scholarly journals Comparison of the Changes in Corneal Endothelial Cells after Pars Plana and Anterior Chamber Ahmed Valve Implant

2015 ◽  
Vol 2015 ◽  
pp. 1-7 ◽  
Author(s):  
Ji Won Seo ◽  
Jong Yeon Lee ◽  
Dong Heun Nam ◽  
Dae Yeong Lee

Purpose. To compare the changes in corneal endothelial cells after pars plana Ahmed glaucoma valve (AGV) implantation with those after the anterior chamber AGV implantation for refractory glaucoma.Methods. The medical records of 18 eyes with pars plana implantation of AGV (ppAGV) were reviewed retrospectively and were compared with 18 eyes with the anterior chamber AGV (acAGV) implant. The preoperative and postoperative endothelial cells, intraocular pressure (IOP), and postoperative complications during the follow-up in both groups were compared.Results. The average follow-up was 18 months. The postoperative endothelial cells in the ppAGV and acAGV groups were 2044 ± 303 and 1904 ± 324, respectively(P=0.25). The average percentage decrease in the endothelial cells in the ppAGV and acAGV groups at 18 months was 12.5% and 18.4%, respectively, and showed significant difference between the 2 groups(P=0.01). No difference in IOP control and the number of postoperative glaucoma medications was observed between the 2 groups.Conclusions. Endothelial cell damage in the ppAGV group for refractory glaucoma appeared to be lower than that in the acAGV group. Therefore, pars plana implantation of AGV may be preferred as it may have lower level of endothelial cell damage while maintaining similar level of IOP control.

2020 ◽  
Vol 2020 ◽  
pp. 1-6
Author(s):  
Yating Tang ◽  
Jie Xu ◽  
Jiahui Chen ◽  
Yi Lu

Purpose. To investigate the long-term changes of corneal endothelial cells (EC) in anterior chamber intraocular lens- (AC-IOL-) implanted eyes. Methods. Retrospective study. We included 37 eyes (25 patients) that received AC-IOL implantation previously in the Eye and ENT Hospital of Fudan University between 1995 and 2016. Follow-up outcomes included the best-corrected visual acuity (BCVA), endothelial cell density, hexagonality, coefficient of variance, and central corneal thickness. Results. In total, 23 eyes (62.16%) with phakic and 14 eyes (37.84%) with aphakic AC-IOLs were included. Among these, 3 eyes (8.11%) were angle-supported AC-IOLs and 34 eyes (91.89%) were Artisan iris-fixated AC-IOLs. The mean age of patients was 41.40 ± 17.17 years, and the mean follow-up time was 12.12 ± 4.71 years in our study. At the follow-up time, corneal decompensation existed in 3 angle-supported AC-IOL eyes with a rate of 100% and 15 iris-fixated AC-IOL eyes with a rate of 44.12%. AC-IOL displacement occurred in 14 (41.18%) iris-fixated AC-IOL eyes. In the 19 iris-fixated AC-IOL eyes without corneal decompensation, significant changes also took place in corneal endothelial cells. The endothelial cell density decreased from 2843.26 ± 300.76 to 2015.58 ± 567.99 cells/mm2 (29.1% loss, P < 0.001 ) and hexagonality decreased from 51.21 ± 7.83 to 42.53 ± 9.17 (%) (16.9% loss, P < 0.001 ). The Kaplan–Meier survival curve also demonstrated the accumulated expectation rates of corneal endothelial cell decomposition for AC-IOLs with a median survival time of 12 years. Conclusion. We reported a significant chronic loss and long-term decompensation destiny of corneal endothelial cells in AC-IOL eyes. Semiannual or annual follow-up and evaluation of endothelial cells should be conducted in AC-IOL-implanted patients.


2021 ◽  
pp. 30-31
Author(s):  
Gargi Verma ◽  
Kishor Kumar

Purpose: To assess the association between anterior chamber depth and endothelial cell loss after phacoemulsication Material and Methods: Ninety patients were recruited for this comparative type of observational study who were further divided into 3 groups according to anterior chamber depth (ACD). All patients underwent phacoemulsication procedure and intraocular implantation. Postoperatively endothelial cell loss (ECL) was calculated by measuring percentage decrease in endothelial cell density of central cornea and regression coefcient between ACD and ECLwas assessed in each group. Results: Endothelial cell loss was signicantly higher in shallow anterior chambers to other groups and the association between ACD and ECLwas signicant only in shallow anterior chamber depth group. Conclusion: Eyes with shallow anterior chamber depth are at higher risk for endothelial cell damage and shows an association between ACD and ECLwhen compared to deep anterior chamber depth.


Blood ◽  
2007 ◽  
Vol 110 (11) ◽  
pp. 3535-3535 ◽  
Author(s):  
Anna D. Petropoulou ◽  
Grigoris T. Gerotziafas ◽  
Kostas Zervas ◽  
A. Mpanti ◽  
Michel Meyer Samama ◽  
...  

Abstract Thalidomide has emerged as a promising treatment for multiple myeloma (MM). Thrombosis is the most serious complication of thalidomide therapy, essentially when it is combined with dexamethasone. The pathogenesis of thrombosis in MM patients (pts) treated with thalidomide is not clear and probably of multi factorial origin. We used the Thrombin Generation test (TGT) and measured the plasma levels of soluble thrombomodulin (sTM) to better clarify the MM-related and thalidomide-related thrombogenicity. TGT was performed in citrated frozen platelet poor plasma (PPP). Blood was obtained from 26 MM pts, Salmon and Durie stage II and III, 62.5 years old (42–77), 9 males and 17 females, 10 treated with thalidomide (100–200mg/d orally) and dexamethasone (40mg/d for 4 days) (TD group) and 16 receiving no treatment (MM group). 13 healthy volunteers formed the control group. Thrombin Generation (TG) was initiated by adding the PPP reagent (Thrombogram-Thrombinoscope®) and the triggering solution (CaCl2 and fluorogenic substrate). We analyzed the endogenous thrombin potential (ETP), the Cmax and the velocity index of TG. The plasma levels of sTM in PPP were measured by a specific ELISA (Diagnostica Stago, France). In the MM group we observed an increase of the ETP, though not significant compared to the controls. The Cmax was almost equal to the control group value, while the velocity index of TG was statistically lower in the MM group compared to controls. In the TD group, a statistically significant increase of ETP was observed as compared to the control group. The Cmax was higher, compared to controls, though not significantly, whereas the velocity index of TG was almost equal to the control group value. There was no significant difference in the TG parameters between MM and TD groups. sTM in the control group was 45±14ng/ml. Both groups of pts had significantly increased sTM plasma levels as compared to the control but the difference between the two groups did not reach significance. Results are shown in Table 1. In patients with MM coexists an increase of sTM, a marker of endothelial cell damage, together with an increased TG capacity. The addition of thalidomide treatment is associated with a slight but not significant increase of ETP and Cmax. The co-existence of endothelial cell damage with increased TG capacity could be associated to the increased thrombotic risk in MM patients treated with thalidomide. This hypothesis will be controlled in a prospective study. Table 1: Thrombogram parameters and sTM plasma levels of studied pts. Control MM group TD group * Results significantly different between the MM and TD groups and the control group (p<0.05 vs the control group) ETP (nM×min) 1399±297 1651±478 1747±448* Cmax (nM) 366±54 342±52 402±99 Velocity Index (nM/min) 198±45 160±19* 184±65 STM (ng/ml) 45±14 84±42* 73±30*


2004 ◽  
Vol 72 (1) ◽  
pp. 598-601 ◽  
Author(s):  
Angela A. Sanchez ◽  
Douglas A. Johnston ◽  
Carter Myers ◽  
John E. Edwards ◽  
Aaron P. Mitchell ◽  
...  

ABSTRACT Candida albicans must penetrate the endothelial cell lining of the vasculature to invade the deep tissues during a hematogenously disseminated infection. We compared 27 C. albicans mutants with their wild-type parent for their capacity to damage endothelial cells in vitro and cause a lethal infection in mice following tail vein inoculation. Of 10 mutants with significantly impaired capacity to damage endothelial cells, all had attenuated virulence. Therefore, the endothelial cell damage assay can be used as a screen to identify some virulence factors relevant to hematogenously disseminated candidiasis.


Author(s):  
Hua Wei ◽  
Qiongfang Zhang ◽  
Jun Li ◽  
Jing Yang ◽  
Bin Huang ◽  
...  

IntroductionThe purpose of this study was to investigate long non-coding RNA (lncRNA) maternally expressed gene 3 (MEG3) effects in vitamin D (Vit. D) treatment in endothelial cell damage induced by diabetes.Material and methodsWe used human umbilical vein endothelial cells (HUVECs) as a research objective in our study and used high glucose in a diabetic cell model. We evaluated cell apoptosis by flow cytometry, inflammatory factors (IL-6, IL-1β and TNF-α) concentrations by ELISA assay, relative gene and protein expression by RT-qPCR and WB assay, and NF-κB(p65) nuclear volume by cellular immunofluorescence.ResultsCompared with the NC (normal control) group, the cell apoptosis rate was significantly increased, inflammatory factor (IL-6, IL-1β and TNF-α) concentrations were significantly up-regulated, lncRNA MEG3 gene expression was significantly depressed, Toll-like receptor 4 (TLR4), myeloid differentiation factor 88 (MyD88) and nuclear factor B p65 (NF-κB(p65)) gene and protein expression levels were significantly increased and NF-κB(p65) nuclear volume was significantly up-regulated (p < 0.001, respectively). With Vit. D supplementation, compared with the Model group, Vit. D improved endothelial cell damage induced by diabetes, while lncRNA MEG3 was significantly increased and the TLR4/MyD88/NF-κB(p65) pathway was significantly depressed dose-dependently (all p < 0.05). With sh-MEG3 transfection, the Vit. D treatment effects were significantly reduced.ConclusionsVit. D improved endothelial cell damage induced by diabetes via lncRNA MEG3 up-regulation in vitro study.


2020 ◽  
Vol 9 (8) ◽  
pp. 2546
Author(s):  
Han Min Lee ◽  
Kyoung Nam Kim ◽  
Kee Sup Park ◽  
Nam Ho Lee ◽  
Sung Bok Lee ◽  
...  

Purpose: We compared the clinical factors, including anterior chamber tube parameters, in patients with and without corneal endothelial cell damage after Ahmed glaucoma valve (AGV) implantation. Methods: In this retrospective and comparative case series, patients who underwent AGV implantation were enrolled consecutively. Serial specular microscopy was performed before and after AGV implantation. Patients were divided into two groups depending on whether there was a significant decrease in corneal endothelial cell density (ECD), which was determined by each patient’s rate of ECD change (%/year), calculated using linear regression analyses. Tube parameters such as the tube-cornea distance (TCD) and tube-cornea angle (TCA) were measured with anterior segment optical coherence tomography. Clinical factors related to the rate of ECD change were evaluated with regression analyses and compared between the two groups. The tipping point at which tube parameters became significantly associated with the rate of ECD change was identified with broken stick regression analyses. Results: There were 30 eyes (32.3%) with ECD damage (group 1) and 63 eyes (67.7%) without damage (group 2). The mean rate of ECD change (%/year) was −18.82 ± 22.97 and 2.14 ± 2.93 in groups 1 and 2, respectively (p < 0.001). The TCA was the only clinical factor associated with the rate of ECD change (regression coefficient, β = 1.254, p < 0.001). The tipping point in the TCA was 26.70° (95% confidence interval, CI: 23.75–29.64°). The mean TCD (mm) was 0.98 ± 0.38 and 1.26 ± 0.39 (p = 0.002), and the mean TCA (degrees) was 28.67 ± 7.79 and 36.35 ± 5.35 (p < 0.001) in groups 1 and 2, respectively. Conclusions: A wider TCA was protectively associated with the rate of ECD change, and the TCA was significantly narrower in patients with ECD damage. When inserting a tube into the anterior chamber, surgeons should therefore try to secure a wide TCA of about 30°. In patients with a narrow TCA after AGV implantation, increased attention should be directed toward whether ECD decreases continuously.


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