Brooks A M, Gillies W E
Glaucoma Investigation and Research Unit, Royal Victorian Eye and Ear Hospital, East Melbourne, Victoria, Australia.
Br J Ophthalmol. 1987 Sep;71(9):706-15. doi: 10.1136/bjo.71.9.706.
A series of 17 patients with stromal atrophy, hypoperfusion, and microneovascularisation of the iris investigated in the Glaucoma Investigation and Research Unit are described, and their iris angiograms were compared with those of normal irides of patients in the same age group seen in general clinics. In all but one of the 17 cases this iris atrophy was associated with glaucoma or ocular hypertension, which appeared to be secondary to the iris changes. The condition was bilateral and presented a typical slit-lamp appearance, with subtle evidence of microneovascularisation. There was neither history nor clinical evidence of previous trauma, heterochromia, or intraocular inflammation. The commonest form of iris atrophy affected the inner third of the iris stroma in a patchy manner, often with sparing above. However, diffuse atrophy occurred in two cases, and there were two cases of 'senile tears' of the iris. Some accompanying atrophy of the pigment epithelium was usual but less prominent. The changes on fluorescein angiography of the iris included the late appearance of dye with a long arteriovenous circulation time, fewer arteries than normal with sectorial hypoperfusion, leakage of dye from the pupil margin and peripupillary neovascularisation, stromal tufts, and sometimes more complex stromal microneovascularisation. An expanded prominent lesser vascular circle was a common feature of the condition. The condition is bilateral and distinct from other forms of iris atrophy. In all cases the iris changes appeared to be secondary to the vascular hypoperfusion and were not consistently associated with evidence of gross vascular disease. All patients had grey (blue) irides, and this may be an aetiological factor. The condition appears common enough to form a significant group of glaucoma patients and to be a separate clinical entity.
本文描述了在青光眼研究单位接受检查的17例患有虹膜基质萎缩、灌注不足和微血管形成的患者，并将他们的虹膜血管造影与在普通诊所就诊的同年龄组正常虹膜患者的进行了比较。在这17例病例中，除1例之外，所有病例的虹膜萎缩均与青光眼或高眼压症相关，而青光眼或高眼压症似乎继发于虹膜改变。该病为双侧性，具有典型的裂隙灯表现，有微血管形成的细微迹象。既往无创伤、异色症或眼内炎症的病史及临床证据。最常见的虹膜萎缩形式为虹膜基质内三分之一呈片状受累，上方常不受累。然而，有2例发生弥漫性萎缩，有2例出现虹膜“老年性撕裂”。通常伴有一定程度的色素上皮萎缩，但不太明显。虹膜荧光素血管造影的改变包括染料延迟出现、动静脉循环时间延长、动脉数量少于正常且有扇形灌注不足、染料从瞳孔边缘渗漏及瞳孔周围新生血管形成、基质丛，有时还有更复杂的基质微血管形成。扩大且突出的较小血管环是该病的常见特征。该病为双侧性，与其他形式的虹膜萎缩不同。在所有病例中，虹膜改变似乎继发于血管灌注不足，且并非始终与明显的血管疾病证据相关。所有患者均为灰色（蓝色）虹膜，这可能是一个病因学因素。该病似乎较为常见，足以构成青光眼患者中的一个重要群体，且为一个独立的临床实体。
