Hollwich F
Klin Monbl Augenheilkd. 1988 Feb;192(2):87-96. doi: 10.1055/s-2008-1050081.
We are indebted to I. Loewenfeld and her ophthalmologist colleague H. S. Thompson for having called for an explanation of the clinical picture of Fuchs's heterochromic cyclitis in their "Critical Review." In the present author's view, the reason why so many different opinions are held concerning the clinical picture and the etiology is that only a few authors (Franceschetti, François, Georgiades, Hollwich, Huber, Kimura, Hogan and Thygeson, Perkins, Sugar and others) have been able to follow up collectives of their own, of up to 50 patients and more, for many years. None of the investigators deny the presence of typical precipitates, observed both under direct light and retroillumination; typical because they are only found in Fuchs's heterochromia and its variation Posner-Schlossman syndrome. The course is inflammation-free, since, in contrast to all other forms of diseases of the anterior uvea, neither external signs of inflammation nor posterior synechiae occur. Etiologically, according to the behavior of the pupil (François 1949, 1954), there is sympathicoparalysis, while according to Amsler and Huber as well as Verrey, Franceschetti and Herrmann there is a corresponding pathologically increased fluorescein permeability of the vessels in the anterior segment and an extreme tendency to bleeding, as shown by the filiform bleeding when the anterior chamber is opened. The sympathicoparalysis also explains the inflammation-free vascular fragility, with escape of cell elements, primarily protein (albumins) and lymphocytes (Verrey, Matteucci, Franceschetti and Hermann, and François) into the aqueous and vitreous. Therefore, the syndrome should no longer be termed "heterochromic cyclitis" but rather "heterochromia complicata" as proposed by E. Fuchs. In view of the somatic features, amounting to a status dysraphicus, the condition is probably connected with a congenital developmental anomaly of the sympathetic nerve (François); these features have been described by Franceschetti, Hollwich, Passow, Perkins, Sugar, Huber and many others. There may also be immunologic factors (Loewenfeld and Thompson); however, research into these is still only at an early stage.
我们要感谢I. 勒文菲尔德及其眼科医生同事H. S. 汤普森,他们在“批判性综述”中呼吁对富克斯异色性睫状体炎的临床症状作出解释。在本文作者看来,对于临床症状和病因存在如此多不同观点的原因在于,只有少数作者(弗朗切谢蒂、弗朗索瓦、乔治亚德斯、霍尔维希、胡贝尔、木村、霍根和蒂格森、珀金斯、休格等人)能够多年跟踪自己收集的多达50名及以上患者的群体。没有一位研究者否认在直接照明和后照法下观察到的典型沉淀物的存在;之所以典型,是因为它们仅见于富克斯异色症及其变异型波斯纳 - 施洛斯曼综合征。病程无炎症,因为与前葡萄膜炎的所有其他形式不同,既没有炎症的外部体征,也没有后粘连。从病因学角度来看,根据瞳孔的表现(弗朗索瓦,1949年,1954年),存在交感神经麻痹,而根据阿姆斯勒和胡贝尔以及韦雷、弗朗切谢蒂和赫尔曼的观点,前节血管存在相应的病理性荧光素通透性增加以及极度的出血倾向,如前房开放时的丝状出血所示。交感神经麻痹也解释了无炎症的血管脆弱性,细胞成分,主要是蛋白质(白蛋白)和淋巴细胞(韦雷、马泰ucci、弗朗切谢蒂和赫尔曼以及弗朗索瓦)进入房水和玻璃体。因此,该综合征不应再称为“异色性睫状体炎”,而应如E. 富克斯所提议的称为“复杂性异色症”。鉴于其相当于发育不全状态的躯体特征,这种情况可能与交感神经的先天性发育异常有关(弗朗索瓦);这些特征已被弗朗切谢蒂、霍尔维希、帕索、珀金斯、休格、胡贝尔和许多其他人描述过。也可能存在免疫因素(勒文菲尔德和汤普森);然而,对此的研究仍处于早期阶段。