Search

Objective To test whether the presence of structural entheseal lesions in psoriasis patients influences the risk for the progression to psoriatic arthritis (PsA). Methods Prospective cohort study on psoriasis patients without clinical evidence of musculoskeletal involvement receiving baseline assessment of structural entheseal lesions and volumetric bone mineral density (vBMD) at entheseal and intra-articular sites by high-resolution peripheral quantitative computed tomography (HR-pQCT). Adjusted relative risks of developing PSA associated with baseline volumetric bone density and the presence of structural entheseal lesions were calculated using multivariable Cox regression models. Results The cohort included 114 psoriasis patients (M/F 72/42) with a mean (SD) follow-up duration of 28.2 (17.7) months, during which 24 patients developed PsA (9.7 /100 patient-years, 95%CI 6.2 to 14.5). Patients with structural entheseal lesions were at higher risk of developing PsA compared to patients without such lesions (21.4/100 patient-years, 95%CI 12.5 to 34.3, HR 5.10, 95%CI 1.53 to 16.99, p=0.008). With respect to vBMD, a 1-standard deviation increase in entheseal, but not intra-articular vBMD was associated with an approximate 30% reduced risk to progress to PsA. Especially, higher cortical vBMD at entheseal segments was associated with a lower risk of developing PsA (HR 0.32 per SD, 95%CI 0.14 to 0.71), and remained robust after multiple imputation of missing data (HR 0.64, 95%CI 0.42 to 0.98). Conclusion Presence of structural entheseal lesions as well as low cortical vBMD at entheseal segments are associated with an increased risk of developing PsA in patients with psoriasis.

Objective Autoantibodies against CD74 (anti-CD74) are associated with ankylosing spondylitis (AS). The present multicenter study, the International Spondyloarthritis Autoantibody (InterSpA) trial, was undertaken to compare the sensitivity and specificity of anti-CD74 and HLA-B27 in identifying patients with nonradiographic axial spondyloarthritis (axSpA). Methods Patients ages 18-45 years with inflammatory back pain of ≤2 years' duration and a clinical suspicion of axSpA were recruited. HLA-B27 genotyping and magnetic resonance imaging of sacroiliac joints were performed in all patients. One hundred forty-nine patients with chronic inflammatory back pain (IBP) not caused by axSpA served as controls, and additional controls included 50 AS patients and 100 blood donors whose specimens were analyzed. Results One hundred patients with inflammatory back pain received a diagnosis of nonradiographic axSpA from the investigators and fulfilled the Assessment of SpondyloArthritis international Society (ASAS) criteria. The mean age was 29 years, and the mean symptom duration was 12.5 months. The sensitivity of IgA anti-CD74 and IgG anti-CD74 for identifying the 100 axSpA patients was 47% and 17%, respectively. The specificity of both IgA anti-CD74 and IgG anti-CD74 was 95.3%. The sensitivity of HLA-B27 was 81%. The positive likelihood ratios were 10.0 (IgA anti-CD74), 3.6 (IgG anti-CD74), and 8.1 (HLA-B27). Assuming a 5% pretest probability of axSpA in chronic back pain patients, the posttest probability, after consideration of the respective positive test results, was 33.3% for IgA anti-CD74, 15.3% for IgG anti-CD74, and 28.8% for HLA-B27. A combination of IgA anti-CD74 and HLA-B27 results in a posttest probability of 80.2%. Conclusion IgA anti-CD74 may be a useful tool for identifying axSpA. The diagnostic value of the test in daily practice requires further confirmation.

Objective: To characterize the specific structural properties of the erosion-prone bare area of the human joint and to search for early microstructural changes in this region during rheumatoid arthritis Methods: An initial cadaveric study was used for exact localization of the bare area of the metacarpal heads, detection of cortical micro-channels (CoMiCs) in this region by high-resolution peripheral computed tomography (HR-pQCT) and, after anatomical dissection, their validation by micro-computed tomography (μCT). In the second part, number and distribution of CoMiCs were analyzed in 105 healthy individuals and 107 RA patients with similar sex and age distribution. Results: HR-pQCT investigation combined with adaptive thresholding allowed detection of CoMiCs in the bare area of cadaveric joints. Their existence in the bare area was additionally validated by μCT. In healthy individuals, the number of CoMiCs increased with age. RA patients showed significantly (p

Objective To assess the 2-year efficacy and safety of the interleukin-17A inhibitor, secukinumab, in active psoriatic arthritis (PsA). Methods In the FUTURE-1 study, 606 patients with active PsA were randomized to secukinumab 10 mg/kg intravenously at baseline, and at weeks 2 and 4, followed by 150 mg or 75 mg subcutaneously (SC) every 4 weeks from week 8, or matching placebo. Patients receiving placebo were re-randomized to secukinumab 150 mg or 75 mg SC from week 16 or week 24, depending upon clinical response. Treatment continued to week 104. Exploratory analysis of all primary and secondary end points, on an intent-to-treat basis, continued to week 104. Results A total of 476 patients (78.5%) completed 104 weeks of treatment. Secukinumab showed sustained efficacy across multiple domains of PsA through week 104, including signs and symptoms, disease activity, quality of life, physical function, skin symptoms, dactylitis, and enthesitis. American College of Rheumatology criteria for 20% improvement response rates were 66.8% with secukinumab 150 mg and 58.6% with secukinumab 75 mg at week 104; Psoriasis Area and Severity Index criteria for 75% improvement response rates were 74.6% and 63.0%, respectively (multiple imputed data). At week 104, 84.3% of patients in the secukinumab 150 mg group and 83.8% in the secukinumab 75 mg group showed no radiographic disease progression (observed data). No new or unexpected safety signals were reported during 2 years of treatment. Immunogenicity to secukinumab was low. Conclusion Secukinumab provided sustained improvements in PsA at 2 years, with very little radiographic progression. Treatment was well tolerated over the long term.

Psoriatic arthritis (PsA) is a chronic inflammatory disease characterized by periarticular bone loss and new bone formation. Current data regarding systemic bone loss and bone mineral density (BMD) in PsA are conflicting. The aim of this study was to evaluate bone microstructure and volumetric BMD in patients with PsA and psoriasis. We performed HR-pQCT scans at the ultradistal and periarticular radius in 50 PsA patients, 30 psoriasis patients and 70 healthy, age- and sex-related controls assessing trabecular bone volume (BV/TV), trabecular number (Tb.N), inhomogeneity of the trabecular network, cortical thickness (Ct.Th) and cortical porosity (Ct.Po) as well as volumetric BMD. Trabecular BMD (Tb.BMD, p=0.021, 12.0%), BV/TV (p=0.020, -11.9%) and Tb.N (p=0.035, 7.1%) were significantly decreased at the ultradistal radius and the periarticular radius in PsA patients compared to controls. In contrast, bone architecture of the ultradistal radius and periarticular radius was similar in patients with psoriasis and healthy controls. Duration of skin disease was associated with low BV/TV and Tb.N in patients with PsA. These data suggest that trabecular BMD and bone microstructure are decreased in PsA patients. The observation that duration of skin disease determines bone loss in PsA supports the concept of subclinical musculoskeletal disease in psoriasis patients. This article is protected by copyright. All rights reserved

Objective To investigate the factors associated with cartilage proteoglycan content in patients with rheumatoid arthritis (RA). Methods A total of 32 RA patients received high-field 3T delayed gadolinium-enhanced magnetic resonance imaging of cartilage (dGEMRIC) to determine cartilage proteoglycan content. Measurements were performed in 3 individual cartilage regions (medial, central, and lateral) of metacarpophalangeal (MCP) joints 2 and 3. T1 dGEMRIC values were then related to disease duration, disease activity, anti–citrullinated protein antibody (ACPA) status, rheumatoid factor (RF) status, and C-reactive protein (CRP) level. Results T1 dGEMRIC values did not differ significantly between MCP joints 2 and 3. Intraclass correlation coefficients were high (>0.92) for all 3 cartilage compartments (medial, central, and lateral). T1 dGEMRIC values were significantly lower in RA patients with longer disease duration (≥3 years) (P = 0.034 for the central compartment) and those with ACPA positivity (P = 0.0002 for the central compartment, P = 0.013 for the lateral compartment). In contrast, no associations were found between cartilage proteoglycan content and disease activity, CRP level, or RF status. Conclusion Decreased cartilage proteoglycan content in RA patients is associated with disease duration and ACPA positivity but not with actual disease activity, CRP level, or RF status. These data suggest that the cumulative burden of inflammation as well as ACPAs are the determinants of cartilage damage in RA.

Rheumatoid arthritis (RA) is a highly bone destructive disease. Although it is well established that RA leads to bone loss and increased fracture risk, current knowledge on the microstructural changes of bone in RA is still limited. The purpose of this study was to assess the microstructure of periarticular and nonperiarticular bone in female and male RA patients and compare it with respective healthy controls. We performed two high-resolution peripheral quantitative computed tomography (HR-pQCT; Xtreme-CT) scans, one of the distal radius and one of the ultradistal radius in 90 patients with RA (60 females, 30 males) and 70 healthy controls (40 females, 30 males) matched for sex, age, and body mass index. Volumetric bone mineral density (vBMD), bone geometry, and bone microstructure including trabecular bone volume fraction (BV/TV), trabecular number (Tb.N), trabecular thickness (Tb.Th), cortical thickness (Ct.Th) and cortical porosity (Ct.Po) were assessed. At the distal and ultradistal radius, trabecular (p = 0.005 and p

Demyelinating polyneuropathy with anti-myelin associated glycoprotein (anti-MAG) antibodies is an immune mediated disorder characterized by proximal and distal symmetric weakness. Electrophysiological measurements depict features characteristic for demyelination, including prolonged distal latency, retarded conduction velocity, delayed or absent F-waves, and, rarely, partial conduction block. We report on a 65-year-old patient who was diagnosed with demyelinating polyneuropathy and anti-MAG antibodies five years before admission. Despite immunosuppressive agents and extracorporeal therapy (plasmapheresis) the disease progressed as assessed by clinical symptoms and neurological tests. Laboratory results showed an increase of serum immunoglobulin M and anti-MAG antibodies over time. Because of progressive disease we decided to treat the patient with immunoadsorption followed by application of the anti-CD20 antibody, rituximab. Six cycles of selective immunoadsorption were performed over three-weekly intervals with a repetitively used column (Globaffin); each cycle consisted of four consecutive daily treatments. Starting at cycle 4 the anti-CD20 antibody rituximab was administered with 375 mg/m(2) after immunoadsorption. The pretreatment anti-MAG antibody level of 10,000 U/mL, indicating disease activity, initially increased during treatment to a maximum of 30,559 U/mL. However, after completion of the six cycles, the anti-MAG level had decreased to 2348 U/mL; 16 months after the last immunoadsorption cycle the anti-MAG level had increased to 4134 U/mL, while the conduction velocity and compound motor action potentials remained stabile. Immunoadsorption in combination with a monoclonal anti-CD20 antibody in patients with demyelinating polyneuropathy with anti-MAG is effective and can be used an alternative treatment option in patients with progressive disease.