Abstract
Objective:
To identify demographic and clinical characteristics associated with time between psoriasis and psoriatic arthritis (PsA).
Methods:
A retrospective, population-based cohort of incident PsA patients ≥18 years (2000–17) from Olmsted County, MN was identified. PsA patients were divided into two groups: patients with concurrent psoriasis and PsA (within 1 year), and patients with psoriasis before PsA (>1 year). Patients with PsA prior to psoriasis were excluded. Age- and sex-adjusted logistic regression models were used to examine factors associated with the time between psoriasis and PsA diagnosis.
Results:
Among 164 patients with incident PsA, 158 had a current or personal history of psoriasis. The mean (SD) age at PsA diagnosis was 46.3 (12.0) years, and 46% were females. The median (interquartile range) time from psoriasis to PsA was 35.5 (0.8–153.4) months. 64 patients (41%) patients had concurrent psoriasis and PsA while 94 (59%) had onset of psoriasis before PsA. The estimated age at onset of psoriasis symptom (OR per 10-year decrease = 1.63, 95% CI: 1.26–2.11) and psoriasis severity (OR = 3.65, 95% CI: 1.18–11.32 for severe vs. mild) were associated with having a psoriasis diagnosis more than one year prior to incident PsA.
Conclusion:
In this population-based study, approximately 60% of the patients had psoriasis before PsA, and the rest had concurrent psoriasis and PsA. Patients with lower age at psoriasis onset or severe psoriasis were more likely to have a longer time to transition from psoriasis to PsA.
Keywords: Psoriatic arthritis, spondyloarthritis, transition
INTRODUCTION
Psoriatic arthritis (PsA) is a heterogeneous disease that may precede, occur concurrently, or occur after the development of psoriasis. The spectrum of disease from psoriasis to PsA offers an opportunity to study the important pathways leading to synovio-entheseal inflammation. Psoriasis precedes psoriatic arthritis more commonly and up to 30% of patients with psoriasis eventually develop inflammatory synovio-entheseal (SE) inflammation (1). This usual sequence represents an opportunity to identify PsA earlier in the disease course (2). A preclinical state, in which synovial inflammation has begun but has not yet become clinically recognized, has been fairly well described in rheumatoid arthritis (RA) and is an emerging area of research in PsA (3,4). In PsA, psoriasis acts as a convenient visual biomarker of future SE inflammation. Why this preclinical phase is prolonged in some and very brief in others is unclear. Genetic factors such as HLA antigen subtypes may be one explanation. While HLA-C*06 antigen is associated with a longer latency period, HLA-B*27 is associated with an increased risk of early progression from psoriasis to overt PsA (5–8). However, some studies show that the time to transition from psoriasis to PsA is not fully explained by genetic factors alone (9). Therefore, clinical, environmental, and immunological changes might play important roles. Our study aimed to identify demographic and clinical characteristics associated with a longer time from psoriasis to PsA compared to diagnosis around the same period of time.
METHODS
Study design and data source.
A retrospective nested case-control study using the resources of the Rochester Epidemiology Project (REP) was performed. The population of Olmsted County, Minnesota, in which resides the city of Rochester, is well suited for investigation of the epidemiology of PsA, as comprehensive medical records for all residents seeking medical care for over five decades are available. The availability of long-term longitudinal data in the REP provides a unique opportunity to study the natural history of psoriatic disease. A record linkage system allows ready access to the medical records from all health care providers for the local population, including the Mayo Clinic, the Olmsted Medical Center and affiliated hospitals, local nursing homes, and the few private practitioners (10,11). This system ensures virtually complete ascertainment of all clinically recognized cases of PsA among the residents of Olmsted County, Minnesota. The population of Olmsted County in 2010 was 144,248 with 74.7% being adults of age ≥18 years. Patients who denied authorization to use their medical records for research were excluded. The study was approved by the Mayo Clinic (18-010851) and Olmsted Medical Center (051-OMC-18) institutional review boards.
Patient population and case ascertainment.
PsA cases were defined as patients fulfilling ClASsification of Psoriatic ARthritis (CASPAR) criteria for PsA (sensitivity of 91.4% and a specificity of 98.7%) (12). ICD-9/10 diagnostic codes for arthralgia, arthritis, monoarthritis, oligoarthritis, polyarthritis, spondylitis, ankylosing spondylitis, arthropathy, psoriatic arthropathy, spondyloarthropathy, and seronegative spondyloarthropathy were used to screen for patients with PsA. Medical record abstraction of all potential cases was performed by PK to ascertain fulfillment of the CASPAR criteria. Olmsted County residents ≥18 years of age fulfilling CASPAR criteria between January 1, 2000 to December 31, 2017, were included in the incidence PsA cohort. Details of the case ascertainment have been described previously (13).
Comparisons.
The date of fulfillment of CASPAR criteria was considered as the time of onset of PsA. Onset of psoriasis was defined as the date of confirmatory diagnosis of psoriasis by a physician (primary care physician, dermatologist, or rheumatologist). If psoriasis was questionable with alternative diagnoses noted, these cases were labeled as not having psoriasis. Probable cases were reviewed by a dermatologist to ascertain case status. PsA patients were divided into two groups: 1) patients with concurrent psoriasis and PsA diagnosis (within one year of each other), and 2) patients with psoriasis onset before PsA (>1 year). Patients with psoriasis development after PsA onset (>1 year) or only a family history of psoriasis were excluded.
Covariates of interest.
Complete medical records from all healthcare providers were identified and reviewed for each patient using a standardized, pre-tested data abstraction form using the Research Electronic Data Capture (REDCap) system for consistency. Information regarding demographics, clinical characteristics, laboratory data, and radiographic features was collected. Symptom onset was defined as first psoriasis eruption and PsA-related musculoskeletal symptom (not explained by other diagnoses) respectively as documented by a clinician in the medical records. Severity of psoriasis was defined based on the body surface area involved, sites involved, and requirement for phototherapy or systemic therapy as documented in the medical records.
Statistical analysis.
Descriptive statistics (medians, percentages, etc.) were used to summarize the data. Chi-square, Fisher’s exact, and rank-sum tests were used to compare characteristics between groups. Logistic regression models adjusted for age and sex were performed to identify factors associated with longer time to development of PsA (>1 year). Trends in time from psoriasis onset to PsA were examined using linear regression models adjusted for age and sex with and without log transformation of the delay to address skewness. Model diagnostics were examined. Analyses were performed using SAS version 9.4 (SAS Institute, Cary, NC) and R 3.6.2 (R Foundation for Statistical Computing, Vienna, Austria).
RESULTS
A total of 164 patients with incident PsA were identified between January 1, 2000 and December 31, 2017. Six patients who had psoriasis onset after PsA (>1 year) or who only had a family history of psoriasis were excluded. The remaining 158 cases with incident PsA were included in the study population. The mean (SD) age was 46.3 (12.0) years at diagnosis, and 46% were females.
Among the 158 total patients, 64 (41%) had concurrent psoriasis and PsA, and 94 (59%) had onset of psoriasis before PsA (Figure 1). The median time from psoriasis diagnosis to PsA incidence was 35.5 (interquartile range: 0.8–153.4) months while the median estimated time from onset of first psoriasis eruption to onset of inflammatory joint pain was 2 (interquartile range: 0–15) years. Among those patients who had psoriasis before PsA, the median time from psoriasis diagnosis to PsA incidence was 118.5 (interquartile range: 47.0–224.6) months (Table 1). The time from the onset of psoriasis to PsA increased by 3% per year between 2000 to 2017 in the subgroup of patients with psoriasis occurring before PsA, but this trend did not reach statistical significance (p=0.09).
Figure 1.
Delay between onset of psoriasis (PSO) and fulfillment of CASPAR criteria for psoriatic arthritis (PsA) in months, according to the date of PsA incidence with a smoother line for trend.
Table 1.
Baseline characteristics of patient groups with concurrent psoriasis and psoriatic arthritis (PsA) and psoriasis before PsA
| Concurrent psoriasis and PsA (N=64) | Psoriasis before PsA (N=94) | Total (N=158) | p value | |
|---|---|---|---|---|
| Months from PsO to PsA, median (IQR) | 0 (0, 2.8) | 118.5 (47.0, 224.6) | 35.5 (0.8, 153.4) | -- |
| Estimated years from first psoriasis eruption to psoriasis diagnosis, median (IQR) | 1 (0, 4) | 1 (0, 7) | 1 (0, 6) | 0.84 |
| Estimated years from first psoriasis symptom onset to PsA symptom onset, median (IQR) | 0 (−2, 2) | 10 (1, 19) | 2 (0, 15) | <0.001 |
| Age at PsA incidence (years), mean (SD) | 43.7 (11.2) | 48.1 (12.3) | 46.3 (12. 0) | 0.029 |
| Sex, female | 28 (44%) | 44 (47%) | 72 (46%) | 0.70 |
| Education Level | 0.073 | |||
| High school or less | 14 (22%) | 18 (19%) | 32 (20%) | |
| Some college or 2yr degree | 17 (27%) | 42 (45%) | 59 (38%) | |
| ≥4yr college degree | 32 (51%) | 34 (36%) | 66 (42%) | |
| Missing | 1 | 0 | 1 | |
| Race | 0.65 | |||
| Black | 2 (3%) | 2 (2%) | 4 (3%) | |
| Asian | 2 (3%) | 6 (6%) | 8 (5%) | |
| Hispanic | 4 (6%) | 5 (5%) | 9 (6%) | |
| Other/Mixed | 1 (2%) | 0 (0%) | 1 (1%) | |
| White | 54 (86%) | 81 (86%) | 135 (86%) | |
| Unknown | 1 | 0 | 1 | |
| BMI (kg/m 2 ) at PsA diagnosis, mean (SD) | 30.1 (6.2) | 31.5 (7.7) | 31.0 (7.1) | 0.41 |
| Missing | 1 | 2 | 3 | |
| Smoking at psoriasis diagnosis | 0.66 | |||
| Current smoker | 12 (19%) | 23 (24%) | 35 (22%) | |
| Former smoker | 19 (30%) | 28 (30%) | 47 (30%) | |
| Never smoker | 33 (52%) | 43 (46%) | 76 (48%) | |
| Smoking at PsA dx | 0.39 | |||
| Current smoker | 12 (19%) | 15 (16%) | 27 (17%) | |
| Former smoker | 19 (30%) | 38 (40%) | 57 (36%) | |
| Never smoker | 33 (52%) | 41 (44%) | 74 (47%) | |
| Alcohol intake at psoriasis diagnosis | 53 (83%) | 68 (72%) | 121 (77%) | 0.13 |
| Alcohol intake at PsA diagnosis | 51 (80%) | 68 (72%) | 119 (75 %) | 0.29 |
| Family history of psoriasis | 19 (37%) | 37 (49%) | 56 (44%) | 0.20 |
| Missing | 13 | 18 | 31 | |
| Estimated Age at onset of first psoriasis symptom (years), mean (SD) | 39 (12) | 30 (14) | 34 (14) | <0.001 |
| Psoriasis 1st diagnosis by: | <0.001 | |||
| Dermatology | 25 (39%) | 60 (64%) | 85 (54%) | |
| Rheumatology | 22 (34%) | 1 (1%) | 23 (15%) | |
| PCP | 17 (27%) | 32 (34%) | 49 (31%) | |
| Other | 0 (0%) | 1 (1%) | 1 (1%) | |
| Psoriasis Seriousness at 1st diagnosis | 0.051 | |||
| Mild (< 2% BSA) | 33 (52%) | 33 (35%) | 66 (42%) | |
| Moderate (2–10% BSA) | 26 (41%) | 42 (45%) | 68 (43%) | |
| Severe (>10% BSA) | 5 (8%) | 18 (19%) | 23 (15%) | |
| No Documentation | 0 | 1 | 1 | |
| Type of psoriasis at first dx | 0.12 | |||
| Chronic plaque psoriasis | 49 (78%) | 85 (90%) | 134 (85%) | |
| Guttate psoriasis | 3 (5%) | 2 (2%) | 5 (3%) | |
| Pustular psoriasis- Generalized | 1 (2%) | 0 (0%) | 1 (1%) | |
| Pustular psoriasis- palms/soles | 3 (5%) | 3 (3%) | 6 (4%) | |
| Sebo-psoriasis | 3 (5%) | 2 (2%) | 5 (3%) | |
| Chronic plaque psoriasis & Guttate psoriasis | 0 (0%) | 1 (1%) | 1 (1%) | |
| Chronic plaque & Pustular psoriasis-palms/soles | 0 (0%) | 1 (1%) | 1 (1%) | |
| Chronic plaque & Sebo-psoriasis | 4 (6%) | 0 (0%) | 4 (3%) | |
| No Documentation | 1 | 0 | 1 | |
| Site of psoriatic lesions at first diagnosis of psor iasis | 0.33 | |||
| Palms and/or soles | 1 (4%) | 3 (10%) | 4 (7%) | |
| Elbows and/or knees | 2 (9%) | 8 (26%) | 10 (19%) | |
| Limbs arms and/or legs | 8 (35%) | 4 (13%) | 12 (22%) | |
| Trunk | 1 (4%) | 1 (3%) | 2 (4%) | |
| Face | 1 (4%) | 0 (0%) | 1 (2%) | |
| Scalp | 7 (30%) | 13 (42%) | 20 (37%) | |
| Intergluteal/perianal | 2 (9%) | 1 (3%) | 3 (6%) | |
| Genital | 1 (4%) | 1 (3%) | 2 (4%) | |
| Missing | 41 | 63 | 104 | |
| Nail involvement at first diagnosis of psoriasis | 23 (43%) | 25 (37%) | 48 (39%) | 0.51 |
| No Documentation/Missing | 10 | 26 | 36 | |
| Family history of PsA | 4 (10%) | 7 (11%) | 11 (11%) | 0.77 |
| Missing | 22 | 32 | 54 | |
| Enthesitis prior to PsA | 17 (27%) | 31 (33%) | 48 (30%) | 0.39 |
| Dactylitis prior to PsA | 30 (47%) | 36 (38%) | 66 (42%) | 0.28 |
| Inflammatory back pain prior to PsA | 6 (9%) | 11 (12%) | 17 (11%) | 0.64 |
| Uveitis | 3 (5%) | 4 (4%) | 7 (4%) | 0.90 |
| Inflammatory bowel disease | 0 (0%) | 1 (1%) | 1 (1%) | 0.41 |
| Rheumatoid factor positive | 2 (3%) | 4 (5%) | 6 (4%) | 0.64 |
| Not done | 5 | 14 | 19 | |
| ESR (mm/hr) at psoriasis diagnosis, mean (SD) | 15.3 (11.5) | 19.8 (18.9) | 17.3 (15. 2) | 0.78 |
| Missing | 40 | 75 | 115 | |
| CRP (mg/L) at psoriasis diagnosis, mean (SD) | 12.2 (16.8) | 10.5 (11.6) | 11.6 (14. 9) | 0.58 |
| Missing | 41 | 80 | 121 | |
| ESR (mm/hr) at PsA diagnosis, mean (SD) | 18.5 (15.3) | 19.1 (18.0) | 18.8 (16. 9) | 0.87 |
| Missing | 9 | 11 | 20 | |
| CRP (mg/L) at PsA diagnosis, mean (SD) | 12.1 (14.1) | 17.9 (32.2) | 15.5 (26. 4) | 0.99 |
| Missing | 20 | 31 | 51 | |
| Radiographic damage | 14 (22%) | 32 (34%) | 46 (29%) | 0.11 |
| Missing | 1 | 0 | 1 |
There was no statistically significant difference between the two groups in terms of demographic features such as sex, race, body mass index, smoking, educational level, or alcohol status. Similarly, no significant differences were observed in family history or PsA-related (enthesitis, dactylitis, uveitis, and inflammatory back pain) factors, laboratory characteristics (rheumatoid factor positivity, high inflammatory markers), or radiographic outcomes between the two groups.
The estimated age at onset of first psoriasis symptom (odds ratio [OR] per 10 year decrease = 1.63, 95% CI: 1.26–2.11), type of psoriasis as chronic plaque psoriasis (OR = 3.14, 95% CI: 1.07 – 9.19), and psoriasis severity (compared to mild, OR = 1.69, 95% CI: 0.84 – 3.40 for moderate and OR = 3.65, 95% CI: 1.18 –11.32 for severe) were more likely in those who had a psoriasis diagnosis more than one year prior to PsA incidence compared to those who had a concurrent diagnosis (Table 2).
Table 2.
Logistic models for psoriasis before psoriatic arthritis adjusted for age at psoriatic arthritis and sex
| Clinical features | Odds Ratio (95% Confidence Interval) |
|---|---|
| Estimated age at onset of 1st psoriasis eruption (per 10 yr decrease)* | 1.63 (1.26–2.11) |
| Education level (reference: high school or less) | |
| Some college or 2yr degree | 2.19 (0.86–5.54) |
| ≥4yr college degree | 0.87 (0.36–2.09) |
| Family history of psoriasis | 1.84 (0.85–3.95) |
| Severity of psoriasis (reference: mild) | |
| Moderate | 1.69 (0.84, 3.40) |
| Severe | 3.65 (1.18, 11.32) |
| Type of psoriasis (Chronic plaque psoriasis) | 3.14 (1.07–9.19) |
| Nail involvement at psoriasis diagnosis | 0.85 (0.40–1.80) |
| Radiographic damage | 1.78 (0.83–3.79) |
Adjusted for sex only
DISCUSSION
In this population-based study, approximately 60% of the patients had psoriasis onset before PsA, and the rest had concurrent psoriasis and PsA. Patients of younger age at first psoriasis symptom or those with severe psoriasis were more likely to have a longer time from the onset of psoriasis to PsA.
There are only a few studies specifically examining the time to transition from psoriasis to PsA and our study provides data from a population-based cohort in the US, which is currently lacking. Tillett et. al reported data on psoriasis to PsA interval from two separate cohorts, namely Clinical Practice Research Datalink (CPRD) and Royal National Hospital for Rheumatic Diseases, Bath PsA cohort (14). Our study showed a slightly lower percentage of PsA patients who had psoriasis before PsA compared to their data from the CPRD and Bath cohort (60 vs. 88.7% and 72% excluding the group with PsA occurring first). The median interval between psoriasis to PsA among patients with psoriasis before PsA in our study was similar to what was seen in the CPRD (9.88 vs. 9) but slightly lower than what was described for the Bath cohort (9.88 vs.13 years). Similarly, a study from the PsART-international web-based registry (Turkey, Italy, and Canada) examining factors associated with time from psoriasis to PsA showed that age at psoriasis onset and family history of psoriasis were associated with psoriasis occurring before PsA similar to our study results (15). In that study, plaque psoriasis and nail involvement were associated with a longer interval between psoriasis and PsA. Severity of psoriasis was not reported in the PsART study, but our study found this to be one of the significant predictors of longer time to transition from psoriasis to PsA. Our study did not find any significant association with plaque psoriasis and time to PsA transition. Nail involvement was found to be negatively associated with a longer time to transition, but this association did not reach statistical significance. This makes sense clinically because nail involvement is one of the strongest predictors of PsA in patients with psoriasis (2,16).
The reason for heterogeneity in the latency period between psoriasis and PsA is unclear. Genetic studies have examined the association of HLA genes with the time to PsA transition. Two genetic variants are of specific interest: HLA-C*06 has been associated with early-onset skin disease in both psoriasis and PsA, and HLA-B*27 with earlier PsA onset (7). However, the clinical-phenotypic variability in the latency of PsA is not fully explained by differences in the status of these two genes; additional clinical and environmental factors likely play a role (2,9). While our study did not examine genetic information, a role for these genes in the two subgroups is possible. Alternatively, it is possible that a longer latency between psoriasis and PsA is simply related to a detection bias; i.e., a longer interval between psoriasis and PsA can be explained by an earlier diagnosis of psoriasis in patients with severe psoriasis. Patients with mild psoriasis might not seek medical care or be formally diagnosed with psoriasis.
Similarly, our study noted an increase in the time interval between the onset of psoriasis and PsA from 2000 to 2017 although not statistically significant. While the low number of patients in our study makes this difficult to interpret, the results could be associated with improved management of psoriasis in recent years. As the data are highly skewed, further evaluation in larger longitudinal PsA cohorts will be necessary to verify our findings.
Our study results have strong implications in psoriatic disease research, especially in the study of prevention of PsA in patients with psoriasis. Studies are being conducted to examine whether early, aggressive treatment of psoriasis patients could halt or stop progression to PsA. However, in our population-based study, approximately 40% of the patients developed PsA concurrently with psoriasis; such a trial would not be relevant in this subgroup with concurrent PsA. Patients enrolled in such trials would be the group with psoriasis with a latency period. Moreover, retrospective studies examining the transition to PsA might provide spurious results if the codes for PsA are entered later but treatment is tailored to the patient with psoriasis and PsA. Similarly, patients who are destined to have PsA within a year might not have enough medication exposure to evaluate the effect. Additionally, spurious conclusions about the transition to PsA may be drawn from considering only one subgroup of patients (i.e., collider bias). Natural history studies such as this one may help to better understand the similarities and differences between these two subgroups (i.e., PsA at the same time as psoriasis or psoriasis first then PsA).
The strengths of our study include the unique record linkage system of the REP, allowing near-complete ascertainment of all clinically recognizable PsA cases in a well-defined population. Furthermore, case ascertainment was done using the validated CASPAR criteria. Unlike administrative coding in most studies, all variables were collected via manual review of the paper and electronic records.
Our study also has several limitations. First, patients with mild psoriasis or PsA may have never presented to the physician or rheumatologist respectively, which may have resulted in an underestimation of psoriasis and PsA cases (17). While PsA cases not fulfilling CASPAR criteria may have been missed, the sensitivity and specificity of the CASPAR criteria were close to 99% when adapted for retrospective use to identify PsA cohort (18). Next, PsA patients with a very long latency period might have been missed. Only symptoms noted in the medical records would be ascertained, and the precision or accuracy of exact symptom onset is uncertain. However, due to the extended study period and availability of near-complete medical history in this population, we believe the vast majority of PsA cases were correctly ascertained. Third, being a retrospective study, detailed documentation of all clinical characteristics may not have been available. To minimize detection bias, data abstraction was done by study investigators using a standardized data abstraction form. Similarly, the population of Olmsted County, Minnesota is predominantly a white population (90%), which may limit the generalizability of study results to other racial or ethnic groups. Lastly, our PsA cohort is not associated with biological samples or genomic data and future studies should examine immunologic and genetic differences between those who have concurrent psoriasis and PsA, and those with psoriasis developing before PsA.
In conclusion, two distinct clinical phenotypes in terms of the time to transition from the onset of psoriasis to PsA were described in our study. Patients with earlier age at psoriasis onset or severe psoriasis were more likely to have a delay in the transition from psoriasis to PsA. This classification might have important implications for epidemiological studies on the natural history of psoriatic disease, and the characteristics related to delay may provide targets for PsA prevention in future studies.
Financial support:
This study was made possible using the resources of the Rochester Epidemiology Project, which is supported by the National Institute on Aging of the National Institutes of Health under Award Number R01AG034676, and Grant Number UL1 TR002377 from the National Center for Advancing Translational Sciences (NCATS), a component of the National Institutes of Health. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health. Paras Karmacharya is supported by T32 AR56950 (7/2020- 6/2021) and T32AR059039 (7/2021-) grants from the National Institute of Arthritis and Musculoskeletal and Skin Diseases, Spondyloarthritis Research and Treatment Network (SPARTAN) fellowship pilot grant, and Group for Research and Assessment of Psoriasis and Psoriatic Arthritis (GRAPPA) Pilot Research Grant. Alí Duarte-García is supported by the Centers for Disease Control and Prevention, the Rheumatology Research Foundation Scientist Development Award, the Robert D. and Patricia E. Kern Center for the Science of Health Care Delivery, and the Eaton Family Career Development Award.
Disclosures:
Dr. Ogdie has served as a consultant for AbbVie, Amgen, BMS, Celgene, Corrona, Gilead, Janssen, Lilly, Novartis, Pfizer, and UCB (less than 10,000 each) and has received grants from Novartis and Pfizer to Penn and from Amgen to Forward (grants more than 10,000). Dr. Davis has received consulting fees and/or honoraria from AbbVie and Sanofi-Genzyme (less than $10,000 each) and research support from Pfizer. No other disclosures relevant to this article. Dr. Ernste has received research support from Octapharma and Genentech (less than $10,000 each).
Footnotes
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Ethical approval information: The study was approved by the Mayo Institutional Review Board (IRB) and the Olmsted Medical Center IRB (18-010851 and 051-OMC-18).
Data sharing statement:
Access to the complete de-identified data can be made available following approval. Requests for additional study-related data can be sent to Paras Karmacharya at paraskarmacharya@gmail.com
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Associated Data
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Data Availability Statement
Access to the complete de-identified data can be made available following approval. Requests for additional study-related data can be sent to Paras Karmacharya at paraskarmacharya@gmail.com