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a Department
of Rheumatology, Århus University Hospital, Århus, Denmark, b Department of Internal Medicine, Randers County
Hospital, Randers, Denmark, c Department of Rheumatology, Viborg County
Hospital, Viborg, Denmark, d Department
of Pathology, Århus Community Hospital, Århus, Denmark, e Department of Molecular Preventive
Medicine, School of Medicine, Tokyo University, Japan
Correspondence to: Dr Kristian Stengaard-Pedersen, Department of Rheumatology, Århus University Hospital, DK-8000 Århus C, Denmark Email: stengaard{at}aaa.dk
Accepted for publication 7 March 2000
OBJECTIVE
To examine
the localisation of monocyte chemoattractant protein 1 (MCP-1) in the
inflamed vessel wall in temporal arteritis (TA) and to measure MCP-1 in
plasma both in patients with TA and patients with polymyalgia
rheumatica (PMR).
METHODS
By
immunohistochemical techniques MCP-1 was localised to the vessel wall
in patients with TA. In TA, PMR, and healthy controls MCP-1 was
quantified by enzyme linked immunosorbent assay (ELISA) in plasma.
RESULTS
MCP-1 was
localised to the majority of mononuclear cells, some smooth muscle
cells, and giant cells in the arterial biopsy specimens from 12 patients with histologically verified TA. In all sections, including
the vasa vasorum, the endothelium stained positive. In the intima 73%
(range 57-91%), in the media 49% (range 32-67%), and in the
adventitia 74% (range of 62-91%) of all cells stained positive. In
plasma MCP-1 was significantly raised in untreated TA (n=33) and
untreated PMR (n=27) compared with healthy controls (n=12). Untreated
TA plasma levels of MCP-1 (mean 391 pg/ml (range 82-778 pg/ml)) were
similar to untreated PMR plasma levels (mean 402 pg/ml (range 29-1153
pg/ml)), and no significant difference was found between the two groups
of patients. In both patients with TA and patients with PMR no
correlation was found between the plasma level of MCP-1 and the
erythrocyte sedimentation rate, haemoglobin concentration, and CD4/CD8 ratio.
CONCLUSIONS
These
results show that MCP-1 plays a part in the disease processes of TA and PMR.
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