Psoriasis vs. psoriatic arthritis. Similarities and differences in the pathophysiology

被引:2
|
作者
Pap, T. [1 ,2 ]
Sunderkotter, C. [3 ]
机构
[1] Westfalische Wilhelms Univ, Inst Muskuloskeletale Med, Albert Schweitzer Campus 1,Gebaude D3, D-48148 Munster, Germany
[2] Univ Klinikum Munster, Albert Schweitzer Campus 1,Gebaude D3, D-48148 Munster, Germany
[3] Martin Luther Univ Halle Wittenberg, Univ Klin & Poliklin Dermatol & Venerol, Halle, Germany
来源
ZEITSCHRIFT FUR RHEUMATOLOGIE | 2017年 / 76卷 / 06期
关键词
Interleukin; 23; 17; Tumor necrosis factor alpha; Immune response; Rheumatoid arthritis; TUMOR-NECROSIS-FACTOR; SKIN INFLAMMATION; DOUBLE-BLIND; MODEL; MICE; USTEKINUMAB; MACROPHAGES; EXPRESSION; CYTOKINES; CELLS;
D O I
10.1007/s00393-017-0342-0
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Psoriasis is a chronic inflammatory skin disease with genetic and (auto) immunological backgrounds. Up to 30% of patients with psoriasis also develop a mostly oligoarticular arthritis with spinal involvement that is termed psoriatic arthritis (PsA) and shows a specific joint pattern which differs from that of rheumatoid arthritis (RA). Both Psa and psoriasis share a commonmain axis, the interleukin (IL) 23/IL17 pathway as well as major overlaps in the functions of tumor necrosis factor alpha (TNFalpha). Recently acquired knowledge supports the concept that in both diseases, similar genetic dispositions and molecular pathways lead to organ-specific disease patterns. In some types of PsA, genetic predisposition and the relevance of acute inflammatory reactions appear to be greater that in psoriasis, while in the latter exogenous factors and T-lymphocyte reactions in the skin seemto have a higher impact. A key difference between PsA and cutaneous psoriasis is the largely irreversible nature of inflammatory joint changes in PsA, whereas cutaneous plaques in psoriasis completely heal. The question of how interdependent both diseases are and whether immunologically primed T-lymphocytes fromcutaneous lesions in PsAmay transmit the disease to the synovial membranes and induce acute inflammation is not precisely known. A detailed analysis of these organ-specific differences may not only provide an explanation for the similar, but partly different efficacy of novel therapeutic strategiesbut may also lead to the development of personalized therapies that take into account the individually different manifestations of the diseases over time.
引用
收藏
页码:477 / 483
页数:7
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