Keratoconus

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Article initiated by:
Brad H. Feldman, M.D., Penny A. Asbell M.D. M.B.A., Theodora Petratos, M.D., Olivia F Dutton
All contributors:
Angeline Nguyen, MD, Hannah Brosman, BS, Colleen Halfpenny, M.D., Zeba A. Syed, MD, S. Grace Prakalapakorn, MD, MPH, Kara M. Cavuoto, M.D., Mary Daly, MD, Naomie Warner, DO, Theodora Petratos, M.D., Brad H. Feldman, M.D., Alex Kozak, Dr. Shivanand Sheth, Vatinee Y. Bunya, MD, MSCE, Linda Rose, MD, PhD, Gustavo Ortiz-Morales, MD, Sezen Karakus, MD, MPH, Benjamin Park, MD, Penny A. Asbell M.D. M.B.A., Shivohn da Silva MBBS, Dr Mohammed Afnan KT (MBBS)
Assigned editor:
Sezen Karakus, MD, MPH
Review:
Assigned status Up to Date
 by Sezen Karakus, MD, MPH on August 26, 2026.


Keratoconus
Prominent Keratoconus Cone
Prominent Keratoconus Cone
DiseasesDB
7158
ICD-10
H18.6
ICD-9
371.60
MedlinePlus
001013
MeSH
D007640


Keratoconus is a bilateral, usually asymmetric corneal ectasia characterized by progressive central or paracentral thinning and steepening, resulting in irregular astigmatism and reduced visual quality. Disease may begin in childhood, when it often progresses more rapidly and requires age-specific surveillance and management.[1][2][3]

Disease Entity

Keratoconus adult eye (ICD-9 #371.60).

Disease

German professor Burchard Mauchart was the first physician to describe keratoconus, in 1748; he referred to it as "staphyloma diaphanum." In 1854, John Nottingham, a British physician, named it "conical cornea." John Horner, a Swiss physician, in 1869 was the first to give the term keratoconus to the disease.[4]

Keratoconus is the most common corneal ectatic disorder where the central or paracentral cornea undergoes progressive thinning and steepening, causing high irregular astigmatism and poor quality of vision. It was thought to be rare, but more awareness among ophthalmologists about the disease led to an increase in diagnosis and prevalence, which varies between regions. It is considerably higher in the Middle East,[5][6][7] India,[8] China,[9] and Australia.[10]

Etiology

The etiology is unknown, but several factors leading to progression have been described. Inheritance and environmental factors are suggested to play a role in the pathogenesis of ectatic corneal diseases, with 8% resulting from genetic mutations and 92% from environmental factors.[11][12][13] The hereditary pattern is neither prominent nor predictable, but positive family histories have been reported. The prevalence of keratoconus is often reported to be 1 in 700.[14]

Keratoconus is associated with atopy and eye rubbing. Eye rubbing and repeated trauma in genetically predisposed individuals results in keratoconus and its progression.[15][16][17] Systemic disorders such as Down syndrome, Leber congenital amaurosis, Ehlers-Danlos Syndrome and other connective tissue disorders are also associated with keratoconus.

Risk Factors

  • Eye rubbing, associated with atopy or vernal keratoconjunctivitis
  • Sleep apnea
  • Connective tissue disorders
  • Floppy eyelid syndrome[18]
  • Retinitis pigmentosa
  • Positive family history
  • Down syndrome
  • Hormonal changes in pregnancy[19]
  • Selective tissue estrogenic activity regulator (STEAR) therapy[20]
  • Hypothyroidism[21]

Pediatric Risk Profile

Children may present with more advanced and more rapidly progressive disease than adults. Eye rubbing, allergic eye disease, and vernal keratoconjunctivitis are particularly important modifiable factors. In a 305-eye pediatric cohort, baseline Kmax ≥55 D predicted faster progression; allergy history was also associated with faster progression in one eye-level analysis. Age, sex, and family history were not consistent predictors within that cohort.[2][22] Children with Down syndrome, connective-tissue disorders, retinitis pigmentosa, Leber congenital amaurosis, or a strong family history warrant a low threshold for corneal imaging when symptoms or refractive findings are suggestive.[2][3]

General Pathology

Keratoconus can show the following pathologic findings: fragmentation of Bowman layer, thinning of stroma and overlying epithelium, folds or breaks in Descemet membrane, and variable amounts of diffuse corneal scarring.

The American Academy of Ophthalmology's Pathology Atlas contains a virtual microscopy image of keratoconus.

Pathophysiology

Histopathology studies demonstrated breaks in or complete absence of Bowman layer, collagen disorganization, scarring, and thinning. The etiology of these changes is unknown, though some suspect changes in enzymes that lead to the breakdown of collagen in the cornea. While a genetic predisposition to keratoconus is suggested, a specific gene has not been identified. Although keratoconus does not fulfill the criteria for inflammatory disease, studies show a significant role of proteolytic enzymes, cytokines, and free radicals (matrix metalloproteinase 9 [MMP-9], interleukin 6 [IL-6], tumor necrosis factor alpha [TNF-α]) even in subclinical disease, showing a quasi-inflammatory characteristic in keratoconus.[23]

Primary Prevention

No preventive strategy has been proven effective to date. Some feel that eye rubbing or pressure (eg, sleeping with the hand against the eye) can cause and/or lead to the progression of keratoconus. Patients should be informed not to rub their eyes. In some patients, avoidance of allergens and treatment of ocular surface disease may help decrease eye irritation and therefore decrease eye rubbing.

Diagnosis

Diagnosis can be made by slit-lamp examination and observation of central or inferior corneal thinning. Computerized videokeratography is useful in detecting early keratoconus and allows following of its progression. Ultrasound pachymetry can also be used to measure the thinnest zone on the cornea. New algorithms using computerized videokeratography have been devised which now allow the detection of forme fruste, subclinical, or suspected keratoconus. These devices may allow better screening of patients for prospective refractive surgery.

History

The majority of cases of keratoconus are bilateral, but often asymmetric. The less-affected eye may show a high amount of astigmatism or mild steepening. Onset is typically in early adolescence and progresses into the mid-20s and 30s. However, cases may begin much earlier or later in life, and progression may also persist beyond the 30s.[24] There is a variable progression for each individual. There is often a history of frequent changes in eyeglass prescription that do not adequately correct vision. Another common progression is from soft contact lenses to toric or astigmatism-correcting contact lenses, to rigid gas-permeable contact lenses. A complete ocular and medical history should be taken, including change in eyeglass prescription, decreased vision, history of eye rubbing, medical problems, allergies, and sleep patterns.

Pediatric Presentation and Natural History

Pediatric keratoconus is commonly defined as disease diagnosed at 18 years of age or younger. Compared with adult disease, it is more likely to be advanced at diagnosis and to demonstrate faster refractive and tomographic progression.[2][3][25] Children may not report gradual monocular visual decline, and apparent progressive myopia, astigmatism, or meridional amblyopia may delay recognition. Published progression estimates vary substantially because studies use different definitions and follow-up periods; therefore, a single percentage should not be applied to all children.[2][26][22]

Physical Examination

A thorough and complete eye exam should be performed on any patient suspected of having keratoconus.

The general health of the eye should be assessed, and appropriate ancillary tests should be done to assess corneal curvature, astigmatism, and thickness. The best potential vision should also be evaluated. Many of the potential exam components are listed below:

  • Measurement of uncorrected visual acuity
  • Measurement of visual acuity with current correction (the power of the present correction recorded) at distance and when appropriate at near
  • Measurement of best-corrected visual acuity (BCVA) with spectacles and hard or gas-permeable contact lenses (with refraction when indicated)
  • Measurement of pinhole visual acuity
  • Retinoscopy to check for scissoring reflex
  • Slit-lamp biomicroscopy of the anterior segment including lid tightness and papillae in upper tarsal conjunctiva
  • Keratometry, computerized topography, computerized tomography, or ultrasound pachymetry

Signs

Early signs of keratoconus include the following:

  • Asymmetric refractive error with high or progressive astigmatism
  • Keratometry showing high astigmatism and irregularity (the axis that does not add to 180 degrees)
  • Scissoring of the red reflex on retinoscopy
  • Inferior steepening, skewed axis, or elevated keratometry values on K reading and computerized corneal topography
  • Corneal thinning, especially in the inferior cornea; maximum corneal thinning corresponds to the site of maximum steepening or prominence
  • Rizzuti sign, a conical reflection on the nasal cornea when a penlight is shone from the temporal side
  • Fleischer ring, an iron deposit often present within the epithelium around the base of the cone; brown in color and best visualized with a cobalt blue filter
  • Vogt striae, which are fine, roughly vertical parallel striations in the stroma; they generally disappear with firm pressure applied over the eyeball and reappear when pressure is discontinued


Later signs of keratoconus include the following:

Munson sign
  • Munson sign, a protrusion of the lower eyelid in downgaze
  • Breaks in Bowman membrane
  • Acute hydrops, a condition where a break in Descemet membrane allows aqueous to enter into the stroma causing severe corneal thickening, decreased vision, light sensitivity, tearing, and pain
  • Stromal scarring after the resolution of acute hydrops, which paradoxically may improve vision in some cases by changing corneal curvature and reducing irregular astigmatism

Symptoms

Symptoms include progressive changes in vision not easily corrected with eyeglasses.

Clinical Diagnosis

Diagnosis is made based on the history of changing refraction, poor best spectacle-corrected vision, scissoring reflex on retinoscopy, and abnormalities in keratometry, corneal topography, and corneal tomography, in association with corneal thinning and inferior steepening; characteristic slit-lamp findings can often be seen.

Diagnostic Procedures

Example of early keratoconus as evidenced on a Placido disk–based topographic evaluation.

Diagnostic procedures include the following:

  • Slit-lamp examination
  • Retinoscopy (assessment of scissor reflex)
  • Hard or gas-permeable contact lens trial, as improved vision with lenses eliminates other sources of poor vision, including amblyopia
  • Measurement of K values
  • Ultrasound pachymetry
  • Computerized corneal topography
  • Tear film biomarkers, like IL-6, TNF-α, and MMP-9, which were overexpressed in tears of keratoconus patients, indicating pathogenesis of keratoconus might involve chronic inflammatory events[27][28][29]
  • Computerized corneal tomography (rotating Scheimpflug, rotating slit-beam photography)


Modern assessment combines anterior and posterior elevation, pachymetric distribution, and corneal curvature. The ABCD system incorporates anterior and posterior radii of curvature in a 3-mm zone centered on the thinnest point, thinnest pachymetry, and best spectacle-corrected distance visual acuity. Corneal biomechanics and epithelial-thickness mapping may provide complementary information. Machine-learning systems for detection and progression prediction are under active study, but performance depends on the device, population, reference standard, and external validation; they should support rather than replace clinical interpretation.[1][30][31]

Example of severe keratoconus as evidenced on a Pentacam Scheimpflug evaluation. Clockwise from top right: the first image displays elevated K readings and high astigmatism consistent with keratoconus, the anterior elevation map shows central protrusion, the posterior elevation map shows a corresponding area of central protrusion, and the pachymetric map displays central thinning. These are all diagnostic of ectasia.

Pediatric Diagnosis and Monitoring

Children with unexplained or increasing myopia or astigmatism, reduced spectacle-corrected acuity, scissoring on retinoscopy, a strong family history, or chronic eye rubbing/allergic eye disease should undergo corneal topography or tomography when feasible. Imaging quality and repeatability must be confirmed because cooperation may be limited. Pediatric progression has no universally accepted definition; serial assessment should consider reproducible change in more than one parameter, including anterior curvature, posterior elevation, pachymetry, refractive error, and visual acuity.[2][26][22] Follow-up is individualized according to age, severity, allergy/eye rubbing, and imaging reliability. Intervals of approximately 3-6 months are commonly used in higher-risk children, with shorter review when progression is suspected.[2][22]

Differential Diagnosis

Management

General Treatment

The goals of treatment are to provide functional visual acuity and to halt changes in the corneal shape if progressing.

For visual improvement and astigmatism management, spectacles or soft toric contact lenses can be used in mild cases. Rigid gas-permeable contact lenses are needed in the majority of cases to neutralize the irregular corneal astigmatism. The majority of patients who can wear hard or gas-permeable contact lenses have a dramatic improvement in their vision. Specialty contact lenses have been developed to better fit the irregular and steep corneas found in keratoconus; these include (but are not limited to) Rose K, custom-designed contact lenses (based on topography and/or wavefront measurements), semi–scleral contact lenses, piggyback lens use (hard lens over soft lens), scleral lenses, hybrid lenses, and PROSE (prosthetic replacement of the ocular surface ecosystem). Patients who become contact lens intolerant or do not have acceptable vision, typically from central scarring, can proceed to surgical alternatives.

Corneal collagen crosslinking (CXL) is the principal disease-modifying treatment for progressive keratoconus. Riboflavin and ultraviolet-A exposure produce additional stromal cross-links and increase corneal biomechanical resistance. The strongest evidence supports epithelium-off CXL: an American Academy of Ophthalmology assessment of randomized trials found reduced progression compared with controls, with improvements in Kmax and visual acuity measures and an acceptable safety profile.[32] Conventional and accelerated epithelium-off protocols are used, although protocol selection depends on corneal thickness, disease severity, device labeling, and surgeon judgment.[33] Evidence comparing transepithelial with epithelium-off treatment has historically been less certain, and outcomes should not be assumed equivalent across protocols.[34] In the United States, Photrexa/KXL epithelium-off treatment was approved for progressive keratoconus in 2016. In October 2025, the FDA approved Epioxa HD/Epioxa with the O2n System and Boost Goggles for epithelium-on CXL in adults and pediatric patients aged 13 years and older (US Food and Drug Administration, 2025).

Medical Therapy

Patients with associated medical conditions should have these attended to properly. Atopic or vernal conjunctivitis should be treated using topical antihistamines, mast cell stabilizers, or anti-inflammatory/immunomodulatory treatments such as topical steroids, cyclosporine, tacrolimus, or lifitegrast.

Since the incidence of sleep apnea is very high in keratoconus, and because this condition may contribute to the pathogenesis of keratoconus and other medical conditions, all keratoconus patients should be questioned regarding sleep habits. Sleep studies and CPAP mask wear, if found necessary, are recommended for at-risk patients.

Medical therapy for patients who have an episode of corneal hydrops involves acute management of the pain and swelling. Patients are usually given a cycloplegic agent and sodium chloride (Muro) 5% ointment and may be offered a pressure patch. After the pressure patch is removed, patients may still need to continue sodium chloride drops or ointment for several weeks to months until the episode of hydrops has resolved. Patients are advised to avoid vigorous eye rubbing or trauma.

Medical Follow-up

Patients with suspected or established progression are followed with repeat refraction, visual acuity, and reproducible corneal imaging. A 3- to 6-month interval is commonly used during active surveillance, with frequency individualized by age, baseline severity, rate of change, eye rubbing/allergy, and imaging reliability. Children and adolescents generally require closer surveillance because progression may be faster. After CXL, follow-up evaluates epithelial healing, haze or infection, visual rehabilitation, and long-term stability; apparent progression should be confirmed with repeatable measurements before retreatment decisions.[2][22][32] Patients with acute hydrops are seen more frequently until resolution.

Pediatric Management

Management in children includes vigorous control of allergic eye disease, repeated counseling to avoid eye rubbing, optical correction, and timely CXL when progression is documented. Because pediatric disease can progress quickly, the threshold for intervention is generally lower than in adults, but prophylactic treatment of every child without evidence of progression remains debated.[2][3][22] A pediatric meta-analysis found that available CXL techniques generally attenuated progression over at least one year; the evidence base was heterogeneous, and standard or accelerated epithelium-off approaches had more consistent improvements than transepithelial protocols.[35] Families should understand that continued progression or later retreatment can occur and that long-term pediatric data are less mature than adult data.

Surgery

The majority of patients with keratoconus can be fitted with contact lenses and their vision significantly improves. When patients become intolerant or no longer benefit from contact lenses, surgery is the next option. If keratoconus is effectively stabilized with corneal crosslinking while patients are still able to achieve adequate visual function with spectacles or contact lenses, further interventions may not be required. Surgical options include intrastromal corneal ring segments (ICRS), corneal allogenic intrastromal ring segments (CAIRS), deep anterior lamellar keratoplasty (DALK), and penetrating keratoplasty (PK).

Non–FDA-approved treatments, which typically have less evidence-based information available on safety and efficacy, include the use of corneal crosslinking experimentally combined with excimer laser treatment, conductive keratoplasty,[36] and/or ICRS.[37] Some surgeons will use phakic intraocular lenses (IOLs) to address high myopia and some astigmatism.

ICRS have also been approved for the treatment of mild to moderate keratoconus in patients who are contact lens intolerant.[37] In these cases, patients must have a clear central cornea and a corneal thickness of >450 μm where the segments are inserted, approximately at the 7 mm optical zone. The advantage of ICRS is that they require no removal of corneal tissue and no intraocular incision, and they leave the central cornea untouched. Most patients will need spectacles and/or contact lenses postoperatively for best vision but will have flatter corneas and easier use of lenses. Different types and sizes of rings and different nomograms have also been developed.[38] [39] However, with ICRS being made of synthetic material, there have been reports of up to a 30% rate of complications, ranging from innocuous to sight threatening.

CAIRS use donor corneal tissue rather than synthetic segments. Early studies suggest improved corneal shape and visual function with potentially favorable biocompatibility, but techniques and nomograms are evolving and long-term comparative evidence remains limited.[40][41][42] Pediatric evidence is especially limited; combined ICRS and accelerated epithelium-off CXL has shown sustained improvement in a retrospective pediatric series, but this does not establish superiority over CXL or other approaches.[43]

DALK involves the replacement of the central anterior cornea, leaving the patient’s endothelium intact.[44] The advantages are that the risk of endothelial graft rejection is eliminated; there is less risk of traumatic rupture of the globe in the incision, since the endothelium and Descemet membrane and some stroma are left intact; and faster visual rehabilitation. Several techniques are utilized including manual dissection and big-bubble technique to remove the anterior stroma while leaving the Descemet layer and endothelium untouched. However, the procedures can be technically challenging, requiring conversion to penetrating keratoplasty, and postoperatively there is the possibility of interface haze leading to a decrease in BCVA; it is not clear if astigmatism is better treated with DALK versus PK. PK has a high success rate and is the standard surgical treatment with a long track record of safety and efficacy. Risks of this procedure include infection and cornea rejection and risk of traumatic rupture at the wound margin. Many patients after PK may still need hard or gas-permeable contact lenses due to residual irregular astigmatism. Any type of refractive procedure is considered a contraindication in keratoconic patients due to the unpredictability of the outcome and risk of leading to increased and unstable irregular astigmatism.

Bowman layer inlay or onlay transplantation has been investigated as a tissue-sparing option for selected advanced keratoconus, particularly when conventional CXL or ring-segment implantation is unsuitable. Medium-term series suggest stabilization with preservation of contact-lens-corrected vision, but availability is limited and comparative evidence is less mature than for CXL or keratoplasty.[42][45] Topography-guided surface ablation combined with CXL, stromal keratophakia, regenerative therapies, and pharmacologic or gene-targeted treatments remain specialized or investigational and should be described as such.[30][41][42]

Surgical Follow-up

Following any corneal surgical procedure, patients need to be followed to complete visual rehabilitation. Most patients still require vision correction with spectacles or contact lenses, and often hard or gas-permeable lenses are required if high levels of astigmatism are present.

All surgical patients need to be followed to ensure wound healing, evaluation for infection, suture removal, and other routine eye care, such as testing for glaucoma, cataracts, and retinal disease. Graft rejection can occur after penetrating keratoplasty, requiring prompt diagnosis and treatment to ensure graft survival.

Complications

  • Infection
  • Poor wound healing
  • Cornea transplant rejection
  • Corneal neovascularization
  • Graft–host junction thinning
  • Glare
  • Irregular astigmatism
  • High refractive error

Prognosis

With early diagnosis, control of modifiable risk factors, appropriate optical rehabilitation, and timely CXL for progression, many patients maintain functional vision without keratoplasty. Long-term follow-up remains important because progression may occur beyond the third decade and after treatment. Pediatric patients require particular vigilance: they often progress faster, may present with more advanced disease, and may require repeat CXL or transplantation during a longer lifetime of risk.[2][3][25][26][22][35] When transplantation is required and the endothelium is healthy, DALK is generally preferred to preserve host endothelium and avoid endothelial rejection, although procedure choice depends on scarring, hydrops-related Descemet injury, anatomy, and surgical expertise.

Additional Resources

  • Cornea Atlas, 2nd Edition. Krachmer, Palay. Elsevier, 2006.
  • External Disease and Cornea, Section 8. Basic and Clinical Science Course, AAO, 2025-2026.
  • Refractive Surgery, Section 13. Basic and Clinical Science Course, AAO, 2025-2026.

References

  1. ↑ 1.0 1.1 Singh RB, Koh S, Sharma N, et al. Keratoconus. Nat Rev Dis Primers. 2024;10. doi:10.1038/s41572-024-00565-3.
  2. ↑ 2.0 2.1 2.2 2.3 2.4 2.5 2.6 2.7 2.8 2.9 Price LD, Larkin DFP. Diagnosis and management of keratoconus in the paediatric age group: a review of current evidence. Eye (Lond). 2023 Dec;37(18):3718-3724.
  3. ↑ 3.0 3.1 3.2 3.3 3.4 Buzzonetti L, Bohringer D, Liskova P, Lang S, Valente P. Keratoconus in Children: A Literature Review. Cornea. 2020 Dec;39(12):1592-1598.
  4. ↑ Sinjab MM. Keratoconus: a historical and prospective review. Oman J Ophthalmol. 2023;16(3):401-414. doi:10.4103/ojo.ojo_70_23
  5. ↑ Hashemi H, Khabazkhoob M, Fotouhi A. Topographic keratoconus is not rare in an Iranian population: the Tehran Eye Study. Ophthalmic Epidemiol. 2013;20(6):385-391. doi:10.3109/09286586.2013.848458
  6. ↑ Assiri AA, Yousuf BI, Quantock AJ, Murphy PJ. Incidence and severity of keratoconus in Asir province, Saudi Arabia [published correction appears in Br J Ophthalmol. 2006;90(8):1071]. Br J Ophthalmol. 2005;89(11):1403-1406. doi:10.1136/bjo.2005.074955
  7. ↑ Millodot M, Shneor E, Albou S, Atlani E, Gordon-Shaag A. Prevalence and associated factors of keratoconus in Jerusalem: a cross-sectional study. Ophthalmic Epidemiol. 2011;18(2):91-97. doi:10.3109/09286586.2011.560747
  8. ↑ Jonas JB, Nangia V, Matin A, Kulkarni M, Bhojwani K. Prevalence and associations of keratoconus in rural maharashtra in central India: the central India eye and medical study. Am J Ophthalmol. 2009;148(5):760-765. doi:10.1016/j.ajo.2009.06.024
  9. ↑ Xu L, Wang YX, Guo Y, You QS, Jonas JB; Beijing Eye Study Group. Prevalence and associations of steep cornea/keratoconus in Greater Beijing. The Beijing Eye Study. PLoS One. 2012;7(7):e39313. doi:10.1371/journal.pone.0039313
  10. ↑ Chan E, Chong EW, Lingham G, et al. Prevalence of keratoconus based on Scheimpflug imaging: the Raine study. Ophthalmology. 2021;128(4):515-521. doi:10.1016/j.ophtha.2020.08.020
  11. ↑ Salomão M, Hoffling-Lima AL, Lopes B, et al. Recent developments in keratoconus diagnosis. Expert Rev Ophthalmol. 2018;13(6):329-341.
  12. ↑ Wheeler J, Hauser MA, Afshari NA, Allingham RR, Liu Y. The genetics of keratoconus: a review. Reprod Syst Sex Disord. 2012;(Suppl 6):001. doi:10.4172/2161-038X.S6-001
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  15. ↑ Mazharian A, Panthier C, Courtin R, et al. Incorrect sleeping position and eye rubbing in patients with unilateral or highly asymmetric keratoconus: a case-control study. Graefes Arch Clin Exp Ophthalmol. 2020;258(11):2431-2439. doi:10.1007/s00417-020-04771-z
  16. ↑ Grieve K, Ghoubay D, Georgeon C, et al. Stromal striae: a new insight into corneal physiology and mechanics. Sci Rep. 2017;7(1):13584. doi:10.1038/s41598-017-13194-6
  17. ↑ Rabinowitz YS, Galvis V, Tello A, Rueda D, García JD. Genetics vs chronic corneal mechanical trauma in the etiology of keratoconus. Exp Eye Res. 2021;202:108328. doi:10.1016/j.exer.2020.108328
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  19. ↑ Spoerl E, Zubaty V, Raiskup-Wolf F, Pillunat LE. Oestrogen-induced changes in biomechanics in the cornea as a possible reason for keratectasia. Br J Ophthalmol. 2007;91(11):1547-1550. doi:10.1136/bjo.2007.124388
  20. ↑ Torres-Netto EA, Randleman JB, Hafezi NL, Hafezi F. Late-onset progression of keratoconus after therapy with selective tissue estrogenic activity regulator. J Cataract Refract Surg. 2019;45(1):101-104. doi:10.1016/j.jcrs.2018.08.036
  21. ↑ Lee R, Hafezi F, Randleman JB. Bilateral keratoconus induced by secondary hypothyroidism after radioactive iodine therapy. J Refract Surg. 2018;34(5):351-353. doi:10.3928/1081597X-20171031-02
  22. ↑ 22.0 22.1 22.2 22.3 22.4 22.5 22.6 Antunes-Foschini R, Doná H, de Mello PHS, et al. Natural history and predictors for progression in pediatric keratoconus. Sci Rep. 2023;13:4940. doi:10.1038/s41598-023-32176-5.
  23. ↑ Lema I, Sobrino T, Durán JA, Brea D, Díez-Feijoo E. Subclinical keratoconus and inflammatory molecules from tears. Br J Ophthalmol. 2009;93(6):820-824.
  24. ↑ Gokul A, Patel DV, Watters GA, McGhee CNJ. The natural history of corneal topographic progression of keratoconus after age 30 years in non-contact lens wearers. Br J Ophthalmol. 2017;101(6):839-844.
  25. ↑ 25.0 25.1 Lin KK, Chen YW, Yeh CT, et al. Comparing the natural progression and clinical features of keratoconus between pediatric and adult patients. Sci Rep. 2022;12:8278.
  26. ↑ 26.0 26.1 26.2 Meyer JJ, Gokul A, Vellara HR, McGhee CNJ. Progression of keratoconus in children and adolescents. Br J Ophthalmol. 2023.
  27. ↑ Lema I, Brea D, Rodríguez-González R, Díez-Feijoo E, Sobrino T. Proteomic analysis of the tear film in patients with keratoconus. Mol Vis. 2010;16:2055-2061.
  28. ↑ Acera A, Vecino E, Rodríguez-Agirretxe I, et al. Changes in tear protein profile in keratoconus disease. Eye (Lond). 2011;25(9):1225-1233. doi:10.1038/eye.2011.105
  29. ↑ Balasubramanian SA, Mohan S, Pye DC, Willcox MD. Proteases, proteolysis and inflammatory molecules in the tears of people with keratoconus. Acta Ophthalmol. 2012;90(4):e303-e309. doi:10.1111/j.1755-3768.2011.02369.x
  30. ↑ 30.0 30.1 Bui AD, Truong A, Pasricha ND, Indaram M. Keratoconus Diagnosis and Treatment: Recent Advances and Future Directions. Clin Ophthalmol. 2023 Sep 16;17:2705-2718.
  31. ↑ Vandevenne MM, Favuzza E, Veta M, Lucenteforte E, Berendschot TT, Mencucci R, Nuijts RM, Virgili G, Dickman MM. Artificial intelligence for detecting keratoconus. Cochrane Database Syst Rev. 2023 Nov 15;11(11):CD014911.
  32. ↑ 32.0 32.1 Cortina MS, Greiner MA, Kuo AN, et al. Safety and efficacy of epithelium-off corneal collagen cross-linking for the treatment of corneal ectasia: a report by the American Academy of Ophthalmology. Ophthalmology. 2024. doi:10.1016/j.ophtha.2024.05.006.
  33. ↑ Raiskup F, Herber R, Lenk J, Pillunat LE, Spoerl E. Crosslinking with UV-A and riboflavin in progressive keratoconus: From laboratory to clinical practice - Developments over 25 years. Prog Retin Eye Res. 2024 Sep;102:101276.
  34. ↑ Ng SM, Ren M, Lindsley KB, Hawkins BS, Kuo IC. Transepithelial versus epithelium-off corneal crosslinking for progressive keratoconus. Cochrane Database Syst Rev. 2021;(3):CD013512.
  35. ↑ 35.0 35.1 Kobashi H, Hieda O, Itoi M, Kamiya K, Kato N, Shimazaki J, Tsubota K, The Keratoconus Study Group Of Japan. Corneal Cross-Linking for Paediatric Keratoconus: A Systematic Review and Meta-Analysis. J Clin Med. 2021 Jun 15;10(12):2626.
  36. ↑ Asbell PA. Is conductive keratoplasty the treatment of choice for presbyopia? Expert Rev Ophthalmol. 2007;Feb:121-130.
  37. ↑ 37.0 37.1 Asbell PA, Holmes-Higgin DK. Intacs corneal ring segments. In: Probst LE, Doane JF, eds. Refractive Surgery: A Color Synopsis. Thieme; 2001.
  38. ↑ Henriquez MA, Izquierdo L Jr, Bernilla C, McCarthy M. Corneal collagen cross-linking before Ferrara intrastromal corneal ring implantation for the treatment of progressive keratoconus. Cornea. 2012;31(7):740-745. doi:10.1097/ICO.0b013e318219aa7a
  39. ↑ Renesto Ada C, Melo LA Jr, Sartori Mde F, Campos M. Sequential topical riboflavin with or without ultraviolet a radiation with delayed intracorneal ring segment insertion for keratoconus. Am J Ophthalmol. 2012;153(5):982-993.e3. doi:10.1016/j.ajo.2011.10.014
  40. ↑ Jacob S, Patel SR, Agarwal A, Ramalingam A, Saijimol AI, Raj JM. Corneal allogenic intrastromal ring segments (CAIRS) combined with corneal cross-linking for keratoconus. J Refract Surg. 2018;34(5):296-303.
  41. ↑ 41.0 41.1 Deshmukh R, Ong ZZ, Rampat R, Alió Del Barrio JL, Barua A, Ang M, Mehta JS, Said DG, Dua HS, Ambrósio R Jr, Ting DSJ. Management of keratoconus: an updated review. Front Med (Lausanne). 2023 Jun 20;10:1212314.
  42. ↑ 42.0 42.1 42.2 Son HS, Friedrich M, Jun AS, Soiberman US. Advancements and innovations in keratoconus management: a review of current practices. J Clin Med. 2025. Oct 23;14(21):7491.
  43. ↑ Albertazzi R, Solis C, Ballesteros-Sánchez A, Mazzotta C, Rocha-de-Lossada C. Intracorneal Ring Segment Implantation with Epithelium-off Accelerated Cross-Linking for Pediatric Keratoconus: A 7-Year Retrospective Analysis. J Cataract Refract Surg. 2026 Jun 22. doi: 10.1097/j.jcrs.0000000000002010. Epub ahead of print. PMID: 42319885.
  44. ↑ Bisbe L, Deveney T, Asbell PA. Big bubble keratoplasty. Expert Rev Ophthalmol. 2009;4(5):553-561.
  45. ↑ Dapena I, Parker JS, Melles GRJ. Potential benefits of modified corneal tissue grafts for keratoconus: Bowman layer 'inlay' and 'onlay' transplantation, and allogenic tissue ring segments. Curr Opin Ophthalmol. 2020 Jul;31(4):276-283.
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