Zusammenfassung
Hintergrund
Obwohl LASIK zur Zeit weltweit der häufigste refraktive Eingriff ist, wurden histopathologische Untersuchungen nur selten veröffentlicht und fast ausschließlich bei Tierversuchen durchgeführt. Das Ziel dieser Arbeit war die histopathologische und immunhistochemische Untersuchung von menschlichen Hornhäuten nach LASIK zur Hyperopiebehandlung.
Patienten und Methode
Klinische, histologische und immunhistochemische Untersuchung von zwei menschlichen Hornhäuten mit irregulärem Astigmatismus und zentraler Narbenbildung nach LASIK zur Hyperopiekorrektur. Die Hornhautscheibchen wurden jeweils während einer perforierenden Keratoplastik entnommen und histologisch sowie immunhistochemisch mit Antikörpern gegen verschiedene Kollagentypen, Proteoglykane und Zytokine untersucht.
Ergebnisse
Beide Hornhäute zeigten lichtmikroskopisch ein für die Hyperopiebehandlung typisches Ablationsprofil mit einer Stromaverdünnung in der mittleren Peripherie und einer „Aufsteilung“ zentral. Im Gegensatz zum Stroma war das Epithel in der mittleren Peripherie auf mehr als 12 Schichten stark verdickt und im Zentrum auf 2–3 Zelllagen stark verdünnt. Zentral war unter dem verdünnten Epithel eine dünne Schichte von Narbengewebe sichtbar. Unter dem Flap im Bereich des Interfaces war praktisch keine Wundheilung nachweisbar. Hier zeigten sich häufig auch artifizielle Spaltbildungen mit nur wenig kreuzenden Kollagenlamellen. Nur im Bereich des Flaprandes waren Spuren von Narbengewebe mit irregulären Kollagenlamellen sichtbar. Hier war auch eine verstärkte Expression von Hepatocyte Growth Factor (HGF) nachweisbar.
Schlussfolgerung
Auch nach LASIK bei Patienten mit Hyperopie ist ähnlich wie nach Myopiebehandlungen ein Wundheilungsprozess nur am Flaprand nachweisbar. Eine überschießende Epithelregeneration in der mittleren Peripherie, wahrscheinlich verursacht durch HGF, sowie eine Epithelverdünnung im Zentrum war für eine partielle Kompensation des ursprünglichen Ablationsprofiles in beiden Hornhäuten verantwortlich und scheint teilweise die Regression nach Hyperopiebehandlungen zu verursachen.
Summary
Purpose
Histopathological examinations after LASIK are rare and have been performed primarily in experimental animals. The aim of the present study was to describe histopathological and immunohistochemical findings of 2 human corneas after hyperopic LASIK.
Methods
Clinical, histological and immunohistochemical investigation of two human corneas with irregular astigmatism and central scar formation after hyperopic LASIK. Corneal buttons were obtained during penetrating keratoplasty.
Results
Histopathologic examination showed central steepening with mid-peripheral flattening in both eyes of the patient after hyperopic LASIK. However, this characteristic ablation profile of the stroma after hyperopic LASIK was partially mitigated and compensated by the epithelium which was significantly thinned in the center and strongly thickened in the mid-periphery. Only traces of wound healing with minimal scar tissue were present at the flap margin in both corneas after hyperopic LASIK. Under the flap it was mostly impossible to detect the interface for certain because the adjacent stroma had a regular and normal appearance in both corneas. However, an artificial space between the superficial flap and the posterior residual stroma with only few collagen lamellae being crossing between these structures was visible in some sections. Immunohistochemistry revealed increased staining of hepatocyte growth factor (HGF) on keratocytes/ fibroblasts at the flap margin in both corneas.
Conclusions
The results of the present study clearly show that similar to myopic LASIK a wound healing response is only found near the flap margin. In hyperopic LASIK the effect of the laser may be diminished by compensatory epithelial thickening in the annular mid-peripheral ablation zone being responsible at least in part for regression in this refractive procedure.
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Literatur
Rosen E (2000) LASIK mania. J Cataract Refract Surg 26: 303–4
Farah SG, Azar DT, Gurdal C, Wong J (1998) Laser in situ kerato- mileusis: literature review of a developing technique. J Cataract Refract Surg 24: 989–1006
Gimbel HV, Penno EE, van Westenbrugge JA, Ferensowicz M, Furlong MT (1998) Incidence and management of intraoperative and early postoperative complications in 1000 consecutive laser in situ keratomileusis cases. Ophthalmology 105: 1839–47
Seiler T (1999) Iatrogenic keratectasia: academic anxiety or serious risk? J Cataract Refract Surg 25: 1307–8
Wright JD Jr, Neubaur CC, Stevens G Jr (2000) Epithelial ingrowth in a corneal graft treated by laser in situ keratomileusis: light and electron microscopy. J Cataract Refract Surg 26: 49–55
Seiler T, Quurke AW (1998) Iatrogenic keratectasia after LASIK in a case of forme fruste keratoconus. J Cataract Refract Surg 24: 1007–9
Speicher L, Göttinger W (1998) Progressive corneal ectasia after laser in situ keratomileusis. Klin Monatsbl Augenheilkd 213: 247–51
Wachtlin J, Langenbeck K, Schrunder S, Zhang EP, Hoffmann F (1999) Immunohistology of corneal wound healing after photo- refractive keratectomy and laser in situ keratomileusis. J Refract Surg 15: 451–8
Amm M, Wetzel W, Winter M, et al (1996) Histopathological com- parison of photorefractive keratectomy and laser in situ keratomi- leusis in rabbits. J Refract Surg 12: 758–766
Lohmann CP, Patmore A, O’Brart D, et al (1997) Regression and wound healing after excimer laser PRK: a histopathological study on human corneas. Eur J Ophthalmol 7: 130–138
Bonnard C, Papermaster DS, Kraehenbuhl JP (1984) The strepta- vidin-biotin bridge technique: Application in light and electron microscope immunocytochemistry. In: Polak JM, Varndell IM (eds) Immunolabelling for electron microscopy. Amsterdam: Elsvier, pp 95–111
Geggel HS, Talley AR (1999) Delayed onset keratectasia following laser in situ keratomileusis. J Cataract Refract Surg 25: 582–586
Argento C, Cosentino MJ, Tytiun A, Rapetti G, Zarate J (2001) Cor- neal ectasia after laser in situ keratomileusis. J Cataract Refract Surg 27: 1440–1448
Philipp WE, Speicher L, Göttinger W (2003) Histological and immunhistochemical findings after laser in situ keratomileusis in human corneas. J Cataract Refract Surg 29: 808–820
Newsome DA, Foidart JM, Hassell JR, et al (1981) Detection of specific collagen types in normal and keratoconus corneas. Invest Ophthalmol Vis Sci 20: 738–50
Nakayasu K, Tanaka M, Konomi H, Hayashi T (1986) Distribution of types I, II, III, IV and V collagen in normal and keratoconus cor- neas. Ophthalmic Res 18: 1–10
Hassell JR, Newsome DA, Hascall VC (1979) Characterization and biosynthesis of proteoglycans of corneal stroma from rhesus mon- key. J Biol Chem 254: 12346–12354
Funderburgh JL, Cintron C, Covington HI, Conrad GW (1988) Immunoanalysis of keratan proteoglycan from corneal scars. Invest Ophthalmol Vis 29: 1116–1124
Wilson SE, Liu JJ, Mohan RR (1999) Stromal-epithelial interactions in the cornea. Prog Retin Eye Res 18: 293–309
Schultz G, Khaw PT, Oxford K, MaCauley S, Van Setten G, Chegini N (1994) Growth factors and ocular wound healing. Eye 8: 184–7
Kaji Y, Mita T, Obata H, et al (1998) Expression of transforming growth factor beta superfamily and their receptors in the corneal stromal wound healing process after excimer laser keratectomy. Br J Ophthalmol 82: 462–3
Wilson SE, He YG, Wenig J, et al (1996) Epithelial injury induces keratocyte apoptosis: hypothesized role for the interleukin-1 system in the modulation of corneal tissue organization and wound healing. Exp Eye Res 62: 325–7
Helena MC, Baerveldt F, Kim WJ, Wilson SE (1998) Keratocyte apoptosis after corneal surgery. Invest Ophthalmol Vis Sci 39: 276–83.
Li DQ, Tseng SC (1996) Differential regulation of cytokine and receptor transcript expression in human corneal and limbal fibro- blasts by epidermal growth factor, transforming growth factor-alpha, platelet-derived growth factor B, and interleukin-1 beta. Invest Oph- thalmol Vis Sci 37: 2068–80
Andresen JL, Ehlers N (1998) Chemotaxis of human keratocytes is increased by platelet-derived growth factor-BB, epidermal growth factor, transforming growth factor-alpha, acidic fibroblast growth factor, insulin-like growth factor-I, and transforming growth factor- beta. Curr Eye Res 17: 79–87
Andresen JL, Ledet T, Ehlers N (1997) Keratocyte migration and peptide growth factors: the effect of PDGF, bFGF, EGF, IGF-I, aFGF and TGF-beta on human keratocyte migration in a collagen gel. Curr Eye Res 16: 605–13
Wilson SE, Kim WJ (1998) Keratocyte apoptosis: implications on corneal wound healing, tissue organization, and disease. Invest Oph- thalmol Vis Sci 39: 220–6
Jester JV, Huang J, Barry-Lane PA, et al (1999) Transforming growth factor(beta)-mediated corneal myofibroblast differentiation requires actin and fibronectin assembly. Invest Ophthalmol Vis Sci 40: 1959–67
Arbelaez MC, Knorz MC (1999) Laser in situ keratomileusis for hyperopia and hyperopic astigmatism. J Refract Surg 15: 406–414
Rosa DS, Febbraro JL (1999) Laser in situ keratomileusis for hyper- opia. J Refract Surg 15 [2 Suppl]: 212–215
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Philipp, W., Speicher, L. & Göttinger, W. Histopathologische und immunhistochemische Befunde nach LASIK bei Hyperopie. Spektrum Augenheilkd 18, 130–134 (2004). https://doi.org/10.1007/BF03163154
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DOI: https://doi.org/10.1007/BF03163154