E-Book, Englisch, 118 Seiten
Mease / Helliwell Atlas of Psoriatic Arthritis
1. Auflage 2008
ISBN: 978-1-84628-897-5
Verlag: Springer
Format: PDF
Kopierschutz: 1 - PDF Watermark
E-Book, Englisch, 118 Seiten
ISBN: 978-1-84628-897-5
Verlag: Springer
Format: PDF
Kopierschutz: 1 - PDF Watermark
Psoriatic arthritis (PsA) is a form of arthritic joint disease associated with the chronic skin scaling and fingernail changes seen in psoriasis. Patients with PsA have a reduced quality of life. This comprehensive visual reference contains over 150 images from a wide gamut of variations of the disease, as well as charts and tables detailing the most up-to-date information on patient susceptibility, incidence, and symptoms.
Philip J. Mease, MD, is a clinical professor at the University of Washington School of Medicine in Seattle, where he has also been chief resident and fellow in rheumatology, and is chief of rheumatology clinical research at the Swedish Hospital Medical Center. He is highly involved in clinical trials of new therapies for a number of rheumatic disease conditions, (including rheumatoid arthritis, ankylosing spondylitis, psoriatic arthritis, osteoarthritis, lupus, fibromyalgia and osteoporosis,) and is a founding organizer of GRAPPA (Group for Research and Assessment of Psoriasis and Psoriatic Arthritis.) Publications include numerous articles and book contributions. Philip Mease also sits on review boards for The Journal of Rheumatology, Arthritis & Rheumatism, and The Annals of the Rheumatic Diseases and has received the Medical Communicator Award of the American College of Rheumatology. Dr Mease chairs / co-chairs three working groups of OMERACT (Outcome Measures in Rheumatology): psoriatic arthritis, fibromyalgia and single joint assessment. He is also on the medical advisory boards of pharmaceutical and biotechnology companies, the Lupus Foundation, the Psoriasis Foundation, and the Northwest Arthritis & Osteoporosis Institute. With a strong interest in education, he is also a part of the speakers' bureaus of the Arthritis Foundation, Lupus Foundation, National Psoriasis Foundation, Wyeth Ayerst, SmithKline Beecham, Genelab Technologies, Proctor & Gamble - to name but a few. Philip S. Helliwell, BM, BCh, is currently senior lecturer in rheumatology at the University of Leeds, Academic Unit of Musculoskeletal & Rehabilitation Medicine. His interests include chronic pain, disability, and communication. He has written about the Moll and Wright classification criteria for diagnosing PsA, making the case for retaining at least the two subgroups of peripheral and axial disease and splitting the peripheral disease into oligo- and polyarthritis.
Autoren/Hrsg.
Weitere Infos & Material
1;Contents;5
2;Contributors;7
3;Introduction;9
3.1;References;10
4;Epidemiology;11
4.1;Incidence and prevalence data for PsA in published studies;12
4.2;Prevalence of PsA among patients with psoriasis;13
4.3;Predominantly DIP joint involvement in PsA;13
4.4;Oligoarthritis in patients with PsA;14
4.5;Symmetric polyarthritis in PsA;14
4.6;Arthritis mutilans in PsA;15
4.7;Spondyloarthritis in PsA;15
4.8;Change in patterns of PsA in 664 patients in an inception cohort;16
4.9;Dactylitis in fingers and toes in PsA;16
4.10;Photograph and radiograph of enthesitis in PsA;17
4.11;Adjusted mean SF-36 health survey scores for PsA sample and UK and USA general populations;17
4.12;Predictive factors for mortality in PsA;18
4.13;Factors associated with remission in PsA;18
4.14;HLA gene complex - chromosome 6;19
4.15;HLA antigens and disease progression in PsA Genetic basis of psoriasis: genome scans;20
4.16;References;21
5;Etiology and Pathophysiology;25
5.1;Etiology;25
5.1.1;Genetic factors;25
5.1.2;Environmental factors;25
5.2;Pathogenesis;26
5.2.1;Synovial membrane characteristics;26
5.2.2;Enthesis;26
5.2.3;Mechanisms of joint destruction;26
5.2.4;Environmental factors in the pathogenesis of RA;27
5.2.5;Histology of psoriatic plaque Vascular morphology in psoriatic and rheumatoid synovium;27
5.2.6;hybridization for VEGF and Ang-2 mRNA in patients with early PsA and RA;28
5.2.7;Synovial membrane characteristics – features of psoriatic synovium;28
5.2.8;MRI showing acute enthesitis;29
5.2.9;Undifferentiated SpA at baseline and 6 months after treatment;29
5.2.10;Distal digit osteolysis in PsA;30
5.2.11;Osteoclasts are prominent in the psoriatic joint Bone and cartilage destruction in PsA;30
5.2.12;Osteoclastogenesis pathway;31
5.2.13;Schematic model of osteolysis in the psoriatic joint;31
5.2.14;References;32
6;Clinical Evaluation;35
6.1;PsA clinical subgroups of Moll and Wright;36
6.2;DIP joint inflammation;37
6.3;Asymmetric oligoarthritis;37
6.4;Classic ankylosing spondylitis;38
6.5;Symmetric polyarthritis;38
6.6;Distinctive mutilation in PsA;39
6.7;Dactylitis in the hand and foot;39
6.8;Entheseal sites in PsA;40
6.9;SAPHO syndrome – palmoplantar pustulosis;40
6.10;SAPHO syndrome – abnormal radioisotope uptake in psoriasis vulgaris Eye disease in PsA;41
6.11;Pitting edema in PsA Relationship between joint symmetry and number of joints in PsA;41
6.12;Juvenile PsA;42
6.13;HIV and PsA;42
6.14;Clinical syndromes that suggest PsA;42
6.15;General diagnostic principles for PsA Flexural psoriasis;43
6.16;Left and right hand of a 67-year-old male at first presentation;44
6.17;Inflammatory articular disease (joint, spine, or entheseal);44
6.18;Screening questions for arthritis;45
6.19;Diagnostic pointers to distinguish PsA from RA;46
6.20;References;47
6.21;Distinguishing PsA from other SpAs;47
7;Imaging;49
7.1;Plain radiographs of patients with arthritis mutilans;50
7.2;Plain radiograph of ‘whittling’ in PsA;50
7.3;Plain radiograph of characteristic changes in finger in chronic PsA – classic periostitis;51
7.4;Inflammatory polyarthritis in chronic PsA;51
7.5;Multiple peri-articular bone erosions in PsA patient receiving combination therapy;52
7.6;PsA with rheumatoid-like features – ulnar deviation of the MCP joints;52
7.7;PsA with rheumatoid-like features – fibular deviation of the toes;53
7.8;Monoarthritis of the right wrist in patient with PsA;53
7.9;Syndesmophytes in PsA;54
7.10;Enthesophytes in PsA;54
7.11;Ultrasonographs showing capsular edema in PsA;55
7.12;Ultrasonography of patellar tendon enthesitis in PsA;55
7.13;Ultrasonographs of plantar fasciitis and patellar tendonitis;55
7.14;Ultrasonography and MRI of plantar faciitis in PsA;56
7.15;MRI of the hands in PsA – capsular-based edema;56
7.16;Use of MRI in early PsA;57
7.17;MRI of knee of HLA-B27-positive patient with PsA;57
7.18;MRI of patient with SAPHO syndrome;58
7.19;Scintigraphy and MRI of patient with SAPHO syndrome;58
7.20;Imaging of sacroiliac joints of patient with HLA-B27-positive PsA;59
7.21;CT scan of pelvis of PsA patient showing sacroiliitis;59
7.22;References;60
8;Skin and Psoriasis;63
8.1;Pathophysiology;63
8.2;The Psoriasis Phenotype;63
8.2.1;MHC and non-MHC psoriasis loci;64
8.2.2;Histopathology of psoriasis;65
8.2.3;Examples of plaque-type psoriasis;65
8.2.4;Examples of plaque-type psoriasis;66
8.2.5;Examples of partially cleared psoriasis;66
8.2.6;Guttate psoriasis;67
8.2.7;Psoriatic flare;67
8.2.8;Distribution of psoriasis;67
8.2.9;Palmoplantar psoriasis;68
8.2.10;Pustular psoriasis;69
8.2.11;Erythrodermic psoriasis;69
8.2.12;Psoriatic nail disease;70
8.2.13;References;70
9;Juvenile Psoriatic Arthritis;73
9.1;Introduction;73
9.2;Clinical Features of Juvenile Psoriatic Arthritis;73
9.2.1;Dactylitis;73
9.2.2;Psoriasis;73
9.2.3;Uveitis;73
9.2.4;Growth Disturbances;74
9.2.5;Other Systemic Manifestations of JPsA;74
9.3;Imaging;74
9.4;Treatment;74
9.5;Outcome and Prognosis;74
9.5.1;Differential diagnosis of musculoskeletal disorders in children;75
9.5.2;Definition of JIA;75
9.5.3;Comparison between the classification systems for JIA, JCA, and JRA;76
9.5.4;JIA and subtypes;76
9.5.5;JPsA;77
9.5.6;Guttate psoriasis;77
9.5.7;Epidemiology of JIA;78
9.5.8;Clinical features of JPsA;78
9.5.9;a) JPsA patterns of joint disease at onset;79
9.5.10;b) Joint involvement in JPsA;79
9.5.11;Oligoarticular-onset JPsA;79
9.5.12;Asymmetrical small joint involvement in JPsA;80
9.5.13;Symmetrical DIP involvement in JPsA Polyarticular JPsA;80
9.5.14;Psoriasis skin rash;80
9.5.15;Destructive small joint disease in JPsA;81
9.5.16;Oligoarticular-onset JIA or oligoarticular JPsA?;81
9.5.17;Knee arthritis and asymmetrical growth;81
9.5.18;Micrognathia;82
9.5.19;JPsA of the left foot and asymmetrical growth;82
9.5.20;Dactylitis;83
9.5.21;Dactylitis in the foot;83
9.5.22;Enthesitis;84
9.5.23;Case history: dactylitis in the left foot;84
9.5.24;Heel and foot pain in children;85
9.5.25;Psoriasis at the umbilicus;85
9.5.26;Acute anterior uveitis;86
9.5.27;Koebner phenomenon;86
9.5.28;Nail changes;86
9.5.29;Chronic anterior uveitis;87
9.5.30;Recommended ophthalmologic monitoring for patients with JIA;87
9.5.31;MSUS image of an adolescent with JPsA;87
9.5.32;Medicines used to treat inflammatory arthritis in children;88
9.5.33;References;89
10;The Management of Psoriatic Arthritis;91
10.1;Therapy of PsA;93
10.2;Therapeutic targets in PsA;93
10.3;Who will progress aggressively?;94
10.4;Measures of PsA outcome;94
10.5;Trial-verified benefit of traditional DMARDs in PsA;95
10.6;Sulfasalazine in PsA: PsARC response at 36 weeks;95
10.7;Leflunomide in PsA: ACR20 and PsARC results;95
10.8;Pathophysiology of PsA;96
10.9;Role of cytokines and cytokine inhibitors in chronic inhibition;96
10.10;Key actions attributed to TNF;97
10.11;Cytokine inhibition;97
10.12;TNF inihibition;98
10.13;Design elements in current PsA trials;99
10.14;Demographics of etanercept phase III trial;99
10.15;Results of phase III trial of etanercept in PsA;100
10.16;Etanercept in PsA: radiographic progression mean change in TSS through 24 months;101
10.17;IMPACT 2: study design/subject disposition;101
10.18;Infliximab in psoriasis/PsA therapy: phase III study;101
10.19;Infliximab reduces inflammation in PsA (IMPACT 2);102
10.20;ADEPT study design;102
10.21;Adalimumab in PsA: ACR response at weeks 12 and 24 ( ADEPT);103
10.22;HAQ mean change from baseline at week 12 and 24 (ADEPT);103
10.23;Adalimumab in PsA: ACR response at weeks 12 and 24 ( ADEPT);103
10.24;Mean change in mTSS at week 24 (ADEPT);104
10.25;Safety issues of anti-TNF therapy;104
10.26;PsA: new therapies on the horizon;105
10.27;T-cell activation requires two signals;105
10.28;PsA open-label study: alefacept;106
10.29;Example of an adaptive aid: a wrist splint;106
10.30;PsA: strategizing therapy choice;106
10.31;References;107
11;Treatment of Psoriasis;109
11.1;Definition of the PASI;110
11.2;Dermatology Life Quality Index;111
11.3;Topical therapies for psoriasis;111
11.4;Overview of phototherapy for psoriasis;113
11.5;Overview of systemic agents for psoriasis;115
11.6;Biologic agents currently available or in late-phase trials for psoriasis;116
11.7;Alefacept, a fully humanized fusion protein;117
11.8;PASI response and efficacy of alefacept in two phase III studies;117
11.9;PASI 75 response to etanercept in a phase II trial;118
11.10;Percentage of patients achieving PASI 75 or PASI 50 in efalizumab- treated ( 1 mg/ kg/ wk) and placebo groups;118
11.11;Adalimumab efficacy at weeks 12, 24 and 60;119
11.12;Randomized placebo-controlled trials with infliximab;120
11.13;References;120
12;Index;125




