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Abstract Number: 1241

Glucocorticoid use Is associated with increase in HDL in Rheumatoid Arthritis Patients

Lisa L. Schroeder1, Xiaoqin Tang2, Mary Chester M. Wasko3 and Androniki Bili4, 1Rheumatology, Geisinger Health System, Danville, PA, 2Biostatistics, Geisinger Center for Health Research, Danville, PA, 3West Penn Allegheny Health System, Temple University School of Medicine, Pittsburgh, PA, 4Rheumatology, Geisinger Medical Center, Danville, PA

Meeting: 2012 ACR/ARHP Annual Meeting

Keywords: glucocorticoids, lipids and rheumatoid arthritis (RA)

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Session Information

Title: Rheumatoid Arthritis - Clinical Aspects II: Clinical Features & Comorbidity/Cardiovascular Disease

Session Type: Abstract Submissions (ACR)

 

Glucocorticoid use is associated with increase in HDL in

Rheumatoid Arthritis Patients

Background/Purpose: Atherogenic lipid profiles are common in active RA, with most common being decreased HDL. Glucocorticoids (GC) use is reported to have variable associations with lipid profiles in RA, and the potential differential effect of GC dose on lipid levels is unknown. We sought to evaluate the association of GC dose with lipid changes in RA.

Methods: Patients with RA diagnosed between 1/1/01-11/30/11, receiving oral or intravenous GC and having lipid levels tested prior to and at least 1 year after treatment with ongoing GC were identified. A cohort of RA patients not on GC was constructed for comparison. GC exposure was calculated as a weighted daily dosage in prednisone equivalents. GC exposure was analyzed as a continuous and as a dichotomous <7.5mg/day (low) vs. ≥7.5mg/day (high) GC dose. Primary outcome was change in HDL in the low vs. high GC groups. Secondary outcomes were changes in LDL, total cholesterol (TC), triglycerides (TG) and TC/HDL in the same fashion. A similar analysis between the patients on GC vs. not on GC was performed. Linear regression models were used to calculate the outcome, adjusting for age, gender, body mass index (BMI), diabetes, HTN, hyperlipidemia, RF, ESR, statin, NSAID, methotrexate (MTX), hydroxychloroquine (HCQ) and TNF-α inhibitor use.

Results: 202 patients on GC and 463 patients not on GC were included. Baseline characteristics are shown in Table 1. The changes in lipid levels according to GC use are shown in Table 2. Any GC and high dose GC use were associated with increased HDL, but no other significant lipid changes, compared to non-GC users. There were no significant differences in HDL or other lipids between the low vs. high GC groups. Sensitivity analysis, excluding patients on statins, showed similar results.

Conclusion: In this RA cohort, any GC and high dose GC (median 10.4 mg/day) use were associated with increased HDL, whereas low dose was not. Although our results need to be replicated in other RA cohorts, these findings are reassuring in this patient population at high risk for cardiovascular disease.

Table 1. Baseline patient characteristics

 

Patients on GC

No GC

 

 

All

N=202

GC <7.5

N=87

GC ≥7.5

N=115

N=463

GC dose * (median)

8.4 (5.6-11.1)

5.2 (5.0-6.2)

10.4 (9.3-14.5)

 

Age (mean ± SD years)

64.7 (11.7)

64.5 (11.2)

64.8 (12.1)

62.8 (11.4)

Female

137 (67.8)

61 (70.1)

76 (66.1)

293 (67.2)

BMI

30.6 (6.5)

N=166

30.4 (6.5)

N=66

30.7 (6.6)

N=100

30.5 (6.2)

N=358

ESR

35.6 (24.8)

N=154

30.8 (22.5)

N=60

38.6 (25.9)

N=94

34.2 (24.5)

N=313

RF

124 (61.4)

41 (47.1)

83 (72.2)

254 (58.3)

Diabetes

88 (43.6)

39 (44.8)

49 (42.6)

161 (36.9)

HTN

136 (67.3)

59 (67.8)

77 (67.0)

302 (69.3)

Hyperlipidemia*

141 (69.8)

53 (60.9)

88 (76.5)

316 (72.5)

HCQ use

42 (20.8)

20 (23.0)

22 (19.1)

106 (24.3)

NSAID use

96 (47.5)

41 (47.1)

55 (47.8)

196 (45.0)

Statin use

74 (36.6)

29 (33.3)

45 (39.1)

163 (37.4)

Anti-TNF use

23 11.4)

10 (11.5)

13 (11.3)

47 (10.8)

MTX use

107 (53.0)

49 (56.3)

58 (50.4)

184 (42.2)

Table 2. Change in lipids according to GC use[1]

 

Any GC

GC <7.5

GC ≥ 7.5

No GC

Pre-treatment HDL

52.4 (15.8)

55.4 (16.0)

50.1 (15.4)

52.2 (15.3)

Highest post-treatment HDL

58.1 (16.6)

60.1 (15.6)

56.5 (17.2)

55.4 (16.0)

Change in HDL

5.7 (11.6)*

4.7 (12.1)

6.5 (11.3)*

3.2 (10.5)*

Pre-treatment TC

191 (43)

197 (34)

187 (48)

194 (43)

Lowest post-treatment TC

189 (41)

193 (36)

186 (45)

186 (41)

Change in TC

2.4 (36.5)

3.6 (3.9)

1.5 (40.3)

7.8 (37.7)

Pre-treatment TC/HDL

3.9 (1.2)

3.8 (1.2)

4.0 (1.2)

4.0 (1.2)

Lowest post-treatment TC/HDL

3.5 (1.0)

3.4 (1.0)

3.5 (1.1)

3.6 (1.2)

Change in TC/HDL

0.39 (0.91)

0.37 (0.94)

0.40 (0.89)

0.35 (0.93)

Pre-treatment LDL

106 (35)

110 (33)

103 (36)

110 (35)

Lowest post-treatment LDL

96 (33)

103 (30)

97 (34)

100 (33)

Change in LDL

6.4 (32.3)

6.9 (28.5)

6.0 (34.8)

9.9 (32.6)

Pre-treatment TG

160 (113)

151 (84.1)

167 (130)

157 (90)

Lowest post-treatment TG

149 (81)

147 (81)

152 (82)

149 (83)

Change in TG

11.1 (90.3)

4.3 (78.4)

16.2 (98.3)

7.8 (68.4)

*Statistically significant findings p-value<0.05:

GC vs. No GC: change in HDL: p=0.006

High GC dose vs. No GC: change in HDL: p=0.012

[1]Adjusted for age, gender, BMI, ESR, RF, DM, HTN, hyperlipidemia, and use of TNF-α inhibitors, MTX, statins, HCQ, and NSAIDs

 



 



Disclosure:

L. L. Schroeder,
None;

X. Tang,
None;

M. C. M. Wasko,
None;

A. Bili,
None.

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