Deposition of eosinophil cationic protein in vascular lesions in temporal arteritis

Article Abstract:

Giant cell, or temporal, arteritis is a chronic inflammatory disease of arteries branching from the aorta, chiefly the temporal and occipital arteries supplying the head. The disease is similar or related to polymyalgia rheumatica. The disorder features infiltration by immune and white blood cells; giant cells contain several nuclei and appear to made of several cells. Affected arteries are narrowed by thickening of the wall, and clots may entirely block blood flow. Patchy necrotic (dead cell) lesions also occur. The role of eosinophils, granular white blood cells, in the disorder is unclear, reflecting the lack of study of the function of these cells in inflammatory processes. Two recent studies suggest that the cells may be involved in vascular (blood vessel) injury, possibly due to deposition of two toxic proteins from the cell's granules. Eosinophil cationic protein (ECP) may facilitate the development of clots both by an effect on the development of clots and by inhibiting heparin, an anticoagulant. The role of eosinophils and ECP deposition was evaluated in temporal artery biopsy specimens from 16 patients. Results were compared with those from negative biopsy specimens used as controls. To detect eosinophils and ECP, antibodies to these were used. Stains previously used to routinely detect eosinophils identified fewer eosinophils. Infiltration by eosinophils and ECP deposition was detected in the biopsy specimens. In 12 specimens, eosinophils were detected in the media, the middle of the arterial wall, and in 10 specimens, cells were detected in the intima, the inner arterial wall. ECP deposits were rather dim in areas containing eosinophils, but bright in areas with necrotic lesions and clots. Arteries from patients with atherosclerosis showed no eosinophils or ECP, while in three of five specimens from patients with polymyalgia rheumatica, reactivity for ECP or eosinophils, but not both, was observed. The study suggests that eosinophil infiltration occurs in the vascular damage of temporal arteritis, and ECP deposits are associated with necrosis and clotting in this disorder. Greater understanding of the actual role played by this protein awaits research into its metabolism and regulation. (Consumer Summary produced by Reliance Medical Information, Inc.)

Eosinophils

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Plasma viscosity in giant cell arteritis as a predictor of disease activity

Article Abstract:

Measuring blood plasma viscosity may be useful in monitoring giant cell arteritis (GCA). GCA is a chronic vascular disease that affects the elderly and is characterized by inflammation throughout the body, headache, weakness and fever. It is usually monitored by erythrocyte sedimentation rate (ESR), which is generally elevated in affected patients. Plasma viscosity and ESR were measured in 31 patients with GCA who took successively lower doses of the anti-inflammatory drug prednisolone. Prior to treatment, all patients had increased plasma viscosity and ESR. As treatment progressed, plasma viscosity correlated significantly with ESR. However, in patients with a high risk of a GCA flare-up, the ESR was within the normal range whereas plasma viscosity levels were above normal. Not only does plasma viscosity appear to be a better predictor of flare ups, it is less sensitive than ESR to factors like age, sex and smoking behavior.

Measurement, Blood plasma

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Circulating soluble adhesion molecules in patients with giant cell arteritis. Correlation between soluble intercellular adhesion molecule-1 (sICAM-1) concentrations and disease activity

Article Abstract:

Blood levels of soluble intercellular adhesion molecule-1 (sICAM-1) appear to increase with disease activity in giant cell arteritis and decrease as the disease remits. Cellular adhesion molecules are prominent in conditions in which white blood cells interact with endothelial membranes, such as infection, cancer, and inflammation. Researchers compared cellular adhesion molecule levels in blood samples from 65 patients with giant cell arteritis and 35 healthy people. Soluble ICAM-1 levels were significantly higher in patients with active vascular inflammation, and lower after corticosteroid antiinflammatory treatment, compared to levels in healthy people. Patients in remission had sICAM-1 levels similar to healthy people.

Spain, Cell adhesion molecules

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