中华眼底病杂志

中华眼底病杂志

重视玻璃体代谢功能 审慎进行玻璃体干预

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玻璃体是由复杂分子结构形成的透明凝胶状组织,占眼球体积的80%;除了支撑作用外,玻璃体还具有调节眼发育、屈光、细胞屏障和参与眼内氧代谢等功能并且参与视网膜等疾病的发生发展过程。年龄、近视和全身病等因素对玻璃体功能均有影响。玻璃体注药和手术等均可能会干扰玻璃体功能,破坏眼内代谢平衡。因此,需要重视玻璃体代谢功能,审慎进行玻璃体干预,以便更好地维持眼内代谢平衡和视功能。

Vitreous is composed of transparent gel-like tissue with complex molecular structure, accounting for 80% of the volume of the eyeball. In addition to support the eye structure, vitreous has important functions such as regulating eye development, refraction and cellular barriers, participating in intraocular oxygen metabolism and the development of retinal diseases. Age, myopia and systemic diseases and other factors have an impact on vitreous function. Intra-vitreous injection and vitreous surgery may interfere with vitreous function, damage the intraocular metabolic balance. To better maintain intraocular metabolic balance and visual function, it is important to study vitreous metabolic function carefully and intervene it cautiously.

关键词: 玻璃体/生理学; 玻璃体/病理生理学; 代谢; 早期医疗干预; 述评

Key words: Vitreous body/physiology; Vitreous body/physiopathology; Metabolism; Early medical intervention; Editorial

引用本文: 高前应. 重视玻璃体代谢功能 审慎进行玻璃体干预. 中华眼底病杂志, 2017, 33(4): 336-340. doi: 10.3760/cma.j.issn.1005-1015.2017.04.003 复制

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1. Donati S, Caprani SM, Airaghi G, et al. Vitreous substitutes: the present and the future [J/OL].Biomed Res Int, 2014, 2014: 351804[2014-05-04]. http://dx.doi.org/10.1155/2014/351804. DOI:10.1155/2014/351804.
2. Su X, Tan MJ, Li Z, et al. Recent progress in using biomaterials as vitreous substitutes [J]. Biomacromolecules, 2015, 16(10): 3093-3102. DOI: 10.1021/acs.biomac.5b01091.
3. Kleinberg TT, Tzekov RT, Stein L, et al. Vitreous substitutes: a comprehensive review [J]. Surv Ophthalmol, 2011, 56(4): 300-323. DOI: 10.1016/j.survophthal.2010.09.001.
4. Filas BA, Zhang Q, Okamoto RJ, et al. Enzymatic degradation identifies components responsible for the structural properties of the vitreous body [J]. Invest Ophthalmol Vis Sci, 2014, 55(1): 55-63. DOI: 10.1167/iovs.13-13026.
5. Skeie JM, Roybal CN, Mahajan VB. Proteomic insight into the molecular function of the vitreous [J/OL]. PLoS One, 2015, 10(5): 0127567[2015-05-28]. https://doi.org/10.1371/journal.pone.0127567. DOI: 10.1371/journal.pone.0127567.
6. Ogawa K. Scanning electron microscopic study of hyalocytes in the guinea pig eye [J]. Arch Histol Cytol, 2002, 65(3): 263-268.
7. Sebag J. To see the invisible: the quest of imaging vitreous[J].Dev Ophthalmol, 2008, 42: 5-28. DOI: 10.1159/000138754.
8. Lacharme T, Almanjoumi A, Aptel F, et al. Twenty-four-hour rhythm of ocular perfusion pressure in non-arteritic anterior ischaemic optic neuropathy [J]. Acta Ophthalmol, 2014, 92(5): 346-352. DOI: 10.1111/aos.12352.
9. Holekamp NM. The vitreous gel: more than meets the eye [J]. Am J Ophthalmol, 2010, 149(1): 32-36. DOI: 10.1016/j.ajo.2009.07.036.
10. Wen B, Urano M, Humm JL, et al. Comparison of Helzel and OxyLite systems in the measurements of tumor partial oxygen pressure (PO2)[J]. Radiat Res, 2008, 169(1): 67-75. DOI: 10.1667/rr0888.1.
11. Beebe DC, Shui YB, Siegfried CJ, et al. Preserve the (intraocular) environment: the importance of maintaining normal oxygen gradients in the eye [J]. Jpn J Ophthalmol, 2014, 58(3): 225-231. DOI: 10.1007/s10384-014-0318-4.
12. Murali K, Kang D, Nazari H, et al. Spatial variations in vitreous oxygen consumption[J/OL]. PLoS One, 2016, 11(3): 0149961[2016-03-01]. https://doi.org/10.1371/journal.pone.0149961. DOI: 10.1371/journal.pone.0149961.
13. Holekamp NM, Shui YB, Beebe DC. Vitrectomy surgery increases oxygen exposure to the lens: a possible mechanism for nuclear cataract formation [J]. Am J Ophthalmol, 2005, 139(2): 302-310. DOI: 10.1016/j.ajo.2004.09.046.
14. Shui YB, Holekamp NM, Kramer BC, et al. The gel state of the vitreous and ascorbate-dependent oxygen consumption: relationship to the etiology of nuclear cataracts [J]. Arch Ophthalmol, 2009, 127(4): 475-482. DOI: 10.1001/archophthalmol.2008.621.
15. Milston R, Madigan MC, Sebag J. Vitreous floaters: etiology, diagnostics, and management [J]. Surv Ophthalmol, 2016, 61(2): 211-227. DOI: 10.1016/j.survophthal.2015.11.008.
16. Foos RY, Wheeler NC. Vitreoretinal juncture. Synchysis senilis and posterior vitreous detachment [J]. Ophthalmology, 1982, 89(12): 1502-1512.
17. Bishop PN, Holmes DF, Kadler KE, et al. Age-related changes on the surface of vitreous collagen fibrils [J]. Invest Ophthalmol Vis Sci, 2004, 45(4): 1041-1046.
18. Syed Z, Stewart MW. Age-dependent vitreous separation from the macula in a clinic population [J]. Clin Ophthalmol, 2016, 10: 1237-1243. DOI: 10.2147/opth.s99635.
19. Kersten E, Paun CC, Schellevis RL, et al.Systemic and ocular fluid compounds as potential biomarkers in age-related macular degeneration[J/OL]. Surv Ophthalmol, 2017, 2017: E1[2017-05-15]. https://doi.org/10.1016/j.survophthal.2017.05.003. DOI: 10.1016/j.survophthal.2017.05.003. [published online ahead of print].
20. Danser AH, van den Dorpel MA, Deinum J, et al. Renin, prorenin, and immunoreactive renin in vitreous fluid from eyes with and without diabetic retinopathy [J]. J Clin Endocrinol Metab, 1989, 68(1): 160-167. DOI: 10.1210/jcem-68-1-160.
21. Takeuchi M, Sato T, Tanaka A, et al. Elevated levels of cytokines associated with th2 and th17 cells in vitreous fluid of proliferative diabetic retinopathy patients[J/OL]. PLoS One, 2015, 10(9): 0137358[2015-09-09]. https://doi.org/10.1371/journal.pone.0137358. DOI: 10.1371/journal.pone.0137358.
22. Monteiro JP, Santos FM, Rocha AS, et al. Vitreous humor in the pathologic scope: insights from proteomic approaches [J]. Proteomics Clin Appl, 2015, 9(1-2): 187-202. DOI: 10.1002/prca.201400133.
23. Conart JB, Berrod JP. Non-traumatic vitreous hemorrhage [J]. J Fr Ophtalmol, 2016, 39(2): 219-225. DOI: 10.1016/j.jfo.2015.11.001.
24. Ghadiali Q, Zahid S, Dolz-Marco R. An assessment of vitreous degeneration in eyes with vitreomacular traction and macular holes [J/OL]. 2017, 2017: 6834692[2017-01-04]. https://doi.org/10.1155/2017/6834692. DOI: 10.1155/2017/6834692.
25. Rakoczy PE, Lai CM, Baines M, et al. Modulation of cathepsin D activity in retinal pigment epithelial cells [J]. Biochem J, 1997, 324 (Pt 3)935-940.
26. 陈国海, 李涛, 郑钦象, 等. 补体C4b及甲状腺素转运蛋白在增生性玻璃体视网膜病变中的表达变化及意义[J]. 中华眼科杂志, 2011, 47(8): 726-731.DOI: 10.3760/cma.j.issn.0412-4081.2011.08.013.Chen GH, Li T, Zheng QX, et al. Differential expression and significance of complement C4b and transthyretin in proliferative vitreoretinopathy[J]. Chin J Ophthalmo, 2011, 47(8): 726-731.DOI: 10.3760/cma.j.issn.0412-4081.2011.08.013.
27. Yu J, Peng R, Chen H, et al. Elucidation of the pathogenic mechanism of rhegmatogenous retinal detachment with proliferative vitreoretinopathy by proteomic analysis [J]. Invest Ophthalmol Vis Sci, 2012, 53(13): 8146-8153. DOI: 10.1167/iovs.12-10079.
28. 李静, 谷威. Ultra Q-YAG玻璃体消融术治疗飞蚊症的临床初步观察[J]. 国际眼科杂志, 2016, 16(7): 1369-1371. DOI: 10.3980/j.issn.1672-5123.2016.7.44.Li J, Gu W. Clinical observation of Ultra Q-YAG vitreolysis for vitreous floaters[J]. Int Eye Sci, 2016, 16(7): 1369-1371. DOI: 10.3980/j.issn.2222-3959.2015.03.01.
29. Abdelkawi SA, Abdel-Salam AM, Ghoniem DF, et al. Vitreous humor rheology after Nd: YAG laser photo disruption [J]. Cell Biochem Biophys, 2014, 68(2): 267-274. DOI: 10.1007/s12013-013-9706-5.
30. Noristani R, Schultz T, Dick HB. Cataract formation after YAG laser vitreolysis: importance of femtosecond laser anterior capsulotomies in perforated posterior capsules [J]. Eur J Ophthalmol, 2016, 26(6): 149-151. DOI: 10.5301/ejo.5000854.
31. Koo EH, Haddock LJ, Bhardwaj N, et al. Cataracts induced by neodymium-yttrium-aluminium-garnet laser lysis of vitreous floaters [J]. Br J Ophthalmol, 2017, 101(6): 709-711. DOI: 10.1136/bjophthalmol-2016-309005.
32. Filas BA, Shah NS, Zhang Q, et al. Quantitative imaging of enzymatic vitreolysis-induced fiber remodeling [J]. Invest Ophthalmol Vis Sci, 2014, 55(12): 8626-8637. DOI: 10.1167/iovs.14-15225.
33. Sampat KM, Garg SJ. Complications of intravitreal injections [J]. Curr Opin Ophthalmol, 2010, 21(3): 178-183. DOI: 10.1097/ICU.0b013e328338679a.
34. Li X, Zarbin MA, Bhagat N. Anti-vascular endothelial growth factor injections: the new standard of care in proliferative diabetic retinopathy? [J]. Dev Ophthalmol, 2017, 60: 131-142. DOI: 10.1159/000459699.
35. Siegfried CJ, Shui YB, Holekamp NM, et al. Oxygen distribution in the human eye: relevance to the etiology of open-angle glaucoma after vitrectomy [J]. Invest Ophthalmol Vis Sci, 2010, 51(11): 5731-5738. DOI: 10.1167/iovs.10-5666.
36. Tavares RLP, Nobrega MJ, Nobrega FAJ, et al. Timing and outcomes after silicone oil removal in proliferative vitreoretinopathy: a retrospective clinical series[J]. Int J Retina Vitreous, 2015, 1: 2. DOI: 10.1186/s40942-015-0002-y.
37. Lange CA, Stavrakas P, Luhmann UF, et al. Intraocular oxygen distribution in advanced proliferative diabetic retinopathy [J]. Am J Ophthalmol, 2011, 152(3): 406-412. DOI: 10.1016/j.ajo.2011.02.014.
38. Gao QY, Fu Y, Hui YN. Vitreous substitutes: challenges and directions [J]. Int J Ophthalmol, 2015, 8(3): 437-440. DOI: 10.3980/j.issn.2222-3959.2015.03.01.
39. Baillif S, Gastaud P.Complications of silicone oil tamponade [J]. J Fr Ophtalmol, 2014, 37(3): 259-265. DOI: 10.1016/j.jfo.2013.11.004.
40. Fu Y, Dong Y, Gao Q. Age-related cataract and macular degeneration: Oxygen receptor dysfunction diseases [J]. Med Hypotheses, 2015, 85(3): 272-275. DOI: 10.1016/j.mehy.2015.05.020.