@article {Jacobsen2148, author = {Soren Jacobsen and Bo Baslund and Hans Ole Madsen and Niels Tvede and Arne Svejgaard and Peter Garred}, title = {Mannose-binding lectin variant alleles and HLA-DR4 alleles are associated with giant cell arteritis.}, volume = {29}, number = {10}, pages = {2148--2153}, year = {2002}, publisher = {The Journal of Rheumatology}, abstract = {OBJECTIVE: To determine whether variant alleles of the mannose-binding lectin (MBL) gene causing low serum concentrations of MBL and/or polymorphisms of HLA-DRB1 are associated with increased susceptibility to polymyalgia rheumatica (PMR) and giant cell arteritis (GCA) or particular clinical phenotypes of PMR/GCA. METHODS: MBL and HLA-DRB1 alleles were determined by polymerase chain reaction in 102 Danish patients with PMR (n = 37) or GCA (n = 65). Two hundred fifty and 193 healthy individuals served as controls for MBL and HLA genotyping, respectively. RESULTS: The prevalence of MBL variant alleles in controls, patients with PMR only, and patients with GCA was 37, 32, and 53\% (p = 0.01), respectively. HLA-DRB1*04 was found in 47\% of patients with PMR only and in 54\% of patients with GCA, which differed significantly from the 35\% found in controls (p = 0.01). HLA-DR4 alleles were not associated with any clinical phenotypes of PMR/GCA, whereas MBL variant alleles were associated with cranial arteritis, high erythrocyte sedimentation rate, and low B-hemoglobin. CONCLUSION: We found MBL variant alleles and HLA-DR4 alleles to be weak susceptibility markers for GCA. In patients with PMR/GCA, MBL variant alleles were associated with signs of increased inflammatory activity and clinical signs of arteritic manifestations. This was not found for HLA-DR4 alleles. These findings indicate that HLA-DR4 and MBL are contributing to the pathophysiology of GCA at different levels in the disease process.}, issn = {0315-162X}, URL = {https://www.jrheum.org/content/29/10/2148}, eprint = {https://www.jrheum.org/content/29/10/2148.full.pdf}, journal = {The Journal of Rheumatology} }