Clinical Rheumatology

https://doi.org/10.1007/s10067-020-04981-0

REVIEW ARTICLE

At the crossroads of gout and psoriatic arthritis: “psout”

Renaud Felten 1,2 & Pierre-Marie Duret 1 & Jacques-Eric Gottenberg 1,2 & Lionel Spielmann 3 & Laurent Messer 3

Received: 9 October 2019 / Revised: 31 January 2020 / Accepted: 7 February 2020

# International League of Associations for Rheumatology (ILAR) 2020

Abstract
Psoriatic arthritis and gout are frequently encountered conditions sharing a number of common risk factors, which render their
independent study difficult. Epidemiological studies have demonstrated a strong link between these diseases, suggesting the
presence of underlying, intertwined pathophysiological mechanisms that currently remain unknown. Indeed, sodium urate
crystals could play a pathogenic role in psoriasis and psoriatic arthritis. In daily practice, the distinction between psoriatic arthritis
associated with hyperuricemia and a gouty arthropathy with psoriasis is complex. Several common pathogenic features suggest a
more intricate relationship than their mere coexistence in the same patient. Thus, the concurrence of these two diseases should be
seen as a novel overlap syndrome, at the boundary between inflammatory and metabolic rheumatism. The present update aims to
clarify the determinants of the link and to define this new nosological entity. Its recognition could have therapeutic implications
that appear essential for treatment optimization in a personalized setting.

Key Points
• What is already known about this subject? Psoriatic arthritis (PsA) and gout have strong interconnections, including comorbidities and pathophys-
iology. One must note that confounding clinical symptoms and radiological signs of PsA and gout are similar and difficult to differentiate in patients
whose radiological lesions become too advanced to be differentiated or with less clearly defined phenotypes.
• What does this study add? The pathogenic role of chronic hyperuricemia in the development and maintenance of PsA is based on epidemiological,
clinical, and fundamental arguments and hence does not appear fortuitous. These two pathological processes can influence each other.
• How might this impact on clinical practice? This new line of thinking regarding the convergence of gout and PsA, involving the role of urate crystals,
could prompt a potential new approach to treatment (urate-lowering therapy) among patients with active/refractory PsA.

Keywords Gout . Hyperuricemia . Psoriasis . Psoriatic arthritis

Abbreviations PsA Psoriatic arthritis

bDMARD Biological disease-modifying antirheumatic PUVA Psoralen and ultraviolet A
drug SUA Serum uric acid
csDMARD Conventional synthetic disease-modifying Tx Treatment
antirheumatic drug
MSU Monosodium urate
MTP Metatarsophalangeal Introduction
NSAID Non-steroidal anti-inflammatory drug
For introductory purposes, we present a clinical observation
that led us to consider the existence of a model reconciling
* Renaud Felten
[email protected] gout with psoriatic arthritis (PsA).
A 40-year-old man with a 15-year history of skin psoriasis,
1
in addition to a family history of psoriasis in a brother and gout
Service de Rhumatologie, Hôpitaux universitaires de Strasbourg, 1
avenue Molière, 67098 Strasbourg, France
in the mother, presented intermittent ankle and knee arthritis,
2
inflammatory spinal pain, and extended skin psoriasis.
Laboratoire d’Immunologie, Immunopathologie et Chimie
Thérapeutique, Institut de Biologie Moléculaire et Cellulaire
Laboratory workup highlighted an inflammatory syndrome
(IBMC), CNRS UPR3572, 15 Rue René Descartes, (C-reactive protein level 27 mg/l, normally < 3.0 mg/l), hy-
67000 Strasbourg, France peruricemia at 556 μmol/l (normal level < 400 μmol/l), and a
3
Service de Rhumatologie, Hospices Civils de Colmar, 39 Avenue de negative immunological profile (rheumatoid factor, anti-
la Liberté, 68024 Colmar Cedex, France citrullinated peptide antibodies, antinuclear antibodies). The
 Clin Rheumatol

search for HLA-B27 was negative. Synovial fluid analysis of with psoriasis and PsA. Risk of incident gout was increased in
the right knee revealed an inflammatory, microorganism-free patients with cutaneous psoriasis (hazard ratio 1.71, 95% con-
fluid (25,000 leucocytes/mm3), with sparse sodium urate crys- fidence interval (CI) 1.36 to 2.15) and with PsA (4.95, 95% CI
tals. X-rays showed extensive pre-vertebral dorsal and lumbar 2.72 to 9.01) [20]. A case–control study comparing 39,111
ankylosis with syndesmophytes, an incipient ischial calcifying patients with gout to 39,111 healthy controls showed an in-
enthesopathy, and bilateral sub- and retro-calcaneal creased risk of incident gout with pre-existing psoriasis and
enthesophytes, associated with erosions and osteoblastic bone risk of psoriasis in gouty patients [7]. Moreover, in a recent
formations next to the first right and left metatarsophalangeal study, an approximately 4-fold increased risk of hyperurice-
(MTP I) joints. Joint ultrasonography of the foot revealed a mia was found associated with PsA in the presence of skin
talocrural effusion associated with MTP I arthritis along with a psoriasis [21]. These data are further confirmed by the results
rice grain appearance without associated tenosynovitis. Given of another larger study comparing 114,623 patients with gout
the above description, which diagnosis(es) should be consid- to 114,623 without gout, showing increased prevalence of
ered: PsA? gout? psoriasis in the former [22]. PsA is threefold more frequent
The coexistence of these two diseases in the same patient in gout patients than in controls, with psoriasis 1.5-fold more
could represent an overlap syndrome, at the boundary be- frequent [22]. Hyperuricemia is common in patients with
tween metabolic and inflammatory rheumatism. This overlap long-duration psoriasis and obesity [23]. The risk of develop-
could be underpinned by the pathogenic role of urate crystals ing psoriasis increases with duration of gout [7]. Cutaneous
[1]. Indeed, as early as the 1970s, several studies showed psoriasis is also more severe with hyperuricemia [24].
hyperuricemia as more common in psoriatic patients than in As outlined above, PsA and gout share many common risk
the general population [1–5]. factors, at times confounding, which render their independent
In the present analysis, we propose to go one step further study difficult. Regardless, epidemiological studies have dem-
and examine this overlap syndrome in its various aspects, in onstrated a strong link between these diseases, thereby sug-
conjunction with the latest scientific advances, while specify- gesting the presence of underlying, closely intertwined path-
ing the main determinants linking gout and PsA. We conduct- ophysiological mechanisms that remain unknown.
ed a narrative-review approach, in order to synthesize litera-
ture by screening relevant literature from 1950 to 2019 using
Medline and the following MeSH terms: “Arthritis,” Pathophysiology
“Psoriatic,” “Psoriasis,” “Gout,” and “Hyperuricemia.” We
also examined grey literature represented by abstract of the Pathogenic role of urate crystals in gout
ACR and EULAR congresses since 2015. In particular, this
analysis aims to define this particular condition and delineate The past decade has been marked by considerable prog-
its potential therapeutic implications. ress in understanding the pathogenic role of urate crystals
and the pathophysiology of gout by processes involving
two fundamental intracellular mechanisms of innate im-
Epidemiology munity: the inflammasome and NETosis, but also more
surprisingly, adaptive immunity.
Link between hyperuricemia/gout and PsA During a gout attack, monosodium urate (MSU) crystals
exhibit a strong affinity for immunoglobulin type G as well
Patients with psoriasis or gout share common epidemiological as complement proteins, which confer pro-inflammatory
features, comorbidities, and risk factors (Fig. 1) [6, 7]. properties. All cells possessing receptors for the Fc fragment
An increase in the catabolism of purine bases was first of immunoglobulin G, such as polymorphonuclear cells,
suspected due to the enhanced epidermal turnover observed macrophages, and synoviocytes, can thus be activated.
during psoriasis. This theory has since been disputed by a During bouts of joint inflammation, urate crystals are inter-
number of studies [8, 9], the level of uricemia seemingly not nalized by phagocytosis and are incorporated into lyso-
correlated with the extent of psoriasis as measured by the somes, inducing an influx of sodium and intracellular water,
Psoriasis Area Severity Index [10]. thereby activating the inflammasome, an oligomeric protein
Numerous patient observations associating gout and psori- complex involved in innate immunity [25]. The intracellular
asis have been reported in the literature. These studies de- protein complex (NLRP3) leads to the activation of caspase-
scribed patients with psoriasis [11–15] and/or PsA [13, 1 and allows the cleavage of pro-interleukin 1β (IL-1β) into
16–19], in whom gout subsequently developed or vice versa IL-1β, the activated form of the pro-inflammatory cytokine.
[19]. A large cohort of US patients, prospectively followed for Intra-articular microcrystals and those present in the tophi
a period of more than 10 years, assessed the risk of gout are able to activate the surrounding cells according to the
developing in a population of 27,751 men and 71,059 women following different mechanisms:
Clin Rheumatol

Fig. 1 Interplay of comorbidities

related to gout, psoriasis, and PsA

& MSU crystals can induce necroptosis or programmed ne- (Th17) cell pathway [35] which is involved in the patho-
crosis of polynuclear neutrophils (PNNs) via the RIPK3 genesis of spondyloarthritis.
receptor and MLKL protein kinases [26].
& Under the influence of MSU crystals, PNNs can be
activated by an alternative mechanism characterized Involvement in PsA (Fig. 2)
by the release of intracellular and intranuclear compo-
nents in networks called neutrophil extracellular traps In psoriasis, plasmacytoid dendritic cells are activated by
(NET); this process is called NETosis. These NETs pathogen-associated molecular patterns after Toll-like re-
expose various cellular structures that play the role ceptor stimulation. Some of these pathogen-associated
of damage-associated molecular patterns, such as his- molecular patterns are present in large numbers in the
tones, mitochondrial DNA, ATP, and urate crystals, psoriatic epithelium, possibly emanating from the exoge-
which, in turn, stimulate Toll-like receptors present nous environment (microbial peptides) or hyperactivated
in surrounding cells and participate in the release of keratinocytes (cathelicidin, DNA, urate crystals) [36].
pro-inflammatory cytokines including IL-1. These two key cell populations, plasmacytoid dendritic
Paradoxically, this NETosis is also involved in the cells and keratinocytes, produce and secrete numerous cy-
resolution of acute gouty arthritis [27] via serine pro- tokines, including IL-1β, IL-6, tumor necrosis factor al-
teases capable of neutralizing pro-inflammatory medi- pha, interferon-alpha (IFN-α), and IFN-gamma (IFN-γ)
ators, thus creating a control feedback loop. [37]. Dendritic cells induce T cell proliferation and differ-
& MSU crystals have been shown to interact with entiation into Th1 and Th17 cells in secondary lymphoid
keratinocytes [28] and synoviocytes [29] via the P2Y6 organs. Self-reactive T cells, in turn, will stimulate
receptor and induce the secretion of pro-inflammatory me- keratinocytes [38] via the release of IL-17 and IFN-γ.
diators including IL-1α, IL-8/CXCL8, and IL-6. They can Involvement of MSU crystals in triggering PsA:
also induce osteoclast differentiation [30] and have an
inhibitory effect on osteoblasts [31], which explains the & MSU crystals have been found in large numbers in psori-
bone erosion. atic skin lesions. Psoriasis-like dermatosis developed in an
& MSU crystals or soluble uric acid also act on adaptive experimental animal model of boa constrictors fed high
immunity, as adjuvants in the humoral response of hepa- doses of uric acid. In humans, hypouricemic treatment
titis B, tuberculosis, and tumors. MSU crystals activate with allopurinol may allow for improving the psoriasis
antigen-presenting cells (dendritic cells), thus promoting of hyperuricemic patients [39]. The origin of uric acid
their antigenic presentation function [32], but also directly may be local, released by hyperactivated keratinocytes,
on T cells via the P2X7 receptor by inducing a pro- or systemic with chronic hyperuricemia [40].
inflammatory response [33]. They can stimulate the pro- & MSU crystals could represent central effectors of cell ac-
liferation of human T cells [34] by activating the c-Myc tivation in psoriasis and PsA in the case of hyperuricemia.
transcription factor [27]. In addition, they promote the These crystals activate, on the one hand, the keratinocytes
differentiation of T lymphocytes toward the T helper 17 themselves through an autocrine effect, and on the other,
 Clin Rheumatol

Fig. 2 Role of uric acid in the pathophysiology of psoriasis: self- inflammatory cytokines, activating dendritic cells. (E) Secretion of IL-
amplification loop. (A) Circulating monosodium urate (MSU) crystals 12 => differentiation of Th1 cells and IL-23 => Th17 cells. (F)
directly activate the synoviocytes. (B) Release of interleukin-6 (IL-6) Stimulation of keratinocytes via the release of tumor necrosis factor-
and CXCL8, thereby stimulating plasmacytoid dendritic cells. (C) alpha and IL-17 and by MSU crystals via P2Y6. (G) Proliferation of
Stimulation of plasmacytoid dendritic cells by MSU crystals via P2Y6 keratinocytes, cutaneous renewal, and release of MSU by catabolism of
receptors and Toll-like receptor 9 (TLR9) and by the release of IL-1 and purine bases. ⇨ Self-amplification loop
IL-6 by macrophages phagocyting the MSU. (D) Release of pro-

epidermal plasmacytoid dendritic cells by binding to their clinically or radiographically (Table 1, Fig. 3). Although
transmembrane receptor P2Y6, which leads to the secre- such patients do not represent the majority of cases, this
tion of pro-inflammatory cytokines (tumor necrosis factor association should be known and considered in daily prac-
alpha, IL-1β, IL-8) [27]. This signal on the surface of tice, especially to avoid misdiagnosing an acute gout flare in
activated dendritic cells stimulates antigen presentation patients with inactive PsA.
and the T lymphocyte response [25]. Finally, in an inflam- Clinically, the topographic distribution of these two afflic-
matory environment, these crystals can induce secretion of tions can be superimposable (i.e., monoarthritis, oligoarthritis,
IL-17 by T cells [35]. or polyarthritis preferentially affecting the knee, ankle, or first
MTP). In both gout and PsA, arthritis is readily associated
with periarticular locoregional erythema.
The involvement of MTP I is characteristic of gout but
Gout and psoriatic arthritis share clinical, can also be observed during PsA, often represented as
biological, and radiographic features dactylitis of the first digit. Unlike onycho-pachydermo-
periostitis, which is typical of PsA (Fig. 3), MTP I arthri-
PsA and gout have strong interconnections, including co- tis and/or a diffuse first toe dactylitis can be encountered
morbidities and pathophysiology. Also, confounding clini- in both conditions [41], therefore appearing as a signifi-
cal symptoms and radiological signs of PsA and gout are cant confounding symptom in this particular context.
similar and difficult to differentiate in patients whose radio- Less than 50% of patients with PsA carry the HLA-B27
logical lesions become too advanced to be differentiated or allele, essentially the axial forms with sacroiliitis [42, 43].
with less clearly defined phenotypes. Indeed, differentiating Hyperuricemia (≥ 360 μmol/l) is common in patients with
a gout attack from a psoriatic arthritis flare can sometimes psoriasis and PsA. In addition, normal uricemia during an
be challenging, even for trained rheumatologists, whether incident gout attack is a common event, so the distinction
Clin Rheumatol

Table 1 Similarities and

differences between gout and PsA PsA Gout
in clinical, biological, and
radiographic aspects Joint impairment Asymmetrical Asymmetrical
Number of joints Oligoarticular Monoarticular or oligoarticular
Accompanying signs Periarticular erythema Periarticular erythema
Impairment in hands and feet Distal Distal
Dactylitis Frequent Possible
Impairment of the first MTP Possible Frequent
Spinal impairment Common Rare
Sacroiliitis Common Exceptional
Hyperuricemia Frequent: about 30% Constant except during an acute bout
MSU crystals on joint puncture 3.3% [44] Theoretically present but can be absent
HLA B27 < 50% 8–10%

MTP metatarsophalangeal, MSU monosodium urate

is difficult in a patient with concomitant psoriasis. In con- erosion and formation phenomena is another important radio-
trast, 3.3% of PsA synovial fluid samples show MSU crys- graphic feature in PsA but can also be encountered in gout
tals [44], but MSU crystals are not systematically proven [48]. Unlike rheumatoid arthritis (RA), neither PsA nor gout is
during a bout of gout. Biological inflammatory syndrome associated with periarticular bone demineralization. Although
is encountered in both diseases in the acute phase and thus often developing remotely from the joint space, intraosseous
is also not discriminating. gouty tophi, if peripheral, can mimic marginal erosions and
Radiographically, the distribution of structural lesions appear as bone resorption from the periphery to the center
according to an asymmetric oligoarticular or polyarticular [49], similar to that of the “pencil-in-cup” pattern observed
mode is one of the characteristics of PsA, although this in PsA [45, 50].
presentation is also frequently encountered in gout. Finally, it is not uncommon to observe complete joint de-
Radiographic features of PsA include joint erosions, joint struction with ankylosis in advanced gouty arthropathies [51].
space narrowing, bony proliferation including Bone proliferation [48] with hyperostosis may occur in gout
periarticular and shaft periostitis, osteolysis including by periarticular bone bridges (e.g., overhanging edges), peri-
“pencil in cup” deformity and acro-osteolysis, ankylosis, osteal bone appositions, and spurs affecting the tarsus (e.g.,
spur formation, and spondylitis [45]. spiny bony outgrowths on the upper surface of the tarsus) or
However, the involvement of distal interphalangeal (DIP) the fingers or engulfing the MTP 1 joint. The presence of
joints, which is typical of PsA, can also be observed in gouty enthesophytes, most often coarse, at the insertion site of the
arthropathy (Fig. 3). In addition, spinal gout is known to exist Achilles tendon or the plantar fascia can be seen in gouty
and is sometimes responsible for posterior facet joint arthritis patients [52] and, once again, does not always allow for dif-
[46] or sacroiliitis, as in PsA [47]. The coexistence of bone ferentiating the two disorders.

Fig. 3 Confounding features

between gout and psoriatic
arthritis (PsA). a Coexistence of
signs of gout and PsA in the same
patient. Phalangeal
resorption, erosion of distal
interphalangeal joints from the
periphery to the center (pencil in a
cup) => PsA. Non-
articular bone erosions
(intraosseous tophus) => gout.
Intraosseous geodes
=> both PsA and gout. b Psoriatic
onycho-pachydermo-periostitis.
“An arthritis of the first digit is not
necessarily gouty”
 Clin Rheumatol

Discussion The World Health Organization defined “multimorbidity”

as the coexistence of two or more chronic conditions in a same
Psoriasis is a complex and multifactorial disease that shares a individual. Multimorbidity has since been associated with re-
common profile and numerous environmental factors with duced quality of life and increased mortality [58]. In contrast,
gout. An accurate diagnosis is challenging for patients whose “comorbidity” has been defined by the occurrence of diseases
background as well as clinical, biological, and radiographic in addition to a main or index disease. According to these
symptoms can encompass both PsA and gout. definitions and to our conception, psout could be considered
In this context, the use of new imaging techniques such a multimorbidity/comorbidity entity. Clinical trial-based dis-
as dual-energy computed tomography (DECT) to identify ease-specific guidelines are not appropriate for patients with
urate crystals in joints could represent a valuable tool for multimorbidity for whom the therapeutic strategy remains
advancing our understanding of the links between these challenging. The understanding and accurate description of
two diseases [53]. This imaging modality has indeed been multimorbidity/comorbidity-specific conditions should im-
used for the diagnosis of sacroiliac gout [54], and urate prove the management of the corresponding patients.
crystals have been detected by DECT in the sacroiliac With this perspective, there is probably no single psout
joints of patients followed for gout but also for but rather a multitude of “psouts” associating varying de-
spondyloarthritis [55]. However, routine practice is usual- grees of PsA and hyperuricemia (symptomatic or not) and
ly accompanied by ultrasonography assessments. The po- evolving over time.
tential of ultrasonography in differentiating gouty or pso- Although the presence of inflammatory arthritis on a
riatic arthropathy has been suggested [56, 57]. In fact, the frequent cardiometabolic background (as comorbidities)
specific ultrasound signs of these two diseases (double is an acceptable rationale for the current cardiovascular
contour sign or tophi for gout and ungual involvement screening and prevention, routine monitoring of acid uric
for PsA) along with clinical or biological signs are incon- levels and asymptomatic treatment of hyperuricemia are
sistent, with the coexistence of both rheumatisms still re- not recommended.
maining a possibility.
The pathogenic role of chronic hyperuricemia in the devel- & Obviously, not all forms of PsA are associated with
opment and maintenance of psoriasis and PsA is based on gout or hyperuricemia, and therefore, rheumatologists
epidemiological, clinical, and pathophysiological arguments should appropriately assess the degree of involvement
and hence does not appear fortuitous. These two pathological of these two pathological processes in their daily prac-
processes can influence each other, even though primarily tice. We believe that this new line of thinking regard-
MSU crystals have a deleterious role on psoriasis and PsA, ing the convergence of gout and PsA, involving the
rather than the opposite. Nevertheless, the epidemiological role of urate crystals, could prompt a potential new
and pathophysiological overlap and the clinical and radiolog- approach to treatment (urate-lowering therapy) among
ical similarities suggest a much narrower interplay between patients with active/refractory PsA.
PsA and gout than the mere coexistence of two common pa- & In clinical practice, because the clear distinction be-
thologies in the same patient. tween an acute gouty attack and a PsA flare can be
The concurrence of these two diseases in the same patient confounding, a knowledge of this association provides
could be considered a novel overlap syndrome, at the bound- the opportunity for appropriate therapeutic adjust-
ary between inflammatory and metabolic rheumatism, for ments. Knowing how to screen a patient at a given time
which we propose the term “psout.” may provide valuable keys for adjusting treatment reg-
The concept of psout has some limitations. First, PsA is a imens, for instance intensifying the psoriasis or PsA
complex and multifactorial disease, which is unlikely based treatment or lowering the hyperuricemia (Fig. 4).
solely on hyperuricemia. The pathogenic role of chronic hy- & In the event of insufficient control of PsA, proposing a
peruricemia in the development and maintenance of psoriasis modification or intensification of the disease-modifying
and PsA is not a conventional representation of the pathogenic treatment with a biologic, for example, is appropriate.
process leading to the development of psoriasis and its arthrit- Recognition of the psout entity leads to further propose
ic manifestations. Indeed, many other environmental triggers an initial hypouricemic therapy in conjunction with this
identified in the development of psoriasis include drug expo- treatment. This in itself represents a concomitant optimi-
sure, streptococcal infections, or viral infections. Second, ele- zation of the disease-modifying treatment of PsA.
ments of the metabolic syndrome such as body mass index
and adipocytokines are key players in determining both dis-
eases, which questions whether their coexistence in the same Clinical trials are needed to further assess the potential role
patient could be fortuitous or related to multimorbidity/ of urate crystals and the effect of reducing uricemia levels in
comorbidity overlap between these diseases. PsA before implementing this particular approach in daily
Clin Rheumatol

Fig. 4 Diagram at the crossroads

of PsA and gout, adaptation of the
therapeutic strategy. bDMARDs:
biological disease-modifying an-
tirheumatic drugs; csDMARDs:
conventional synthetic disease-
modifying antirheumatic drugs;
NSAIDs: non-steroidal anti-in-
flammatory drugs; PsA: psoriatic
arthritis; PUVA: psoralen and ul-
traviolet A; SUA: serum uric acid;
Tx: treatment

practice. A clinical trial designed to assess the efficacy and which has a hypouricemic effect [63]. Once again, a clin-
safety of allopurinol plus standard of care versus intensifica- ical trial evaluating the benefit of treatment with
tion of PsA therapy plus standard of care in patients with leflunomide versus methotrexate in patients with PsA
hyperuricemia and poorly controlled joint manifestations in and hyperuricemia could be of great interest because of
PsA could also be considered. Indeed, lowering uricemia no randomized controlled trials conducted in PsA to date,
levels decreases the risk of incident gout attacks but may also in contrast to a study of rheumatoid arthritis [64].
reduce synovial inflammation and joint destruction in PsA, The presence of several rheumatic conditions influencing
given the pro-inflammatory role of MSU crystals. each other in the same individual, such as osteoarthritis and
At the dawn of personalized medicine, it is becoming in- chondrocalcinosis, is frequently encountered in clinical prac-
creasingly necessary to have a thorough understanding of tice. In this sense, psout could represent a new model by
these diseases in their complexity by taking into account co- integrating the latest data on the mechanisms of action of urate
morbidities to accurately adjust treatment. Moreover, it has crystals in their environment in the pathophysiology of psori-
been well established that inflammatory rheumatism in itself atic arthritis, which is still poorly known.
represents a cardiovascular risk factor to be managed [59] just
like hyperuricemia [60]. Despite no recommendation suggest-
ing the treatment of isolated hyperuricemia, this optimization Conclusion
of PsA therapy by adding urate-lowering therapy may also
enable better management of the cardiovascular risk factors As in “rhupus,” combining lupus and rheumatoid arthritis,
of these patients, thereby fulfilling one of the objectives of the the existence of psout, combining psoriasis/PsA and gout,
current recommendations [61]. This point is further is corroborated by the concomitant existence of a common
highlighted by a recent study comparing 318 patients with background and pathophysiology as well as an intricate
PsA who had hyperuricemia to 318 matched patients with clinical, biological, and radiological presentation, which
PsA without hyperuricemia. These hyperuricemic patients could, in the near future, justify an adapted diagnostic
had more concurrent comorbidities (cardiovascular and and therapeutic strategy.
metabolic diseases, as well as a higher prevalence of kid-
ney stones) and higher creatinine level than those without Authors’ contributions RF, PMD, LS, and LM: conception of the concept
hyperuricemia. Over the follow-up, patients with persistent of “psout,” article design, manuscript writing, drafting, and revision.
hyperuricemia frequently showed myocardial infarction, JEG: article design, manuscript drafting, and revision.
heart failure, and renal impairment [23]. Most recently,
hyperuricemia has been found independently associated Compliance with ethical standards
with cardiovascular diseases in psoriatic patients [62].
Disclosures None.
Finally, in a “psouty” patient, the use of non-steroidal
anti-inflammatory drugs may be deleterious given the
Consent for publication The patient gave his informed consent before
high cardiovascular risk, whereas conversely, certain basic the writing of the case report. Details that might disclose the identity of
treatments could be favored, in particular leflunomide, the patient have been removed.
 Clin Rheumatol

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