非家族遗传性先天性白内障危险因素研究
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摘要
目的
先天性白内障(congenital cataract)是儿童第二位的致盲眼病,是出生时或出生后第一年内发生的晶状体混浊,病因复杂。大约三分之一的病例与遗传有关,三分之一患儿是环境因素所致,其余三分之一原因不清。了解环境不利因素在先天性白内障发生中的危险性,对预防先天性白内障的发生有重要意义。
方法
收集2005～2008年在第四军医大学西京医院收治的无先天性白内障家族史的72例先天性白内障患者资料,在儿科门诊按就诊顺序取72例与白内障患儿出生时间相差在一年以内的、性别相同,发育良好,未患白内障的儿童作为对照,进行了病例对照研究。应用spss 13.0软件对调查的25个因素进行单因素和多因素Logistic回归分析。
结果
多因素Logistic回归分析显示先天性白内障的主要危险因素是患缺血缺氧性脑病(OR=6.42,95%CI 1.35～30.47)、患者母亲孕期营养不良(OR=2.55,95%CI 1.17～5.56)、患者母亲孕期服用药物(OR=4.49,95%CI 1.74～11.55)、患者出生后吸氧(OR=5.63,95%CI 1.45～21.84)。
结论
患者母亲孕期营养不良、服用药物和吸氧均为先天性白内障发病的危险因素,与以往的研究结果相似。缺血缺氧性脑病是先天性白内障的危险因素却少有报道。这为我们预防先天性白内障发生提供了新思路。
Purpose
Congenital cataract, which is the second cause of blindness in childhood, is defined as the lens opacity occurred within the first year of birth. Its causes are very complex. It is known that about one third of the cases are related to inheritance, one third of the cases are induced by environmental factors, and the reasons for the remaining one third of the cases are not clear. The aim of this study is to understand the risk factors in development of non-inheriditary cataract.
Methods
We collected 72 congenital cataract cases without the family history of congenital cataract at in-patient department of Xijing Hospital from 2005 to 2008. 72 age and gende matched , non cataract cases were obtained from the out-patient department of pediatric.This is a case-control study. 25 candidate factors were surveied with questionaire and analysed with SPSS 13.0 software with single and multiple logistic regression analysis.
Results
Logistic regression analysis showed that the major risk factors for congenital cataract are suffering from hypoxic ischemic encephalopathy (OR=6.42,95%CI 1.35-30.47), malnutrition during pregnancy (OR = 2.55,95%CI 1.17-5.56), taking medicines during pregnancy (OR = 4.49,95%CI 1.74-11.55) and having oxygen therapy (OR = 5.63,95%CI 1.45-21.84).
Conclusion
From our present study we concluded that malnutrition and taking medicines during pregnancy and having oxygen therapy after birth are the risk factors for congenital cataract.This is coinsistant with the previous studies. To our knowledge, it is the first time to report that hypoxic-ischemic encephalopathy is a risk factor for congenital cataract. This gives us the clues to prevent the non-heritarty congenitl catatract.
先天性白内障(congenital cataract)是儿童第二位的致盲眼病,是出生时或出生后第一年内发生的晶状体混浊,病因复杂。大约三分之一的病例与遗传有关,三分之一患儿是环境因素所致,其余三分之一原因不清。了解环境不利因素在先天性白内障发生中的危险性,对预防先天性白内障的发生有重要意义。
方法
收集2005～2008年在第四军医大学西京医院收治的无先天性白内障家族史的72例先天性白内障患者资料,在儿科门诊按就诊顺序取72例与白内障患儿出生时间相差在一年以内的、性别相同,发育良好,未患白内障的儿童作为对照,进行了病例对照研究。应用spss 13.0软件对调查的25个因素进行单因素和多因素Logistic回归分析。
结果
多因素Logistic回归分析显示先天性白内障的主要危险因素是患缺血缺氧性脑病(OR=6.42,95%CI 1.35～30.47)、患者母亲孕期营养不良(OR=2.55,95%CI 1.17～5.56)、患者母亲孕期服用药物(OR=4.49,95%CI 1.74～11.55)、患者出生后吸氧(OR=5.63,95%CI 1.45～21.84)。
结论
患者母亲孕期营养不良、服用药物和吸氧均为先天性白内障发病的危险因素,与以往的研究结果相似。缺血缺氧性脑病是先天性白内障的危险因素却少有报道。这为我们预防先天性白内障发生提供了新思路。
Purpose
Congenital cataract, which is the second cause of blindness in childhood, is defined as the lens opacity occurred within the first year of birth. Its causes are very complex. It is known that about one third of the cases are related to inheritance, one third of the cases are induced by environmental factors, and the reasons for the remaining one third of the cases are not clear. The aim of this study is to understand the risk factors in development of non-inheriditary cataract.
Methods
We collected 72 congenital cataract cases without the family history of congenital cataract at in-patient department of Xijing Hospital from 2005 to 2008. 72 age and gende matched , non cataract cases were obtained from the out-patient department of pediatric.This is a case-control study. 25 candidate factors were surveied with questionaire and analysed with SPSS 13.0 software with single and multiple logistic regression analysis.
Results
Logistic regression analysis showed that the major risk factors for congenital cataract are suffering from hypoxic ischemic encephalopathy (OR=6.42,95%CI 1.35-30.47), malnutrition during pregnancy (OR = 2.55,95%CI 1.17-5.56), taking medicines during pregnancy (OR = 4.49,95%CI 1.74-11.55) and having oxygen therapy (OR = 5.63,95%CI 1.45-21.84).
Conclusion
From our present study we concluded that malnutrition and taking medicines during pregnancy and having oxygen therapy after birth are the risk factors for congenital cataract.This is coinsistant with the previous studies. To our knowledge, it is the first time to report that hypoxic-ischemic encephalopathy is a risk factor for congenital cataract. This gives us the clues to prevent the non-heritarty congenitl catatract.
引文
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[6] Palmquist BM, Philipson B, Barr PO. Nuclear cataract and myopia during hyperbaric oxygen therapy[J]. Br J Ophthalmol, 1984, 68: 113-117.
[7] Schaal S, Beiran I, Rubinstein I, et al. Lenticular oxygen toxicity[J]. Invest Ophthalmol Vis Sci, 2003, 44: 3476-3484.
[8] Freel CD, Gilliland KO, Mekeel HE, et al. Ultrastructural characterization and Fourier analysis of fiber cell cytoplasm in the hyperbaric oxygen treated guinea pig lens opacification model[J]. Exp Eye Res. 2003,76(4):405–415
[9] Simpanya MF, Ansari RR, Suh KI, et al. Aggregation of lens crystallins in an in vivo hyperbaric oxygen guinea pig model of nuclear cataract: dynamic light-scattering and HPLC analysis[J].Invest Ophthalmol Vis Sci. 2005,46(12):4641-4651.
[2] Leach RM, Rees PJ, Wilmshurst P. ABC of oxygen: Hyperbaric oxygen therapy[J]. BMJ 1998;317:1140-1143.
[3] Tibbles PM, Edelsberg JS. Hyperbaric-oxygen therapy[J]. N Engl J Med 1996;334:1642-1648.
[4] Bishop.A. Role of oxygen in wound healing[J]. J Wound Care. 2008;17(9):399-402.
[5] Sen CK, Khanna S, Gordillo G, et al. Oxygen,oxidants and antioxidants in wound healing: an emerging paradigm[J]. Ann NY Acad Sci , 2002;57:239-249.
[6] Schmetterer L, Findl O, Strenn K, et al. Role of NO in the O2 and CO2 responsiveness of cerebral and ocular circulation in humans[J]. Am J Physiol. 1997 ;273(6 Pt 2):R2005-2012.
[7] Thom SR, Bhopale V, Fisher D, et al. Stimulation of nitric oxide synthesis in cerebral cortex due to elevated partial pressures of oxygen: an oxidative stress response[J]. J Neurobiol. 2002;51(2):85-100.
[8] Landers MB, 3rd. Retinal oxygenation via the choroidal circulation[J]. Trans Am Ophthalmol Soc 1978;76:528-556.
[9] Rivera JC. Decompression Sickness among Divers: An Analysis of 935 Cases[J]. Mil Med 1964;129:314-334.
[10] Fitzpatrick DT. Visual manifestations of neurologic decompression sickness[J]. Aviat Space Environ Med 1994;65:736-738.
[11] Butler FK Jr. Diving and hyperbaric ophthalmology[J].Surv Ophthalmol 1995;39:347-366.
[12] Hayreh SS, Zimmerman MB. Central retinal artery occlusion: visual outcome[J]. Am J Ophthalmol 2005;140:376-391.
[13] Duker JS, Brown GC. Recovery following acute obstruction of the retinal and choroidal circulations - a case history[J]. Retina 1988;8:257-260.
[14] Ros MA, Magargal LE, Uram M. Branch retinal artery obstruction: a review of 201 eyes[J]. Ann Ophthalmol 1989;21 :103-107.
[15] Glacet-Bemard A, Coscas G, Chabanel A, et al. Prognostic factors for retinal vein occlusion: a prospective study of 175 cases[J]. Ophthalmology 1996;103:551-560.
[16] Henderson LT, Slade JB. Central retinal artery occlusion and hyperbaric oxygen therapy[J]. Undersea Hyperb Med 2004;31 :309.
[17] Weinberger AW, Siekmann UP, Wolf S, et al. Treatment of acute centralretinal artery occlusion (CRAO) by hyperbaric oxygen therapy (HBO)-Pilot study with 21 patients[J].Klin Monatsbl Augenheilkd 2002;219:728-734.
[18] Beiran I, Goldenberg I, Adir Y, et al. Early hyperbaric oxygen therapy for retinal artery occlusion[J]. Eur J Ophthalmol 2001;11: 345-350.
[19] Vucetic M, Jensen PK, Jansen EC. Diameter variations of retinal blood vessels during and after treatment with hyperbaric oxygen[J].Br J Ophthalmol 2004;88:771-775.
[20] Coscas G, Gaudric A. Natural course of nonaphakic cystoid macular edema[J]. Surv Ophthalmol 1984;28 (Suppl):471-484.
[21] Miyamoto H, Ogura Y, Wakano Y, Honda Y. The long term results of hyperbaric oxygen treatment for macular edema with retinal vein occlusion[J]. Nippon Ganka Gakkai Zasshi 1993;97: 1065-1069.
[22] Vinores SA, YoussriAI, Luna JD, et al. Upregulation of vascular endothelial growth factor in ischemic and non-ischemic human and experimental retinal disease[J]. Histol Histopathol 1997;12:99-109.
[23] Pfoff DS, Thom SR. Preliminary report on the effect of hyperbaric oxygen on cystoid macular edema[J]. J Cataract Refract Surg 1987;13: 136-140.
[24] Okinami S, Nihira M, Iwaki M, Sunakawa M, Arai I. Hyperbaric oxygen therapy for cystoid macular edema in uveitis[J]. Jpn J Clin Ophthalmol 1992;46:199-201.
[25] Chang YH, Chen PL, Tai MC, et al. Hyperbaric oxygen therapy ameliorates the blood-retinal barrier breakdown in diabetic retinopathy[J]. Clin Experiment Ophthalmol 2006;34:584-589.
[26] Averous K, Erginay A, Timsit J, et al. Resolution of diabetic macular oedema following high altitude exercise[J]. Acta Ophthalmol Scand. 2006;84(6):830-1.
[27] Bristow JH, Kassar B, Sevel D. Gas gangrene panophthalmitis treated with hyperbaric oxygen[J]. BrJ Ophthalmol 1971;55: 139-42.
[28] Yohai RA, Bullock JD, Aziz AA, Markert RJ. Survival factors in thino-orbital-cerebral mucormycosis[J]. Surv Ophthalmol 1994;39:3-22.
[29] Kronish JW, McLeish WM. Eyelid necrosis and periorbital necrotizing fasciitis. Report of a case and rewew of the literature[J]. Ophthalmology 1991;98:92-98.
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