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首页> 外文期刊>Amyloid: the international journal of experimental and clinical investigation : the official journal of the International Society of Amyloidosis >Amyloid arthropathy associated with multiple myeloma: Polyarthritis without synovial infiltration of CD20+ or CD38+ cells
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Amyloid arthropathy associated with multiple myeloma: Polyarthritis without synovial infiltration of CD20+ or CD38+ cells

机译：与多发性骨髓瘤相关的淀粉样变性病：多关节炎，没有滑膜浸润CD20 +或CD38 +细胞

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摘要

Objectives: To describe histological, immunohistochemical and ultrastructural features of synovial biopsies of amyloid arthropathy associated with multiple myeloma (MM). Methods: Synovial biopsies from affected joints of two patients with MM and amyloid arthropathy were examined with light and electron microscopy, and immunohistochemically for expression of CD3, CD8, CD20, CD38, CD68, Ki-67 and vWF. Results were compared to values from osteoarthritis (OA, n=26), rheumatoid arthritis (RA, n=24) and normal (n=15) synovial membranes. Results: There was no or only mild lining hyperplasia. Vascular density was not elevated, and there were few Ki-67+ proliferating cells in the stroma. The Krenn synovitis score classified one specimen as "low-grade" and one as "high-grade" synovitis. CD68+ and CD3+ cells were the predominant mononuclear inflammatory cells, whereas CD20+ and CD38+ cells were absent from both synovial membrane and synovial fluid sediment. Electron microscopy demonstrated amyloid phagocytosis by synovial macrophages. In hierarchical clustering the two amyloid arthropathy specimens were more closely related to OA than to RA or normal synovium. Conclusions: This first detailed immunohistological analysis of MM-associated amyloid arthropathy suggests that it is a chronic synovitis that evolves despite the loss of humoral immunity seen in advanced MM. Instead, amyloid phagocytosis by synovial macrophages likely triggers and perpetuates local disease.
机译：目的：描述与多发性骨髓瘤（MM）相关的淀粉样变性病滑膜活检的组织学，免疫组化和超微结构特征。方法：对两名MM和淀粉样变性病患者的关节滑膜活检进行光镜和电镜检查，并免疫组织化学检测CD3，CD8，CD20，CD38，CD68，Ki-67和vWF的表达。将结果与骨关节炎（OA，n = 26），类风湿性关节炎（RA，n = 24）和正常（n = 15）滑膜的值进行比较。结果：没有或仅有轻度的内膜增生。血管密度没有升高，并且基质中几乎没有Ki-67 +增殖细胞。克伦滑膜炎评分将一个标本归为“低度”，将一个标本归为“高度”。 CD68 +和CD3 +细胞是主要的单核炎性细胞，而滑膜和滑液沉积物均不存在CD20 +和CD38 +细胞。电子显微镜显示滑膜巨噬细胞吞噬了淀粉样蛋白。在分级聚类中，两个淀粉样变性病标本与OA的关系比与RA或正常滑膜的关系更紧密。结论：首次对MM相关的淀粉样变性关节病进行了详细的免疫组织学分析，表明这是一种慢性滑膜炎，尽管在晚期MM中体液免疫力下降，但仍在发展。相反，滑膜巨噬细胞对淀粉样蛋白的吞噬作用可能触发并延续局部疾病。

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