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Updated: Jun 7, 2026

An Immunohistopathologic Study to Profile the Folate Receptor Beta Macrophage and Vascular Immune Microenvironment in Giant Cell Arteritis
Published on: February 8, 2019
Adherence to dietary recommendations and the risk of developing giant cell arteritis: A nested Case-Control study
P Kwanyuen1, K Wadström2, E Sonestedt3
1Rheumatology, Department of Clinical Sciences, Malmö, Lund University, Malmö, Sweden.
Objectives:
To investigate the relation between adherence to dietary recommendations, the quantified intake of the components of these recommendations, and the risk of developing giant cell arteritis (GCA).
Methods:
Participants in the Malmö Diet and Cancer Study cohort who subsequently developed GCA were identified through register linkage and validated in a structured review. Four controls, matched for age, sex, and year of inclusion, were selected per case. Diet quality was assessed using the Swedish Dietary Guidelines Score (SDGS, range 0-5). The relations for the SDGS, adherence to recommendations for each component and total intake of each component with development of GCA were assessed using logistic regression, adjusted for total energy intake, leisure-time physical activity and alcohol intake. Potential misreporters of total energy intake were excluded.
Results:
There were 193 incident cases of GCA. High adherence to dietary guidelines (SDGS 4-5 vs 0-1) was associated with subsequent development of GCA (adjusted odds ratio 2.70; 95% CI 1.43-5.10). In adjusted models, adherence to recommended intake of added sugar, fish and shellfish and vegetables and fruit was associated with an increased risk of GCA. A reduced risk was seen with higher quantified consumption of added sugar, and an increased risk with higher intakes of fiber and fish and shellfish.
Conclusions:
An overall high diet quality was independently associated with an increased risk of GCA. This is compatible with the concept of an increased risk of GCA in subjects with a healthy metabolic profile, and of metabolic regulation of early disease mechanisms in GCA.
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