Patients with higher apolipoprotein A-I levels at greater risk for giant cell arteritis
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Key takeaways:
- Apolipoprotein A-I levels were significantly associated with the development of subsequent giant cell arteritis.
- Metabolic profiles associated with lower cardiovascular risk may increase the risk for GCA.
Patients who eventually developed giant cell arteritis demonstrated significantly higher levels of apolipoprotein A-I at baseline, according to population-based data published in Arthritis Research & Therapy.
“Previous work from our group indicated that obesity and diabetes were associated with a reduced risk for giant cell arteritis, and that there was also an inverse relation with total cholesterol,” Carl Turesson, MD, PhD, of Lund University and Skåne University Hospital, in Malmö, Sweden, told Healio. “However, the relation between apolipoproteins and development of GCA has not been investigated.”
![A quote from Carl Turesson, MD, PhD, saying, "[These findings] underlie the healthy metabolic profile that characterizes individuals who develop GCA."](/~/media/slack-news/rheumatology/misc/infographics/2024/rh0224wadstrom_graphic_01.jpg?w=800)
To examine the link between apolipoprotein levels and subsequent GCA development, Turesson and colleagues conducted a nested case-control study of data from the population-based Malmö Diet Cancer Study. By linking study data to medical registries, the researchers matched each patients who developed GCA after inclusion to four control individuals randomly selected from the cohort. Logistic regression models were used to compare the groups and reveal potential predictors of GCA.
The analysis included 30,447 residents (average age, 58 years; 60.2% women) of Malmö, Sweden, 100 of whom developed GCA after their initial screening — which was between 1991 and 1996 — and before Dec. 31, 2011. Serum concentrations of apolipoprotein A-I and apolipoprotein B were collected at baseline from non-fasting blood samples.
According to the researchers, patients who later developed GCA had significantly higher apolipoprotein A-I at baseline vs. controls, with a mean level of 168.7 mg/dL vs. 160.9 mg/dL (OR = 1.57; 95% CI, 1.18-2.1). This association was still significant after adjusting for BMI and physical activity (OR = 1.48; 95% CI, 1.09-1.99), the researchers added. Compared with controls, those who developed GCA demonstrated similar levels of apolipoprotein B, at a mean of 109.3 mg/dL vs. 110.4 mg/dL (OR = 0.99; 95% CI, 0.74-1.32).
One limitation of the study was that apolipoprotein levels were only assessed at one point in time. Also, the “limited” number of men in the study — 19 among GCA cases and 76 of the matched controls — means their results should be interpreted with caution, Turesson and colleagues wrote.
“These findings may be helpful for understanding the pathogenesis of GCA and for further research on novel treatments and diagnostics,” Turesson said. “They also underline the healthy metabolic profile that characterizes individuals who develop GCA. This is encouraging, as it tells us that efforts to prevent unfavorable metabolic effects of glucocorticosteroids in such patients are done from a good starting point.”
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