All of us Vs Keratoconus


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Post Info TOPIC: Article of Theo Seiler, MD, PhD
Deb


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Date: Sat Mar 6 12:27 PM, 2021
Article of Theo Seiler, MD, PhD
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An excellent article by Dr Seiler (please see the attached)

'During the past 40 years, 2 main causes for keratoconus have been identified: eye rubbing and reduced biomechanical stiffness of the cornea. The coincidence of keratoconus and atopic conjunctivitis was described already 100 years ago, but it took another 50 years to understand that it is the mechanical trauma to the connective tissue eye shell that induces ectasia.1,2 Intraocular pressure spikes of up to 300 mm Hg accompany eye rubbing and lead to extension of cornea and sclera, both viscoelastic tissues.3 Although some hardliners of the eye rubbing hypothesis advocate this as the only cause of keratectasia (no rubbing—no conus), we have good reasons to believe that pathology processes other than rubbing are involved in the progression of keratectasia: (1) we have many keratoconus patients who never had episodes of eye rubbing, (2) keratoconus is a bilateral disease, but eye rubbing is in approximately 50% of the cases single handed, and the association between patient-reported unilateral eye rubbing and greater asymmetry in corneal curvature (steep K-reading) is weak, and (3) sclera is more viscous than cornea, and therefore, we would expect a stronger effect on scleral extension than on cornea; however, to my knowledge, an effect of eye rubbing on myopia progression has not been reported so far.4,5

Increased elasticity (reduced stiffness) of keratoconus cornea compared with normal cornea was reported by Andreassen et al in 1980, and Edmund found in 1988 a significantly reduced Young modulus of the cornea in keratoconus eyes.6,7 The ocular rigidity coefficient describing scleral and corneal biomechanical expansion, however, did not differ between normal and keratoconus eyes.8 In addition, modern methods of measuring ocular rigidity such as the ocular response analyzer primarily failed to discriminate between keratoconus and normal eyes.

Based on these considerations, we established the working hypothesis that eye rubbing and reduced biomechanical stiffness of the cornea contribute interactively to the genesis of keratoconus. The proportion of each causal mechanism may vary significantly from patient to patient, and we may find strong rubbers with normal corneas and no rubbers with weak corneas both ending up in progressive keratoconus. By means of in vivo Brillouin spectroscopy, we measured a high variation of the corneal bulk modulus in nonkeratoconus eyes even higher than the average difference between 20- and 60-year-old corneas.9 This surprising result supports the working hypothesis and requests of any modern therapy of keratoconus to address both causal arms: stiffening of the cornea and to stop rubbing by means of topical treatment of the itching eye.

The landmark article on elasticity of crosslinked human cornea (and previous papers in German) covered the biomechanical arm of keratoconus therapy only.10 It documents convincingly that, by means of corneal crosslinking (CXL) using the Dresden protocol, the stiffness of the human cornea can be enhanced significantly. Although, at first glance, this looks impressive, a one treatment fits all, however, may lead to overcrosslinked and undercrosslinked corneas. Undercrosslinked corneas continue to progress and such treatment failures were reported in 4% to 10% of the cases. On the other hand, in less than 10% of the crosslinked corneas a too strong effect of CXL was found leading to continued flattening of the cornea with a constant flattening rate for more than 10 years.11 We interpreted this as a consequence of overcrosslinking. Such a mismatch of achieved vs required CXL could be easily avoided by choosing the right irradiation time to obtain a certain radiant exposure (in J/cm2 ). If we only would know how much CXL a cornea needs to achieve normal stiffness! A preoperative determination of the biomechanical parameters by means of clinical Brillouin spectroscopy or other elastometric techniques was necessary to customize the amount of CXL.

The landmark article was the starting signal for a series of publications on CXL that accumulated until today to more than 2500 clinical and basic science articles (PubMed research January 2021).10 The 2-layer model proposed in the article was verified clinically a few years later by the demarcation line visible at the slitlamp or in anterior segment optical coherence tomography.12 Meanwhile, we also learned that it is not only riboflavin and ultraviolet A that determines the success of CXL but also the intrastromal oxygen that represents the bottleneck of clinical CXL and limits the applicability of accelerated CXL.13 Despite some improvements of CXL, the parameters 5.4 J/cm2 for radiant exposure and 0.1% of riboflavin concentration are still valid today and are used in most of the hundreds of thousands of clinical treatments across the world.'

 



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Optometrist

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Posts: 14
Date: Sat Mar 6 3:51 PM, 2021
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I highly intelligent article with very crucial points!

I was reading the following, on the clinical side and was aghast by it!

 https://www.kcfreedom.org/download.spark?id=2385881&aBID=48159



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contact lens.pdf (387.5 kb)
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Date: Sat Mar 6 3:59 PM, 2021
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All the more reason why screening of family members is advisable as per concluded in this attached study.



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