Accuracy of intraocular lens power calculation for cataract surgery after deep anterior lamellar keratoplasty.

BACKGROUND: The purpose of this study was to assess the accuracy of intraocular lens power (IOL) formulas for cataract surgery after deep anterior lamellar keratoplasty (DALK). METHODS: This retrospective study included eyes which had previously undergone DALK and underwent standard phacoemulsification with monofocal IOL implantation between January 2012 and January 2021 at Ospedali Privati Forlì "Villa Igea" (Forlì, Italy). The predicted spherical equivalent (SE) was calculated using the Barrett Universal II, Emmetropia Verifying Optical (EVO), Haigis, Hoffer Q, Hoffer QST, Holladay 1, Holladay II, Kane and SRK/T formulas. Prediction error (PE) was calculated as the actual postoperative SE refraction minus the SE predicted refraction. RESULTS: Eighty-two eyes of 82 patients were included. The mean PE was negative using all formulas. Friedman test revealed a statistically significant difference of the median absolute PE (MedAE) among the different IOL formulas (P = 0.005). On the basis of the MedAE, the formulas were ranked as follows: SRK/T (0.805 D), Kane (0.810 D), EVO (0.845 D), Hoffer QST (0.847 D), Barrett (0.895 D), Holladay 1 (0.915 D), Haigis (1.010 D) and Hoffer Q (1.070 D) formulas. CONCLUSIONS: All formulas had a tendency towards a myopic refractive shift in post-DALK eyes. Although the SRK/T, Kane, EVO and Hoffer QST formulas were more accurate, predictability of refractive outcomes was lower than in virgin eyes.

Clinical Outcomes of Preloaded Descemet Membrane Endothelial Keratoplasty Grafts With Endothelium Tri-Folded Inwards.

PURPOSE: To evaluate the initial outcomes and complications of Descemet membrane endothelial keratoplasty (DMEK) using donor tissues tri-folded with the endothelium inwards, preloaded at the Eye Bank, and delivered with bimanual pull-through technique. DESIGN: Prospective, noncomparative, interventional case series. METHODS: Setting: Eye bank and tertiary care eye department. PATIENT POPULATION: Forty-six consecutive eyes of 41 patients with Fuchs endothelial dystrophy with or without cataract operated between November 2016 and March 2017. INTERVENTION: DMEK tissues prepared with SCUBA technique and punched to a diameter of 8.25 mm were preloaded with the endothelium tri-folded inwards in an intraocular lens (IOL) cartridge with a 2.2-mm opening filled with the same tissue culture medium contained in the vial used for shipment to the surgeon. Standardized DMEK was performed as a single procedure (n = 15) or in combination with phacoemulsification and IOL implantation (n = 31) within 48 hours from preparation using a bimanual pull-through technique. MAIN OUTCOME MEASURES: Preparation and surgical times, intraoperative and postoperative complications, best spectacle-corrected visual acuity (BSCVA), endothelial cell density (ECD), and graft detachment rate. RESULTS: Preparation time averaged 26.2 ± 4.1 minutes (range 17-36 minutes), while the surgical time from opening of the stoppers to air fill of the anterior chamber never exceeded 9 minutes (range 3-9 minutes). Surgery was uneventful in all cases. Postoperative complications included graft detachment in 9 of 46 cases (19.6%), successfully managed in all cases by single rebubbling within 6 days from surgery, and glaucoma irresponsive to conservative treatment in 1 of 46 cases (2.1%). In all eyes without comorbidities (35 of 40 eyes) BSCVA was 20/25 (0.097 logMAR) or better as early as 3 months after surgery. Six months postoperatively, ECD was available in 24 of 25 eyes with an endothelial cell loss calculated as a percentage of the preoperative value determined at the eye bank (ranging from 2500 to 2800 cells/mm2) of 29.5% ± 14.8% (range 8.3%-52.1%). CONCLUSIONS: Delivering a preloaded DMEK tissue, tri-folded with the endothelium inwards, minimizes surgical time and costs without negatively affecting the outcomes of the procedure.

Mechanism of inflammation in age-related macular degeneration.

Age-related macular degeneration (AMD) is a multifactorial disease that represents the most common cause of irreversible visual impairment among people over the age of 50 in Europe, the United States, and Australia, accounting for up to 50% of all cases of central blindness. Risk factors of AMD are heterogeneous, mainly including increasing age and different genetic predispositions, together with several environmental/epigenetic factors, that is, cigarette smoking, dietary habits, and phototoxic exposure. In the aging retina, free radicals and oxidized lipoproteins are considered to be major causes of tissue stress resulting in local triggers for parainflammation, a chronic status which contributes to initiation and/or progression of many human neurodegenerative diseases such as AMD. Experimental and clinical evidences strongly indicate the pathogenetic role of immunologic processes in AMD occurrence, consisting of production of inflammatory related molecules, recruitment of macrophages, complement activation, microglial activation and accumulation within those structures that compose an essential area of the retina known as macula lutea. This paper reviews some attractive aspects of the literature about the mechanisms of inflammation in AMD, especially focusing on those findings or arguments more directly translatable to improve the clinical management of patients with AMD and to prevent the severe vision loss caused by this disease.

Genetic predictors of response to photodynamictherapy.

In Western countries, therapeutic management of patients affected by choroidal neovascularization (CNV) secondary to different typologies of macular degeneration represents a major health care problem. Age-related macular degeneration is the disease most frequently associated with CNV development. Schematically, CNVs can be distinguished into classic and occult subtypes, which are characterized by variable natural history and different responsiveness to some therapeutic procedures. At present, the dramatic vision loss due to CNV can be mainly treated by two interventional strategies, which are utilizable in either single or combined modalities: photodynamic therapy with verteporfin (PDT-V), and intravitreal administration of drugs acting against vascular endothelial growth factor. The combined use of PDT-V and anti-angiogenic drugs represents one of the most promising strategies against neovascular macular degeneration, but it unavoidably results in an expensive increase in health resource utilization. However, the positive data from several studies serve as a basis for reconsidering the role of PDT-V, which has undergone a renaissance prompted by the need for a more rational therapeutic approach toward CNV. New pharmacogenetic knowledge of PDT-V points to exploratory prospects to optimize the clinical application of this intriguing photothrombotic procedure. In fact, a Medline search provides data regarding the role of several single nucleotide polymorphisms (SNPs) as genetic predictors of CNV responsiveness to PDT-V. Specifically, correlations between SNPs and different levels of PDT-V efficacy have been detected by examining the gene variants influencing (i) thrombo-coagulative pathways, i.e. methylenetetrahydrofolate reductase (MTHFR) 677C>T (rs1801133), factor V (F5) 1691G>A (rs6025), prothrombin (F2) 20210G>A (rs1799963), and factor XIII-A (F13A1) 185G>T (rs5985); (ii) complement activation and/or inflammatory processes, i.e. complement factor H (CFH) 1277T>C (rs1061170), high-temperature requirement factor A1 (HTRA1) promoter -512G>A (rs11200638), and two variants of the C-reactive protein (CRP) gene (rs2808635 and rs876538); and (iii) production and bioavailability of vascular endothelial growth factor (VEGFA -2578C>A [rs699947] and rs2146323). This article critically evaluates both the clinical plausibility and the opportunity to utilize the most important SNP-response interactions of PDT-V for an effective upgrade of the current anti-CNV therapeutic scenario. In addition, the pharmacogenetics of a very severe post-PDT-V adverse event, i.e. a decrease in acute vision, is briefly discussed. A comprehensive appraisal of the findings reviewed in this article should be carefully considered to design future trials aimed at verifying (after proper genotypic stratification of the enrolled patients) whether these innovative pharmacogenetic approaches will be able to improve the multifaceted interventional management of neovascular macular degeneration.

Clear cell renal cell carcinoma associated with bilateral atypical acute posterior multifocal placoid pigment epitheliopathy.

BACKGROUND/OBJECTIVE: Clear cell renal cell carcinoma (CCRCC) is a malignant neoplasm frequently associated with an increase in circulating immune complexes (CIC). Acute posterior multifocal placoid pigment epitheliopathy (APMPPE) is a disease involving the chorioretinal structures of the eye, and it is commonly observed in association with several immunogenic disorders. We report here the clinical association between humoral immunologic modifications during tumoral diseases (long-standing CIC increase) and chorioretinal changes resembling atypical APMPPE. CASE REPORT: A 52-year-old white male affected by metastatic CCRCC is described. Histopathologic review of his surgically removed organs (kidney and lung), periodical laboratory immunologic tests and ophthalmologic examinations, including fluorescein and indocyanine green angiographies, were performed. RESULTS: The patient underwent total left nephrectomy (May 1997) and total left pneumonectomy (March 2001) for the presence of stage III CCRCC and CCRCC lung metastasis, respectively. On both occasions, postoperative immunotherapy was started. From June 1997 to February 2003, laboratory analyses demonstrated the presence of marked CIC peaks. During the follow-up period, an atypical APMPPE pattern, complicated by asynchronous choroidal neovascularization, occurred in both eyes. CONCLUSIONS: Long-standing tumorous disease, through a pathogenic mechanism triggered by CIC spreading, can be responsible, over time, for a progressive choroidal occlusive microangiopathy (atypical APMPPE pattern), associated with a high risk of poor visual outcome. Therefore, bilateral APMPPE could be related to a systemic disease able to increase CIC levels.