Giant-Cell or Temporal Arteritis: a Review

Harrison, C. V.

doi:10.1136/jcp.1.4.197

Cited by 102 publications

(39 citation statements)

References 26 publications

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“…Therewas evidence of involvement of the carotid system in the optic atrophy which occurred four months before death. The histological appearances of the mesaortitis were identical with giant cell arteritis; the distribution and appearances of lesions in the pulmonary, splenic, and renal muscular arteries were similar to those described in certain instances of this disease (Harrison, 1948;Heptinstall, Porter, and Barkley, 1954;Lander and Bonnin, 1956;Ainsworth and Gresham, 1961). However, neither the involvement of small arteries and arterioles of the heart, spleen, and kidneys, nor the presence of an acute haemolytic process reported here, have been associated with giant cell arteritis.…”

Section: Discussionsupporting

confidence: 70%

Necrotizing arteritis with giant cells associated with haemolytic anaemia

Flanagan¹,

McCracken²,

Jones³

et al. 1965

J Clin Pathol

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SYNOPSIS Necrotizing arteritis with giant cells, involving the aorta, pulmonary and coronary arteries, and coronary, splenic, and renal arterioles was found at necropsy in a 74-year-old male who had died with severe haemolytic anaemia associated with cold haemagglutinins.The clinical and pathological features of this case are shared by well-recognized forms of necrotizing angiitis, in particular giant cell arteritis, but do not conform satisfactorily with any of these disorders. Cold agglutinin haemolytic anaemia in this instance suggests the possibilitv of an autoimmune aetiology.The absence of a completely satisfactory classification of the various forms of necrotizing angiitis reflects the considerable overlap of clinical and pathological features among these conditions. This report of a patient whose features were not typical of any one syndrome gives weight to the concept that the various forms of necrotizing angiitis are a spectrum of vascular disease which includes giant cell arteritis, Wegener's granulomatosis, the ChurgStrauss (1951) syndrome, and polyarteritis nodosa. CASE REPORTA 74-year-old man entered hospital on 20 April 1963, because of jaundice of one day's duration. He had had chronic cough with sputum and exertional dyspnoea for many years. He had experienced gradual loss of vision of the left eye and left parotid swelling four months before admission. The parotid swelling subsided slowly and spontaneously. One month later he had increasing shortness of breath and a right pleural effusion. Thrombophlebitis developed in the right calf a week later. The thrombophlebitis resolved following penicillin, tetracycline, and anticoagulant therapy.When he was admitted, fundal examination showed left optic atrophy. He was severely anaemic (Hb 6-9 g. per 100 ml. to a titre of 1/512 at 4°C., and 1/32 at 20°C.; there was no agglutination at 37°C., but there was a positive direct antiglobulin test at this temperature. There was no Donath-Landsteiner antibody present. Thrombotest (Owren) showed 11-5% coagulation activity. Plasma protein was 5-8 g. per 100 ml. On paper strip plasma protein electrophoresis, there were two haptoglobin bands, an intense band with the beta-globulins and a less intense one with the alpha-globulins.Hyland screening tests for lupus erythematosus, thyroiditis, and rheumatoid arthritis were each negative. Immuno-chemical studies to identify further the cold haemagglutinin were not done nor was it possible to ascertain any blood group specificity.Serum bilirubin was 3-4 mg. per 100 ml.; alkaline phosphatase, 15 King-Armstrong units per 100 ml.; serum glutamic-pyruvic transaminase, 10 Sigma-Frankel units per 100 ml.; urea 51 mg. per 100 ml. Urine analysis was normal.The patient had progressive severe respiratory distress and died 36 hours after admission to hospital. NECROPSYBoth upper lobes of the lungs were studded with emphysematous blebs and cysts. The lower lobes were wet, heavy, and speckled with many small collections of pus. There was 30 ml. of clear pericardial effusion. The myoc...

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Section: Discussionsupporting

confidence: 70%

Necrotizing arteritis with giant cells associated with haemolytic anaemia

Flanagan¹,

McCracken²,

Jones³

et al. 1965

J Clin Pathol

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“…The granulomatous inflammation variant without giant cells has been previously recognized (Crosby & Wadsworth 1948, Harrison 1948, Bevan et al 1968). Many sections should be studied since involvement may be focal around the circumference and segmental along the blood vessel; this latter feature being referred to as the 'skip areas' by Albert, Ruchman & Keltner 1976 and Klein, Campbell, Hunder & Carney…”

Section: Discussionmentioning

confidence: 88%

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

Mambo

1979

Histopathology

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Thirty-two cases of temporal arteritis were reviewed. All patients were adults with a mean age of 69.6 years, and no sex predominance. The erythrocyte sedimentation rate was raised and there was a good response to steroid therapy in the 29 patients who were adequately documented and followed up. Detailed histopathological study of the temporal artery biopsies showed three main histopathological variants; 12 cases (37.5%) had predominantly intimal proliferative changes, four cases (12.5%) had granulomatous inflammation without giant cells and 16 (50%) had granulomatous inflammation with giant cells. The predominantly intimal change variant, consisting of a cellular proliferation of fibroblasts and myointimal cells with little or no changes in the media represent an active pathological process and not a healed disease as has been previously suggested. The internal elastic lamina showed abnormal features in all three morphological variants. The need to recognize this variant, the temporal relationship between these variants and the need to study multiple sections are discussed. Biopsy of clinically normal temporal arteries in patients suspected of having temporal arteritis is recommended as some of these vessels may show disease. No correlation was observed between the clinical picture and the histopathological findings.

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“…The ‘classic' description of a positive temporal artery biopsy has been described as granulomatous inflammation in all layers, primarily centered at the internal elastic lamina, accompanied by intimal hyperplasia and breaks in the internal elastic lamina [4,5,6]. The internal elastic lamina has been suggested as a possible target of the inflammatory reaction [1].…”

Section: Discussionmentioning

confidence: 99%

“…The current literature describes a positive biopsy as revealing chronic granulomatous inflammation - consisting of epithelioid histiocytes, multinucleated giant cells, T lymphocytes, and macrophages - concentrated at the level of the internal elastic lamina [4,5,6]. Intimal hyperplasia and fragmentation of the internal elastic lamina are also frequently seen on histopathology.…”

Section: Introductionmentioning

confidence: 99%

Studies on the Histopathology of Temporal Arteritis

et al. 2016

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Aims: The aim of this paper was to identify the location and to grade the severity of most significant inflammation within positive temporal artery biopsies along with other key clinical and histologic characteristics. Methods: Charts and pathology slides for 70 patients diagnosed with temporal arteritis at the University of Wisconsin (UW) Hospital and Clinics from 1989 to 2015 were reviewed. A subset of 48 specimens was immunostained for CD68 and graded on a scale from 0 to +++; the location of staining was recorded. Results: The most severe granulomatous inflammation was in the media and adventitia in 13% (9/70) of the biopsies; the remaining had uniform full thickness inflammation. Of the slides that were stained with CD68, 94% (45/48) were positive. In 42% (19/45), the stained cells were found mainly in the muscularis and adventitia. Seven percent (3/45) of the slides had staining solely around the internal elastic lamina, and 2% (1/45) had staining limited to the intima. Conclusions: With a few exceptions, granulomatous inflammation in positive temporal artery biopsies is most evident at the media and adventitia or is uniform throughout the layers of the artery. Our study lends support to the theory that the muscularis and adventitia may play an inciting role in the pathogenesis of temporal arteritis.

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Giant-Cell or Temporal Arteritis: a Review

Cited by 102 publications

References 26 publications

Necrotizing arteritis with giant cells associated with haemolytic anaemia

Necrotizing arteritis with giant cells associated with haemolytic anaemia

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

Studies on the Histopathology of Temporal Arteritis

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