Key Points
Question
What are the prognostic factors for the clinical course of psoriasis?
Findings
In this 10-year cohort study of 721 patients with recent-onset psoriasis, 52% of the patients with plaque phenotype, high disease activity, and scalp lesions developed severe disease, compared with 11% of patients with low disease activity at inclusion.
Meaning
Patient characteristics at onset can help to estimate the long-term course of psoriasis with good discriminatory power.
Abstract
Importance
Psoriasis is a heterogeneous disease. Improved understanding of prognosis and long-term outcomes in new-onset psoriasis may improve care.
Objective
To describe the clinical course of psoriasis and identify possible indicators of long-term outcomes.
Design, Setting, and Participants
The Stockholm Psoriasis Cohort was a noninterventional inception cohort study enrolling patients between 2001 and 2005. The present study was conducted from January 15, 2019, to February 5, 2021. At enrollment and 10 years, patients were examined by dermatologists and rheumatologists. Data from examinations were complemented by questionnaires, medical records, and registers. A total of 721 patients with recent-onset psoriasis (<12 months duration), 15 years or older were recruited using advertising and referrals from a broad range of health care settings.
Main Outcomes and Measures
Disease severity and psoriatic arthritis (PsA). Recursive partitioning and regression models were implemented to identify probable indicators of long-term outcomes.
Results
A total of 721 patients (median [interquartile range] age, 39 [27-55] years; 405 [56%] women), including 542 (75%) with plaque-onset and 174 (24%) with guttate-onset psoriasis, were enrolled. The median follow-up was 9.6 years (interquartile range, 8.8-10.4 years). The cumulative incidence of severe psoriasis at 12 years from enrollment was 21%. Among 509 patients examined clinically after 10 years, 77 of 389 patients (20%) with plaque onset and 56 of 116 (48%) with guttate onset had minimal disease activity without treatment, and 120 of 509 (24%) had PsA. Recursive partitioning identified strata with distinct risks for severe skin disease and PsA: the cumulative incidence of severe disease in patients with plaque phenotype, above-median disease activity, and scalp lesions was 52% (95% CI, 41%-64%), compared with 11% (95% CI, 8%-14%) in patients with below-median disease activity at inclusion; and 48 of 82 patients (59%) with peripheral enthesitis had PsA after 10 years compared with 37 of 304 patients (12%) without initial joint pain (P < .001). Smoking (hazard ratio, 1.70; 95% CI, 1.10-2.63) and activating genes in the interleukin-23 (IL-23) pathway (odds ratio, 1.55; 95% CI, 1.14-2.11) were also significantly associated with a severe disease course. Systemic therapy at or before enrollment was associated with a lower risk for severe disease at 10 years compared with later initiation of systemic therapy (odds ratio, 0.24; 95% CI, 0.06-0.90).
Conclusions and Relevance
The findings of this cohort study suggest that combinations of clinical characteristics at onset and activating genes in the IL-23 pathway are significantly associated with the clinical course of psoriasis, whereas joint pain and peripheral enthesitis may indicate the probability of PsA. Patients within those categories merit specialist referral and closer follow-up. The possibility of modifying the disease course with early systemic intervention should be tested.
This cohort study examines the disease course in patients with psoriasis over a 10-year follow-up period to identify factors that may be used in prognosis.
Introduction
Psoriasis is a serious immune-mediated skin disease with estimated prevalence ranging from 0.1% to 11.4% worldwide.1 Psoriasis is clinically heterogeneous, with the main phenotypes at onset being plaque psoriasis and guttate psoriasis, the latter with a more acute onset and often associated with infection.2,3,4 The disease substantially affects both the body and psyche, and is associated with comorbidities including psoriatic arthritis (PsA), cardiovascular disease, and depression.5
Although considerable progress has been made on the knowledge of the pathogenesis and treatment of psoriasis, our understanding of its clinical course is limited and stems from retrospective studies.6 Therefore, prospective observational inception cohort studies that describe the clinical course of psoriasis, identify prognostic factors for disease severity, and investigate the use of early systemic treatment have repeatedly been deemed key research priorities.6,7,8 Such data would help reduce prognostic uncertainty, facilitate identification of patients who merit closer follow-up or specialist referrals, and give insight into the possibility of disease course modification. Therefore, we set up the Stockholm Psoriasis Cohort, a 10-year prospective, inception cohort study to describe the clinical course of psoriasis, identify prognostic factors for the disease course, and explore the use of early systemic treatment on long-term outcomes.
Methods
Study Design and Oversight
The Stockholm Psoriasis Cohort was a prospective observational study of patients with recent-onset psoriasis and population-matched controls. Herein, we present findings from the analyses on the clinical course of the disease. The study was approved by the Stockholm Ethics Committee, and all patients provided written informed consent; participants did not receive financial compensation. This study followed the Strengthening the Reporting of Observational Studies in Epidemiology (STROBE) reporting guideline for cohort studies.
Study Population and Data Collection
Patients aged 15 years or older with their first onset of psoriasis lesions on nonhairy skin within the past 12 months were eligible. Patients were mainly recruited from the Stockholm area, Sweden, between 2000 and 2005 from dermatology clinics, general practitioners, school nurses, sexual health centers, and youth clinics. The study was also advertised in daily newspapers and in the magazine and website of the Swedish Psoriasis Association. The present study was conducted from January 15, 2019, to February 5, 2021.
Individuals were screened via a telephone interview conducted by a dermatologist or a study nurse. Patients who were deemed to fulfill the study inclusion criteria were examined by 2 dermatologists (L.M. and M.S.) and patients with a clinically convincing diagnosis were included. Because the study was limited to new-onset psoriasis, individuals with a history of skin lesions compatible with psoriasis were excluded.
Clinical examinations were performed using standardized forms at enrollment and at 10 years. Patients with subjective joint problems were seen by a rheumatologist (P.L.) for comprehensive joint examination. Relevant patients were also seen by another rheumatologist (U.L.) at 10 years for a similar joint examination. Information from the examinations was combined with medical records, data on outpatient and inpatient care from the National Patient Register,9 prescriptions from the Prescribed Drug Register,10 and death and emigration from the Total Population Register.11
The data collected have been described in detail.12 In brief, psoriasis phenotypes and clinical manifestations were classified according to established terminology.13 Plaque psoriasis comprised nummular and large plaque types and guttate psoriasis was defined as acute onset of small, coin-like lesions. Family history of psoriasis and potential precipitating factors, including infection, defined as acute symptoms requiring anti-infective treatment within 10 days of onset of psoriasis, and stressful life events, defined as events with a profound effect on the patients within 2 months of disease onset, were elicited. The rheumatologic examinations included evaluation of the presence of arthrosynovitis, tenosynovitis, axial enthesitis, peripheral enthesitis, dactylitis, and tender and swollen joint counts.
Outcomes and Covariates
Skin disease severity was measured using the Psoriasis Area Severity Index (PASI) and the static Physician’s Global Assessment (s-PGA).14,15 The PASI evaluates 4 body regions (head, trunk, upper extremities, and lower extremities) for erythema, induration, and scaling. Scores range between 0 and 72, with higher scores denoting more severe disease. The s-PGA describes severity on a 7-point scale, ranging from 1 (clear) to 7 (severe).15
Disease severity at clinical examinations was defined using combinations of current treatment and the PASI score: complete remission (free of lesions and no treatment for 2 years), minimal disease activity (0 ≤ PASI < 1 without treatment), mild disease (1 ≤ PASI < 5 or topical treatment), moderate disease (5 ≤ PASI < 10 or phototherapy), or severe disease (PASI ≥ 10 or systemic treatment). Given that treatment with systemic agents is a valid marker for psoriasis disease severity in observational research,16 the first instance of severe disease was defined as the first event consistent with severe psoriasis: a filled prescription of systemic treatment for psoriasis (from the Prescribed Drug Register, eTable 1 in the Supplement) or a PASI score exceeding 10 at clinical examination.
In patients examined rheumatologically, the presence of inflammatory joint disease was assessed according to criteria of the Swedish Psoriatic Arthritis Register.17 Patients with inflammatory joint disease were classified as having PsA if they fulfilled the CASPAR criteria18 unless the joint symptoms had another apparent cause. No radiographs were available; therefore, evidence of juxta-articular new bone formation was excluded from the assessment of CASPAR in this study, albeit patients still had to have a score of 3 on the CASPAR tool to be classified as having PsA. Because CASPAR was not available at the time of enrollment examinations, data from enrollment were re-evaluated for conformity in classification between the examinations. Patients who reported joint pain but elected not to see the study rheumatologist were assessed for the presence of PsA using an algorithm combining information from the dermatologic examination, medical records, and the National Patient Register (eMethods and eTable 2 in the Supplement).
Indicators of severe disease, minimal disease activity, and PsA included the following variables measured at enrollment: sex, age, smoking (current vs never or former smoker), body mass index, nail involvement, scalp lesions, joint pain, infection precipitation, s-PGA level, and peripheral enthesitis. Furthermore, 21 genetic variants were included in analysis of skin disease severity and phenotype based on their potential role in the disease or its treatment as described.19
Early systemic treatment was defined as systemic treatment at or before enrollment. Later systemic treatment comprised systemic agents initiated thereafter until the 10-year examination. Time to initiation of systemic therapy was stratified into quartiles: initiation before or at enrollment and initiation in the first, second, or third tertiles of follow-up.
All enrolled patients (cohort A) were included in analyses of baseline characteristics and development of severe psoriasis. All other analyses were conducted on patients who participated in the 10-year examination (cohort B).
Statistical Analysis
Comparisons among groups were conducted using χ2 tests for categorical variables. Relative risks (RRs) were derived using binomial generalized linear models with a log link function. Time-to-event analysis was implemented to estimate the cumulative incidence of severe disease.
To identify subgroups with distinct risks for developing mild disease, severe disease, and PsA, recursive partitioning analyses were implemented using hypothesized clinical predictors and baseline phenotype as covariates (eMethods in the Supplement). The resulting models were internally validated with C-indices excluding ties on predictor groups. To further explore clinical factors that indicate the probable disease course, univariate and multivariable models stratified by onset phenotype were implemented. Cox proportional hazard regression models were fitted to assess predictors of severe disease and logistic regression models were fitted to assess predictors of minimal disease activity and PsA at 10 years. For the genetic markers, we tested for allele frequency differences for all single nucleotide variants using logistic regression, with sex and age as covariates and without adjustments for multiple testing.
The proportions of patients with severe disease at the 10-year clinical examination stratified by early and late systemic treatment were compared using a χ2 test and logistic regression controlling for the variables that were found to be significantly associated with development of severe psoriasis in the multivariable analysis described above. Sensitivity analyses using multiple imputation of missing data, including end points were performed to explore the potential impact of loss to follow-up and missing predictors (eMethods in the Supplement).
Analyses were implemented in R, version 3.4.2 (R Foundation for Statistical Computing) for recursive partitioning analyses, Stata, version 14.2 (StataCorp LLC) for multiple imputation, and SAS, version 9.2 (SAS Institute Inc) for all other analyses.
Results
In total, 765 individuals were examined clinically. Forty-three patients were excluded owing to uncertain diagnosis or erroneous personal identification numbers. Hence, 721 participants were included in the study (cohort A); of these, 405 patients (56%) were women and 316 (44%) were men; median age was 39 years (interquartile range [IQR], 27-55 years). All patients in cohort A were followed up using administrative registers and electronic medical records. During follow-up, 35 participants died. Among the 686 patients alive at 10 years, 177 (26%) did not participate in the follow-up; 509 (74%) were interviewed and examined clinically (cohort B). Median time from onset to enrollment was 6 months (IQR, 3-10 months) and median time from enrollment to the 10-year examination was 9.6 years (IQR, 8.8-10.4 years).
Disease Onset and Course
The number of patients with plaque phenotypes at onset was 542 (75%); guttate, 174 (24%); and other phenotypes, 5 (1%). Baseline characteristics for patients with plaque and guttate onset are presented in the Table. We found 4 genetic variants associated with guttate onset, IL13 (rs20541), IL12B (rs3212227), HLA-C*06, and NFKBIL1 (rs2255798) (eTable 3 in the Supplement).
Table. Baseline Patient Characteristics.
| Characteristic | No. (%) | |
|---|---|---|
| Guttate phenotype (n = 174) | Plaque phenotype (n = 542) | |
| Age, median (IQR), y | 31 (22-41) | 45 (30-58) |
| Sex | ||
| Men | 66 (37.9) | 248 (45.8) |
| Women | 108 (62.1) | 294 (54.2) |
| BMI, mean (SD) | 24.1 (4.5) | 25.3 (4.4) |
| Smoking, No./total No. (%) | 64/171 (37.4) | 196/536 (36.6) |
| Comorbidity profile | ||
| Diabetes | 2 (1.2) | 21 (3.9) |
| Hypercholesterolemia | 19 (10.9) | 148 (27.3) |
| Hypertension | 26 (14.9) | 197 (36.4) |
| Obesity | 11 (6.3) | 74 (13.7) |
| Depression | 5 (2.9) | 25 (4.6) |
| Potential precipitating factorsa | ||
| Infection | 126 (72.4) | 75 (13.8) |
| Life crisis | 57 (32.7) | 258 (47.6) |
| Genetic weight | ||
| First degree | 64 (26.3) | 177 (32.7) |
| Second degree | 22 (12.6) | 81 (14.9) |
| Higher degree, none, or unknown | 88 (50.6) | 284 (52.4) |
| Disease severity, median (IQR) | ||
| PASIb | 4.1 (2.8-6.4) | 2.8 (1.5-4.7) |
| s-PGAc | 3 (3-4) | 3 (2-4) |
| Joints | ||
| Self-reported joint pain | 49 (28.1) | 236 (43.5) |
| Peripheral enthesitis, No./total No. (%) | 16/166 (9.6) | 93/516 (18.0) |
| Psoriatic arthritis | 10 (5.8) | 89 (17.0) |
| Pattern of joint involvement | ||
| Axial | 1 (10.0) | 2 (2.2) |
| Peripheral | 6 (60.0) | 61 (68.5) |
| Peripheral and axial | 3 (30.0) | 26 (29.2) |
| Pattern of peripheral arthritis | ||
| Oligoarthritis, No./total No. (%) | 7/10 (70.0) | 62 (69.7) |
| Polyarthritis, No./total No. (%) | 3/10 (30.0) | 27 (30.3) |
| Tender joint count, median (IQR) | 1 (0-11) | 1 (0-5) |
| Swollen joint count, median (IQR) | 0 (0-2) | 0 (0-2) |
Abbreviations: BMI, body mass index (calculated as weight in kilograms divided by height in meters squared); IQR, interquartile range; PASI, Psoriasis Area Severity and Severity Index; s-PGA, static Physician Global Assessment Index.
Not mutually exclusive.
The PASI evaluates 4 body regions (head, trunk, upper extremities, and lower extremities) for erythema, induration, and scaling. Scores range between 0 and 72, with higher scores denoting more severe disease.
The s-PGA describes disease severity on a 7-point scale, ranging from 1 (clear) to 7 (severe).
Among the 389 patients with plaque onset who were examined clinically at 10 years (cohort B), 346 (89%) retained plaque phenotype, 13 (3%) had nonplaque phenotypes, and 30 (8%) were in complete remission. Among the 116 patients with guttate onset in cohort B, 75 (65%) had plaque phenotype at 10 years, 4 (3%) had nonplaque phenotypes, and 37 (32%) were in complete remission.
Disease severity at onset and 10 years in cohort B are presented in Figure 1. In 389 patients with plaque onset, the proportion of patients with severe disease increased from 7% (n = 27) at onset to 12% (n = 45) at 10 years (P = .02) (Figure 1A). Conversely, in 116 patients with guttate onset, the proportion of patients with severe disease decreased from 19% (n = 22) at onset to 4% n = 5) at 10 years (P < .001) (Figure 1B). Among the 50 patients with severe disease at the 10-year clinical examination, 22 had a PASI score greater than or equal to 10, and 10 of those did not receive previous systemic treatment for moderate to severe psoriasis. At the 10-year clinical examination 77 of 389 patients (20%) with plaque onset and 56 of 116 patients (48%) with guttate onset had minimal disease activity; 120 of 509 patients (24%) had developed PsA.
Figure 1. Disease Severity and Clinical Manifestations From Onset to 10 Years.
Distribution of disease severity at enrollment and at 10 years in patients with plaque-onset (A) and guttate-onset (B) psoriasis. The transparent fields between the bars illustrate the flow of patients between disease severity categories at enrollment and the 10-year clinical examination.
Among patients with plaque onset, 11 of 27 (41%) individuals with severe disease at onset had severe disease at 10 years compared with 34 of 362 (9%) patients with mild or moderate disease at onset (RR, 4.3; P < .001). Conversely, 59 of 253 (23%) patients with mild disease at onset had minimal disease activity at 10 years compared with 18 of 136 (13%) patients with moderate or severe disease at onset (RR, 1.8; P < .001). Among patients with guttate onset, 4 of 22 (18%) of those with severe disease at onset had severe disease at 10 years compared with 1 of 94 (1%) patients with mild or moderate disease at onset (P = .001). There was no significant association between disease severity at onset and minimal disease activity at 10 years in patients with guttate onset. Among the 721 patients enrolled in the study, the estimated cumulative incidence of severe psoriasis at 12 years from enrollment was 21% in all patients, 23% in patients with plaque phenotype, and 13% in patients with guttate phenotype at onset. The prevalence of PsA increased from 18% (69 of 389) to 26% (102 of 389) in patients with plaque onset (P < .001) and from 4% (5 of 116) to 14% (16 of 116) in those with guttate onset (P = .02).
Prognostic Factors and Outcomes
Examples of the benign and severe disease course are presented in Figure 2. In patients with plaque onset, male sex, high s-PGA score, scalp lesions, smoking, and an IL23R genotype increased the risk of severe disease (eTable 4 and eTable 5 in the Supplement). The same factors decreased the probability of minimal disease activity at 10 years, whereas previous infection and an NKBIA genotype increased the probability of minimal disease activity (eTable 4 and eTable 6 in the Supplement). In patients with guttate onset, older age, high s-PGA score, an IL12B genotype, and lack of the HLA-C*06 genotype increased the risk of severe disease (eTables 4 and 5 in the Supplement), whereas previous infection, no scalp lesions, and an LCE genotype increased the probability of minimal disease activity at 10 years (eTables 4 and 6 in the Supplement). Joint pain and peripheral enthesitis at enrollment increased the risk of PsA at 10 years in both plaque and guttate onset. Coefficients from models based on multiple imputation data did not differ substantially from the main analyses (eTable 7 in the Supplement).
Figure 2. Examples of Severe and Benign Disease Course Along With Predictors of Disease Course.
A patient with mild plaque psoriasis at onset (A) and severe disease at follow-up (B). A patient with severe guttate psoriasis at onset (C) and minimal disease activity (D) at follow-up.
Recursive partitioning analyses identified 3 subgroups with distinct risks for development of severe psoriasis, mild disease, and PsA (Figure 3 and eFigure in the Supplement). For severe disease, patients with an s-PGA score exceeding 3 at enrollment with nonguttate phenotypes and scalp lesions had the highest risk of severe disease, with an estimated 12-year cumulative incidence of 52% (95% CI, 41%-64%), compared with 11% (95% CI, 8%-14%) for patients with an s-PGA score of 3 or below at enrollment. Patients with guttate onset had the highest probability of having minimal disease activity at 10 years: 49% (57 of 116) compared with 33% (59 of 177) in patients with nonguttate onset without scalp lesions, and 11% (23 of 216) among those with nonguttate onset and scalp lesions. Patients with peripheral enthesitis at enrollment were more likely to have PsA at 10 years: 59% (48 of 82) compared with 25% (24 of 97) of those with self-reported joint problems but no enthesitis, and 12% (37 of 304) of those patients without self-reported joint pain. The C-indices for the models were 0.794 for severe disease, 0.821 for mild disease, and 0.794 for PsA.
Figure 3. Outcomes for the Identified Groups for Severe Psoriasis, Minimal Disease Activity at 10 Years, and Psoriatic Arthritis.
Cumulative incidence of severe disease beyond 10 years (A), proportion of patients with minimal disease activity at 10 years (B), and proportion of patients with psoriatic arthritis at 10 years. For panel A, group 1, the static Physician Global Assessment Index (s-PGA) was ≤3; for group 2, s-PGA was >3 in guttate onset or s-PGA was >3 in nonguutate onset without scalp lesions; for group 3, s-PGA was >3 in nonguttate onset with scalp lesions. For panel B, group 1 was the guttate onset; group 2 was nonguttate onset without scalp lesions; and group 3 was nonguttate onset with scalp lesions. For panel C, group 1 was no joint pain; group 2 was joint pain but no enthesitis; and group 3 was enthesitis. eTable 5 in the Supplement presents further details.
In total, 66 patients initiated systemic treatment before the 10-year examination. Patients who initiated systemic therapy at enrollment or before were less likely to have severe disease at the 10-year clinical examination (6 of 16 [38%]) compared with patients who initiated systemic treatment thereafter (33 of 50 [65%]) (P = .04). The differences remained significant after adjustments for s-PGA score, smoking, PsA, and scalp lesions at enrollment (odds ratio, 0.24; 95% CI, 0.06-0.90). The proportions of patients with severe disease at the 10-year examination stratified by timing of the systemic therapy initiation are presented in Figure 4.
Figure 4. Proportion of Patients With Severe Psoriasis at the 10-Year Clinical Examination Stratified by Time to Systemic Initiation.
Error bars indicate exact binomial 95% confidence limits.
Discussion
This inception cohort study of 721 participants with recent onset psoriasis found that plaque psoriasis exhibited a notable persistence in its overall disease course from onset. Forty-eight percent of the participants with severe disease at onset had severe disease at the 10-year clinical examination compared with 14% of participants with mild or moderate disease at onset (RR, 4.3; P < .001). Guttate-onset psoriasis had a favorable prognosis, with 48% of the patients having minimal disease activity at 10 years. In addition, 20% of participants with plaque-onset psoriasis had minimal disease activity without treatment at 10 years. The prevalence of PsA increased from 18% to 26% in participants with plaque onset and from 4% to 14% in participants with guttate onset.
Based on disease characteristics at onset, the study identified subgroups with an elevated risk of developing severe psoriasis or PsA. Participants with greater than mild symptoms (s-PGA score >3), plaque phenotype, and scalp lesions were almost 5 times more likely to develop severe psoriasis than participants with mild symptoms or less (s-PGA score ≤3) at enrollment (52% vs 11%; P < .001). Similarly, participants with peripheral enthesitis were more than 4 times more likely to have PsA at 10 years compared with participants without self-reported joint pain (59% vs 12%; P < .001).
The study also found that participants who initiated systemic therapy at or before enrollment were less likely to have severe disease at the 10-year clinical examination (6 of 16 [38%]) compared with participants who initiated systemic treatment thereafter (33 of 50 [65%]) (P = .04).
To our knowledge, this is the first study that has enrolled participants with recent-onset psoriasis and followed them prospectively over an extended period; therefore, comparable studies may not exist. However, the study supports the notion that guttate psoriasis has a fairly favorable prognosis.20 The factors for the probability of severe disease for participants with plaque-onset psoriasis in this study included scalp psoriasis, smoking, sex, and an IL23R single nucleotide variant and partially corroborates previous cross-sectional and retrospective studies.19,21,22 The finding that the same factors decrease the probability of minimal disease activity at 10 years strengthens the notion that these factors are important for the disease course. In line with previous research, subjective joint pain and peripheral enthesitis were associated with the development of PsA.23,24 However, in contrast to previous findings25 nail manifestations were not statistically significant indicators for probable development of PsA.
Strengths and Limitations
The study was designed to describe the clinical course of psoriasis and identify prognostic factors; it was therefore suited to address these objectives. The inception cohort design removed recall and survivorship biases, enabling accurate description of the disease course and the prognosis at onset. The comprehensive recruitment strategy should render the study participants broadly representative of the population with recent-onset psoriasis. Clinical examination of all participants by a specialist dermatologist ensures diagnostic accuracy and minimizes misclassification bias. Low attrition rates and data linkage to population-based registers facilitate accurate estimates of the long-term outcomes.
The study has limitations. As with all non–population-based observational research with less than complete follow-up, there may be selection and attrition bias. There is a risk of chance findings given that we explored multiple outcomes, especially in the analysis of genetic variants. Radiographs were not available for the assessment of PsA, resulting in a potential underestimation of PsA prevalence. However, any underestimation would be limited given that CASPAR requires only 1 criterion (ie, negative rheumatoid factor, nail lesions, or dactylitis) to classify individuals with psoriasis and inflammatory joint pain as having PsA. Even though patients were recruited within 1 year of the first onset of psoriasis, several patients were treated before enrollment, influencing the measure of baseline disease severity. The Prescribed Drug Register only contains data on dispensed prescriptions; therefore, a prescription for a systemic agent for treatment of psoriasis that was never filled would not be included in the definition of severe disease, resulting in a potential underestimation of the cumulative incidence of severe disease. Furthermore, the Swedish population is mostly of White race, potentially affecting generalizability.
Conclusions
The findings from this study contribute to the knowledge about the disease course of psoriasis, reducing prognostic uncertainty. In the light of the persistent nontreatment and undertreatment of both psoriasis and PsA,26 the identified subgroups with elevated risk for severe skin disease and PsA merit close follow-up or specialist referrals to facilitate timely and appropriate intervention. Our study also suggests that early systemic intervention may be beneficial for the long-term prognosis of psoriasis, supporting a long-standing notion in dermatology practice.27 However, the number of individuals in the analyses was limited and treatment was not randomized. Therefore, causality cannot be determined and this finding should be tested in randomized clinical trials.
eMethods. Detailed Methods
eMethods. Detailed Methods
eTable 1. Treatments and Corresponding ATC Codes Used to Define Severe Psoriasis
eTable 2. PsA Status at Enrollment and Follow-up by Examination Method
eTable 3. Marker Information and Association Analyzed in Patients With a Guttate Onset vs Plaque Onset
eTable 4. Prognostic Factors for the Clinical Remission at Ten Years, Severe Psoriasis and Psoriatic Arthritis (PsA)
eTable 5. Marker Information and Association With Remission at Ten Years and Severe Disease During Follow-up Analyzed in Patients With a Plaque Onset
eTable 6. Marker Information and Association With Remission at Ten Years and Severe Disease During Follow-up Analyzed in Patients With a Guttate Onset
eTable 7. Prognostic Factors for the Development of Mild Psoriasis, Moderate to Severe Psoriasis and Psoriatic Arthritis (PsA) in Complete Case Analysis and Multiple Imputation Analysis
eFigure. Classification Trees
eReferences
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Associated Data
This section collects any data citations, data availability statements, or supplementary materials included in this article.
Supplementary Materials
eMethods. Detailed Methods
eMethods. Detailed Methods
eTable 1. Treatments and Corresponding ATC Codes Used to Define Severe Psoriasis
eTable 2. PsA Status at Enrollment and Follow-up by Examination Method
eTable 3. Marker Information and Association Analyzed in Patients With a Guttate Onset vs Plaque Onset
eTable 4. Prognostic Factors for the Clinical Remission at Ten Years, Severe Psoriasis and Psoriatic Arthritis (PsA)
eTable 5. Marker Information and Association With Remission at Ten Years and Severe Disease During Follow-up Analyzed in Patients With a Plaque Onset
eTable 6. Marker Information and Association With Remission at Ten Years and Severe Disease During Follow-up Analyzed in Patients With a Guttate Onset
eTable 7. Prognostic Factors for the Development of Mild Psoriasis, Moderate to Severe Psoriasis and Psoriatic Arthritis (PsA) in Complete Case Analysis and Multiple Imputation Analysis
eFigure. Classification Trees
eReferences