Original language | English (US) |
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Pages (from-to) | 1309-1310 |
Number of pages | 2 |
Journal | British Journal of Dermatology |
Volume | 182 |
Issue number | 5 |
DOIs | |
State | Published - May 1 2020 |
ASJC Scopus subject areas
- Dermatology
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In: British Journal of Dermatology, Vol. 182, No. 5, 01.05.2020, p. 1309-1310.
Research output: Contribution to journal › Letter › peer-review
}
TY - JOUR
T1 - Autoimmune disease development before and after cutaneous lupus erythematosus diagnosis
AU - Shi, K. Y.
AU - Kunzler, E.
AU - Hynan, L. S.
AU - Chong, B. F.
N1 - Funding Information: K.Y. Shi E. Kunzler L.S. Hynan B.F. Chong ben.chong@utsouthwestern.edu University of Texas Southwestern Medical Center Department of Dermatology Dallas TX U.S.A. University of Texas Southwestern Medical Center Department of Population and Data Sciences and Psychiatry Dallas TX U.S.A. National Center for Advancing Translation Sciences of the National Institutes of Health UL1TR001105 National Institute of Arthritis and Musculoskeletal and Skin Diseases K23AR061441 Funding sources: this study was supported, in part, by the National Institute of Arthritis and Musculoskeletal and Skin Diseases of the National Institutes of Health under Award Number K23AR061441; the Rheumatology Research Foundation Career Development R Bridge Funding Award; and by the National Center for Advancing Translation Sciences of the National Institutes of Health under Award Number UL1TR001105. The content is solely the responsibility of the authors and does not necessarily represent the official views of the University of Texas Southwestern Medical Center at Dallas and its affiliated academic and healthcare centres, the National Center for Research Resources and the National Institutes of Health. Conflicts of interest: B.F.C. is an investigator for Daavlin Corporation, Biogen Incorporated, and Pfizer Incorporated, and has received honoraria from Viela Bio as a consultant. We recently reported in a cross‐sectional study that 17·8% of patients with cutaneous lupus erythematosus (CLE) without SLE had coexisting autoimmune disease(s). Thus, we conducted a retrospective cohort study to characterize the timing and prevalence of autoimmune diseases in patients in relation to their CLE diagnosis. We also identified demographic and clinical factors associated with additional autoimmune conditions. Dear Editor , Previous studies showed that patients with systemic lupus erythematosus (SLE) had an increased risk of developing additional autoimmune diseases. All patients had at least one clinic visit with dermatology with ≥ 1 additional visit with either dermatology or rheumatology. Patients who had drug‐induced CLE were excluded. The primary outcome was the presence of ≥1 ‘new‐onset’ (diagnosed > 6 months after CLE diagnosis) or ‘prior‐onset’ (diagnosed prior to ‘new‐onset’) autoimmune disease, as defined by Hayter and Cook. We performed univariate (Mann–Whitney We retrospectively reviewed patient records from February 2006 to March 2018 from the University of Texas Southwestern (UTSW) Medical Center and Parkland Health and Hospital System in Dallas, TX, U.S.A. This study was approved by the UTSW Institutional Review Board. CLE without SLE was diagnosed based on clinicopathological correlation and did not satisfy Systemic Lupus International Collaborating Clinics criteria. U ‐test, χ 2 ‐test or Fisher's exact test), survival (log‐rank test) and logistic regression analyses in SPSS version 25 (IBM, Armonk, NY, U.S.A.) to identify risk factors associated with autoimmune diseases. After 269 patients were screened, 118 patients with CLE without a prior diagnosis of SLE were identified. Thirteen (11·0%) had subacute CLE (SCLE) and 105 (89·0%) had chronic cutaneous lupus, of which 87 cases were discoid lupus. Fifteen (12·7%) patients had 16 prior‐onset autoimmune diseases. The most common were autoimmune thyroid disease ( n = 4; 3·4%) and Sjögren syndrome ( Sjögren syndrome was significantly associated with SCLE ( The median time from CLE diagnosis to new‐onset autoimmune disease was 7·3 years (interquartile range 4·9–15·2). For new‐onset diseases, the time to SLE progression (median 7·9 years) was not significantly different compared with the development of other diseases (median 7·3 years; a). n = 3; 2·5%), the frequencies of which were higher than the reported general population prevalences of 1·4% and 0·01%, respectively. P = 0·03). Other diseases did not have a significant association with CLE subtype. Nineteen (16·1%) patients with CLE had 23 new‐onset diseases, with 14 cases of SLE and three cases of autoimmune thyroid disease. Overall, the constellation of diagnoses was similar to our previous findings. P = 0·93) (Fig. Timing and accumulation of new‐onset autoimmune disease after cutaneous lupus erythematous ( CLE ) diagnosis. (a) Timing distribution of new‐onset autoimmune diagnoses after CLE diagnosis showed that system lupus erythematosus ( SLE ) did not progress differently than other autoimmune diseases. (b) Survival analysis of new‐onset autoimmune disease development in patients with CLE grouped by antinuclear antibody ( ANA ) status ( ANA positive: ≥ 1 : 160 titre, at any time during follow‐up). Patients with CLE with positive ANA showed a greater risk of developing new‐onset autoimmune diseases over time than those with negative ANA . P ‐value was determined by log‐rank test. Based on univariate analyses, at the time of CLE diagnosis, patients with prior‐onset autoimmune disease had more antinuclear antibody (ANA) positivity (60% vs. 13%; Sex, race/ethnicity, smoking status, family history of autoimmunity and CLE subtype were not significant risk factors. Patients with new‐onset disease were more likely to be ANA positive at any point during follow‐up (90% vs. 37%; P < 0·001), defined as ≥ 1 : 160 titre to increase specificity for autoimmunity. P < 0·001). Logistic regression analysis also showed that positive ANA [odds ratio (OR) 10·0; p < 0·0001] was associated with prior‐onset disease. Positive ANA (OR 16·3; P < 0·001) and younger age at the time of CLE diagnosis [OR 1·04 (per 10 year decrease); P = 0·04] were associated with new‐onset disease. Accounting for differential follow‐up time, survival analysis showed that ANA positivity was still associated with the development of a new‐onset autoimmune disease ( b). Notably, 30 of 86 (35%) patients who had an ANA titre < 1 : 160 at CLE diagnosis seroconverted by the end of follow‐up, with 15 of 30 (50%) acquiring new‐onset autoimmune diseases. P = 0·002) (Fig. Compared with a SLE cohort from our institution, patients with CLE acquired a similar number of prior and new‐onset autoimmune diseases (data not shown). Prior‐onset diagnoses in patients with CLE were heterogeneous and aligned with the collection of diseases found in SLE. In contrast, new‐onset autoimmune conditions were predominantly SLE, at rates similar to those found in previous reports. In spite of this, the frequency of all non‐SLE autoimmune diseases in our cohort (21·2%) was still higher than that reported in the general population (4·5%). Finally, ANA positivity was significantly associated with prior‐onset and new‐onset autoimmune diseases. The limitations of this study included its retrospective design, resulting in missing data, and lack of a control group and paediatric patients, who were not seen in our clinics. We found that patients with CLE without SLE had an elevated risk of developing comorbid autoimmune conditions throughout their lifetimes. Rates of secondary autoimmunity in our cohort were similar to those for patients with SLE. Thus, we recommend careful history taking and targeted reviews for symptoms of autoimmune disease (e.g. overt symptoms of thyroid disease and sicca symptoms), especially in patients with CLE and ANA positivity. For patients with CLE and an initially negative ANA, periodic repeat testing may be important in assessing the risk of developing additional autoimmunity. Acknowledgments: we thank Rebecca Vasquez, Andrew Kim, Daniel Grabell, Noelle Teske, Tina Vinoya, Jack O'Brien, Danielle Lin, Jenny Raman and Justin Raman for recruiting patients. We thank Dr Arash Mostaghimi for his critical review of this manuscript, and Rose Cannon for help with the submission of this manuscript. We thank participants of the University of Texas Southwestern CLE Registry for their contributions to lupus research.
PY - 2020/5/1
Y1 - 2020/5/1
UR - http://www.scopus.com/inward/record.url?scp=85076878079&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85076878079&partnerID=8YFLogxK
U2 - 10.1111/bjd.18631
DO - 10.1111/bjd.18631
M3 - Letter
C2 - 31647114
AN - SCOPUS:85076878079
SN - 0007-0963
VL - 182
SP - 1309
EP - 1310
JO - British Journal of Dermatology
JF - British Journal of Dermatology
IS - 5
ER -