Comparative evaluation of progression rate in keratoconus before and after collagen crosslinking

Posted Posted in cornea

progression, keratoconus, collagen, crosslinking

2017 Nov 9. pii: bjophthalmol-2017-311017. doi: 10.1136/bjophthalmol-2017-311017. [Epub ahead of print]

Comparative evaluation of progression rate in keratoconus before and after collagen crosslinking.

Abstract

PURPOSE:

To compare the rate of disease progression in keratoconus before and after corneal collagen crosslinking (CXL).

METHODS:

145 eyes were followed without CXL (no-CXL group) for a median duration of 31 months whereas 45 eyes were followed up for 41 months before (pre-CXL) and after (post-CXL) accelerated, epithelium-off crosslinking. Progression was defined based on significant slope found in linear mixed effect models against time. Swept-source optical coherence tomography was used for measurement of anterior steep keratometry, anterior flat keratometry (Ant Kf), anterior average keratometry (Ant Avg K); posterior steep keratometry, posteriorflat keratometry (Post Kf), posterior average keratometry (Post Avg K) and corneal thickness.

RESULTS:

The patients in pre-CXL group were significantly younger (26.3±5.48 years) compared with the patients in no-CXL group (32.7±10.24 years) (P=0.004). Significant differences were observed during baseline examination for all parameters (P≤0.035) between pre-CXL and no-CXL groups except Ant Cyl and Post Cyl. During observation period, statistically significant differences were noted between pre-CXL and no-CXL groups in the progression rate of Ant Kf, Ant Avg K, Post Kf and Post Avg K (P≤0.045). After CXL, the progression rate in post-CXL group was comparable to that in no-CXL group. All corneal parameters remained stable in no-CXL group throughout the follow-up period.

CONCLUSIONS:

Serial tomographic examination is useful to document disease progression before and after CXL. In our study, a decrease in progression rate of corneal parameters was noted after CXL. In cases with stable corneal parameters over time, careful monitoring can be considered instead of collagen crosslinking.

progression, keratoconus, collagen, crosslinking:

cornea; imaging; treatment other

PMID:
29122823
DOI:
10.1136/bjophthalmol-2017-311017

Optical Coherence Tomography Predictors of Risk for Progression to Non-Neovascular Atrophic Age-Related Macular Degeneration

Posted Posted in Retina

Optical Coherence Tomography, Progression, Non-Neovascular, Atrophic, Age-Related Macular Degeneration

2017 Aug 25. pii: S0161-6420(16)32460-5. doi: 10.1016/j.ophtha.2017.06.032. [Epub ahead of print]

Optical Coherence Tomography Predictors of Risk for Progression to Non-Neovascular Atrophic Age-Related Macular Degeneration.

Abstract

PURPOSE:

Appearance of geographic atrophy (GA) on color photography (CP) is preceded by specific features on spectral-domain optical coherence tomography (SD OCT). We aimed to build SD OCT-based risk assessment models for 5-year new onset of GA and central GA on CP.

DESIGN:

Prospective, longitudinal study.

PARTICIPANTS:

Age-Related Eye Disease Study 2 Ancillary SD OCT study participants with age-related macular degeneration (AMD) with bilateral large drusen or noncentral GA and at least 1 eye without advanced disease (n = 317).

METHODS:

For 1 eye per participant, qualitative and quantitative SD OCT variables were derived from standardized grading and semiautomated segmentation, respectively, at baseline. Up to 7 years later, annual outcomes were extracted and analyzed to fit multivariate logistic regression models and build a risk calculator.

MAIN OUTCOME MEASURES:

New onset of CP-visible GA and central GA.

RESULTS:

Over a follow-up median of 4.0 years and among 292 AMD eyes (without advanced disease at baseline) with complete outcome data, 46 (15.8%) developed central GA. Among 265 eyes without any GA on baseline CP, 70 (26.4%) developed CP-visible GA. Final multivariate models were adjusted for age. In the model for GA, the independent predicting SD OCT factors (P < 0.001-0.03) were: hyperreflective foci and retinal pigment epithelium (RPE) layer atrophy or absence, followed by choroid thickness in absence of subretinal drusenoid deposits, photoreceptor outer segment loss, RPE drusen complex volume, and RPE drusen complex abnormal thinning volume. For central GA, the factors (P < 0.001) were RPE drusen complex abnormal thinning volume, intraretinal fluid or cystoid spaces, hyperreflective foci, and RPE layer atrophy or absence. The models yielded a calculator that computes the probabilities of CP-visible, new-onset GA and central GA after 1 to 5 years.

CONCLUSIONS:

For AMD eyes with large drusen and no advanced disease, we built a novel risk assessment model-based on age and SD OCT segmentation, drusen characteristics, and retinal pathology-for progression to CP-visible GA over up to 5 years. This calculator may simplify SD OCT grading and with future validation has a promising role as a clinical prognostic tool.

PMID:
28847641
DOI:
10.1016/j.ophtha.2017.06.032

Risk factors for Rapid Glaucoma Disease Progression

Posted Posted in glaucoma

Risk Factor, Glaucoma, Progression

2017 Jun 14. pii: S0002-9394(17)30241-6. doi: 10.1016/j.ajo.2017.06.003. [Epub ahead of print]

Risk factors for Rapid Glaucoma Disease Progression.

Abstract

PURPOSE:

To determine the intraocular and systemic risk factor differences between a cohort of rapid glaucoma disease progressors and non-rapid disease progressors.

DESIGN:

Retrospective case control study Methods SETTING: Five private ophthalmology clinics STUDY POPULATION: 48 rapidly progressing eyes (progression ≥1dB mean deviation (MD)/year) and 486 non-rapidly progressing eyes (progression <1dB MD/year). Patients were eligible if they had a diagnosis of glaucoma from their ophthalmologist and if they had greater than or equal to 5 Humphrey visual fields (24-2) conducted. Patients were excluded if their sequential visual fields showed an improvement in MD or if they had greater than 5dB MD variation in between visits. Patients with obvious neurological fields were excluded.

OBSERVATION PROCEDURE:

Clinical and demographic data (age, gender, CCT, IOP, refraction, medications) as well as medical, surgical and ocular histories were collected.

MAIN OUTCOME MEASURES:

Risk factor differences between the cohorts were measured using the independent t-test, Wald chi-squared and binomial regression analysis.

RESULTS:

Rapid progressors were older, had significantly lower CCT and baseline IOPs and were more likely to have pseudoexfoliation, disc haemorrhages, ocular medication changes and IOP lowering surgery. They also had significantly higher rates of cardiovascular disease and hypotension. Subjects with cardiovascular disease were 2.33 times more likely to develop rapidly progressive glaucoma disease despite significantly lower mean and baseline IOPs.

CONCLUSION:

Cardiovascular disease is an important risk factor for rapid glaucoma disease progression irrespective of IOP control.

PMID:
28624324
DOI:
10.1016/j.ajo.2017.06.003
Risk Factor, Glaucoma, Progression
Optic nerves damaged by glaucoma. Not from article