糖皮质激素性青光眼35例临床分析

目的:探讨糖皮质激素性青光眼的病因,临床特点及预防治疗。方法:对35例(64眼)糖皮质激素性青光眼患者资料进行分析。结果:35例中,男24例,女11例,年龄9～59(平均28.8)岁。局部应用糖皮质激素27例(77%),全身用药8例(23%)。19眼停用糖皮质激素后眼压得到控制;22眼给予局部和全身使用抗青光眼药物治疗后,眼压得到控制;13眼眼压未得到控制,通过手术治疗。结论:糖皮质激素性青光眼多发生于青年男性,滥用糖皮质激素药物是发生糖皮质激素性青光眼的重要原因,强调要合理应用糖皮质激素,避免医源性青光眼的发生。     

妥布霉素地塞米松滴眼液致激素性青光眼

目的 探讨妥布霉素地塞米松滴眼液引起激素性青光眼的原因、治疗方法和预防措施.方法 回顾分析11例(20眼)局部长期应用妥布霉素地塞米松眼液致激素性青光眼患者的临床资料.结果 所有患者确诊后均停用妥布霉素地塞米松眼液,其中17眼(85%)停用后眼压降至正常,2眼(10%)经用抗青光眼药物治疗后眼压得到控制,1眼(5%)经药物降眼压处理后眼压仍控制不良,进行手术治疗.结论 长期不规范应用妥布霉素地塞米松眼液可引起激素性青光眼,因此强调合理用药.     

糖皮质激素性青光眼临床分析

目的探讨糖皮质激素性青光眼的病因、临床特点及预防治疗。方法对32例（57眼）糖皮质激素性青光眼患者资料进行分析。结果32例中,男性21例,女性11例。年龄11～58岁,平均29.3岁。局部应用糖皮质激素25例,（78.1%）,全身用药7例（21.9%）。17眼停用激素后眼压得到控制;28眼给予局部和全身使用抗青光眼药物治疗后,眼压得到控制;12眼眼压未得到控制,通过手术治疗。结论糖皮质激素性青光眼多发生于年轻男性,滥用糖皮质激素药物是发生糖皮质激素性青光眼的重要原因,强调要合理应用糖皮质激素,避免医源性青光眼的发生。     

小儿糖皮质激素性高眼压和青光眼46例临床分析

目的:分析小儿糖皮质激素性高眼压和青光眼的病因、临床特点及治疗效果.方法:回顾分析46例84眼糖皮质激素性高眼压和青光眼患者病史,并给予相应的治疗.结果:患儿46例经停用激素、局部或联合全身应用降眼压药物后,眼压均能控制正常.结论:小儿糖皮质激素性高眼压和青光眼中,用药剂量、持续时间、药物种类对其发生都有影响,治疗后均可得到满意的疗效.     

联合毛果芸香碱滴眼液治疗眼外伤房角后退继发性青光眼

目的探讨联合毛果芸香碱滴眼液治疗外伤引起房角后退继发性青光眼的临床疗效。方法回顾性分析山东省眼科医院2007年8至2012年7收治12例(12只眼)眼外伤房角后退继发性青光眼患者的临床资料,患者均有眼球钝挫伤史且超生生物显微镜(UBM)和前房角镜检查可见外伤眼有不同程度的房角后退,入院眼压为(48.50±3.10)mm Hg,瞳孔直径为(5.15±0.70)mm。治疗:积极治疗原发性损伤,控制炎症,口服及静脉给予降眼压药物联合局部应用0.5%马来酸噻吗洛尔滴眼液、1%布林佐胺滴眼液、酒石酸溴莫尼定滴眼液降眼压治疗3～5 d,眼压不再下降,记录眼压为(35.00±3.55)mm Hg,此时加用0.5%毛果芸香碱滴眼液每日4次。详细记录患者治疗转归,观察眼压变化。结果加用毛果芸香碱眼滴眼液24 h后眼压为(21.90±3.87)mm Hg,平均下降(13.10±1.10)mm Hg。治疗前后瞳孔直径缩小(2.10±0.31)mm。4例患者最终逐渐减量药物致停,眼压正常;8例患者眼压降低后行小梁切除术控制眼压。结论毛果芸香碱滴眼液可以应用于眼外伤房角后退继发性青光眼患者,在减轻炎症的的基础上,联合应用毛果芸香碱滴眼液能够有效的降低眼压。     

24例糖皮质激素性青光眼临床分析

目的：分析糖皮质激素性青光眼病因及治疗结果。方法：回顾24例糖皮质激素性青光眼患者的激素使用及其治疗经过,进行分析。结果：9例患者停用糖皮质激素类眼水后眼压降至正常范围,11例患者降眼压处理后眼压控制,随访9－16月眼压无升高。4例患者经停用糖皮质激素类眼水、降眼压处理后眼压控制不良,手术治疗。结论：目前的药物或手术治疗对大多数病例效果较好。临床上常常发现许多患者滥用糖皮质激素,希望引起临床医师注意。     

儿童糖皮质激素性青光眼或高眼压23例临床分析

目的探讨儿童糖皮质激素性青光眼或高眼压的病因、临床特点、治疗方法和预防措施.方法对23例(46只眼)儿童糖皮质激素性青光眼或高眼压患者进行回顾性分析.结果23例中,男性16例,女性7例;年龄3～14岁,平均(8.81±15.32)岁,均为局部使用,合并全身使用6例,平均用药时间(14±23.18)个月.所有患者均因结膜炎或其他外眼病.所有患者均具有开角型青光眼或高眼压的临床表现.结论滥用药物是发生儿童糖皮质激素性青光眼或高眼压的重要原因,并提出了临床上可以避免的诱致儿童糖皮质激素性青光眼或高眼压5种常见原因.     

曲伏前列腺素治疗残余性青光眼的疗效

目的:观察曲伏前列腺素对残余青光眼的降眼压效果。方法:对12例14眼残余青光眼患者(21mmHg≤眼压≤30mmHg)滴用曲伏前列腺素滴眼液,每晚1次,共观察3mo,记录用药前、用药后1wk;1,2,3mo的眼压。结果:所有患者用药后降眼压效果明显,3mo内平均降眼压幅度在37.69%～38.44%之间。结论:曲伏前列腺素可以作为残余青光眼眼压不甚高的患者的首选降眼压药物。     

选择性激光小梁成形术治疗糖皮质激素性青光眼的疗效观察

背景糖皮质激素在眼科治疗过程中的应用日益广泛,而糖皮质激素的局部长期应用存在诱发青光眼的潜在危险。近年来的研究表明,选择性激光小梁成形术（SLT）可用于糖皮质激素性青光眼的治疗,但其疗效需要进一步评价。目的观察SLT治疗糖皮质激素性青光眼的降眼压效果。方法采用回顾性系列病例分析设计,对经复旦大学眼耳鼻喉科医院眼科确诊的糖皮质激素性青光眼患者9例9眼行360。SLT治疗,年龄25～52岁。其中5例5眼为准分子激光角膜原位磨镶术（LASIK）术后长期（4—6周）使用糖皮质激素滴眼液所致,4例4眼因视网膜中央静脉阻塞（CRVO）黄斑水肿接受玻璃体腔内注射0．1ml曲安奈德（4．0mg）所致。在接受SLT治疗前,虽然所有患者均无青光眼和高眼压病史,但这些患者使用糖皮质激素后出现了高眼压,所以均接受了最大可耐受剂量的降眼压治疗。所有患者行SLT治疗前停止使用糖皮质激素2～12个月,术前眼压为35～44mmHg（1mmHg=0．133kPa）。患者随访6个月,观察术眼治疗前及治疗后不同时间点的眼压变化。采用重复测量方差分析法分析治疗后各时间点术眼眼压的差异。结果所有患者均只接受1次SLT治疗。SLT治疗前患者的平均眼压为（40．0±2．9）mmHg,治疗后1h、1周及1、3、6个月的眼压分别为（37．9±8．1）、（34．9±5．9）、（27．6±6．7）、（21．6±6．9）和（17．9±2．9）mmHg。治疗后1、3、6个月时的平均眼压均较术前明显下降,差异均有统计学意义（P〈0．05）。本组患者中2例2眼因眼压控制不良分别于SLT治疗后1个月和3个月接受了滤过性手术,SLT治疗后6个月,1例患者仍然需要使用2种局部降眼压药物控制眼压,6例患者无需使用降眼压药物。结论在纳入的9眼中,SLT有效降低了6眼糖皮质激素性青光眼患眼的眼压,降眼压疗效出现于治疗后1个月,随访期内眼压保持稳定。     

2%美开朗与0.5%噻吗心安滴眼液治疗开角型青光眼与高眼压症的临床对照研究

目的以噻吗心安滴眼液作对照,在原发性开角型青光眼和高眼压症患者中评价美开朗滴眼液的降眼压、内在拟交感活性作用。方法选择开角型青光眼和高眼压症患者50例50眼,随机分为美开朗组和噻吗心安组2组,各25例25眼。美开朗组滴用2%美开朗眼液,噻吗心安组滴用0.5%噻吗心安眼液,一日2次,共12周,比较两种滴眼液的降眼压作用及局部和全身副作用。结果两组患者用药后眼压均下降,与用药前相比均有显著性差异(P<0.01)。两组间眼压下降值无显著性差异(P>0.05)。用药12周,美开朗组心率平均降低3.6次,噻吗心安组心率平均降低6.5次,两者相比有显著性差异。结论美开朗滴眼液对开角型青光眼和高眼压症患者具有明显的降眼压作用,和噻吗心安滴眼液局部降眼压作用相同,但对心率的抑制作用比噻吗心安小。     

Strabisme Alternant - Etude clinique - traitement

The author defines motor and sensory alternation: the term alternation should not be used in isolation, it should always be accompanied by the name of the parameter concerned. Sensory alternation is always found together with motor alternation but the reverse is not true.The examining criteria for a diagnosis of sensory alternation are given, sensory alternation must not be confused with alternating inhibition. Working from clinical observations of cases of motor alternating strabismus, the author selects 2 types of binocular sensory relations which allow one to differentiate between:- cases of primary alternating strabismus- cases of secondary alternating strabismusThese forms will develop in different ways; in both cases a cure is possible providing that the right treatment is prescribed and once prescribed carefully followed, etc. It is always a case of serious forms of strabismus whose developmental period is spread over several years.According to the authors, the frequency of cases of true primary strabismus is from 1–3%, the frequency of cases of secondary alternating strabismus varies according to the type of therapy practised on cases of monocular strabismus with amblyopia. These latter will become cases of alternating strabismus under the influence of certain types of therapy carried out over several years (penalization, rocking, alternated occlusion, etc...).Experimental data on kittens confirm clinical data; kittens placed in abnormal environments during the sensitive period will show modification in the distribution of cortical cells and the absence of binocular cells (either because the excitation of the two eyes was not simultaneous, or not identical: artificial strabismus, occlusion, opaque glasses). This disturbances become irreversible after a certain period of exposure (a function of age, length of exposure, etc...).It is thus necessary to bear in mind: 1) the iatrogenic risks of certain orthoptic treatments, 2) the necessity for a binocular form of treatment as soon as possible, as once a certain stage is passed, cortical plasticity diminishes and the elaboration of normal binocular relations becomes impossible.

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Effects of Adenosine Agonists on Intraocular Pressure and Aqueous Humor Dynamics in Cynomolgus Monkeys

The effects of single or multiple topical doses of the relatively selective A₁adenosine receptor agonists (R)-phenylisopropyladenosine (R-PIA) and N⁶-cyclohexyladenosine (CHA) on intraocular pressure (IOP), aqueous humor flow (AHF) and outflow facility were investigated in ocular normotensive cynomolgus monkeys. IOP and AHF were determined, under ketamine anesthesia, by Goldmann applanation tonometry and fluorophotometry, respectively. Total outflow facility was determined by anterior chamber perfusion under pentobarbital anesthesia. A single unilateral topical application of R-PIA (20–250 μg) or CHA (20–500 μg) produced ocular hypertension (maximum rise=4.9 or 3.5 mmHg) within 30 min, followed by ocular hypotension (maximum fall=2.1 or 3.6 mmHg) from 2–6 hr. The relatively selective adenosine A₂antagonist 3,7-dimethyl-1-propargylxanthine (DMPX, 320 μg) inhibited the early hypertension, without influencing the hypotension. Neither 100 μg R-PIA nor 500 μg CHA clearly altered AHF. Total outflow facility was increased by 71% 3 hr after 100 μg R-PIA. In conclusion, the early ocular hypertension produced by topical adenosine agonists in cynomolgus monkeys is associated with the activation of adenosine A₂receptors, while the subsequent hypotension appears to be mediated by adenosine A₁receptors and results primarily from increased outflow facility.