用超声波描绘接受生物制剂治疗的银屑病关节炎的临床过程。

Mayumi Ota, Yoshimasa Nobeyama, Akihiko Asahina
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摘要

银屑病关节炎(PsA)是一种慢性炎症性关节疾病,被视为银屑病的一种特殊亚型。使用超声波对 PsA 进行长期评估的研究尚属空白。本研究的目的是利用超声波造影术了解开始使用生物制剂后关节病变的变化,并为超声波造影术在 PsA 患者长期随访中的应用提供证据。我们回顾性地招募了 17 名接受生物制剂治疗的日本 PsA 患者,他们均符合银屑病关节炎的分类标准。我们使用 18 兆赫的高频线性探头通过多普勒和 B 模式记录了超声图像。在接受生物制剂治疗前,所有受检患者(100%)都患有肌腱内翻炎和伸肌腱炎,而只有六名患者(35.3%)的肌腱出现纤维状脱落(LFP)。随着时间的推移,疼痛的数字评分量表得分以及超声波检查结果(包括内翻炎、伸肌腱炎和 LFP)的程度都发生了明显变化。此外,这些超声波检查结果之间也会随着时间的推移而发生明显变化。该研究确定了开始使用生物制剂后特定 PsA 病变的改善过程。研究发现,肌腱炎、伸肌腱炎和 LFP 的改善过程各不相同。这些结果可能有助于加深对 PsA 发病机制的理解。
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Clinical course of psoriatic arthritis treated with biologics delineated with ultrasonography.

Psoriatic arthritis (PsA) is a chronic, inflammatory articular disease regarded as a specific subtype of psoriasis. Long-term assessment for PsA using ultrasonography has not yet been investigated. The present study was conducted to delineate the changes in articular lesions after the initiation of biologics using ultrasonography, and to provide the evidence of the utility of ultrasonography in long-term follow-up of PsA patients. We retrospectively recruited 17 Japanese PsA patients treated with biologics who met the classification criteria for psoriatic arthritis. Ultrasonographic images were recorded using a high-frequency linear 18 MHz probe through Doppler- and B-modes. Before the treatment with biologics, all examined patients (100%) had enthesitis and extensor tendinitis, while only six patients (35.3%) had loss of the fibrillar pattern of the tendon (LFP). There were significant changes over time in the numerical rating scale score for pain, and in the degree of ultrasonographic findings, including enthesitis, extensor tendinitis, and LFP. Also, there were significant changes over time between these ultrasonographic findings. The study identified the improvement course for a specific PsA lesion after the initiation of biologics. The improvement courses in enthesitis, extensor tendinitis, and LFP were found to differ from each other. These results may contribute to deeper understanding of the pathogenesis of PsA.

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