Herrmann V
Z Gesamte Inn Med. 1985 Jul 15;40(14):417-23.
On the basis of previous (n = 23) and current muscle biopsies (n = 25) as well as five animal-experimental investigations, the paper deals with the cause and the manifestation of perifascicular muscle-fiber atrophy. A deteriorated trophic situation of the subfascial or marginal muscle fibers in patients suffering from immunocomplex vasculopathies in connection with a reduced supply of blood to the muscles is seen as the cause of the areactive weight loss (atrophy). This is accompanied by a considerably reduced capillary supply of blood to the muscle fibers. Even in normal conditions, the portion of collateral vessels and capillaries is lower in the subfascial region than in the center of the fascicle. When the blood supply is disturbed, the marginal fibers are in a trophic situation worse than that of the central muscle fibers. They become atrophied. In responsive patients, the muscle fibers regenerate and recapillarize during the convalescence period. This can be shown histochemically by means of the alkaline phosphatase reaction. The extent of perifascicular musclefiber atrophy can be fixed in quantitative terms by the method of Baumli and Mumenthaler. Where a second biopsy is indicated, results can be obtained regarding the changes in the perifascicular atrophy as a consequence of the therapy provided.
基于先前的23例和当前的25例肌肉活检以及五项动物实验研究,本文探讨了束周肌纤维萎缩的病因及表现。患有免疫复合物血管病的患者,其筋膜下或边缘肌纤维的营养状况恶化,同时肌肉血液供应减少,这被视为无反应性体重减轻(萎缩)的原因。这伴随着肌肉纤维的毛细血管血液供应显著减少。即使在正常情况下,筋膜下区域的侧支血管和毛细血管比例也低于肌束中心。当血液供应受到干扰时,边缘纤维的营养状况比中央肌纤维更差。它们会萎缩。在有反应的患者中,肌纤维在恢复期会再生并重新形成毛细血管。这可以通过碱性磷酸酶反应进行组织化学显示。束周肌纤维萎缩的程度可以通过鲍姆利和穆门塔勒的方法进行定量测定。在需要进行第二次活检的情况下,可以获得关于治疗后束周萎缩变化的结果。