Six Domains

WWW.6-DOMAINS.COM IS NOT INTENDED FOR US, UK OR IRELAND AUDIENCES

About Psoriatic Arthritis

Psoriatic arthritis: A heterogeneous disease

Professor Pascal Richette, Dr Frank Behrens and Professor Oliver FitzGerald share their expertise on the different phenotypes of psoriatic arthritis and importance of considering all six domains of the disease.

Psoriatic arthritis is a heterogeneous disease involving up to six domains1 (see Figure 1). Every patient with psoriatic arthritis is unique: Each will present with his/her own combination of these domains, with varying severity and disease burden levels. Regardless of the individual’s combination, psoriatic arthritis has a substantial effect on patients’ lives.1
fig-11
Fig. 1 The prevalence of the six domains of psoriatic arthritis2-21
Download the consultation tool

Dysregulation of cytokines

The chronic inflammatory state of psoriatic arthritis is a consequence of the overproduction of pro-inflammatory cytokines.22 Chronic changes to the inflammatory signalling pathways can affect cells in the joints and skin, causing symptoms of psoriatic disease, such as swelling and tenderness of the joints.22,23 Current research suggests that each domain is driven by the dysregulation of a different combination of cytokines24-42 (see Figure 2).
19407-Celgene-web-graphs
Fig.2 Map of cytokines by each domain24-42

The distinct features of psoriatic arthritis and rheumatoid arthritis

The clinical features of psoriatic arthritis clearly distinguish it from rheumatoid arthritis (see Figure 3).43,44 Psoriatic arthritis and rheumatoid arthritis are both autoimmune diseases characterised by pain, swelling and stiffness of the joints.43,44 However, psoriatic arthritis is usually associated with a negative serologic test for rheumatoid factor and is commonly asymmetric, presenting enthesitis and dactylitis, beyond the peripheral joint involvement (see Figure 1).45,46
Celgene__Figure-3-1-1
Fig.3 Prominent clinical features of psoriatic arthritis and rheumatoid arthritis43, 44, 45, 47
The pattern of joint involvement and bone erosion is different in psoriatic arthritis and rheumatoid arthritis.48-51 Bone changes in psoriatic arthritis include erosion and new bone formation, whereas new bone formation is not associated with rheumatoid arthritis.48-51
Psoriatic arthritis is characterised by enthesitis (inflammation of the entheses).50 Enthesitis in psoriatic arthritis is extra-articular, can have a mechanical trigger, and is associated with pain and new bone formation. On the other hand, patients with rheumatoid arthritis experience primary synovitis (see Figures 4a and 4b).50,51
Secondary synovitis may also occur with enthesitis in psoriatic arthritis. This is when synovitis occurs after the release of pro-inflammatory molecules from the entheses, and is different to the primary synovitis seen in rheumatoid arthritis.50
Psoriatic arthritis bone erosion
Psoriatic-Arthritis-bone-erosion
Fig.4a Psoriatic arthritis bone erosion50,51
Rheumatoid arthritis bone erosion
Rheumatoid-Arthritis-bone-erosion
Fig.4b Rheumatoid arthritis bone erosion48-51
 
In psoriatic arthritis, the radiographic progression is knowingly slower than in rheumatoid arthritis.52-58 The modified Total Sharp Score (mTSS) was created to measure joint changes in rheumatoid arthritis and has been modified to account for the clinical features of psoriatic arthritis.58 Randomised controlled trials using mTSS have been used to illustrate this difference in average progression rate (see Figure 5).52-57
Celgene__Figure-5-1-1
Fig. 5 Radiographic progression rates in PsARCTs from 2007 to 201552-57

Comorbid conditions

Many patients with psoriatic arthritis have comorbid conditions59, with 42% having three or more comorbidities.60 The most frequently reported comorbidities are hypertension59, obesity59, depression1 and cardiovascular problems1.
One study of 611 patients with psoriatic arthritis identified the prevalence of the following most common comorbidities:59
37.1% Hypertension
30% Obesity
20.7% Hyperlipidaemia
20.7% Depression
/anxiety
Fig. 6 - Most common comorbidities of psoriatic arthritis
Patients with psoriatic arthritis are more likely to experience comorbidities than patients with psoriasis.61 In addition to this, recent studies have also shown that patients affected by psoriatic disease are more likely to have liver disease (especially non-alcoholic fatty liver disease) compared to patients with rheumatoid arthritis.62
Commonly associated comorbidities of psoriatic arthritis59, 61- 63

References
1. Kavanaugh A, et al. Rheumatol Ther 2016;3:91–102
2. Kyriakou A, et al. Sci World J 2014; Article ID 508178;
3. Lee E, et al. J Exp Med 2004;199:125–30;
4. Lowes M, et al. J Invest Dermatol 2008;128:1207–11
5. Yao Y, et al. PLoS One 2008;3:e2737
6. Taylan A, et al. Rheumatol Int 2012;32:2511
7. Limon-Camacho L, et al. J Rheumatol 2012;39:830–5.
8. Van Kuijk A and Tak P. Curr Rheumatol Rep 2011;13:353–9
9. Ritchlin C, et al. J Rheumatol 1998;25:1544–52
10. Menon B, et al. Arthritis Rheumatol 2014;66:1272–81
11. Celis R, et al. Arthritis Res Ther 2012;14:R93
12. Spadaro A, et al. Ann Rheum Dis 2002;6:174–6
13. Molteni S and Reali E. Psoriasis: Targets and Therapy 2012;2:55–66
14. Siegel E, et al. Curr Opin Rheumatol 2015;27:111–7
15. Lories R, et al. Nat Med 2012;18:1018–9
16. Ebihara S, et al. Autoimmunity 2015;29:1–8
17. Ruutu M, et al. Arthritis Rheum 2012;64;2211–22
18. Sherlock J, et al. Nat Med 2012;18:1069–77
19. Yamamoto M, et al. J Invest Dermatol 2015;135:445–53
20. Reinhardt A, et al. Arthritis Rheumatol 2016;68:2476–86
21. Coates LC, et al. Lancet 2015;386:2489–98.
22. Mease PJ, et al. Drugs 2014;74:423–41.
23. Schafer P. Biochem Pharmacol 2012;83:1583–90.
24. Van Kuijk A and Tak P. Curr Rheumatol Rep 2011;13:353–9
25. Ritchlin C, et al. J Rheumatol 1998;25:1544–52
26. Menon B, et al. Arthritis Rheumatol 2014;66:1272–81
27. Celis R, et al. Arthritis Res Ther 2012;14:R93
28. Spadaro A, et al. Ann Rheum Dis 2002;6:174–6
29. Molteni S and Reali E. Psoriasis: Targets and Therapy 2012;2:55–66  
 
30. Siegel E, et al. Curr Opin Rheumatol 2015;27:111–7
31. Lories R, et al. Nat Med 2012;18:1018–9
32. Ebihara S, et al. Autoimmunity 2015;29:1–8
33. Ruutu M, et al. Arthritis Rheum 2012;64;2211–22
34. Sherlock J, et al. Nat Med 2012;18:1069–77
35. Yamamoto M, et al. J Invest Dermatol 2015;135:445–53.
36. Reinhardt A, et al. Arthritis Rheumatol 2016;68:2476–86
37. Taylan A, et al. Rheumatol Int 2012;32:2511
38. Limon-Camacho L,et al. J Rheumatol 2012;39:830–5.
39. Lee E, et al. J Exp Med 2004;199:125–30
40. Lowes M, et al. J Invest Dermatol 2008;128:1207–11
41. Yao Y, et al. PLoS One 2008;3:e2737
42. Kyriakou A, et al. Sci World J 2014;Article ID 508178.
43. Gottlieb A, et al. J Am Acad Dermatol 2008;58:851–64.
44. Scutellari P, et al. Eur J Radiol 1998;27(suppl 1):S31–38.
45. Coates LC, et al. Arthritis Rheumatol 2016;68:1060–71.
46. Moll JMH and Wright V. Semin Arthritis Rheum 1973;3:55–78.
47. Helliwell PS. Clin Rheum 2015;33:S44-47
48. McGonagle D, et al. Lancet 1998;352:1137–40.
49. McGonagle D & McDermott MF. PLoS Med 2006;3:e29.
50. Schett G, et al. Nat Rev Rheumatol 2017;13:731–41.
51. Ritchlin CT, et al. N Engl J Med 2017;376:957–70
52. Ravindran J, et al. Arthritis Care Res 2010;62:86–91.
53. Gladman DD, et al. Arthritis Rheum 2007;56:476–88.
54. Kavanaugh A, et al. Arthritis Rheum 2012;64:2504–17.
55. Kavanaugh A, et al. Ann Rheum Dis 2014;73:1020–6
56. van der Heijde D, et al. Arthritis Rheum 2016;68:1914–21
57. Strand V & Sharp JT. Arthritis Rheum 2003;48:21–34.
58. van der Heijde, et al. Ann Rheum Dis 2005; 64(Suppl II):ii61–4.
59. Husted JA, et al. Arthritis Care Res (Hoboken) 2011;63:1729–35  
 
60. Husted JA, et al. J Rheumatol 2013;40:1349–56.
61. Edson-Heredia E, et al. J Eur Acad Dermatol Venereol 2015;29:955–63.
62. Ogdie A, et al. J Rheumatol 2014;41:2315–22.
63. Ogdie A, et al. J Invest Dermatol 2017 [Epub]
64. Wervers K, et al. J Rheumatol 2018;45:1526–31
65. Nossent J & Gran JT. Scand J Rheumatol 2009;38:251–5
66. Coates L, et al. Arthritis Rheum 2013;65:1504–9
67. Lindqvist U, et al. J Rheum 2008;35:668–73
68. Husni M. Rheum Dis Clin N Am 2015;41:677–698
69. Queiro-Silva R, et al. Ann Rheum Dis 2003;62:68–70
70. Singh J et al. Arth care res 2019;71:5–32
71. Kavanaugh A, et al. Rheumatol Ther 2016;3:91–102
72. van Mens L, et al. Rheumatology (Oxford) 2018;57:283–90
73. van Mens L, et al. Ann Rheum Dis 2017;77:251–7
74. Huscher D, et al. ACR 2015: Abstract 679
75. Veale DJ & Fearon U. RMD Open 2015;1:e000025
76. Dures E, et al. Patient 2017;10:455–62
77. Wilsdon TD, et al. Cochrane Database Syst Rev 2017, Art. No.: CD012722
78. Xu U, et al. Am Health Drug Benefits 2018;11:408–17
79. Lebwohl M, et al. J Am Acad Dermatol 2014;70:871–81
80. van de Kerkhof P, et al. J Eur Acad Dermatol Venereol 2015;29:2001–210
81. Gossec L, et al. Ann Rheum Dis 2014;73:1012–19
82. Lubrano E, et al. Clin Exp Rheumatol
2015;33(5 Suppl 93):S51–4
83. FitzGerald O, et al. Ann Rheum Dis 2012;71:358–62
84. Waxman R & Helliwell P. Ann Rheum Dis 2018;77:467–8
 
 

Survey