Next Article in Journal
Folate Receptor Alpha Autoantibodies in the Pediatric Acute-Onset Neuropsychiatric Syndrome (PANS) and Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcal Infections (PANDAS) Population
Previous Article in Journal
Can Artificial Intelligence Replace Humans for Detecting Lung Tumors on Radiographs? An Examination of Resected Malignant Lung Tumors
 
 
Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
Journals
JPM
Volume 14
Issue 2
10.3390/jpm14020165
jpm-logo
Submit to this Journal Review for this Journal Propose a Special Issue
► Article Menu

Article Menu

share Share announcement Help format_quote Cite question_answer Discuss in SciProfiles thumb_up
...
Endorse textsms
...
Comment
first_page
settings
Order Article Reprints
Font Type:
Arial Georgia Verdana
Font Size:
Aa Aa Aa
Line Spacing:
Column Width:
Background:
Systematic Review

Psoriasis and Fibromyalgia: A Systematic Review

by
Martina D’Onghia
1,
Francesco Ursini
2,3,
Elisa Cinotti
1,*,
Laura Calabrese
1,
Linda Tognetti
1,
Alessandra Cartocci
1,
Laura Lazzeri
1,
Bruno Frediani
4,
Pietro Rubegni
1 and
Emanuele Trovato
1
1
Department of Medical, Surgical and Neurological Sciences, Dermatology Section, University of Siena, 53100 Siena, Italy
2
Medicine and Rheumatology Unit, IRCCS Istituto Ortopedico Rizzoli, 40136 Bologna, Italy
3
Department of Biomedical and Neuromotor Sciences (DIBINEM), University of Bologna, 40126 Bologna, Italy
4
Rheumatology Unit, Department of Medicine, Surgery and Neurosciences, University of Siena, 53100 Siena, Italy
*
Author to whom correspondence should be addressed.
J. Pers. Med. 2024, 14(2), 165; https://doi.org/10.3390/jpm14020165
Submission received: 28 November 2023 / Revised: 21 January 2024 / Accepted: 28 January 2024 / Published: 31 January 2024
(This article belongs to the Section Mechanisms of Diseases)
Browse Figure
Versions Notes

Abstract

:
Psoriasis is a chronic inflammatory cutaneous condition characterized by several comorbidities, including musculoskeletal disorders. While the association with psoriatic arthritis has been widely addressed in literature, the aim of the present systematic review was to identify all available evidence on the relationship between psoriasis and fibromyalgia, a musculoskeletal syndrome primarily characterized by chronic widespread pain. We followed the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines, and MedLine and Web of Science (WOS) databases were searched for literature up to March 2023. After the removal of duplicate records, a total of 11 articles were deemed eligible for inclusion in a qualitative synthesis. Our results suggested that psoriatic patients had a higher prevalence of fibromyalgia (8–30%), with a very high impact on symptoms of psoriasis. Moreover, fibromyalgic patients had a slightly increased prevalence of psoriasis (2.2–6.7%) compared to the control groups. Finally, several studies demonstrated the substantial impact of fibromyalgia on psoriatic outcome measures in patients with concomitant psoriatic arthritis. In conclusion, available data support a potential interplay between psoriasis and fibromyalgia, but further research is encouraged in this area.

1. Introduction

Fibromyalgia (FM) is a chronic syndrome primarily characterized by widespread pain, fatigue, and sleep disturbances but also by a variety of associated symptoms, including cognitive impairment, anxiety, and depression [1]. Fibromyalgia mainly affects women over 50 years old, reaching an estimated global prevalence of 2% to 3% [2]. The severe symptom burden of FM negatively influences patients’ social functioning and quality of life, resulting in high direct and indirect costs [3].
The real nature of FM is still controversial. Pathogenesis encompasses both central and peripheral mechanisms involved in pain processing through a complex interplay between genetic, immunological, inflammatory, endocrine, social, and cognitive components [4].
Although FM is recognized as a distinct condition, a growing body of literature has focused on the association between FM and other diseases not necessarily defined by chronic pain, such as neurological, gastrointestinal, and mental health illnesses [5]. Within this context, recognizing FM comorbidity is crucial due to its impact on overall self-perceived health status: indeed, a misdiagnosis could result in inaccurate assessment of the severity of the primary disease (often overestimated), which may impact how the underlying condition is managed and treated.
Compared to the general population, FM is particularly common in chronic inflammatory arthropathies, including psoriatic arthritis (PsA) [6], a complex inflammatory musculoskeletal disease with the highest prevalence among 30–60-year-old patients and with no sex differences [7]. PsA may occur in around ~30% of patients with skin psoriasis (PsO) [7], and it is also associated with higher risk of developing comorbidities, including uveitis, inflammatory bowel disease, and metabolic syndrome, with a significant impact on quality of life [8]. Although the precise mechanisms underlying PsA pathogenesis are poorly understood, several immune-inflammatory pathways have been identified, leading to the development of novel therapeutic strategies [9]. However, a sizable portion of PsA patients still report unsatisfactory results following such treatments and experience residual pain and fatigue [10]. Given some clinical similarities between these conditions, it can be difficult to differentiate PsA-associated polyenthesitis from concurrent FM, and it is yet to be quantified how much of treatment failure in PsA patients may be attributed to concurrent FM [11]. Furthermore, while the relationship between FM and rheumatic disorders has received considerable interest, little is known about the association between FM and PsO, although—beyond joint complaints—many FM symptoms are also frequent in PsO, such as fatigue [12], sleep disturbances [13], and cognitive impairment [14].
Despite several comorbidities that have been reported in FM patients, this condition is not classically considered to be associated with cutaneous findings, and the available literature on this topic is still limited. However, current evidence has shown objective differences in the skin biopsies of FM patients compared with healthy subjects [15]. Particularly, multiple studies have described increased mast cell and inflammatory cytokines counts [16,17], altered collagen metabolism [18], cutaneous microcirculatory changes, autonomic nervous system dysfunction, and increased cutaneous opioid receptors in the skin of FM patients [16]. It is well accepted that the impact of PsO, a chronic immune-mediated inflammatory disease, extends far beyond the skin. Psoriasis affects approximately 125 million people worldwide, with a mean age of onset between 30 and 50 years [19], representing a huge health problem for patients and society [20]. The pathogenesis of psoriasis is multifaceted, resulting from the interaction between environmental, genetic, and immunologic factors [21]. The constellation of systemic-associated comorbidities, including cardiometabolic, gastrointestinal, kidney diseases, malignancy, infection, and psychiatric disorders, highlights the importance of correct management of those patients, which is often challenging [22,23].
On this background, the aim of this systematic review was to identify all available data on the prevalence of FM in PsO patients and to synthetize what is known regarding the relationship between PsO severity and FM.

2. Materials and Methods

2.1. Search Strategy

MedLine (via PubMed), Web of Science (WOS). And Cochrane Central Register of Controlled Trials (CENTRAL) databases were searched up to 10 March 2023. The main search in MedLine was performed using the string “(fibromyalgia” OR “chronic fatigue syndrome” OR “chronic fatigue disorder”) AND (“psoriasis” OR “psoriatic arthritis” OR “spondylarth*”)”, while the main search in CENTRAL was performed using the string “(“fibromyalgia” OR “chronic fatigue syndrome” OR “chronic fatigue disorder”) AND (“psoriasis” OR “psoriatic arthritis” OR “spondyloarthritis”)”. Finally, the main search in WOS was performed using the string “[TS= ((“fibromyalgia” OR “chronic fatigue syndrome” OR “chronic fatigue disorder”) AND (“psoriasis” OR “psoriatic arthritis” OR “spondylarth*”))]”. Additionally, relevant keywords were used in different combinations for free-hand search, and the bibliography of selected articles was reviewed. The decision to include the keywords “chronic fatigue syndrome” was adopted to increase the sensitivity of the search strategy (e.g., identification of studies centered on chronic fatigue syndrome (CFS) but also including individuals satisfying criteria for FM, given the clinical overlap between the two clinical entities), although the focus of our article was FM. A similar rationale was used for including the keywords “psoriatic arthritis” and “spondyloarthritis”.
The search was designed and performed by one author (MD) under the supervision of a senior investigator (FU). No date restriction was applied. We followed the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines [24] for preparing our manuscript.

2.2. Eligibility Criteria

For the purpose of this study, only articles written in the English language were considered eligible. To be included in the final review, studies had to be published as full-text original articles in international, peer-reviewed journals. Randomized controlled trials (RCT), quasi-RCT (trials in which allocation to treatment was made by alternation, use of alternate medical records, date of birth, or other expected methods), prospective or retrospective cohort studies, and cross-sectional studies were deemed eligible. The population, intervention, comparator, outcome (PICO) framework was used to build the search question. All studies meeting the following criteria were included in the final review:
-
Population: adult patients diagnosed with FM or PsO;
-
Intervention: not applicable;
-
Comparison: healthy controls or no control group;
-
Outcome:
  • Studies assessing the prevalence of PsO in FM patients.
  • Studies assessing the prevalence of FM in PsO patients.
  • Studies assessing the association between severity of FM clinical features (composite measures of symptoms severity, pain, tender point count, stiffness, fatigue, physical functioning, sleep, depression, anxiety, cognitive dysfunction, QoL) and outcomes measures in PsO and vice versa.
Studies focused on PsA only, without adequate subanalysis to extrapolate information related to cutaneous domain, were excluded.

2.3. Study Selection Process and Data Extraction

After removal of duplicate records, three reviewers (MD, ET, and LC) independently screened titles and abstracts for the first-step evaluation. Following the screening phase, two reviewers (MD and ET) independently evaluated the full text of the remaining articles to determine eligibility for inclusion in the final review. Disagreements among the reviewers were resolved by discussion with a third senior investigator (FU) until reaching a final consensus. A detailed flowchart of the study selection process is reported in Figure 1. Additional studies were identified using bibliographical information of relevant articles.

2.4. Quality Assessment

The quality of studies was evaluated using the Newcastle-Ottawa Quality Assessment Scale (NOS) [25], extensively used to assess the risk of bias in cohort and cross-sectional studies (Table 1).

3. Results

3.1. Results of the Systematic Search

The search strategy identified 254 records in PubMed, 278 in WOS, and 43 in CENTRAL. In addition, a manual search identified one relevant article. After the removal of duplicates, a total of 361 studies proceeded to review. Of those, 302 articles were excluded following screening of titles and abstracts, and full text evaluation was performed on 59 articles. A total of eleven articles were deemed eligible for inclusion in qualitative synthesis, including ten cross-sectional studies and one longitudinal cohort studies (Figure 1). Quality assessment, performed using the NOS scale, showed that the overall risk of bias was high, since none of the included studies scored > 7, widely used as a cut-off for defining high quality (Table 1).

3.2. FM in PsO Patients: Higher Prevalence and Impact on Outcome Measures

Two of the selected articles reported the prevalence of FM in PsO patients and the aftermath of comorbid FM on PsO disease activity [33,35] (see Table 2).
Thune et al. [35] investigated the consequences of FM in a cross-sectional study of 1269 consecutive PsO patients. Among them, 230 (14.1%) had musculoskeletal pain not fulfilling the American College of Rheumatology (ACR) 1990 criteria for FM [37], while 105 (8.3%), mostly women (97.6%), fulfilled the criteria. Of note, 9% of patients had chronic widespread pain (CWP) not satisfying the 1990 FM criteria because of an insufficient tender point count. However, it is possible to anticipate that some of these patients may fulfil the 2016 ACR criteria that abolished the tender point count favoring subjective reporting of widespread pain.
Although psoriasis extent did not differ between patients with and without FM, the two groups differed in terms of disease locations and phenotype. Specifically, the involvement of the head and palmoplantar pustulosis were more frequent in FM patients, while small lesions of the trunk and extremities were more common in individuals not satisfying FM criteria. No correlation was found between FM symptoms and extent of PsO (R < 0.25). On the other hand, tender point count, visual analogue scale (VAS) pain score, prevalence of sleep disturbances, morning tenderness, and daytime fatigue were higher in FM + PsO patients when compared to non-FM (all p < 0.05). In total, 27 patients (28.2%) with FM were diagnosed with PsA and 16 patients with possible PsA. By comparison, only 44/230 patients (19%) with musculoskeletal complaints but without FM were diagnosed as having PsA.
In 2020, Mathkhor et al. [33] published the results of a cross-sectional study on 70 PsO patients and 70 age- and sex-matched controls from the general population. Patients with a diagnosis of PsA were excluded from the study. The overall prevalence of CWP not fulfilling the FM criteria in PsO patients was 52.9% (n = 37), while the overall prevalence of FM in PsO was 30% (n = 21), predominantly women (85.7%, p < 0.05). Psoriasis area severity index (PASI) score was higher in PsO + FM patients when compared to non-FM (respectively 57.9 ± 4.6 vs. 15.5 ± 4.6, p < 0.05). Lastly, FM-allied symptoms, such as morning stiffness, sleep disturbances, anxiety, fatigue, headache, and irritable bowel syndrome, were higher in PsO individuals when compared to the control group (p < 0.05).

3.3. PsO in FM Patients: A Controversial Association

In 2014 Laniosz et al. [32] performed a cross-sectional study to investigate the prevalence of dermatologic diseases and skin-related symptoms in 897 patients with a confirmed diagnosis of FM, reporting an overall prevalence of PsO of 2.2%, a figure that seems comparable to what is observed in the Western general population [38].
Erdogan et al. [29] in their study evaluated skin findings and skin-related symptoms in 105 female FM patients and 105 matched controls. From their analysis, PsO did not appear to be overrepresented in the FM population compared to the control group (p = 0.498).
Finally, Kridin et al. [26] conducted a population-based study from a large database from Israel. A total of 18,598 FM patients were enrolled as cases, and age- and gender-matched randomly to controls without FM (n = 36,985). The prevalence of PsO was higher in FM patients compared to control subjects (6.7% vs. 4.8%, respectively; OR, 1.4; 95% C.I.: 1.3–1.5; p < 0.001) with the greatest association seen in patients between 30 and 49 years (1.5; 95% CI: 1.3–1.8; p < 0.001) and males (OR: 1.8; 95% C.I.: 1.4–2.3; p < 0.001).
This association was robust to a multivariate analysis accounting for age, gender, ancestry, socioeconomic status, and healthcare utilization (OR, 1.3; 95% C.I.: 1.2–1.4; p < 0.001). Finally, patients with coexisting FM and PsO presented with a significantly older age, a higher mean body mass index (BMI), and frequency of smoking when compared to FM only patients.

3.4. FM in PsA Patients: Results on PsO Outcome Measures

Two of the reviewed studies demonstrated that PASI score was statistically higher in patients with concomitant FM and PsA [28,30]. In a cross-sectional study by Elsawy et al. [28], patients with PsA and FM had higher median PASI levels compared to PsA only [14.4 (0.9–49.6) vs. 8.3 (0.0–45.7), p = 0.043]; furthermore, there was a positive correlation between the Fibromyalgia Impact Questionnaire (FIQ) and PASI (R = 0.488, p = 0.018). Median Dermatology Life Quality Index (DLQI) was numerically higher but did not reach the level of statistical significance [13 (3–24) vs. 9 (0–30), p = 0.073]. Similarly, Iannone et al. [30] confirmed a higher PASI score in patients with coexisting PsA + FM compared to PsA only [0.2 (0.5) 0.4 vs. (1.4) 0.6, p = 0.0006], but no significant differences were observed with regard to onychopathy.
On the other hand, Brinkman et al. [27] did not find any significant difference in PASI score comparing PsA + FM versus PsA only patients [3 (0.8–8.6) vs. 2.1 (0.2–6.3), p = 0.22].
Again, Kancharla et al. [31] did not find any significant difference regarding age at onset, duration, or severity of PsO, evaluated through Body Surface Area (BSA) score or PASI, comparing PsA patients with and without FM; in univariate logistic regression, PASI was not associated with the risk of having comorbid FM [OR: 1.01 (0.88–1.15), p = 0.90] and no correlation of either FM Symptom Severity Scale (SSS), Widespread Pain Index (WPI), or FIQ was noted with severity of skin involvement measured by PASI or the duration of skin disease.
Furthermore, Ulus et al. [36] pointed out how psoriasis duration was higher among PsA + FM when compared to only PsA patients; however, Polachek et al. [34] did not find any difference in PsO duration between PsA patients with and without FM.

4. Discussion

Psoriasis is a chronic skin disease with a profound impact on patients’ well-being and quality of life, comparable to that observed in other chronic diseases such as cardiovascular diseases, diabetes, end-stage renal diseases, or cancer [39]. Furthermore, the disease burden of PsO is worsened by a higher risk of comorbidities such as arthritis, obesity, cardiometabolic derangement, psychiatric illness, and malignancy [40].
Although it is somewhat intuitive that rheumatological complaints in PsO patients can often be attributed to coexistent PsA, musculoskeletal pain is highly prevalent in PsO patients even in the absence of clinical, serological, and imaging features suggestive of PsA. A Danish population-based survey reported a prevalence of musculoskeletal pain of 68.3%, in contrast with the prevalence of PsA that was only about 20% [41].
This discrepancy may represent a limit in sensitivity to demonstrate subtlest inflammatory abnormalities—especially at the enthesis—but it is also possible to speculate that a link exists between PsO and other musculoskeletal disorders, including FM.
Fibromyalgia, on the other hand, is a well-established aggravating factor in rheumatic diseases, and its misrecognition may lead to important consequences, in particular overinvestigation and overtreatment [42].
Unfortunately, the results of our systematic review clearly demonstrate that this topic has been poorly explored. Indeed, while several articles describe the association between PsA and FM (outside the scope of this review), little is known about the relationship between pure skin PsO and FM.
Overall, we found only two studies reporting data on the prevalence of FM in PsO, suggesting that it is higher (8–30%) than that observed in the general population [33,35]. Despite this, we feel that comorbid FM can, at least in part, fill the gap between the highly reported musculoskeletal pain and the true prevalence of PsA in PsO patients.
Although the putative pathways connecting PsO to FM are still unknown, some speculative hypotheses can be made based on available data. Despite the frequent consideration of physicians that psoriasis is not particularly associated with skin symptoms, cutaneous pain is reported by up to 42% of patients with PsO [43,44], and it is associated with several subjective unpleasant feelings such as pruritus, unpleasantness, aches, sensitivity, heat/burning, tenderness, and cramping. Specifically, PsO patients describe their pain as a stinging, hot, burning pain, suggesting a neurogenic origin, even though this topic has not been widely investigated in literature [45].
In this context, chronic nociceptive skin stimulation may subsequently lead to central sensitization [46], a mechanism supposed to underly FM associated with other painful diseases such as osteoarthritis [47]. Another possible explanation for the increased prevalence of FM in PsO may lie in the common underlying pathogenetic pathways associated with dysfunctional neurotransmitter systems, particularly the increased level of substance P [48,49]. Furthermore, inflammatory mechanisms are emerging as potential contributors to FM pathogenesis [50]. Interestingly, the distinctive signature of FM includes pro-inflammatory cytokines, which also play a role in the pathogenesis of PsO [51,52]. The results of several studies have shown the presence of increased levels of IL6 [53], IL8 [54], [55] and TNF-α [53,56] in FM patients, giving additional support to this linkage. Notably, Pernambuco et al. [57] found higher levels of IL17A in FM patients, which represents one of the major immunologic cytokines that drives the psoriatic disease [58]. Overall, the imbalance between pro-inflammatory and anti-inflammatory cytokines could underlie a common pathogenetic pathway associated with both FM and psoriatic disorders by contributing to the induction and maintenance of pain [59].
In addition to the increased number of inflammatory cytokines, a statistically significant increase in the number of mast cells, as well as increased mast cell degranulation have been shown in the skin of FM patients [16]. All of these processes have been shown to lead to increased pruritus, burning, and other forms of neuropathic discomfort.
Other possible puzzle pieces can be found in the literature, such as the widespread occurrence of FM-allied symptoms in PsO patients.
Fatigue is a crucial symptom of FM [60] and there is a large clinical overlap between FM and chronic fatigue syndrome (CFS) [61]. Fatigue, on the other hand, is reported frequently (nearly 50% in [12]) in PsO patients, and PsO itself is associated with a 48% increase of subsequent development of CFS [62]. Although the mechanisms leading to fatigue in PsO are far from being ascertained, crucial molecular and cellular players of PsO immunopathogenesis [63,64] are believed to contribute by exploiting both central and peripheral mechanisms.
Sleep disturbances affect more than 90% of patients with FM [65]; similarly, the prevalence of insomnia in PsO has been reported in 5.9–44.8% of patients, while the prevalence of OSA and restless leg syndrome (RLS) ranged from 36–82% and 6–15%, respectively [66].
Further, FM and PsO share an increased risk of psychiatric diseases. The bidirectional association between FM and depression or anxiety has been widely demonstrated in literature [67], as the role of depression in PsO is well known, traditionally explained as a response to psychosocial factors and impaired quality of life, even though a recent hypothesis evoked the dysregulation of common inflammatory and immunological pathways in depression and PsO [68]. Intriguingly, a study by Pinho de Oliveira Ribeiro et al. [69] suggested that DMARDs, such as methotrexate, used to treat severe PsO and PsA, conferred the highest risk of depression, anxiety, and suicidal ideation. On this basis, since FM and PsO are individually related to psychosocial disability, the coexistence of both may worsen depression, influencing management and treatment of those patients and increasing the risk of drug interaction and adverse effects, in a vicious circle.
Another intriguing link between those two conditions may be represented by obesity. It is known that obesity has a cardinal role in pathogenesis of skin diseases, including PsO, by producing adipokines, a group of proinflammatory cytokines involved in immunity and responsible for a chronic low-grade inflammatory state [70]. The overexpression of leptin in obese patients has been shown to reduce T regulatory cells (T-regs) and amplify the local inflammation, as reflected by higher IL-17 and IL-23 in obese subjects compared to controls. Moreover, IL-6 can break homeostasis in immune tolerance by inhibiting TGFβ-driven T-reg differentiation and promoting Th17 differentiation [71,72]. Based on the current knowledge, FM and obesity share common pathophysiological mechanisms, in which obesity seems to represent an aggravating factor and a potential trigger in FM patients, while FM may favor or worsen the development of obesity. Another possible hypothesis is that obesity may “trigger” FM symptoms by fueling the low-grade inflammatory background [73]. Accordingly, the effect of therapeutic weight loss may provide potential benefit in the comprehensive treatment of both PsO and FM patients.
From an epidemiological point of view, data indicate that the occurrence of both FM and PsO varies in relation to demographic characteristics, such as age, gender, and geographic region, but also according to the diagnostic criteria used to define the primary condition [2,74,75]. We found that FM patients with PsO were mostly middle-aged women, which is not particularly surprising since FM has a strong female predominance [26,29,32]. Conversely, there is lack of agreement on specific gender differences in PsO, and a slight male predominance was reported in recent studies [76]. Nevertheless, our results showed that FM was more frequent in female patients with PsO [33,35], suggesting a possible differential gender distribution of FM in the setting of this cutaneous disease. However, further research is required to determine the underlying mechanisms to explain this relationship.
Our review attempted to shed light on the relationship between FM and PsO and opens many new avenues for research, but despite its potential, some limitations must be acknowledged. First, literature on skin findings in FM patients is still lacking, and the few available studies are characterized by high heterogeneity regarding design, sample size, adequate age- and gender-matched control group, demographic characteristics of patients (such as gender ratio), severity of PsO, and classification criteria used. Second, in some studies, the presence of FM was defined using the 1990 ACR criteria, based on tender point count; however, a large overlap between FM tender points and potential enthesitis sites is now recognized that can lead to misclassification [77,78,79].
Finally, most of the eligible studies had a cross-sectional design; hence, distinction between higher PsO disease activity precipitating secondary FM versus comorbid FM inflating PsO disease activity cannot be ascertained.

5. Conclusions

In conclusion, our review suggests that a relationship between Pso and FM is likely to exist, although the mechanisms are far from being clear. Comorbid FM can represent an aggravating factor reverberating on some features of PsO and an amplifier of pain, fatigue, and physical disability, leading to poor QoL independently from the primary skin disease. For these reasons, to achieve global well-being, it seems important to evaluate the presence of comorbid FM, so that the clinicians can make appropriate decisions on the management and treatment of the underlying condition, as well as instituting nonpharmacological or pharmacologic treatment for FM. Future studies are mandatory to shed light on causative mechanisms beyond the possible association between these disorders.

Author Contributions

Conceptualization, M.D. and F.U.; methodology, M.D.; data curation, A.C.; writing—original draft preparation, M.D.; writing—review and editing, E.T. and E.C.; visualization, L.C., L.T. and L.L.; supervision, P.R. and B.F. All authors have read and agreed to the published version of the manuscript.

Funding

This research received no external funding.

Institutional Review Board Statement

Not applicable.

Informed Consent Statement

Not applicable.

Data Availability Statement

Data are available upon request to the corresponding author.

Conflicts of Interest

The authors declare no conflicts of interest.

References

  1. Bair, M.J.; Krebs, E.E. Fibromyalgia. Ann. Intern. Med. 2020, 172, 33–48. [Google Scholar] [CrossRef]
  2. Sarzi-Puttini, P.; Giorgi, V.; Marotto, D.; Atzeni, F. Fibromyalgia: An update on clinical characteristics, aetiopathogenesis and treatment. Nat. Rev. Rheumatol. 2020, 16, 645–660. [Google Scholar] [CrossRef]
  3. D’Onghia, M.; Ciaffi, J.; Ruscitti, P.; Cipriani, P.; Giacomelli, R.; Ablin, J.N.; Ursini, F. The economic burden of fibromyalgia: A systematic literature review. Semin. Arthritis Rheum. 2022, 56, 152060. [Google Scholar] [CrossRef]
  4. Siracusa, R.; Paola, R.D.; Cuzzocrea, S.; Impellizzeri, D. Fibromyalgia: Pathogenesis, Mechanisms, Diagnosis and Treatment Options Update. Int. J. Mol. Sci. 2021, 22, 3891. [Google Scholar] [CrossRef]
  5. Fitzcharles, M.A.; Perrot, S.; Hauser, W. Comorbid fibromyalgia: A qualitative review of prevalence and importance. Eur. J. Pain. 2018, 22, 1565–1576. [Google Scholar] [CrossRef] [PubMed]
  6. Duffield, S.J.; Miller, N.; Zhao, S.; Goodson, N.J. Concomitant fibromyalgia complicating chronic inflammatory arthritis: A systematic review and meta-analysis. Rheumatology 2018, 57, 1453–1460. [Google Scholar] [CrossRef]
  7. FitzGerald, O.; Ogdie, A.; Chandran, V.; Coates, L.C.; Kavanaugh, A.; Tillett, W.; Leung, Y.Y.; deWit, M.; Scher, J.U.; Mease, P.J. Psoriatic arthritis. Nat. Rev. Dis. Primers 2021, 7, 59. [Google Scholar] [CrossRef]
  8. Cigolini, C.; Fattorini, F.; Gentileschi, S.; Terenzi, R.; Carli, L. Psoriatic arthritis: One year in review 2022. Clin. Exp. Rheumatol. 2022, 40, 1611–1619. [Google Scholar] [CrossRef] [PubMed]
  9. Veale, D.J.; Fearon, U. The pathogenesis of psoriatic arthritis. Lancet 2018, 391, 2273–2284. [Google Scholar] [CrossRef] [PubMed]
  10. Conaghan, P.G.; Alten, R.; Deodhar, A.; Sullivan, E.; Blackburn, S.; Tian, H.; Gandhi, K.; Jugl, S.M.; Strand, V. Relationship of pain and fatigue with health-related quality of life and work in patients with psoriatic arthritis on TNFi: Results of a multi-national real-world study. RMD Open 2020, 6, e001240. [Google Scholar] [CrossRef]
  11. Marchesoni, A.; De Marco, G.; Merashli, M.; McKenna, F.; Tinazzi, I.; Marzo-Ortega, H.; McGonagle, D.G. The problem in differentiation between psoriatic-related polyenthesitis and fibromyalgia. Rheumatology 2018, 57, 32–40. [Google Scholar] [CrossRef]
  12. Skoie, I.; Dalen, I.; Ternowitz, T.; Jonsson, G.; Kvivik, I.; Norheim, K.; Omdal, R. Fatigue in psoriasis: A controlled study. Br. J. Dermatol. 2017, 177, 505–512. [Google Scholar] [CrossRef]
  13. Jensen, P.; Zachariae, C.; Skov, L.; Zachariae, R. Sleep disturbance in psoriasis: A case-controlled study. Br. J. Dermatol. 2018, 179, 1376–1384. [Google Scholar] [CrossRef] [PubMed]
  14. Gisondi, P.; Sala, F.; Alessandrini, F.; Avesani, V.; Zoccatelli, G.; Beltramello, A.; Moretto, G.; Gambina, G.; Girolomoni, G. Mild cognitive impairment in patients with moderate to severe chronic plaque psoriasis. Dermatology 2014, 228, 78–85. [Google Scholar] [CrossRef]
  15. Kim, S.H. Skin biopsy findings: Implications for the pathophysiology of fibromyalgia. Med. Hypotheses 2007, 69, 141–144. [Google Scholar] [CrossRef] [PubMed]
  16. Blanco, I.; Béritze, N.; Argüelles, M.; Cárcaba, V.; Fernández, F.; Janciauskiene, S.; Oikonomopoulou, K.; de Serres, F.J.; Fernández-Bustillo, E.; Hollenberg, M.D. Abnormal overexpression of mastocytes in skin biopsies of fibromyalgia patients. Clin. Rheumatol. 2010, 29, 1403–1412. [Google Scholar] [CrossRef] [PubMed]
  17. Salemi, S.; Rethage, J.; Wollina, U.; Michel, B.A.; Gay, R.E.; Gay, S.; Sprott, H. Detection of interleukin 1beta (IL-1beta), IL-6, and tumor necrosis factor-alpha in skin of patients with fibromyalgia. J. Rheumatol. 2003, 30, 146–150. [Google Scholar]
  18. Sprott, H.; Müller, A.; Heine, H. Collagen cross-links in fibromyalgia syndrome. Z. Rheumatol. 1998, 57, S52–S55. [Google Scholar] [CrossRef]
  19. Greb, J.E.; Goldminz, A.M.; Elder, J.T.; Lebwohl, M.G.; Gladman, D.D.; Wu, J.J.; Mehta, N.N.; Finlay, A.Y.; Gottlieb, A.B. Psoriasis. Nat. Rev. Dis. Primers 2016, 2, 16082. [Google Scholar] [CrossRef]
  20. Meneguin, S.; de Godoy, N.A.; Pollo, C.F.; Miot, H.A.; de Oliveira, C. Quality of life of patients living with psoriasis: A qualitative study. BMC Dermatol. 2020, 20, 22. [Google Scholar] [CrossRef]
  21. Boehncke, W.H.; Schön, M.P. Psoriasis. Lancet 2015, 386, 983–994. [Google Scholar] [CrossRef]
  22. Takeshita, J.; Grewal, S.; Langan, S.M.; Mehta, N.N.; Ogdie, A.; Van Voorhees, A.S.; Gelfand, J.M. Psoriasis and comorbid diseases: Epidemiology. J. Am. Acad. Dermatol. 2017, 76, 377–390. [Google Scholar] [CrossRef] [PubMed]
  23. De Simone, C.; Calabrese, L.; Balato, A.; Cannavò, S.P.; Dattola, A.; Esposito, M.; Fargnoli, M.C.; Giuffrida, R.; Hansel, K.; Musumeci, M.L.; et al. “Psoriasis in Women of Childbearing Age” Task Force. Psoriasis and its management in women of childbearing age: Tools to increase awareness in dermatologists and patients. G. Ital. Dermatol. Venereol. 2020, 155, 434–440. [Google Scholar] [CrossRef]
  24. Liberati, A.; Altman, D.G.; Tetzlaff, J.; Mulrow, C.; Gøtzsche, P.C.; Ioannidis, J.P.A.; Clarke, M.; Devereaux, P.J.; Kleijnen, J.; Moher, D. The PRISMA statement for reporting systematic reviews and meta-analyses of studies that evaluate health care interventions: Explanation and elaboration. Ann. Intern. Med. 2009, 151, 65–94. [Google Scholar] [CrossRef] [PubMed]
  25. Wells, A.; Shea, B.; O’Connell, D.; Peterson, J.; Welch, V.; Losos, M.; Tugwell, P. The Newcastle-Ottawa Scale (NOS) for Assessing the Quality of Nonrandomised Studies in Meta-Analyses. 2013. Available online: http://www.ohri.ca/programs/clinical_epidemiology/oxford.asp (accessed on 27 November 2023).
  26. Kridin, K.; Vanetik, S.; Damiani, G.; Cohen, A.D. Big data highlights the association between psoriasis and fibromyalgia: A population-based study. Immunol. Res. 2020, 68, 135–140. [Google Scholar] [CrossRef] [PubMed]
  27. Brikman, S.; Furer, V.; Wollman, J.; Borok, S.; Matz, H.; Polachek, A.; Elalouf, O.; Sharabi, A.; Kaufman, I.; Paran, D.; et al. The Effect of the Presence of Fibromyalgia on Common Clinical Disease Activity Indices in Patients with Psoriatic Arthritis: A Cross-sectional Study. J. Rheumatol. 2016, 43, 1749–1754. [Google Scholar] [CrossRef]
  28. Elsawy, N.A.; Helal, A.H.; Abd ElHamid, H.A.; Abdel-Fattah, Y.H. Fibromyalgia in patients with psoriatic arthritis: Impact on disease activity indices, fatigue and health-related quality of life. Int. J. Rheum. Dis. 2021, 24, 189–196. [Google Scholar] [CrossRef] [PubMed]
  29. Erdogan, H.K.; Sas, S.; Acer, E.; Bulur, I.; Altunay, I.K.; Erdem, H.R. Cutaneous findings in fibromyalgia syndrome and their effect on quality of life. Dermatol. Sinica 2016, 34, 131–134. [Google Scholar] [CrossRef]
  30. Iannone, F.; Nivuori, M.; Fornaro, M.; Venerito, V.; Cacciapaglia, F.; Lopalco, G. Comorbid fibromyalgia impairs the effectiveness of biologic drugs in patients with psoriatic arthritis. Rheumatology 2020, 59, 1599–1606. [Google Scholar] [CrossRef]
  31. Kancharla, H.; Jain, S.; Mishra, S.; Acharya, N.; Grover, S.; Dogra, S.; Sharma, A. Fibromyalgia influences health-related quality of life and disease activity in psoriatic arthritis. Rheumatol. Int. 2022, 42, 511–517. [Google Scholar] [CrossRef]
  32. Laniosz, V.; Wetter, D.A.; Godar, D.A. Dermatologic manifestations of fibromyalgia. Clin. Rheumatol. 2014, 33, 1009–1013. [Google Scholar] [CrossRef] [PubMed]
  33. Mohammed, J.Q.; Mathkhor, A.J.; Abdullah, A.H.; Khudhairy, A.S.; Nasrullah, H.H. Fibromyalgia in patients with psoriasis. World Fam. Med. 2020, 18, 45–49. [Google Scholar] [CrossRef]
  34. Polachek, A.; Furer, V.; Zureik, M.; Nevo, S.; Mendel, L.; Levartovsky, D.; Wollman, J.; Aloush, V.; Tzemach, R.; Elalouf, O.; et al. Role of ultrasound for assessment of psoriatic arthritis patients with fibromyalgia. Ann. Rheum. Dis. 2021, 80, 1553–1558. [Google Scholar] [CrossRef] [PubMed]
  35. Thune, P.O. The prevalence of fibromyalgia among patients with psoriasis. Acta Derm. Venereol. 2005, 85, 33–37. [Google Scholar] [CrossRef] [PubMed]
  36. Ulus, Y.; Akyol, Y.; Bilgici, A.; Kuru, O. The impact of the presence of fibromyalgia on fatigue in patients with psoriatic arthritis: Comparison with controls. Adv. Rheumatol. 2019, 60, 1. [Google Scholar] [CrossRef] [PubMed]
  37. Wolfe, F.; Smythe, H.A.; Yunus, M.B.; Bennett, R.M.; Bombardier, C.; Goldenberg, D.L.; Tugwell, P.; Campbell, S.M.; Abeles, M.; Clark, P.; et al. The American College of Rheumatology 1990 Criteria for the Classification of Fibromyalgia. Report of the Multicenter Criteria Committee. Arthritis Rheumatol. 1990, 33, 160–172. [Google Scholar] [CrossRef]
  38. Icen, M.; Crowson, C.S.; McEvoy, M.T.; Dann, F.J.; Gabriel, S.E.; Kremers, H.M. Trends in incidence of adult-onset psoriasis over three decades: A population-based study. J. Am. Acad. Dermatol. 2009, 60, 394–401. [Google Scholar] [CrossRef]
  39. Moller, A.H.; Erntoft, S.; Vinding, G.R.; Jemec, G.B. A systematic literature review to compare quality of life in psoriasis with other chronic diseases using EQ-5D-derived utility values. Patient Relat. Outcome Meas. 2015, 6, 167–177. [Google Scholar]
  40. Kim, N.; Thrash, B.; Menter, A. Comorbidities in psoriasis patients. Semin. Cutan. Med. Surg. 2010, 29, 10–15. [Google Scholar] [CrossRef]
  41. Felbo, S.; Terslev, L.; Sørensen, I.; Skov, L.; Zachariae, C.; Østergaard, M. Musculoskeletal Pain in Patients with Psoriasis and its Influence on Health-related Quality of Life: Results from a Danish Population-based Survey. Acta Derm. Venereol. 2021, 101, adv00553. [Google Scholar] [CrossRef]
  42. Cohen, H. Controversies and challenges in fibromyalgia: A review and a proposal. Ther. Adv. Musculoskelet. Dis. 2017, 9, 115–127. [Google Scholar] [CrossRef]
  43. Ljosaa, T.; Rustoen, T.; Mørk, C.; Stubhaug, A.; Miaskowski, C.; Paul, S.; Wahl, A. Skin pain and discomfort in psoriasis: An exploratory study of symptom prevalence and characteristics. Acta Derm. Venereol. 2010, 90, 39–45. [Google Scholar] [CrossRef]
  44. Patruno, C.; Napolitano, M.; Balato, N.; Ayala, F.; Megna, M.; Patrì, A.; Cirillo, T.; Balato, A. Psoriasis and skin pain: Instrumental and biological evaluations. Acta Derm. Venereol. 2015, 95, 432–438. [Google Scholar] [CrossRef]
  45. Ayasse, M.T.; Buddenkotte, J.; Alam, M.; Steinhoff, M. Role of neuroimmune circuits and pruritus in psoriasis. Exp. Dermatol. 2020, 29, 414–426. [Google Scholar] [CrossRef]
  46. Latremoliere, A.; Woolf, C.J. Central sensitization: A generator of pain hypersensitivity by central neural plasticity. J. Pain. 2009, 10, 895–926. [Google Scholar] [CrossRef]
  47. Lluch Girbes, E.; Nijs, J.; Torres-Cueco, R.; López Cubas, C. Pain treatment for patients with osteoarthritis and central sensitization. Phys. Ther. 2013, 93, 842–851. [Google Scholar] [CrossRef]
  48. Russell, I.J.; Orr, M.D.; Littman, B.; Vipraio, G.A.; Alboukrek, D.; Michalek, J.E.; Lopez, Y.; Mackillip, F. Elevated cerebrospinal fluid levels of substance P in patients with the fibromyalgia syndrome. Arthritis Rheumatol. 1994, 37, 1593–1601. [Google Scholar] [CrossRef]
  49. Nakamura, M.; Toyoda, M.; Morohashi, M. Pruritogenic mediators in psoriasis vulgaris: Comparative evaluation of itch-associated cutaneous factors. Br. J. Dermatol. 2003, 149, 718–730. [Google Scholar] [CrossRef] [PubMed]
  50. O’Mahony, L.F.; Srivastava, A.; Mehta, P.; Ciurtin, C. Is fibromyalgia associated with a unique cytokine profile? A systematic review and meta-analysis. Rheumatology 2021, 60, 2602–2614. [Google Scholar] [CrossRef] [PubMed]
  51. Coimbra, S.; Oliveira, H.; Reis, F.; Belo, L.; Rocha, S.; Quintanilha, A.; Figueiredo, A.; Teixeira, F.; Castro, E.; Rocha-Pereira, P.; et al. Interleukin (IL)-22, IL-17, IL-23, IL-8, vascular endothelial growth factor and tumour necrosis factor-alpha levels in patients with psoriasis before, during and after psoralen-ultraviolet A and narrowband ultraviolet B therapy. Br. J. Dermatol. 2010, 163, 1282–1290. [Google Scholar] [CrossRef] [PubMed]
  52. Singh, R.; Koppu, S.; Perche, P.O.; Feldman, S.R. The Cytokine Mediated Molecular Pathophysiology of Psoriasis and Its Clinical Implications. Int. J. Mol. Sci. 2021, 22, 12793. [Google Scholar] [CrossRef] [PubMed]
  53. Tsilioni, I.; Russell, I.J.; Stewart, J.M.; Gleason, R.M.; Theoharides, T.C. Neuropeptides CRH, SP, HK-1, and Inflammatory Cytokines IL-6 and TNF Are Increased in Serum of Patients with Fibromyalgia Syndrome, Implicating Mast Cells. J. Pharmacol. Exp. Ther. 2016, 356, 664–672. [Google Scholar] [CrossRef] [PubMed]
  54. Theoharides, T.C.; Tsilioni, I.; Bawazeer, M. Mast Cells, Neuroinflammation and Pain in Fibromyalgia Syndrome. Front. Cell Neurosci. 2019, 13, 353. [Google Scholar] [CrossRef] [PubMed]
  55. Totsch, S.K.; Sorge, R.E. Immune System Involvement in Specific Pain Conditions. Mol. Pain 2017, 13, 1744806917724559. [Google Scholar] [CrossRef] [PubMed]
  56. Ohgidani, M.; Kato, T.A.; Hosoi, M.; Tsuda, M.; Hayakawa, K.; Hayaki, C.; Iwaki, R.; Sagata, N.; Hashimoto, R.; Inoue, K.; et al. Fibromyalgia and microglial TNF-α: Translational research using human blood induced microglia-like cells. Sci. Rep. 2017, 7, 11882. [Google Scholar] [CrossRef] [PubMed]
  57. Pernambuco, A.P.; Schetino, L.P.; Alvim, C.C.; Murad, C.M.; Viana, R.S.; Carvalho, L.S.; Reis, D.Á. Increased levels of IL-17A in patients with fibromyalgia. Clin. Exp. Rheumatol. 2013, 31 (Suppl. S79), S60–S63. [Google Scholar] [PubMed]
  58. Blauvelt, A.; Chiricozzi, A. The Immunologic Role of IL-17 in Psoriasis and Psoriatic Arthritis Pathogenesis. Clin. Rev. Allergy Immunol. 2018, 55, 379–390. [Google Scholar] [CrossRef]
  59. Peck, M.M.; Maram, R.; Mohamed, A.; Ochoa Crespo, D.; Kaur, G.; Ashraf, I.; Malik, B.H. The Influence of Pro-inflammatory Cytokines and Genetic Variants in the Development of Fibromyalgia: A Traditional Review. Cureus 2020, 12, e10276. [Google Scholar] [CrossRef]
  60. Vincent, A.; Benzo, R.P.; O Whipple, M.; McAllister, S.J.; Erwin, P.J.; Saligan, L.N. Beyond pain in fibromyalgia: Insights into the symptom of fatigue. Arthritis Res. Ther. 2013, 15, 221. [Google Scholar] [CrossRef]
  61. Zambolin, F.; Duro-Ocana, P.; Faisal, A.; Bagley, L.; Gregory, W.J.; Jones, A.W.; McPhee, J.S. Fibromyalgia and Chronic Fatigue Syndromes: A systematic review and meta-analysis of cardiorespiratory fitness and neuromuscular function compared with healthy individuals. PLoS ONE 2022, 17, e0276009. [Google Scholar] [CrossRef]
  62. Tsai, S.-Y.; Chen, H.-J.; Chen, C.; Lio, C.-F.; Kuo, C.-F.; Leong, K.-H.; Wang, Y.-T.T.; Yang, T.-Y.; You, C.-H.; Wang, W.-S. Increased risk of chronic fatigue syndrome following psoriasis: A nationwide population-based cohort study. J. Transl. Med. 2019, 17, 154. [Google Scholar] [CrossRef]
  63. Brenu, E.W.; Huth, T.K.; Hardcastle, S.L.; Fuller, K.; Kaur, M.; Johnston, S.; Ramos, S.B.; Staines, D.R.; Marshall-Gradisnik, S.M. Role of adaptive and innate immune cells in chronic fatigue syndrome/myalgic encephalomyelitis. Int. Immunol. 2014, 26, 233–242. [Google Scholar] [CrossRef]
  64. Dantzer, R.; Kelley, K.W. Twenty years of research on cytokine-induced sickness behavior. Brain Behav. Immun. 2007, 21, 153–160. [Google Scholar] [CrossRef]
  65. Bigatti, S.M.; Hernandez, A.M.; Cronan, T.A.; Rand, K.L. Sleep disturbances in fibromyalgia syndrome: Relationship to pain and depression. Arthritis Rheum. 2008, 59, 961–967. [Google Scholar] [CrossRef]
  66. Gupta, M.A.; Simpson, F.C.; Gupta, A.K. Psoriasis and sleep disorders: A systematic review. Sleep. Med. Rev. 2016, 29, 63–75. [Google Scholar] [CrossRef] [PubMed]
  67. Henao-Pérez, M.; López-Medina, D.C.; Arboleda, A.; Bedoya Monsalve, S.; Zea, J.A. Patients With Fibromyalgia, Depression, and/or Anxiety and Sex Differences. Am. J. Mens. Health 2022, 16, 15579883221110351. [Google Scholar] [CrossRef] [PubMed]
  68. Holsken, S.; Krefting, F.; Schedlowski, M.; Sondermann, W. Common Fundamentals of Psoriasis and Depression. Acta Derm. Venereol. 2021, 101, adv00609. [Google Scholar] [CrossRef] [PubMed]
  69. Pinho de Oliveira Ribeiro, N.; Rafael de Mello Schier, A.; Ornelas, A.C.; Pinho de Oliveira, C.M.; Nardi, A.E.; Silva, A.C. Anxiety, depression and suicidal ideation in patients with rheumatoid arthritis in use of methotrexate, hydroxychloroquine, leflunomide and biological drugs. Compr. Psychiatry 2013, 54, 1185–1189. [Google Scholar] [CrossRef] [PubMed]
  70. Kunz, M.; Simon, J.C.; Saalbach, A. Psoriasis: Obesity and Fatty Acids. Front. Immunol. 2019, 10, 1807. [Google Scholar] [CrossRef] [PubMed]
  71. Bettelli, E.; Carrier, Y.; Gao, W.; Korn, T.; Strom, T.B.; Oukka, M.; Weiner, H.L.; Kuchroo, V.K. Reciprocal developmental pathways for the generation of pathogenic effector TH17 and regulatory T cells. Nature 2006, 441, 235–238. [Google Scholar] [CrossRef] [PubMed]
  72. Chehimi, M.; Vidal, H.; Eljaafari, A. Pathogenic Role of IL-17-Producing Immune Cells in Obesity, and Related Inflammatory Diseases. J. Clin. Med. 2017, 6, 68. [Google Scholar] [CrossRef]
  73. D’Onghia, M.; Ciaffi, J.; Lisi, L.; Mancarella, L.; Ricci, S.; Stefanelli, N.; Meliconi, R.; Ursini, F. Fibromyalgia and obesity: A comprehensive systematic review and meta-analysis. Semin. Arthritis Rheum. 2021, 51, 409–424. [Google Scholar] [CrossRef] [PubMed]
  74. White, K.P.; Harth, M. Classification, epidemiology, and natural history of fibromyalgia. Curr. Pain Headache Rep. 2001, 5, 320–329. [Google Scholar] [CrossRef] [PubMed]
  75. Parisi, R.; Symmons, D.P.; Griffiths, C.E.; Ashcroft, D.M. Identification and Management of Psoriasis and Associated ComorbidiTy (IMPACT) project team. Global epidemiology of psoriasis: A systematic review of incidence and prevalence. J. Investig. Dermatol. 2013, 133, 377–385. [Google Scholar] [CrossRef]
  76. Iskandar, I.Y.K.; Parisi, R.; Griffiths, C.E.M.; Ashcroft, D.M. Global Psoriasis Atlas Systematic review examining changes over time and variation in the incidence and prevalence of psoriasis by age and gender. Br. J. Dermatol. 2021, 184, 243–258. [Google Scholar] [CrossRef] [PubMed]
  77. Almodóvar, R.; Carmona, L.; Zarco, P.; Collantes, E.; González, C.; Mulero, J.; Sueiro, J.L.F.; Gratacós, J.; Torre-Alonso, J.C.; Juanola, X.; et al. Fibromyalgia in patients with ankylosing spondylitis: Prevalence and utility of the measures of activity, function and radiological damage. Clin. Exp. Rheumatol. 2010, 28 (Suppl. S63), S33–S39. [Google Scholar] [PubMed]
  78. Marchesoni, A.; Atzeni, F.; Spadaro, A.; Lubrano, E.; Provenzano, G.; Cauli, A.; Olivieri, I.; Melchiorre, D.; Salvarani, C.; Scarpa, R.; et al. Identification of the clinical features distinguishing psoriatic arthritis and fibromyalgia. J. Rheumatol. 2012, 39, 849–855. [Google Scholar] [CrossRef]
  79. Salaffi, F.; Sarzi-Puttini, P. Old and new criteria for the classification and diagnosis of fibromyalgia: Comparison and evaluation. Clin. Exp. Rheumatol. 2012, 30 (Suppl. S74), 3–9. [Google Scholar]
Jpm 14 00165 g001
Figure 1. PRISMA—compliant study selection flow chart.
Figure 1. PRISMA—compliant study selection flow chart.
Jpm 14 00165 g001
Table 1. Quality assessment of included studies according to the Newcastle—Ottawa Scale (NOS).
Table 1. Quality assessment of included studies according to the Newcastle—Ottawa Scale (NOS).
Author, YearItem S1Item S2Item S3Item S4Item C1Item E1Item E2Item E3Score
Kridin, 2020 [26]b *ba *a *a *da *c******
Brinkman, 2016 [27]a *a *cccb *cc***
Elsawy, 2021 [28]a *a *cccb *cd***
Erdogan, 2016 [29]a *a *a *a *a *ca *c******
Iannone, 2020 [30]b *cccca *a *d***
Kancharla, 2022 [31]a *a *cccb *cd***
Laniosz, 2014 [32]bbcccdcc-
Mathkhor, 2020 [33]a *ba *a *a *ca *c*****
Polachek, 2021 [34]a *a *cccb *cc***
Thune, 2005 [35]a *a *cccb *cd***
Ulus, 2019 [36]a *ba *ba *ca *c****
Legend: C, Comparability; E, Exposure; S, Selection. The stars (*) obtained by each article are summed up to obtain a final score, representing the overall quality of the study, reported in the last column.
Table 2. Summary of systematic review assessing the association between fibromyalgia and psoriasis.
Table 2. Summary of systematic review assessing the association between fibromyalgia and psoriasis.
Author, YearCountryRecruitmentYearPatients
(% F)		Patients Age, Years,
Mean (SD)		Controls (%F)DesignFM CriteriaPsO or PsA Criteria
Thune, 2005 [35]NorwayConsecutive outpatient1997–20001269 (56) PsO patients49.5 (12.8)NRCross sectionalACR 1990Clinical examination
Laniosz, 2014 [32]USAOutpatient2008845 (90.6) FM patients 48.9NRCross sectionalACR 1990/ACR 2010/ACR 2011Clinical examination
Brinkman, 2016 [27]IsraelConsecutive outpatient2013–201473 (57.7) PsA patients51.7 (13.5)NRCross sectionalACR 2010/ACR 1990CASPAR
Erdogan, 2016 [29]TurkeyInpatientNR105(100) FM patients45.5 (8.7)105(100)Cross sectionalACR 2010Dermatological examination
Ulus, 2019 [36]TurkeyInpatient2017–201850 (72) PsA patients 47 (23–64) *NRCross sectionalCASPARACR 2010
Iannone, 2020 [30]ItalyOutpatient2010–2017238 (53) PsA patients49.2 (12)NRCohort studyCASPARACR 2010/ACR1990
Kridin, 2020 [26]IsraelHealth Care Database201718,598 (91) FM patients56.5 (14.1)36,985 (91)Cross sectionalEHREHR
Mathkhor, 2020 [33]IraqOutpatient and inpatient2018–202070 (57) PsO patients50.7 (7.3)70 (57)Cross sectionalACR 1990Clinical examination
Elsawy, 2021 [28]EgyptOutpatient consecutive2017–201860 (43.3) PsA patients49.30 (11.69)NRCross sectionalCASPARACR 2016
Polacheck, 2021 [34]IsraelConsecutive outpatient2018–2020156 (56) PsA patients 52.7 (12.7)NRCross sectionalCASPARACR 2016
Kancharla, 2022 [31]IndiaConsecutive outpatient2014–2015102 (50) PsA patients 43.4 (12.4)NRCross sectionalCASPARACR 2010
* age expressed as median (minimum-maximum). Legend: ACR, American College of Rheumatology; CASPAR, ClASsification criteria for Psoriatic Arthritis; EHR, electronic health record; FM, fibromyalgia; NR, non-reported; PsA, Psoriatic arthritis; PsO, Psoriasis.
Disclaimer/Publisher’s Note: The statements, opinions and data contained in all publications are solely those of the individual author(s) and contributor(s) and not of MDPI and/or the editor(s). MDPI and/or the editor(s) disclaim responsibility for any injury to people or property resulting from any ideas, methods, instructions or products referred to in the content.

Share and Cite

MDPI and ACS Style

D’Onghia, M.; Ursini, F.; Cinotti, E.; Calabrese, L.; Tognetti, L.; Cartocci, A.; Lazzeri, L.; Frediani, B.; Rubegni, P.; Trovato, E. Psoriasis and Fibromyalgia: A Systematic Review. J. Pers. Med. 2024, 14, 165. https://doi.org/10.3390/jpm14020165

AMA Style

D’Onghia M, Ursini F, Cinotti E, Calabrese L, Tognetti L, Cartocci A, Lazzeri L, Frediani B, Rubegni P, Trovato E. Psoriasis and Fibromyalgia: A Systematic Review. Journal of Personalized Medicine. 2024; 14(2):165. https://doi.org/10.3390/jpm14020165

Chicago/Turabian Style

D’Onghia, Martina, Francesco Ursini, Elisa Cinotti, Laura Calabrese, Linda Tognetti, Alessandra Cartocci, Laura Lazzeri, Bruno Frediani, Pietro Rubegni, and Emanuele Trovato. 2024. "Psoriasis and Fibromyalgia: A Systematic Review" Journal of Personalized Medicine 14, no. 2: 165. https://doi.org/10.3390/jpm14020165

APA Style

D’Onghia, M., Ursini, F., Cinotti, E., Calabrese, L., Tognetti, L., Cartocci, A., Lazzeri, L., Frediani, B., Rubegni, P., & Trovato, E. (2024). Psoriasis and Fibromyalgia: A Systematic Review. Journal of Personalized Medicine, 14(2), 165. https://doi.org/10.3390/jpm14020165

Note that from the first issue of 2016, this journal uses article numbers instead of page numbers. See further details here.

Article Metrics

Back to TopTop