Abstract
To evaluate whether reducing eyelid muscular force through the administration of botulinum toxin type A (BTX-A) to the orbicularis oculi muscles of patients with keratoconus affected corneal parameters indicative of disease progression. In this prospective parallel randomized clinical trial, 40 eyes of 40 patients with keratoconus were randomized into equally sized control and BTX-A groups. Patients in the BTX-A group received subcutaneous BTX-A injections into the orbicularis muscle. The control group received no intervention. Palpebral fissure height, best spectacle-corrected visual acuity (BSCVA), and corneal topographic parameters were evaluated at baseline and at 3-, 6-, 12-, and 18-month follow-ups. The mean ± standard deviation vertical palpebral fissure heights were 9.74 ± 1.87 mm and 9.45 ± 1.47 mm at baseline in the control and BTX-A groups, respectively, and 10.0 ± 1.49 mm and 9.62 ± 1.73 mm at 18 months, with no significant difference between the groups (p=0.337). BSCVA values were 0.63 ± 0.56 and 0.60 ± 0.27 at baseline in the control and BTX-A groups (p=0.643), and 0.52 ± 0.59 and 0.45 ± 0.26 at 18 months, again with no significant difference between the groups (p=0.452). In addition, there were no statistical differences between the groups at 18 months for the three keratometry topographic parameters: flattest (K1), steepest (K2), and mean (Km) keratometry (p=0.562). BTX-A inhibition of eyelid force generation did not result in detectable changes in corneal parameters in keratoconic patients during 18 months of follow-up.
Highlights
Keratoconus is generally a progressive, bilateral cone-like ectasia of the cornea that affects approximately 1 in 2,000 people in the general population, which is usually diagnosed in young adult patients[1]
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Various factors can result in the deterioration of keratoconus, in cluding ultraviolet-B light, atopy, mechanical eye rubbing, and improperly fitting contact lenses[2]
Summary
Keratoconus is generally a progressive, bilateral cone-like ectasia of the cornea that affects approximately 1 in 2,000 people in the general population, which is usually diagnosed in young adult patients[1]. It is characterized by localized corneal thinning and protrusion, which lead to high myopia and irregular astigmatism that reduces visual quality. The pathophysiology of keratoconus remains poorly defined, but its etiology is known to be multifactorial and it is an autosomal dominant trait with variable phenotypic expression[2]. It is associated with many ophthalmic and systemic conditions, such as Down syn-
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