Fuchs Uveit Sendromunda Santral Kornea Kalınlığı

1. 1Ulucanlar Eye Training And Research Hospital, Ankara, Turkey
2. 2Balikesir University Faculty Of Medicine, Department Of Ophthalmology, Balikesir, Turkey

Sorumlu Yazar: Fuchs’ uveitis syndrome is a unique condition characterized by chronic, low-grade and mostly asymptomatic ocular inflammation leading to complications like cataract, glaucoma, or severe vitreous opacities. Although the diagnosis of FUS is entirely clinical, it is often misdiagnosed mostly because of the vitreous involvement which is not commonly recognized as an association with FUS.3,10-12 The etiology of this particular entity is still unclear. Infectious etiologies like Herpes simplex virus,13 toxoplasma-toxocara-histoplasma3 and rubella,14 hereditary associations15,16 and neurogenic dysfunction theories17,18 are being argued to clarify the underlying pathology. The effect of intraocular inflammation on corneal endothelium has been studied both in experimental4,5 and in clinical studies.6,8,9 In an experimental model, MacDonald et al.5 injected serum bovine albumin intravitreally and created an ocular inflammation. They showed that ongoing inflammation causes a breakdown in apical junctions of corneal endothelium leading to compromised barrier function. They also detected a breakdown in endothelial pump sites. These two conditions have resulted in an increment of the corneal thickness. Different studies have also demonstrated polymegathism and polymorphism of endothelial cells in specular microscopic examinations.6,7,19,20 The endothelial changes that occur in the active inflammatory phase are believed to be temporary and return to normal after the inflammation subsides. Ozdamar et al.8 and Evereklioglu et al.9 studied CCT in Behçet’s disease patients. Both studies have found that the CCT values of patients with active inflammation are greater than inactive Behçet’s disease and control group. The mean CCT value of the active Behçet’s disease patients was found to be approximately 30-40 µm thicker. They also emphasized that this CCT increase was temporary and returned to normal values as the active inflammation subsided. Differently from Behçet’s disease, inflammation is always low-grade and chronic in FUS. One of the characteristic clinical features of this typical inflammatory pattern is the presence of diffusely spread, fine, stellate or medium-sized round non-pigmented KPs.2,3,12 As we mentioned before, KPs are blamed for changing the endothelium metabolism.7 To see if the corneal endothelium is affected by the chronic inflammation due to FUS, we evaluated CCT values of patients with this specific uveitic entity. As it is directly influenced by the endothelial function, CCT is an ideal parameter to evaluate the endothelial changes.22,23 To the best of our knowledge, this study is the first and only study to evaluate CCT in FUS. Since we excluded bilateral involvement, we had chance to compare the involved and uninvolved eyes in same patient which neutralizes the subjects variations. In our study, the mean CCT of the involved eye was 561.1±43.7 µm and in the uninvolved eye was 564.6±45.7 µm. Whereas the mean CCT value of the control group was 547.7±36.9 µm. The CCT values of patients with FUS both in involved and uninvolved eyes were higher than those of the control subjects. This difference was significant only for the uninvolved eyes. These results may be considered as evidence showing that the chronic inflammation in FUS does not disturb the endothelial functions as much as in acute inflammatory conditions and that the cornea is thicker than the normal population probably due to hereditary factors. Elevated IOP or glaucoma is considered to be the most serious problem of FUS.2 Its incidence is reported to vary between 6.3% and 59% in a review by Jones.21 Elevated IOP has been reported in 12.7% of patients in Tugal-Tutkun et al.’s12 study and in 24% in Norrsell and Sjödell’s2 study in accordance with our result which is 25.5%. The thickness of the cornea is closely related to IOP measurements with thicker cornea leading to higher IOP readings. Ocular Hypertension Treatment Study (OHTS) had revealed that CCT is also an independent risk factor for glaucoma conversion of ocular hypertension.24 In the meta-analysis of 80 studies, Doughty and Zaman25 reported that 20 µm change in CCT corresponded to 1 mmHg change in IOP. Although statistical significance appeared only for the uninvolved eyes of FUS patients, the mean CCT of FUS patients in both involved and uninvolved eyes were approximately 20 µm thicker than the control group, which may result in approximately 1 mmHg higher IOP readings. The mean IOP of involved (14.4±7.2 mmHg) and uninvolved eyes (14.6±3.4 mmHg) were approximately 1.5 mmHg higher when compared to the mean IOP of the control group (12.9±2.4 mmHg). The higher IOP readings in FUS patients might be attributable to their thicker corneas. Although elevated IOP is an important problem in FUS and is observed in 25.5% of our patients, interestingly, the mean IOP was lower in most of the involved eyes (55%) when compared with the uninvolved eyes. Bouchenaki and Herbort10 had reported similar finding regarding the IOP difference between healthy and affected eyes of their FUS patients. The mean IOP was lower in 50% of affected eyes in their series. As a conclusion, although an acute ocular inflammation affects endothelial functions and thus the corneal thickness as reported in previous studies,4-6,8,9 a chronic inflammation does not affect the corneal endothelial functions and corneal thickness as much as the acute ocular inflammatory conditions. However, higher CCT readings in FUS patients may result in high IOP measurements. Address for Correspondence/Yazisma Adresi: Pinar Çakar Özdal MD, Ulucanlar Eye Training and Research Hospital, Ankara, Turkey Gsm: +90 530 349 49 75 E-mail: pinarozdal@hotmail.com Received/Gelis Tarihi: 31.01.2013 Accepted/Kabul Tarihi: 01.03.2013