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2名感染弓形虫的兄弟姐妹的骨骼肌病理学

Skeletal muscle pathology in 2 siblings infected with Toxoplasma gondii.

作者信息

Calore E E, Minkovski R, Khoury Z, Seguro A C, Perez Calore N M, Cavaliere M J

机构信息

Pathology Section, Emílio Ribas Institute, Sao Paulo, Brazil.

出版信息

J Rheumatol. 2000 Jun;27(6):1556-9.

Abstract

Skeletal muscle can be the site of inflammatory diseases that lead to muscle weakness, pain, and increased myogenic serum enzymes. Most of these inflammatory myopathies are idiopathic. In some cases inflammatory myopathies are due to infectious agents. We describe the pathological aspects of muscle biopsies of 2 Brazilian siblings who acquired toxoplasmosis at the same time and in similar conditions. One developed a tetraplegia that was confirmed to be due to inflammatory myositis due to toxoplasma. The other developed myocarditis, with heart failure, without skeletal muscle weakness. In both cases many toxoplasma organisms were observed in the muscle biopsies, but in case 1 only was there an inflammatory myopathy with myofiber necrosis; the inflammatory cells were predominantly macrophages with some CD4+ cells and rare CD20+ cells. In case 1, expression of CD54 was observed in many inflammatory cells as well in endothelial cells, but only in endothelial cells in case 2. After treatment with clindamycin and corticosteroids both cases had only partial improvement, case 1 with a residual muscle weakness and case 2 with residual cardiac insufficiency (requiring digoxin). These cases show that the presence of the parasite in myofibers is not enough to induce an inflammatory myositis with muscle cell necrosis. This suggests that immunological disturbances may contribute to the development of inflammatory myositis due to toxoplasma.

摘要

骨骼肌可能是导致肌肉无力、疼痛和肌源性血清酶升高的炎症性疾病的发病部位。这些炎症性肌病大多是特发性的。在某些情况下,炎症性肌病是由感染因子引起的。我们描述了2名巴西同胞兄弟姐妹的肌肉活检病理情况,他们在相同时间、相似条件下感染了弓形虫病。其中一人出现四肢瘫痪,经证实是由弓形虫引起的炎症性肌炎所致。另一人则患上心肌炎并伴有心力衰竭,但没有骨骼肌无力症状。在这两个病例的肌肉活检中均观察到许多弓形虫生物体,但仅在病例1中出现了伴有肌纤维坏死的炎症性肌病;炎症细胞主要是巨噬细胞,还有一些CD4 +细胞和罕见的CD20 +细胞。在病例1中,许多炎症细胞以及内皮细胞中均观察到CD54的表达,但在病例2中仅在内皮细胞中观察到。经克林霉素和皮质类固醇治疗后,两个病例均仅有部分改善,病例1残留肌肉无力,病例2残留心功能不全(需要使用地高辛)。这些病例表明,肌纤维中存在寄生虫不足以诱发伴有肌肉细胞坏死的炎症性肌炎。这表明免疫紊乱可能在弓形虫所致炎症性肌炎的发病过程中起作用。

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