: temporal arteritis (8 patients), polymyalgia rheumatica (10 patients), rheumatoid arthritis (4 patients), and a group of miscellaneous diseases unrelated to inflammatory rheumatic diseases (10 patients). There were a number of similarities between age‐related alterations in the arteries and the changes in giant‐cell arteritis. The most important differences were the inflammatory cellular infiltration of the media, the perifocal accumulation of fibronectin, and the occurrence of deposits of fibrin/fibrinogen and fibrin/fibrinogen degradation products. In addition, alpha‐2 macroglobulin, lysozyme and factor VIII were also noted in giant‐cell arteritis. The alterations in giant‐cell arteritis show a number of similarities to the changes following experimental vascular injury of the rabbit aorta. The nature of the findings in human giant‐cell arteritis, as well as the similarity to the experimental arteritis, indicate that giant‐cell arteritis may reflect a non‐specific reaction to injury, independent of the cause of the disease.