Session Information
Session Type: Abstract Submissions (ACR)
Background/Purpose: The influence of smoking on the severity of cutaneous manifestations in adults with moderate to severe SLE was assessed in an ongoing international, multi-center, double-blind, randomized, placebo-controlled study.
Methods: Adult subjects with SLE (n=431; 94.7% female; median disease duration 6.3 years; 59% white; 37% Hispanic; median age 40; mean SLEDAI 2K 11.3) were assessed for mucocutaneous disease activity and smoking history at baseline. Subjects were classified as Current (within 1 year) (n=61) or Past (stopped >1 year)/Never Smokers (n=365). The 426 subjects who had Cutaneous Lupus Activity and Severity Index (CLASI), SLEDAI 2K, and smoking history available at baseline are included in this analysis.
Results: Based on SLEDAI 2K scoring at baseline 79.4%, 67.1%, and 45.2% had an inflammatory rash, alopecia, or mucosal ulcers, respectively, with no significant differences between smokers and non-smokers. Current smokers had significantly higher CLASI scores and were more likely to have moderate or severe rash (CLASI ≥10) (Table 1). There was no significant difference in CLASI scores between Past/Never smokers (7.1±6.6/7.0±6.3 P=0.890).
Table 1. |
|||||
|
Smoking History |
Significance |
|||
Current |
N |
Never/Past |
N |
||
CLASI activity score (mean ± SD) |
13.1±10.6 |
61 |
7.0±6.3 |
365 |
P<0.001† |
CLASI damage (mean ± SD) |
3.7±6.2 |
61 |
2.2±4.5 |
365 |
P=0.087† |
CLASI <10 (%) |
44.3% |
27 |
75.3% |
275 |
P<0.001‡ |
CLASI ≥10 (%) |
55.3% |
34 |
24.7% |
90 |
|
SLEDAI Rash present |
83.6% |
51 |
78.9% |
288 |
NS‡ |
SLEDAI Alopecia present |
73.8% |
45 |
65.8% |
240 |
NS‡ |
SLEDAI Mucosal ulcers present |
44.3% |
27 |
45.5% |
166 |
NS‡ |
†2 sample t-test; ‡Chi-square test |
This observation was consistent across geography, races, ethnicities, and SLE medications at baseline (Table 2). There was no relationship between smoking and cutaneous damage.
Table 2. |
||||||
Smoking |
Never/Past |
Current |
||||
Mean CLASI |
SD |
N |
Mean CLASI |
SD |
N |
|
Race/Ethnicity |
|
|
|
|
|
|
American-Indian |
5.4 |
5.1 |
20 |
NA |
NA |
0 |
Asian |
9.5 |
7.0 |
65 |
NA |
NA |
0 |
Black |
6.5 |
3.7 |
27 |
8.4 |
6.9 |
5 |
Other |
5.0 |
3.6 |
56 |
20.0 |
1.4 |
2 |
White |
6.9 |
6.8 |
197 |
13.3 |
10.9 |
54 |
Hispanic/Latino |
5.5 |
4.4 |
148 |
9.3 |
7.2 |
11 |
Not Hispanic/Latino |
7.9 |
7.2 |
217 |
14.0 |
11.1 |
50 |
Medications |
|
|
|
|
|
|
Antimalarials |
|
|
|
|
|
|
No |
6.9 |
6.3 |
104 |
13.1 |
12.0 |
10 |
Yes |
7.0 |
6.3 |
261 |
13.1 |
10.4 |
51 |
Immunosuppressive |
|
|
|
|
|
|
No |
7.6 |
6.5 |
184 |
11.9 |
10.6 |
33 |
Yes |
6.3 |
6.1 |
181 |
14.5 |
10.6 |
28 |
Corticosteroids |
|
|
|
|
|
|
No |
6.7 |
5.9 |
53 |
11.0 |
9.4 |
10 |
Yes |
7.0 |
6.4 |
312 |
13.5 |
10.8 |
51 |
CLASI: Cutaneous Lupus Activity and Severity Index; SD: standard deviation |
Conclusion: Previous studies have shown that smoking is associated with an increased risk of cutaneous lupus. In agreement with a previous single center study, here we show in a large, multinational and multiethnic cohort that current smoker SLE subjects have higher CLASI activity scores than past or non-smokers. The CLASI seems more sensitive to detect these differences of inflammatory skin involvement in subjects with moderate to severe SLE than the SLEDAI 2K mucocutaneous descriptors (rash, alopecia, mucous ulcers). The lack of difference in the frequency of mucocutaneous manifestations based on SLEDAI 2K between current smokers and past/never smokers is in apparent contrast to published data but is a consequence of the study eligibility criteria enriching for patients with active mucocutaneous disease. The consistency of the relationship between smoking and higher CLASI activity but not chronicity scores in SLE subjects with skin involvement across geographies, races, ethnicities, and SLE medications suggest that smoking may actively worsen skin disease in SLE. As CLASI activity is similar in past smokers and never smokers, smoking cessation should be emphasized in the management of SLE with cutaneous involvement.
Disclosure:
V. P. Werth,
Medimmune,
5,
University of Pennsylvania,
7;
M. A. Khamashta,
MedImmune,
9;
G. G. Illei,
AstraZeneca,
1,
MedImmune,
3;
S. Yoo,
AstraZeneca,
1,
MedImmune,
3;
L. Wang,
AstraZeneca,
1,
MedImmune,
3;
W. Greth,
AstraZeneca,
1,
MedImmune,
3.
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