McLean Nancy S Johnstone, Ward Daniel A, Hendrix Diane V H, Donnell Robert L, Ilha Marcia R S
Department of Small Animal Clinical Sciences, College of Veterinary Medicine, University of Tennessee, Knoxville, TN 37996, USA.
J Am Vet Med Assoc. 2008 Mar 1;232(5):715-21. doi: 10.2460/javma.232.5.715.
A 7-month-old 16.6-kg (36.5-lb) sexually intact female Golden Retriever was evaluated because of progressive severe bilateral membranous conjunctivitis, oral lesions, nasal discharge, and cough.
Histologic examination of conjunctival biopsy specimens revealed findings consistent with ligneous conjunctivitis. Circulating plasminogen activity was repeatedly low, and congenital plasminogen deficiency was identified as the underlying cause of the ocular, oral, and respiratory lesions.
Topical and subconjunctival administrations of fresh frozen plasma (FFP), topical administration of cyclosporine, and oral administration of azathioprine had no effect on the conjunctival membranes. Excision of the membranes followed by intensive treatment with topical applications of heparin, tissue plasminogen activator, corticosteroid, and FFP and IV administration of FFP prevented membrane regrowth. Intravenous administration of FFP increased plasma plasminogen activity to within reference limits, improved respiratory and oral lesions, and resulted in weight gain; discontinuation of this treatment resulted in weight loss, signs of depression, and worsening of lesions. After euthanasia because of disease progression, necropsy findings included mild hydrocephalus; multifocal intestinal hemorrhages; and fibrinous plaques in the oral cavity, nasopharynx, trachea, esophagus, and pericardium. Microscopically, the plaques were composed of fibrin and poorly organized granulation tissue. Fibrin thrombi were present within vessels in the lungs, oral cavity, and trachea.
In dogs, congenital plasminogen deficiency can occur and may be the underlying cause of ligneous conjunctivitis. A combination of surgical and medical treatments may improve conjunctival membranes, and administration of FFP IV appears to be effective in treating nonocular signs of plasminogen deficiency.
一只7个月大、体重16.6千克（36.5磅）的未绝育雌性金毛寻回犬因进行性严重双侧膜性结膜炎、口腔病变、鼻分泌物和咳嗽而接受评估。
结膜活检标本的组织学检查结果与木样结膜炎一致。循环纤溶酶原活性反复降低，先天性纤溶酶原缺乏被确定为眼部、口腔和呼吸道病变的根本原因。
局部及结膜下给予新鲜冷冻血浆（FFP）、局部应用环孢素以及口服硫唑嘌呤对结膜均无效果。切除结膜膜后，局部应用肝素、组织纤溶酶原激活剂、皮质类固醇和FFP并静脉给予FFP进行强化治疗可防止膜再生。静脉给予FFP可使血浆纤溶酶原活性提高至参考范围内，改善呼吸道和口腔病变，并导致体重增加；停止该治疗会导致体重减轻、抑郁迹象和病变恶化。因疾病进展实施安乐死后，尸检结果包括轻度脑积水；多灶性肠出血；以及口腔、鼻咽、气管、食管和心包的纤维蛋白斑块。显微镜下，这些斑块由纤维蛋白和组织不良的肉芽组织组成。肺、口腔和气管的血管内存在纤维蛋白血栓。
在犬中，可发生先天性纤溶酶原缺乏，可能是木样结膜炎的根本原因。手术和药物治疗相结合可能改善结膜，静脉给予FFP似乎对治疗纤溶酶原缺乏的非眼部体征有效。
