Study | Study design/ Indication | No. of Eyes | Follow-up, Months | Criteria for Progression | UV device/ Riboflavin | Outcome | |||||
---|---|---|---|---|---|---|---|---|---|---|---|
– | – | – | – | – | – | Overall | Pre-op K (D) | ΔK (D) | ΔUCVA | ΔBCVA | Δ Refraction (D) |
Henriquez et al, 2011 [14] | Prospective, randomised/ Keratoconus | 20; 10 treated, 10 FE control | 12 | 1. ↑ Kmax of 1.00 D/1 year 2. ↓ visual acuity 3. New contact lens fitting > once in 2 years |
UV-X 1000; IROC AG/ Riboflavin 0.1% w dextran | Improved UCVA. Reduction in mean-K, max-K and min-K, mean SE, anterior and posterior elevation values. | - | Mean Max K (treated): -2.66 (P = 0.04) | Treated: From 1.18 ± 0.80 to 0.46 ± 0.36 (LogMAR) (P < 0.001) | Treated: From 0.20 ± 0.18 to 0.09 ± 0.09 (LogMAR) (P = 0.06) | Mean SE (treated): -2.25 (P = 0.01) |
Hersh et al, 2011 [28] | Prospective randomised/ Keratoconus and post-laser ectasia | 142; 71 treated, 41 sham control, 30 FE control | 12 | ↑ 1D in steepest K, 1D cyl, 0.5D MRSE/24 months | UV-X; IROC AG/ Riboflavin 0.1% w dextran 20% | Improved UDVA and CDVA. Reduced max-K and mean-K. | Mean max K (treated): 58.6 ± 9.62 | Treated: -1.7 ± 3.9 (P < 0.001) | Treated: From 0.84 ± 0.34 to 0.77 ± 0.37 (LogMAR) (P = 0.04) | Treated: From 0.35 ± 0.24 to 0.23 ± 0.21 (LogMAR) (P < 0.001) | MRSE (treated): -0.86 (P = 0.07) |
O’Brart et al, 2011 [2] | Blind, randomised, prospective, bilateral/Keratoconus | 46; 24 treated, 22 FE control | 18 | 1. ↓ UCVA/ BSCVA > 1 line 2. Worsening refractive/corneal astigmatism, K or cone apex power by 0.75D /18 months |
In-house manufactured device using Roithner Lasertechnik diodes and CMB Vega X-linker/ Riboflavin 0.1% | Improved BSCVA. Reduced Orbscan II-simulated K, 3mm K, simulated astigmatism, cone apex power, root mean square, coma, spherical aberration, secondary astigmatism and pentafoil | Mean SIM K (treated): 47.1 Mean SIM K (control): 47.8 |
Treated: -0.62 (P < 0.001) Control: +0.14 (P = 0.3) |
Treated: +0.06 (SDE) Control: -0.01 (SDE) (P = 0.2) |
Treated: +0.12 (SDE) Control: +0.13 (SDE) (P = 0.01) |
Mean SE (treated): +0.82 Mean SE (control): +0.11 (P = 0.2) |
Wittig-Silva et al, 2008 [3] | Prospective, randomised/ Keratoconus | 66: 33 treated; 33 control | 12 | 1. ↑ ≥ 1D in Kmax 2. ↑ astigmatism with manifest subjective refraction ≥ 1D 3. ↑ of 0.50D in MRSE 4. ↓ ≥ 0.1mm in back optic zone radius of best fitting contact lens |
IROC UV-X/ Riboflavin 0.1% w dextran 20% | Improved BSCVA and reduced Kmax. | Mean Kmax (treated): 52.70 ± 4.5 Mean Kmax (control): 50.80 ± 4.30 (P = 0.073) |
Treated: -1.45 ± 1.00 (P < 0.002) Control: +1.28 (P < 0.001) |
- | Treated: -0.12 (P = 0.07) (LogMAR) |
MRSE: no diff in both treated and control |
Wittig-Silva et al, 2014 [4] | Prospective, randomised/ Keratoconus | 46 treated, 48 control | 36 | Subjective ↓ in vision and ≥ 1 of the following in 12 months: 1. ↑ ≥ 1D in steepest simulated K 2. ↑ astigmatism with manifest subjective refraction ≥ 1D 3. ↓ ≥ 0.1mm in back optic zone radius of best fitting contact lens |
UV-X 1000; IROC/ Riboflavin 0.1% w dextran 20% | Improved UCVA and BSCVA, reduction in Kmax. Significant reduction in corneal thickness. | Kmax (treated): 52.87 ± 4.31 Kmax (control): 51.18 ± 4.03 (P = 0.052) |
Treated: -1.03 ± 0.19 Control: +1.75 ± 0.38 (P < 0.001) |
Treated: -0.15 ± 0.06 Control: +0.10 ± 0.04 (LogMAR) (P = 0.001) |
Treated: -0.09 ± 0.03 Control: -0.05 ± 0.03 (LogMAR) (P = 0.347) |
Treated: -0.61 ± 0.41 Control: -0.79 ± 0.42 (P = 0.752) |
Lang et al, 2015 [30] | Prospective, randomised, blinded, placebo controlled/ Keratoconus | 29 | 37 | 1. ↑ ≥ 1D in Kmax/1 year 2. Clinically significant Δ refraction |
-/Riboflavin 0.1% | Corneal refractive power decreased in treatment group but increased in control group. | Kmax (treatment): 47.3 ± 2.2 Kmax (control): 50.9 ± 5.7 (P = 0.05) |
Treatment: -0.35 ± 0.58 Control: +0.11 ± 0.61 (P = 0.02) |
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