Accelerated corneal endothelial cell loss in two patients with granulomatosis with polyangiitis following phacoemulsific
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CASE REPORT
Open Access
Accelerated corneal endothelial cell loss in two patients with granulomatosis with polyangiitis following phacoemulsification Fang-Chi Hsiao1,2†, Hung-Ta Chen3†, Kuan-Jen Chen1,2, Yi-Jen Hsueh1,2,4, Yaa-Jyuhn James Meir5, Tsai-Te Lu6, Chao-Min Cheng6, Wei-Chi Wu1,2 and Hung-Chi Chen1,2,4*
Abstract Background: Generally, the loss rate of human endothelial cells (HCEC) in routine cataract surgery is 8.5%. When the corneal endothelial cells density (ECD) drops, the HCEC may decompensate to keep cornea dehydration which leads to corneal edema. Granulomatosis with polyangiitis (GPA) is an uncommon autoimmune disease involving multiple organs including eyes such as conjunctivitis, scleritis, uveitis, and corneal ulcer. In this study, we report two cases of GPA whose corneal ECD decreased significantly after phacoemulsification cataract surgery. Case presentation: In the first case of 69-year-old male with GPA, the ECD dropped 39.6% (OD) four months after phacoemulsification and 38.1% (OS) six months postoperatively respectively. At the final follow-up, the residual ECD was only 55% in the right eye in the 49th month, and 56% remained in the left eye in the 39th month. In the second case of 54-year old female, left ECD dropped 63.9% at the 4th month after surgery and 69.6% ECD remained at the 15th month postoperatively while similar ECD of right eye before and after left eye surgery. Conclusion: Extensive preoperative ophthalmic evaluation and meticulous postoperative inflammation control should be applied to prevent severe loss of HCEC in GPA patients. Keywords: Granulomatosis with polyangiitis, Phacoemulsification, Cataract, Corneal, Endothelial cell density (ECD)
Background Granulomatosis with polyangiitis (GPA) is a systematic autoimmune disease with prevalence of 0.003% in America [1, 2], with 50–60% patients presenting with ocular manifestation lifetime [3]. The suspected etiology is activated dendritic cells that present autoantigen and prime type 1 T helper cells inducing macrophage migration, maturation and causing granuloma and tissue destruction. * Correspondence: [email protected] All authors meet the ICMJE authorship criteria. † Fang-Chi Hsiao and Hung-Ta Chen contributed equally to this work. HTC made the conception of this work with HCC. 1 Department of Ophthalmology, Chang Gung Memorial Hospital, No. 5, Fuxing Street, Guishan District, Linkou, Taoyuan 33305, Taiwan 2 Department of Medicine, Chang Gung University College of Medicine, Taoyuan, Taiwan Full list of author information is available at the end of the article
Chronic T cells activation promotes B cells secretion of antineutrophil cytoplasmic antibodies (ANCAs) targeting proteinase 3 (PR3) or myeloperoxidase (MPO) which trigger neutrophil activation and lead to vasculitis [4]. The clinical manifestations include flu-like symptoms, hearing loss, otitis media, bloody rhinorrhea, sinusitis, pulmonary disease, renal, cutaneous, neurologic problems and also conjunctivitis, scleritis, corneal ulceration, or uveitis [5, 6]. I
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