Objectives. To develop a scoring system for evaluating the extrasynovial soft tissue inflammation of the shoulders in patients with polymyalgia rheumatica (PMR) and elderly-onset rheumatoid arthritis with PMR-like onset (pm-EORA) using ultrasound. Methods. We analyzed stored power Doppler (PD) images obtained by the pretreatment examination of 15 PMR patients and 15 pm-EORA patients. A semiquantitative scoring system for evaluating the severity of PD signals adjacent to the anterior aspect of the subscapularis tendon was designed. Results. A four-point scale scoring for the hyperemia on the subscapularis tendon was proposed as follows in brief: 0 = absent or minimal flow, 1 = single vessel dots or short linear-shape signals, 2 = long linear-shape signals or short zone-shape signals, or 3 = long zone-shape signals. This scoring system showed good intra- and interobserver reliability and good correlation to quantitative pixel-counting evaluation. By using it, we demonstrated that inflammation in PMR is dominantly localized in extrasynovial soft tissue as compared with pm-EORA. Conclusions. We proposed a reliable semiquantitative scoring system using ultrasound for the evaluation of extrasynovial soft tissue inflammation of the shoulders in patients with both PMR and pm-EORA. This system is simple to use and can be utilized in future investigations.
A 59-year-old man who presented with continuous fever, livedo reticularis, and left leg ischemia with multiple tibial artery stenosis and renal artery aneurysm, as demonstrated by arteriography, was diagnosed with polyarteritis nodosa (PAN) 6 years ago. Although he frequently relapsed in spite of intensive immunosuppressive therapies, the disease activity of PAN was controlled with repeated rituximab (RTX) therapies and steroid doses were tapered safely. Peripheral CD19 B-cells disappeared soon after the 1st administration of RTX. Although CD19 B-cells remained absent, 3.1% of CD3CD20 T-cells were observed in the peripheral blood prior to the 2nd administration of RTX. Recent studies have suggested the pathogenic role of CD3CD20 T-cells in autoimmune diseases in the context of RTX therapy; therefore, their roles in the pathogenesis of PAN also need to be considered.
Semiquantitative scoring for subacromial bursa (SAB), subdeltoid bursa (SDB), and subcoracoid bursa by both gray-scale (GS) and power Doppler (PD) ultrasonography was performed in 15 patients with polymyalgia rheumatica (PMR) (72.6 ± 7.7 years old) and 15 patients with elderly onset rheumatoid arthritis with PMR-like onset (pm-EORA) (70.7 ± 7.0 years old) before starting treatment. The GS grades of SAB were significantly higher in the shoulders with pm-EORA than in the shoulders with PMR. The GS and PD scores of SAB and the PD scores of SDB were significantly higher in pm-EORA than in PMR cases. The sums of GS and/or PD scores for the three bursae were significantly higher in pm-EORA than in patients with PMR. The sums of GS and PD scores for SAB were significantly higher in pm-EORA than in PMR cases. Moderate to severe proliferative synovitis of the shoulder bursae, especially in SAB, is a key feature for discriminating pm-EORA from PMR.
The consecutive reports and stored images of ultrasound examinations for 100 symptomatic ankles of 74 patients with rheumatoid arthritis (RA) were reviewed for the presence or absence of retrocalcaneal bursitis (RCB) and Achilles tendon enthesitis (ATE). The ankles were classified into 4 categories based on the presence or absence of RCB or ATE. The number of RCB(−)/ATE(−), RCB(+)/ATE(−), RCB(+)/ATE(+), and RCB(−)/ATE(+) ankles was 62, 16, 12, and 10, respectively. When classifying patients into early RA and established RA, the percentage of RCB(−)/ATE(+) ankles with early RA was significantly lower than that with established RA (P = .00595). The disease duration was significantly longer in the RCB(−)/ATE(+) ankles than in the RCB(+)/ATE(−) ankles (median [interquartile range]: 15.29 [8.69] months vs 3.6 [3.06] months, P = .0247). It was speculated that RCB precedes or accompanies ATE in the early phase of RA, which suggests that entheseal inflammation in RA arises from synovial tissues.
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