青光眼的药物治疗

早期治疗青光眼的药物是由局部的β受体（β－R）阻滞剂、肾上腺素能药、缩瞳药和口服碳酸酐酶抑制剂（CAIs)组成。近期治疗青光眼的药物又增加有：降低眼内压（IOP）药（如前列腺素）、局部应用的CAIs和α2－肾上腺素能促进剂。β－R阻滞剂仍为治疗青光眼的一线药物。但β－R阻滞剂进行单一药物治疗时对降低IOP无效，且有不良反应。建议选用前列腺素，局部的CAIs和α2－肾上腺素能促进剂。     

作用于肾上腺素α受体的治疗青光眼药物研究进展

青光眼是一类以眼压升高为特征的疾病,如果眼内压长期持续偏高,会使人致盲。本文主要就作用于肾上腺素α受体的治疗青光眼药物的研究进展进行简要综述。     

青光眼药物治疗的新进展

青光眼是一种多元性的视神经和视网膜病变。全世界大约有 70 0万病人因青光眼而失明。眼压升高是青光眼发病过程中的主要危险因素。本文简要地回顾目前常用的药物疗法 ,并介绍正在研发中的新降眼压药的药效和药理机制。     

青光眼滤过手术的抗疤痕药物研究进展

青光眼滤过手术的目的在于形成房水引流新通道,从而降低眼内压。滤过道成纤维细胞增生、疤痕形成阻塞滤道,是导致手术失败的主要原因。自20世纪80年代以来,随着国内外学者对抗疤痕药物研究的不断深入,许多抗疤痕药都已投入青光眼滤过手术的临床使用中,其对改善滤过泡功能、降低眼压、提高手术成功率起到明显作用,但毒副作用和并发症应该引起重视。现将报道较多的抗疤痕药的研究、使用进展及其应用前景作一综述。1 5-氟尿嘧啶(5-fluorouracil,5-Fu)作为叶酸拮抗药,5-Fu的作用机制是通过非竞争性的酶抑制作用,阻止叶酸还原为四氢叶酸,从而抑…     

青光眼巩膜生物力学研究进展

青光眼的最终结局是视神经损伤、视力丧失,早期诊治是青光眼病人保持良好视功能的最有效措施,然而青光眼复杂的发病机制目前尚不清楚。巩膜生物力学特征在青光眼发病过程中具有不可忽略的作用,近年来全球眼科医生与生物力学研究者在合作探究青光眼巩膜生物力学知识方面已取得很多研究成果,现对这些研究成果进行概括,以利于更深入地了解青光眼的发病机制,为青光眼的防治提供新思路,并探索一些有前景的新型的青光眼治疗途径。     

晚期青光眼的手术治疗

晚期青光眼又称为近绝对期青光眼 ,眼压多持续升高 ,视野成管状 ,视功能严重受损 ,治疗上有很大风险。我院自1991年 6月至 2 0 0 1年 8月对 2 8例 ( 31眼 )晚期青光眼进行了抗青光眼手术 ,现报道如下。1　资料与方法1.1　一般资料 :晚期青光眼患者共 2 8例 ( 31眼 ) ,其中男性     

青光眼治疗药物的疗效和安全性

青光眼是一种老年性眼病。原发性开角型青光眼有典型的三联征：眼内压力升高、视神经乳头变性(乳头退缩凹陷)和视野缩小。近年来已上市了多种新型青光眼治疗药(表1)，本文着重介绍有关作用机理、疗效和安全性。     

抗青光眼药物合用时对肾脏的损害

青光眼是一组以特征性视神经萎缩和视野缺损为共同特征的疾病,其病因通常是因为眼内压异常升高,超过了眼睛所能耐受的最高限度,以致造成了视神经受压及供血不足,轴浆流中断引起视神经损害,视野缺损,若未能得到及时正确的诊断和治疗,最终将导致患眼失明.对于早期发现的开角型青光眼患者,通常不主张采用手术治疗,而以药物降低或控制眼压,保护视神经,保存视功能,而原发性闭角型青光眼一经确诊,首选手术治疗,但手术前也必须先用药物控制眼压,以提高手术的成功率.因此,对于青光眼患者而言,降眼压药物的使用显得至关重要.     

青光眼治疗药物的研究进展

青光眼造成的失明通常是不可逆的,眼压升高被认为是青光眼的最重要危险因素。降眼压治疗可以延缓青光眼的发生和进展,是目前临床治疗青光眼的主要策略。视神经保护可能是青光眼治疗的新方向。从传统降眼压药物、新型降眼压药物、视神经保护药物3个方面对青光眼治疗药物进行综述和探讨。     

Ahmed青光眼阀置入术治疗难治性青光眼

目的探讨Ahmed青光眼阀植入术治疗难治性青光眼的手术方法及疗效。方法用Ahmed青光眼阀植入术治疗难治性青光眼27例(27眼),其中新生血管性青光眼11眼、葡萄膜炎性青光眼3眼、无晶体眼青光眼7眼、外伤性青光眼6眼。其中有5眼曾行小梁切除术后失败。结果术后随访1～3年。术前眼压36～70mmHg,平均(41.12±10.04)mmHg,末次随访时平均眼压(20.04±9.15)mmHg,手术前后眼压存在显著性差异(P<0.01)。其中术后不用药物治疗眼压控制在21mmHg以下者15眼,联合局部降眼压药物治疗眼压控制在21mmHg以下者7眼,总有效率为81.48%。术后9眼视力较前有不同程度提高,最好视力达0.2。结论Ahmed青光眼阀植入术治疗难治性青光眼,操作简便,疗效满意,是目前值得推荐的治疗方法。     

Effects of antiglaucoma drugs on ocular blood flow in ocular hypertensive rabbits

In search of antiglaucoma agents which can increase the ocular blood flow and effectively lower the intraocular pressure (IOP), numerous antiglaucoma drugs were investigated to determine their ability to increase the ocular pulsatile blood flow in ocular hypertensive rabbits with the intraocular pressure artificially raised to 40 mmHg. It was found that various antiglaucoma drugs increased ocular pulsatile flow; these included (with percent increase) ethoxzolamine (36–56%), pilocarpine (65%), physostigmine (43–83%), echothiophate (23–62%), timolol (28–42%), levobunolol (37–55%), betaxolol (35%), and epinephrine (61%). Metipranolol, metoprolol, and clonidine had no effect on pulsatile blood flow. These results indicate that most antiglaucoma drugs, with the exception of a few, can enhance the ocular pulsatile blood flow in ocular hypertensive rabbits. © 1993 Wiley-Liss, Inc.     

Generic drugs for the treatment of ocular conditions: changing the treatment landscape

As global spending on medicinal products continues to rise, the availability of lower-cost generic substitutes is increasingly driving health care decision-making. US FDA does not require strict demonstration of human bioequivalence and/or therapeutic studies for the approval of generic ophthalmic compounds. Bioequivalence between generic and innovator compounds is presumed on the basis of matching active and inactive ingredient profiles. Generic compounds may differ from innovator agents with regards to performance under environmental stress, relative acidity and bottle size/rigidity. Matching ingredient profiles may therefore not result in consistently comparable drug compositions and clinical effects.     

Current and emerging medical therapies for glaucoma

Glaucoma is a multifactorial optic neuropathy in which there is a characteristic acquired loss of retinal ganglion cells, at levels beyond normal age-related baseline loss, and corresponding atrophy of the optic nerve. Although asymptomatic in its earlier stages, the disease is nevertheless one of the leading global causes of irreversible blindness. Although elevated intraocular pressure (IOP) is one of the most important risk factors and lowering of IOP is the only proven treatment so far, the definition of glaucoma has evolved from a disease caused by increased IOP to one characterised by an IOP-sensitive, progressive optic neuropathy. In recent years, safer and better tolerated topical medications have been developed to control IOP more effectively, thereby limiting the need for surgery. New research has also noted the importance of diurnal IOP variation as a critical risk factor for progression of glaucomatous optic neuropathy (GON) and subsequent visual field loss. Moreover, new discoveries have further elucidated the basic pathophysiological and genetic mechanisms underlying the elevated levels of IOP, as well as the cellular mechanisms of GON. As our understanding of these complex pathways continues to improve, development opportunities for new therapeutic modalities will be enhanced.     

The pathogenesis and medical management of glaucoma

The term glaucoma applies to a group of diseases in which an elevated pressure in the eye causes optic nerve damage resulting in visual loss. Current medical and surgical treatment of glaucoma is designed to lower intraocular pressure to a level at which no further optic nerve damage occurs. This review serves to describe the following aspects of glaucoma and its treatment: aqueous humor dynamics and elevation of intraocular pressure; the pathogenesis of glaucomatous optic nerve damage; the nature of visual loss from glaucoma; the modern medical management of glaucoma; and a discussion of a new drug, forskolin, with potential for clinical use in the treatment of glaucoma.     

比马前列素滴眼液的药理和临床应用

比马前列素是合成的前列酰胺F2α衍生物，通过增加小梁网通道和葡萄膜巩膜通道的房水流出而降低眼内压（IOP），被认为是目前降眼压作用最强的局部抗青光眼药物。主要用于开角型青光眼（POAG）或高眼压症（OHT）的患者，全身不良反应较少。现主要综述该药的药理作用、药动学及临床应用。     

An update on bimatoprost in glaucoma therapy

Bimatoprost, a prostamide, effectively lowers intraocular pressure (IOP) in patients with open-angle glaucoma and ocular hypertension. In clinical trials, bimatoprost has demonstrated superiority to the β-adrenergic antagonist timolol and has consistently provided ～ 1 – 2 mmHg greater mean IOP lowering than the prostaglandin latanoprost. Bimatoprost is more effective than either timolol or latanoprost in allowing patients to reach the low target pressures that best protect the visual field. Patients on bimatoprost therapy achieve low pressures throughout the day and night. Moreover, 1-year trials have shown that the efficacy of bimatoprost is sustained with long-term use. The most common side effects have been conjunctival hyperaemia, graded as trace or mild, and eyelash growth. No safety concerns have arisen in postmarketing surveillance. Bimatoprost appears to be a valuable new agent for glaucoma therapy.     

复方樟柳碱注射液联合盐酸卡替洛尔滴眼液治疗开角型青光眼的临床研究

目的 探讨复方樟柳碱注射液联合盐酸卡替洛尔滴眼液治疗开角型青光眼的临床疗效。方法 选取辽宁省朝阳市中心医院2017年1月—2019年6月收治的开角型青光眼患者82例（150眼）作为研究对象。将患者随机分为对照组与观察组,每组各41例。对照组给予盐酸卡替洛尔滴眼液治疗,每日早午饭后滴1滴眼液于结膜囊内,手指压迫内眦角泪囊部5 min, 2次/d,治疗4周。观察组患者在对照组的基础上联合复方樟柳碱注射液治疗,于患眼同侧颞浅动脉旁皮下注射樟柳碱2 mL, 1次/d,14 d为一个疗程,连续治疗2个疗程。观察两组患者的临床疗效,比较治疗前后两组患者的眼压、视力、视野平均缺损（MD）、视野神经宽度、以及眼部血管眼动脉（OA）、睫状后短动脉（PCA）、视网膜中央动脉（CRA）的血管收缩期峰值血流速度（PSV）、舒张末期容量（EDV）、阻力指数（RI）、搏动指数（PI）等指标。结果 治疗后,观察组改善率为96.05%,显著高于对照组的81.08%（P<0.05）。治疗后,两组视力水平显著升高,眼压均显著下降（P<0.05）;观察组视力水平和眼压显著优于对照组（P<0.05）。治疗后与随访3个月,观察组MD与视神经宽度水平均显著高于治疗前（P<0.05）。治疗后,两组CRA、PCA的PSV、EDV呈升高趋势,观察组与治疗前相比差异显著（P<0.05）,且与对照组相比差异明显（P<0.05）。与治疗前相比,观察组OA的PSV、EDV值显著升高,差异有统计学意义（P<0.05）。随访3个月,与治疗前相比,观察组CRA的PSV降低,EDV升高（P<0.05）,PCA和OA的PSV、EDV均降低（P<0.05）,观察组随访3个月的CRA的PSV较对照组低、EDV更高,PCA的PSV、EDV较对照组低（P<0.05）。结论 复方樟柳碱注射液联合盐酸卡替洛尔滴眼液治疗开角型青光眼患者可有效控制眼压,同时还具有较好的视神经保护作用,主要表现为改善视野平均缺损、视神经宽度、眼血管血流参数,延缓视功能损害,疗效显著,值得临床推广。     

Current status of unoprostone for the management of glaucoma and the future of its use in the treatment of retinal disease

Imatinib mesylate is a selective and potent small-molecule inhibitor of tyrosine kinases, including Kit, platelet-derived growth factor receptor, and the BCR–Abl fusion protein. Kit plays an important role in gastrointestinal stromal tumours (GISTs) and is one of the most exciting therapeutic targets discovered so far. Clinical trials have consistently shown the dramatic efficacy of imatinib mesylate in patients with GIST. This article will review the development and pharmacology of this small-molecule inhibitor and summarise the clinical trials of imatinib mesylate for the treatment of GIST. Although imatinib mesylate has significantly improved the outcomes of most patients with advanced GIST, unanswered questions remain: what is the role of imatinib mesylate in the pre- and postoperative settings? What is the mechanism of the antitumour activity of imatinib? How do you manage patients whose tumours are refractory to imatinib mesylate?     

Fixed-combination and emerging glaucoma therapies

Ocular hypotensive agents are the only approved pharmacotherapy for glaucoma. Despite significant advances during the past two decades, a large proportion of glaucoma patients require more than one drug. The most recent additions to the armamentarium of antiglaucoma drugs are fixed-combination products for the glaucoma patient who is insufficiently responsive to monotherapy. Fixed-combination products have the combined efficacy of two ocular hypotensive drugs, and the convenience of a two-drug treatment regimen in a single container, which may aid patient adherence to treatment. Available fixed-combination products consist of timolol 0.5% as an invariant with brimonidine 0.2%, dorzolamide 2%, travoprost 0.004%, latanoprost 0.005% or bimatoprost 0.03%. Research on more advanced antiglaucoma medications continues. Promising new directions appear to be the Rho-kinase inhibitors, microtubule-disrupting agents, serotonergics and cannabimimetics. Efforts continue to improve existing antiglaucoma drugs in an attempt to design second-generation cholinomimetics, adrenergics, prostaglandins and prostamides.