New-Onset Guttate Psoriasis: A Long- Term Follow-Up Study
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Research Article Dermatology 2023;239:188–194 Received: February 1, 2022 Accepted: October 20, 2022 DOI: 10.1159/000527737 Published online: December 8, 2022 New-Onset Guttate Psoriasis: A Long- Term Follow-Up Study Eran Galili Shir Rubinstein Levy Ido Tzanani Oz Segal Anna Lyakhovitsky Aviv Barzilai Sharon Baum Downloaded from http://karger.com/drm/article-pdf/239/2/188/3922414/000527737.pdf by guest on 22 June 2023 Department of Dermatology, Tel Aviv University, Tel Aviv, Israel Keywords the end of follow-up period (mean 6.2 years [±3.1]), 49.1% (n Guttate psoriasis · Psoriasis vulgaris · Autoimmune disease = 59) of the patients reported active persistent psoriasis. A switch to the psoriasis vulgaris phenotype occurred in 17.5% (n = 21) of the study cohort. Persistent psoriasis was associ- Abstract ated with male sex (OR = 2.1, p < 0.05), multiple disease flares Background: Guttate psoriasis (GP), a distinct variant of pso- (>3; OR = 9.1, p < 0.001), switch to the vulgaris phenotype riasis, is more common in children and adolescents. The (OR = 4.16, p < 0.001), and palmoplantar involvement (OR = long-term course of these patients has sparsely been exam- 5.2, p < 0.01). Conclusion: A persistent disease course is com- ined, with few studies reporting the rates of relapse, persis- mon among patients with new-onset GP, with most retain- tence, and further development of the psoriasis vulgaris ing their guttate phenotype throughout the disease course. phenotype. Objectives: The objective of this study was to Persistency was associated with male sex, multiple GP flares, characterize the long-term outcomes of new-onset GP and switching to the vulgaris phenotype, and palmoplantar in- elucidate the potential factors associated with a persistent volvement. © 2022 The Author(s). disease course. Methods: This was a retrospective cohort Published by S. Karger AG, Basel study. Patients diagnosed with new-onset GP between 2009 and 2020 with a follow-up period of at least 1 year, were en- rolled. The examinees were evaluated by dermatologists. Introduction Detailed data retrieved from the examinees’ medical files in- cluded demographics, disease characteristics, treatment, Guttate psoriasis (GP) is a variant of psoriasis that has and comorbidities. A structured telephone questionnaire distinct epidemiological, clinical, and histological charac- was used to determine the current psoriasis status: type, se- teristics. Unlike psoriasis vulgaris (PV), GP is more com- verity, and extent. At the end of follow-up, patients with a mon in children and adolescents than in adults [1], it af- persistent disease course, defined as having lesions at least fects people of all races, as well as men and women [2]. a year after disease onset, were compared with patients in GP manifests as several small (2–10 mm diameter) “drop- complete remission without further psoriasis symptoms. Re- like” scaly plaques. As an immune-mediated disorder, its sults: A total of 120 patients (mean age 28.8 years [±15.2], 58.3% women) with new-onset GP flare were identified. At Eran Galili and Shir Rubinstein Levy contributed equally to this work. Karger@karger.com © 2022 The Author(s). Correspondence to: www.karger.com/drm Published by S. Karger AG, Basel Eran Galili, egalily @ gmail.com This is an Open Access article licensed under the Creative Commons Attribution-NonCommercial-4.0 International License (CC BY-NC) (http://www.karger.com/Services/OpenAccessLicense), applicable to the online version of the article only. Usage and distribution for com- mercial purposes requires written permission.
onset is typically 1–3 weeks following an acute infection, sant, and phosphodiesterase 4 inhibitor), phototherapy, and topi- such as streptococcal tonsillitis [3–5]. Immunohisto- cal steroids. Current psoriasis severity and extent were rated according to chemical analysis of the tonsils and skin lesions in pa- validated patient-reported scales: the Patient Global Assessment of tients with GP demonstrated shared T-cell clones, sug- Psoriasis (PGA) scale and Patient Report of Extent of Psoriasis In- gesting that GP is caused by autoimmune cross-reactivity volvement (PREPI) scale collected from all study participants us- to streptococcal antigen [6]. Additional risk factors for ing a structured telephone questionnaire [14–17]. At the time of GP include stressful life events and family history of pso- interview, occurring at least a year since the first GP onset, those with psoriatic lesions within the last 3 months were defined as hav- riasis [7]. Prognosis is considered better than other types ing persistent psoriasis, while those without any psoriatic lesions of psoriasis because of rapid involution even without within the last 3 months were defined as having complete remis- treatment within a few weeks to months following its ap- sion. pearance [8]. The PREPI scale is composed of a single question for measuring Data evaluating the natural history of GP are scarce, body surface area (BSA) affected by psoriasis, “If you had to take the palm of your hand and cover up all of the patches of psoriasis particularly the question of long-term outcomes. The re- on your body today, how many palms of your hand do you think ported rates of persistent disease course, lasting over a that it would take?” Patients were also instructed that “One palm year are 25–38.9% over a follow-up period of 5–10 years of your hand is equal to about 1% of your BSA” and “Do not in- Downloaded from http://karger.com/drm/article-pdf/239/2/188/3922414/000527737.pdf by guest on 22 June 2023 [9–11]. Risk factors for a prolonged disease course could clude areas in which psoriasis has faded, leaving only changes in not be identified in most studies, possibly because of the the color of the skin.” The PGA is a five-point severity scale, as previously reported, from 0 = clear to 4 = severe (very marked small sample size [10]. Additionally, the risk of acquiring plaque elevation, scaling, and erythema). Pruritus was rated using the vulgaris phenotype is yet to be fully characterized. Pf- the Itch Scale (“no itching” at the 0 point to “severe itching” at the ingstler et al. [9] revealed that the risk of acquired vul- 10 end of the scale). The change in the clinical picture from the GP garis was higher in patients with prolonged GP disease for to PV phenotype was determined by the clinician based on chang- a year. Svedbom et al. [12] and Ko et al. [10] reported op- es in the clinical shape of the lesions from small guttate-sized pap- ules to large scaly plaques with one or more of the following: in- posing findings, as a majority versus a minority of pa- volvement of the extensor body parts, scalp, or palmoplantar sur- tients with a persistent disease course had acquired the faces. Patients were also questioned about having comorbidities: Vulgaris phenotype. However, no previous study has re- arthritis (whether they were diagnosed by a physician or reported ported the clinical importance of this event. In this study, morning stiffness), diabetes, hyperlipidemia, hypertension we aimed to evaluate the long-term outcomes of new- (whether they were given a physician diagnosis), and obesity (cal- culated BMI over 30). A follow-up period of less than 12 months onset GP and to elucidate which factors are associated and other preexisting psoriasis variants served as the exclusion cri- with a prolonged disease course and acquired PV pheno- teria. type. The authors confirm that the ethical policies of the journal, as noted on the journal’s author guidelines page, were adhered to. Ethical approval for this study was obtained from the Research Materials and Methods Ethics Committee of the Sheba Medical Center (no. SMC-7082- 20). Written informed consent was obtained from participants. This retrospective study included patients with first episode of GP that occurred between 2009 and 2020. The patients were eval- Statistical Analysis uated by board-certified dermatologists at the Dermatology De- Values are presented as mean (standard deviation) or number partment of the Sheba Medical Center, Israel. The GP was diag- (percentage). Categorical variables were compared using the χ2 nosed clinically. Detailed data were retrieved from the patients’ test, and continuous variables were tested using the independent medical records. The data retrieved included demographics, dis- samples t test. All statistical tests were two-sided, and statistical ease characteristic and recurrence, treatments applied, response to significance was set at p < 0.05. All data were included in an Excel treatments, family history of psoriasis, and comorbidities. The GP- document, and statistical analyses were performed using SPSS flaring triggers were also recorded. The triggers were deemed rel- (IBM SPSS Statistics for Windows, version 23.0. Released 2015; evant when they occurred up to 3 weeks before the GP flare. Acute IBM Corp., Armonk, NY, USA). streptococcal tonsillitis was diagnosed based on upper respiratory tract symptoms with at least one of the following criteria: throat culture positive for group A β-hemolytic Streptococcus or positive antistreptolysin O (ASLO) titer (>200 μ/mL, taken up to 5 weeks Results from the onset of symptoms). Of note, the antibody level measured by the ASLO titer starts to rise at 1–3 weeks after a streptococcal Baseline Characteristics and Disease Course of the infection and peaks at 3–5 weeks but cannot be detected at 5–6 weeks and thereafter [13]. Disease treatments were grouped based Study Population on reported product efficacy, with biological treatment being the In total, 120 patients with new-onset GP were included most potent, followed by oral agents (acitretin, immunosuppres- in this retrospective cohort study. Mean age was 28.8 Guttate Psoriasis: Long-Term Follow-Up Dermatology 2023;239:188–194 189 DOI: 10.1159/000527737
Fig. 1. Prevalence of persistent psoriasis by follow-up years. Rates of disease persisten- cy remained elevated for the entire range of Downloaded from http://karger.com/drm/article-pdf/239/2/188/3922414/000527737.pdf by guest on 22 June 2023 follow-up periods (lasting 1–12 years). years (±15.2) with 58.3% females. A total of 36.1% of the sistent disease was also associated with palmoplantar in- patients had a family member with psoriasis. The upper volvement at the first GP flare (OR = 3.1; CI, 1.0–9.4) or respiratory tract infection (URTI) was regarded as a trig- at least one of the GP flares (OR = 5.2; CI, 1.8–15.5). gering event in 63.3% of the first GP episodes. During Among patients with persistent disease, severe disease follow-up, a single GP flare occurred in a minority of the (BSA >10%) was not affected by the disease phenotype patients (40.8%), while most patients had multiple GP (43.8% of the PV phenotype vs. 25.6% of the GP pheno- flares (2–3 flares, 26.7%; over 3 flares, 32.5%). Of all the type, p = 0.18). However, the disease phenotype did affect patients with GP, 17.5% (n = 21) further developed the treatment potency, as 43.8% with the vulgaris phenotype PV phenotype. compared to 11.6% with the guttate phenotype being treated with oral or biological treatment (OR = 5.9; CI, Factors Associated with Persistent Psoriasis 1.5–23). Comorbidities, family history of psoriasis, or GP All study patients completed a telephonic question- triggering factors were not associated with persistent dis- naire to assess their current disease state. At that time ease. (average follow-up period of 6.2 years (±3.1)), persistent psoriatic lesions were reported in 49.1% (n = 59) of pa- Factors Associated with Acquired PV Phenotype tients, while the rest had complete remission (50.9%, n = Patients with only GP episodes (n = 99) were com- 61). Disease persistence remained high throughout the pared with patients who acquired the PV phenotype (n = follow-up period (1–12 years), as illustrated in Figure 1. 21), as reported in Table 2. The follow-up period was sim- Patient-reported disease severity scales were calculat- ilar in both groups. Patients with multiple GP flares (>3) ed for patients with persistent disease. A BSA of >10%, were found to have higher odds of acquiring the PV phe- indicating severe disease, was reported in 30.5% of the notype than those with nontransformed GP (52.4% vs. patients. The mean PGA was 1.6 (±0.8), and mean itch 28.3%; OR = 2.8; CI, 1.1–7.3; respectively). The PV phe- index was 3.1 (±3.4) with 54.2% of the patients reporting notype switch was underrepresented among patients with consistent itchiness. Of those with persistent disease, a single GP flare, compared to nontransformed GP (19.9% 72.9% retained the guttate phenotype, while the remain- vs. 45.5%; OR = 0.28; CI, 0.1–0.9, respectively). Addition- ing 27.1% acquired the vulgaris phenotype. ally, the PV phenotype was associated with scalp involve- Persistent disease was compared with disease remis- ment in previous GP flares (81% vs. 50%; OR = 4.3; CI, sion (Table 1). Persistent disease was associated with male 1.3–13.5). Furthermore, patients with the PV phenotype sex (OR = 2.1; confidence interval [CI], 1.0–4.4), vulgaris were more commonly prescribed potent treatment. Oral phenotype switch (OR = 4.2; CI, 1.4–12.3), and having or biological treatment at the first GP and over the disease more than three GP flares (OR = 9.1; CI, 3.5–23.4). Per- course, respectively, were prescribed in 23.8% and 42.9% 190 Dermatology 2023;239:188–194 Galili/Levy/Tzanani/Segal/Lyakhovitsky/ DOI: 10.1159/000527737 Barzilai/Baum
Table 1. Characteristics of patients with persistent GP versus complete remission Characteristic Persistent disease Complete remission OR CI 95% p Value (N = 59) (N = 61) Follow-up, years, mean (SD) 6.5 (3.3) 5.7 (2.9) 1.09 0.97–1.22 0.08 Age at first event, years, mean (SD) 27.9 (14.3) 29.3 (16.3) 0.99 0.97–1.01 0.44 Female gender (%) 29 (49.2) 41 (67.2) 0.47 0.22–0.98 0.04 Family history of psoriasis 25 (42.2) 18 (30.0) 1.71 0.80–3.65 0.16 Missing data n=1 n=1 Episodes, n (%) 1 7 (11.9) 42 (68.9) 0.06 0.02–0.15 0.001 2–3 20 (33.3) 12 (19.6) 2.09 0.91–4.80 0.07 Over 3 32 (54.2) 7 (11.5) 9.14 3.57–23.38 0.001 Area involved Trunk 50 (90.9) 54 (94.7) 0.55 0.12–2.44 0.43 Limbs 52 (94.5) 55 (96.5) 0.63 0.10–3.92 0.61 Head 24 (43.6) 28 (49.1) 0.80 0.38–1.68 0.56 Downloaded from http://karger.com/drm/article-pdf/239/2/188/3922414/000527737.pdf by guest on 22 June 2023 Diffuse 23 (41.8) 27 (47.4) 0.79 0.37–1.68 0.55 Missing data N=4 N=4 URTI anticipating GP flare At first GP episode 37 (62.7) 39 (63.9) 0.94 0.45–1.99 0.88 At some GP episodes 41 (67.2) 41 (69.2) 1.11 0.51–2.40 0.78 With confirmed streptococcal infection a 13 (65.0) 10 (40.0) 2.78 0.82–9.42 0.95 Missing data N = 39 N = 36 Hand and foot involvement At first GP episode 15 (30.0) 5 (12.2) 3.08 1.03–9.40 0.04 At some GP episodes 21 (42.0) 5 (12.2) 5.21 1.75–15.52 0.002 Missing data N = 18 N = 11 Scalp involvement At first episode 30 (50.8) 26 (43.3) 1.35 0.65–2.78 0.41 At some GP episodes 38 (64.4) 28 (46.7) 2.06 0.99–4.31 0.05 Missing data N=0 N=1 Comorbidity, n (%) Arthritis 12 (20.3) 6 (9.8) 2.34 0.81–6.71 0.10 Hypertension 5 (8.5) 3 (4.9) 1.79 0.40–7.85 0.43 Hyperlipidemia 6 (10.2) 3 (4.9) 2.18 0.52–9.19 0.27 Diabetes 4 (6.8) 1 (1.6) 4.36 0.47–40.24 0.15 Obesity 5 (8.5) 6 (9.8) 0.84 0.24–2.94 0.79 Disease state Transformed to vulgaris phenotype 16 (27.1) 5 (8.2) 4.16 1.41–12.27 0.006 Most potent treatment at first GP episode Topical 4 (7.0) 10 (16.9) 0.37 0.10–1.25 0.10 Phototherapy 48 (84.2) 46 (78.0) 1.50 0.58–3.86 0.39 Oral agentsb 5 (8.8) 3 (5.1) 1.79 0.40–7.88 0.43 Biological 0 (0) 0 (0) Missing data N=2 N=2 Most potent treatment along disease course Topical 5 (8.5) 10 (16.4) 0.47 0.15–1.47 0.19 Phototherapy 42 (71.2) 43 (70.5) 1.03 0.47–2.27 0.93 Oral agentsb 8 (13.6) 5 (8.2) 1.75 0.54–5.71 0.34 Biological 4 (6.8) 3 (4.9) 1.40 0.30–6.57 0.66 CI, confidence interval; GP, guttate psoriasis; OR, odds ratio; URTI, upper respiratory tract infection; SD, standard deviation; ASLO, antistreptolysin O. Guttate Psoriasis: Long-Term Follow-Up Dermatology 2023;239:188–194 191 DOI: 10.1159/000527737
Table 2. Characteristics of patients who initially presented with GP and acquired PV phenotype (n = 21) compared to patients with nontransformed GP phenotype (n = 99) Characteristic PV (n = 21), GP (n = 99), OR CI p Value N (%) N (%) Follow-up, years, mean (SD) 6.2 (2.6) 6.1 (3.2) 1.00 0.86–1.17 0.07 Age at first event, years, mean (SD) 23.1 (14.5) 29.8 (15.3) 0.96 0.93–1.00 0.36 Female gender (%) 11 (52.4) 59 (59.6) 0.74 0.29–1.92 0.54 Family history of psoriasis 11 (52.4) 32 (32.7) 2.26 0.87–5.89 0.08 Missing data N=1 N=2 GP episodes, n (%) 1 4 (19.0) 45 (45.5) 0.28 0.08–0.90 0.02 2–3 6 (28.3) 26 (26.3) 1.12 0.39–3.20 0.82 Over 3 11 (52.4) 28 (28.3) 2.78 1.06–7.29 0.03 Area involved Trunk 18 (94.7) 86 (92.5) 1.46 0.17–12.65 0.72 Limbs 18 (94.7) 89 (95.7) 0.80 0.08–7.66 0.85 Downloaded from http://karger.com/drm/article-pdf/239/2/188/3922414/000527737.pdf by guest on 22 June 2023 Head 8 (42.1) 44 (47.3) 0.81 0.29–2.19 0.67 Diffuse 8 (42.1) 42 (45.2) 0.88 0.32–2.39 0.80 Missing data N=2 N=6 URTI anticipating GP flare At first GP episode 10 (47.6) 66 (66.7) 0.45 0.17–1.17 0.10 At some GP episodes 5 (23.8) 14 (14.1) 0.55 0.21–1.45 0.27 With confirmed streptococcal infectiona 4 (66.7) 19 (48.7) 2.10 0.34–12.86 0.41 Missing data 17 60 Hand and foot involvement At first GP episode 6 (35.3) 14 (18.9) 2.33 0.73–7.40 0.14 At some GP episodes 7 (41.2) 19 (25.7) 2.02 0.67–6.07 0.20 Missing data N=5 N = 24 Scalp involvement At first episode 12 (57.1) 44 (44.9) 1.63 0.63–4.23 0.30 At some GP episodes 17 (81.0) 49 (50.0) 4.25 1.33–13.54 0.01 Missing data N=0 N=1 Comorbidity, (%) Arthralgia/Arthritis 5 (23.8) 13 (13.1) 2.06 0.64–6.60 0.21 Hypertension 1 (4.8) 7 (7.1) 0.65 0.07–5.64 0.70 Hyperlipidemia 1 (4.8) 8 (8.1) 0.56 0.06–4.80 0.60 Diabetes 1 (4.8) 4 (4.0) 1.18 0.12–11.19 0.88 Obesity 1 (4.8) 10 (10.4) 0.44 0.05–3.67 0.44 Most potent treatment at first GP episode Topical 2 (10.0) 12 (2.5) 0.77 0.16–3.78 0.75 Phototherapy 14 (70.0) 80 (83.3) 0.46 0.15–1.39 0.16 Oral agentsb 4 (20.0) 4 (4.2) 5.75 1.30–25.36 0.01 Biological 0 (0) 0 (0) Most potent treatment along disease course Topical 3 (14.3) 12 (12.1) 1.20 0.30–4.72 0.79 Phototherapy 9 (42.9) 76 (76.8) 0.22 0.08–0.60 0.002 Oral agents b 5 (23.8) 8 (8.1) 3.55 1.03–12.25 0.03 Biological 4 (19.0) 3 (3.0) 7.52 1.54–36.6 0.004 CI, confidence interval; GP, guttate psoriasis; OR, odds ratio; URTI, upper respiratory tract infection; SD, standard deviation; ASLO, antistreptolysin O. a Throat culture positive for group A β-hemolytic Streptococcus or positive ASLO titer (>200 U/mL, taken up to 5 weeks from the onset of symptoms). b Acitretin, immunosuppressants, and phosphodiesterase 4 inhibitors. 192 Dermatology 2023;239:188–194 Galili/Levy/Tzanani/Segal/Lyakhovitsky/ DOI: 10.1159/000527737 Barzilai/Baum
of the patients with the PV phenotype versus 7.1% and ment approaches. This seems unlikely from our study, as 11.1% of the nontransformed GP patients (ORs = 6 and we found similar comorbidities in both GP and acquired 4.1; Cis, 2.1–17.5 and 1.6–14.5, respectively). Sex, family PV phenotypes; however, there is a need for different history of psoriasis, comorbidities, or GP triggering fac- treatment potency. tors were found to be associated with acquiring the PV Other studies have also reported rates of chronic pso- phenotype. riatic disease. However, these ambiguously define the endpoint of the disease phenotype. Pfingstler et al. [9] re- ported that in a retrospective cohort of 79 patients with Discussion GP, more than a single GP episode was regarded as equiv- alent to plaque psoriasis, occurring in approximately 25% This study assessed the long-term outcomes of new- of the patients. Martin et al. [11] reported that over a fol- onset GP. In almost half of the patients (49.1%), persistent low-up period of 10 years, 5 of 15 (33.3%) patients devel- psoriatic lesions that presented more than a year after GP oped persistent psoriasis. Furthermore, in their study, onset were recorded at the end of follow-up. Although the multiple GP events were recorded in most of the patients. switch to the vulgaris phenotype was significantly associ- While it is well documented that GP is associated with a Downloaded from http://karger.com/drm/article-pdf/239/2/188/3922414/000527737.pdf by guest on 22 June 2023 ated with persistent disease, it only occurred in a minor- family history of psoriasis [7], in our study, it did not pre- ity of these patients. Overall, 17.5% of the patients devel- dict a switch to the vulgaris phenotype or a persistent dis- oped PV phenotypes during the follow-up period. Addi- ease course. Additionally, the data from our study did not tionally, persistent psoriasis was also associated with male identify URTIs to be associated with persistent disease or sex, over three GP flares, and palmoplantar involvement. development of the vulgaris phenotype. This contrasts The long-term outcomes of new-onset GP have been with the results of a study by Pfingstler et al. [9] who rarely described. A recent comprehensive study by Sved- showed that patients with the acquired vulgaris pheno- bom et al. [12] prospectively evaluated 116 patients with type were less likely to test positive for streptococci infec- GP and reported persistent disease rates of 68% at 10 tion. However, only one subgroup of his cohort was test- years of follow-up. Importantly, in our study, disease per- ed for throat infections. sistence remained elevated during the entire follow-up Additionally, we identified several predictors associ- period (up to 12 years), highlighting the clinical signifi- ated with a persistent course of psoriasis. At the onset of cance of this finding. Contrary to our findings, in the GP, persistent disease course predictors were male sex study by Svedbom et al. [12], the majority of patients with and palmoplantar involvement. However, it is unknown persistent disease ultimately acquired the vulgaris pheno- whether early therapeutic interventions are helpful in type. Ko et al. [10] also reported a persistent GP course of lowering the risk of persistence. Along the GP disease over a year in 38.9% of their retrospective cohort of 36 course over three GP flares, the acquired vulvar pheno- patients. In line with our findings, only 15% of patients type was also found to be associated with a persistent dis- with a persistent disease course transformed to plaque ease course. psoriasis, while the rest remained with a guttate pheno- This study has several limitations, including its retro- type. spective nature, although of a considerably large scale. In our study, persistent disease end-phenotype affect- Second, the endpoint disease severity and extent were ed prognosis, as a significantly larger proportion of the based on patient reports; however, validated scales were PV phenotype needed oral or biological agents. To the used [14–17]. Third, we could not differentiate between best of our knowledge, this is the first study to assess the bacterial and viral URTI triggers because these data were clinical importance of acquired PV phenotypes among unavailable for most patients. Further research is re- patients with persistent GP. Although patient-reported quired to validate our findings. severity scales did not differ between the groups, they were completed under treatment. In our study, well- known psoriatic comorbidities were similarly distributed Conclusions among the entire spectrum of GP presentations, includ- ing those who ultimately acquired the PV phenotype. In a long-term follow-up study, a persistent GP course Further studies are needed to assess whether the persis- of greater than 1 year was common among patients with tent GP phenotype should practically be regarded as new-onset GP. A minority of patients with persistent dis- “small plaque” PV, with similar comorbidities and treat- ease acquire the vulgaris phenotype, with a negative im- Guttate Psoriasis: Long-Term Follow-Up Dermatology 2023;239:188–194 193 DOI: 10.1159/000527737
pact on disease prognosis. Persistent GP was associated Funding Sources with male sex, over three GP flares, switch to the vulgaris The study was conducted without funding sources. phenotype, and palmoplantar involvement. Author Contributions Key Message Eran Galili and Sharon Baum: conception and design. Eran A persistent disease course was found to be common among Galili, Shir Rubinstein Levy, Ido Tzanani, and Oz Segal: data ac- patients with new-onset guttate psoriasis. quisition and analysis. Anna Lyakhovitsky, Aviv Barzilai, and Sha- ron Baum: supervision. All authors: critical revision and final ap- proval of the version to be published. Statement of Ethics This study was approved by the Human Research Ethics Com- Data Availability Statement mittee of the Sheba Medical Center (No. SMC-7082-20) and was conducted in accordance with the Declaration of Helsinki. Written The data that support the findings of this study are available on Downloaded from http://karger.com/drm/article-pdf/239/2/188/3922414/000527737.pdf by guest on 22 June 2023 informed consent was obtained from participants. request from the corresponding author. The data are not publicly available due to privacy or ethical restrictions. Further inquiries can be directed to the corresponding author, Eran Galili. Conflict of Interest Statement The authors have no conflicts of interest to declare. References 1 Langley RGB, Krueger GG, Griffiths CEM. 7 Naldi L, Peli L, Parazzini F, Carrel CF. Family 13 Sato H, Ishikawa H. Unspecific increase of Psoriasis: epidemiology, clinical features, and history of psoriasis, stressful life events, and antistreptolysin-O titer in acute guttate pso- quality of life. Ann Rheum Dis. 2005;64(Sup- recent infectious disease are risk factors for a riasis. J Dermatol. 1977;4(5):187–91. pl 2):ii18–25. first episode of acute guttate psoriasis: results 14 Valenzuela F, Paul C, Mallbris L, Tan H, Pa- 2 Psoriasis G. Overview of Guttate Psoriasis, of a case-control study. J Am Acad Dermatol. pacharalambous J, Valdez H, et al. Tofacitinib Pathophysiology of Guttate Psoriasis, Epide- 2001;44(3):433–8. versus etanercept or placebo in patients with miology of Guttate Psoriasis. 2020. (accessed 8 Durham GA, Morgan JK. A y-year follow-up moderate to severe chronic plaque psoriasis: March 30, 2020) Available from: https: // study of ninety patients with psoriasis. Br J patient-reported outcomes from a Phase 3 emedicine.medscape.com/article/1107850- Dermatol. 1974;91(1):7–11. study. J Eur Acad Dermatol Venereol. 2016; overview#a3. 9 Pfingstler LF, Maroon M, Mowad C. Guttate 30(10):1753–9. 3 Leung DYM, Travers JB, Giorno R, Norris psoriasis outcomes. Cutis. 2016;97(2):140–4. 15 Shikiar R, Bresnahan BW, Stone SP, Thomp- DA, Skinner R, Aelion J, et al. Evidence for a 10 Ko HC, Jwa SW, Song M, Kim MB, Kwon KS. son C, Koo J, Revicki DA. Validity and reli- streptococcal superantigen-driven process in Clinical course of guttate psoriasis: long-term ability of patient reported outcomes used in acute Guttate psoriasis. J Clin Invest. 1995; follow-up study. The J Dermatol. 2010;37(10): psoriasis: results from two randomized clini- 96(5):2106–12. 894–9. cal trials. Health Qual Life Outcomes. 2003;1: 4 Baker BS, Bokth S, Powles A, Garioch JJ, Lew- 11 Martin BA, Chalmers RJG, Telfer NR. How 53. is H, Valdimarsson H, et al. Group A strepto- great is the risk of further psoriasis following 16 Dommasch ED, Shin DB, Troxel AB, Margo- coccal antigen-specific T lymphocytes in gut- a single episode of acute guttate psoriasis?. lis DJ, Gelfand JM. Reliability, validity and re- tate psoriatic lesions. Br J Dermatol. 1993; Arch Dermatol. 1996;132(6):717–8. sponsiveness to change of the Patient Report 128(5):493–9. 12 Svedbom A, Mallbris L, Larsson P, Nikamo P, of Extent of Psoriasis Involvement (PREPI) 5 Telfer NR, Chalmers RJG, Whale K, Colman Wolk K, Kjellman P, et al. Long-term out- for measuring body surface area affected by G. The role of streptococcal infection in the comes and prognosis in new-onset psoriasis. psoriasis. Br J Dermatol. 2010;162(4):835–42. initiation of guttate psoriasis. Arch Dermatol. JAMA Dermatol. 2021;157(6):1–8. 17 Raychaudhuri SK, Maverakis E, Raychaud- 1992;128(1):39–42. huri SP. Diagnosis and classification of pso- 6 Diluvio L, Vollmer S, Besgen P, Ellwart JW, riasis. Autoimmun Rev. 2014;13(4–5):490–5. Chimenti S, Prinz JC. Identical TCR β-chain rearrangements in streptococcal angina and skin lesions of patients with psoriasis vulgaris. J Immunol. 2006;176:7104–11. 194 Dermatology 2023;239:188–194 Galili/Levy/Tzanani/Segal/Lyakhovitsky/ DOI: 10.1159/000527737 Barzilai/Baum
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