Low HDL Cholesterol and high risk of autoimmune disease: Two population-based cohort studies including 117341 individuals
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Low HDL Cholesterol and high risk of autoimmune disease : Two population-based cohort studies including 117341 individuals. / Madsen, Christian M.; Varbo, Anette; Nordestgaard, Börge G.
In: Clinical Chemistry, Vol. 65, No. 5, 2019, p. 644-652.Research output: Contribution to journal › Journal article › Research › peer-review
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TY - JOUR
T1 - Low HDL Cholesterol and high risk of autoimmune disease
T2 - Two population-based cohort studies including 117341 individuals
AU - Madsen, Christian M.
AU - Varbo, Anette
AU - Nordestgaard, Börge G.
PY - 2019
Y1 - 2019
N2 - BACKGROUND: HDL is quantitatively the most important lipoprotein in most species and mechanistic evidence points toward a role for HDL in normal immune function. We tested the hypothesis that concentrations of HDL cholesterol are associated with risk of autoimmune disease. METHODS: From 2 studies of the general population-the Copenhagen General Population Study and the Copenhagen City Heart study-we included 107954 and 9387 individuals with baseline measurements of HDL cholesterol. These were followed with the national Danish Patient Registry from baseline in 2003-2015 or 1991-1994 through 2017, during which time 4078 and 1101 individuals developed autoimmune disease in the 2 studies. RESULTS: In the Copenhagen General Population Study, compared to individuals with HDL cholesterol ≥2.0 mmol/L (77 mg/dL), the multifactorially adjusted hazard ratios for any autoimmune disease were 1.06 (95% CI, 0.94-1.19) for individuals with HDL cholesterol of 1.5-1.99 mmol/L (58-77 mg/dL), 1.18 (95% CI, 1.04-1.35) for individuals with HDL cholesterol of 1.0-1.49 mmol/L (39-58 mg/dL), and 1.84 (95% CI, 1.52-2.22) for individuals with HDL cholesterol < 1.0 mmol/L (39 mg/dL) (Pfor trend <0.001). These results were similar when excluding events within 5 years of baseline, in women and men separately, for events at baseline, irrespective of low-grade inflammation or triglyceride concentrations, for the apolipoprotein A1 part of HDL, and for more restrictive end point definitions. Finally, the Copenhagen City Heart Study provided independent confirmation. CONCLUSIONS: Low HDL cholesterol level is associated with high risk of autoimmune disease in individuals from the general population. Our observational findings cannot determine causality.
AB - BACKGROUND: HDL is quantitatively the most important lipoprotein in most species and mechanistic evidence points toward a role for HDL in normal immune function. We tested the hypothesis that concentrations of HDL cholesterol are associated with risk of autoimmune disease. METHODS: From 2 studies of the general population-the Copenhagen General Population Study and the Copenhagen City Heart study-we included 107954 and 9387 individuals with baseline measurements of HDL cholesterol. These were followed with the national Danish Patient Registry from baseline in 2003-2015 or 1991-1994 through 2017, during which time 4078 and 1101 individuals developed autoimmune disease in the 2 studies. RESULTS: In the Copenhagen General Population Study, compared to individuals with HDL cholesterol ≥2.0 mmol/L (77 mg/dL), the multifactorially adjusted hazard ratios for any autoimmune disease were 1.06 (95% CI, 0.94-1.19) for individuals with HDL cholesterol of 1.5-1.99 mmol/L (58-77 mg/dL), 1.18 (95% CI, 1.04-1.35) for individuals with HDL cholesterol of 1.0-1.49 mmol/L (39-58 mg/dL), and 1.84 (95% CI, 1.52-2.22) for individuals with HDL cholesterol < 1.0 mmol/L (39 mg/dL) (Pfor trend <0.001). These results were similar when excluding events within 5 years of baseline, in women and men separately, for events at baseline, irrespective of low-grade inflammation or triglyceride concentrations, for the apolipoprotein A1 part of HDL, and for more restrictive end point definitions. Finally, the Copenhagen City Heart Study provided independent confirmation. CONCLUSIONS: Low HDL cholesterol level is associated with high risk of autoimmune disease in individuals from the general population. Our observational findings cannot determine causality.
U2 - 10.1373/clinchem.2018.299636
DO - 10.1373/clinchem.2018.299636
M3 - Journal article
C2 - 30745290
AN - SCOPUS:85065500696
VL - 65
SP - 644
EP - 652
JO - Clinical Chemistry
JF - Clinical Chemistry
SN - 0009-9147
IS - 5
ER -
ID: 235786481