muramidase and Polymyalgia-Rheumatica

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.

Topics: Aged; alpha-Macroglobulins; Antigens; Factor VIII; Female; Fibrin Fibrinogen Degradation Products; Fibronectins; Giant Cell Arteritis; Glycosaminoglycans; Histocytochemistry; Humans; Male; Microscopy, Electron; Middle Aged; Muramidase; Polymyalgia Rheumatica; von Willebrand Factor

We suggest that polymyalgia rheumatica with giant cell arteritis (PR-GCA) is an arachidonic acid metabolites mediated disease which can be diagnosed more accurately and monitored more precisely for therapeutic benefits by the serial determinations of the major urinary prostaglandin F, serum urinary lysozymes, serum acid phosphatase, and serum angiotensin converting enzyme rather than by the erythrocyte sedimentation rate, and, when necessary by temporal artery biopsy. The pathogenetic role proposed for prostaglandins (PG) and, even more precisely perhaps, the leukotrienes in this disease is consistent with the several published clinical observations that non-steroidal anti-inflammatory drug treatment produces in some cases a therapeutic paradox of symptomatic relief with concurrent, if clinically silent, progression of the arteritis, even to blindness. Furthermore, the impressive response of PR-GCA to low maintenance dose steroid therapy, a clinical conundrum for decades, is rationally explained on the basis of depressed or obstructed PG metabolism early on in the metabolic cascade. These views warrant clinical evaluation, confirmation or correction in whole or in part, and may increase our understanding of PR-GCA.

Topics: Acid Phosphatase; Anti-Inflammatory Agents; Arachidonic Acid; Arachidonic Acids; Aspirin; Blood Sedimentation; Humans; Models, Biological; Muramidase; Peptidyl-Dipeptidase A; Polymyalgia Rheumatica; Prostaglandins; Prostaglandins F