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FRI0686 Negative associations for fasting blood glucose, cholesterol and triglyceride levels with the development of giant cell arteritis
  1. K Jakobsson1,2,
  2. LT Jacobsson1,3,
  3. AJ Mohammad4,5,
  4. KJ Warrington6,
  5. EL Matteson6,
  6. C Turesson1,2
  1. 1Department of Clinical Sciences, Malmö, Lunds University
  2. 2Department of Rheumatology, Skåne University Hospital, Malmö
  3. 3Department of Rheumatology & Inflammation Research, The Sahlgrenska Academy, University of Gothenburg, Institute of Medicine, Gothenburg
  4. 4Department of Rheumatology, Skåne University Hospital, Lund, Sweden
  5. 5Vasculitis and Lupus Clinic, Addenbrooke's Hospital, Cambridge, United Kingdom
  6. 6Division of Rheumatology, Mayo Clinic College of Medicine and Science, Rochester, Minnesota, United States

Abstract

Background Giant cell arteritis (GCA) is the most common vasculitis among patients age >50 years in north European countries. Although ethnic factors and age clearly play a role, the etiology of the disease is largely unknown. Studies of predictors are therefore of major interest. A meta-analysis of observational studies demonstrated that patients with GCA have a significantly reduced prevalence of diabetes at the time of diagnosis (1).

Objectives To investigate metabolic features prior to diagnosis of GCA in a nested case-control study.

Methods Individuals who developed GCA after inclusion in a population-based health survey (the Malmö Preventive Medicine Project; N=33346) were identified by linking the health survey database to the local patient administrative register and the national patient register. A structured review of medical records was performed. Four controls for every validated case, matched for sex, year of birth and year of screening, were selected from the database. Fasting blood samples had been obtained and analyzed using standard methods as part of the health survey. Potential predictors of GCA were examined in conditional logistic regression models.

Results There were 76 cases with a confirmed clinical diagnosis of GCA (61% female; 65% biopsy positive; 95% fulfilled the ACR criteria for GCA). The mean age at diagnosis was 70 years, and the median time from screening to diagnosis was 20 years (range 2–32). The cases had significantly lower fasting blood glucose (fB-glucose) at baseline screening compared to controls [mean 4.7 vs 5.1 mmol/l, odds ratio (OR) 0.49 per mmol/l; 95% confidence interval (CI) 0.30–0.79]. Current smokers had a reduced risk of GCA (OR 0.35; 95% CI 0.18–0.70). The negative association between baseline fB-glucose and GCA remained significant in analysis adjusted for smoking (OR 0.46 per mmol/l; 95% CI 0.28–0.76). Both cholesterol (mean 5.6 vs 6.0 mmol/l) and triglyceride levels (median 1.0 vs 1.2 mmol/l) were lower among the cases at baseline screening, with significant negative associations with subsequent GCA in crude and smoking-adjusted (ORs with 95% CIs 0.66 per mmol/l; 0.46–0.94 for cholesterol, 0.33 per mmol/l; 0.16–0.69 for triglycerides) models. The effect of fB-glucose on the risk of GCA was stronger in men compared to women (smoking-adjusted ORs per mmol/l 0.11; 95% CI 0.03–0.37, and 0.77; 95% CI 0.50–1.18, respectively). Apart from this, results were similar in women and men.

Conclusions Development of GCA was associated with lower fB-glucose, lower cholesterol and triglyceride levels at baseline, all adjusted for current smoking. These findings are in line with the previous findings of a reduced prevalence of diabetes mellitus at the time of diagnosis of GCA (1). This suggests that metabolic factors influence the development of GCA.

References

  1. Ungprasert P et al Mod Rheumatol. 2016;26(3):410–414.

References

Disclosure of Interest None declared

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