Electron microscopy of giant-cell (temporal) arteritis.

Abstract

Definitive histological studies of giant-cell (temporal) arteritis have been published by several workers (Harrison, 1948;Heptinstall, Porter, and Barkley, 1954;McCormick and Neuberger, 1958). The lesions are fairly uniform and have involved all layers of many different arteries and veins-large and small, intracranial as well as extracranial. The distinctive histological finding in this disease has been a giantcell reaction with disruption of the internal elastic membrane. Aetiological factors are unknown. Biopsy specimens from a patient with a classical clinical and pathological case of giant-cell (temporal) arteritis have been examined electron microscopically. This report describes the ultrastructural details of this diseased artery. CASE REPORTA 64-year-old man was referred to the Saint Louis University Hospital in July 1967 by Dr. James Mulvill, Alton, Illinois, with a main complaint of right frontotemporal headaches for three months. He also had noted malaise, weight loss, and mild intermittent fever. His past history was remarkable for a partial loss of vision in the right eye for eight years with an attack of gout two years ago. He took digitalis and probenecid regularly and quinidine intermittently. He denied arthralgia and myalgia, and had no symptoms of cerebral dysfunction. He never noted redness or tenderness of the temporal regions.Examination revealed normal vital signs. The temporal arteries were firm and cord-like with weak pulsations, but were not tender, and there were no signs of inflammation surrounding them. There were no bruits and pulses were good in the extremities. Funduscopic examination showed mild arteriosclerotic changes bilaterally with old perimacular exudates on the right. There was a central scotoma of the right visual field. There was no evidence of recent ocular disease. The cause of his old visual loss was not ascertained. The remainder of the general and neurological examination was normal.Laboratory studies were normal except for erythrocytic sedimentation rate of 116 mm/hr, a diabetic glucose tolerance test, and serum uric acid 7-0 mg%. There was no eosinophilia, serum protein electrophoresis was Hartford Foundation. normal, and cerebrospinal fluid was normal. Mercury-203 chlormerodrin brain scan was normal. An electroencephalogram showed mild, diffuse, slow dysrhythmia. Radiographs of chest, skull, and paranasal sinuses were normal except for bilateral maxillary sinusitis.The left superficial temporal artery was biopsied. The lumen was obliterated in some regions. Histological sections (Fig. 1) demonstrated a marked inflammatory reaction associated with proliferative changes of intima, media, and adventitia. Numerous eosinophils, lymphocytes, and plasma cells were present. The intima had a nodular proliferation. At the junction of the intima and media many giant cells were seen. Some were of foreignbody type, but most were of the Langhan's type. No tuberculoid granulomata were noted.The patient was treated with prednisone 30 mg per day for one month and then the drug w...

Temporal (granulomatous) arteritis: a histopathological study of 32 cases

“…This study attempted todefine the histopathology seen in casessufferingfrom temporal arteritis on the basis of the material available in our institution. The patient and clinical data, as well as the main pathological findings, are similar to thosedocumented in the literature (Wilske & Healey 1967 ~9 6 4 , 1965, O'Brien 1978) and ultrastructural (Smith, 1969, Parker et al 1975) data exist that implicate damaged vascular elastic tissue as the antigen responsible for the inflammation.…”

Giant‐cell (Temporal) Arteritis Following a Bypass Operation for Cerebral Infarction

“…The finding of circulating immune complexes (9) and of anti-IgG activity in artery biopsy specimens (7,10) supports the concept of an immunological disease. There is one report describing the ultrastructure of an involved temporal artery (11). It confirmed light microscopic findings and the relationship of the fragmented internal elastic lamina to macrophages and giant cells, which appeared to be phagocytosing masses of fibrilar material.…”

Lymphocyte proliferation to artery antigen as a positive diagnostic test in polymyalgia rheumatica.

“…It is tempting to suggest that they are present in the internal elastic lamina as there are several studies which suggest that these fibres are initially involved in the disease process, and it has been suggested that it is here that the disease originates (Kimmelstiel, Gilmour, and Hodges, 1952). There is initial swelling and fragmentation, then a surrounding granulomatous reaction (Harrison, 1948;Smith, 1969). Histological changes have been described in temporal arteries in association with advancing age (Kimmelstiel and others, 1952).…”