睑缘炎、睑板腺功能障碍与干眼症

睑板腺通过分泌睑脂组成泪膜脂质层 ,防止泪液过度蒸发 ,促进泪膜稳定性。睑缘炎和睑板腺功能障碍破坏正常的睑脂分泌 ,使泪液蒸发过强 ,是蒸发过强型干眼症的最常见原因。目前对睑板腺和泪膜脂质层功能评价的认识尚不足。本文就睑缘和睑板腺的功能特点和临床评价、睑缘炎和睑板腺功能障碍与干眼症的关系以及治疗进展进行综述     

糖尿病患者睑板腺功能障碍病理机制的研究进展

睑板腺功能障碍是一种以睑板腺终末导管阻塞和(或)睑酯分泌的质或量异常为主要特征的慢性、弥漫性睑板腺病变,临床上可引起泪膜异常和眼表炎症反应,从而导致眼部刺激症状,严重时可能损伤角膜从而影响视功能。睑板腺功能障碍可分为睑酯低排出型和高排出型,低排出型又进一步分为腺泡萎缩型和阻塞型。随着对糖尿病研究的进展,发现在糖尿病早期,患者的睑板腺组织即受到慢性损伤,导致其结构和功能均发生变化,糖尿病患者睑板腺功能障碍的发病率更高,程度更严重。而引起糖尿病患者睑板腺功能障碍的因素很多而且复杂,目前机制并不是很清楚,文章就国内外学者对糖尿病睑板腺功能障碍病理机制的研究进展作一综述。     

睑板腺功能障碍发病机制及患病危险因素

睑板腺功能障碍(meibomian gland dysfunction,MGD)是一种慢性、弥漫性睑板腺异常,以睑板腺终末导管阻塞和(或)睑板腺分泌物的质量和数量改变为特征,可引起泪膜异常、眼部刺激症状、炎性反应以及眼表疾病.MGD发病主要与睑板腺分泌异常以及睑板腺终末导管阻塞有关,炎症是发病的关键.此外泪液特殊前蛋白和细胞凋亡在发病过程中也起到一定作用.     

睑缘炎、睑板腺功能障碍与干眼症

睑板腺通过分泌睑脂组成泪膜脂质层，防止泪液过度蒸发，促进泪膜稳定性。睑缘炎和睑板腺功能障碍破坏正常的睑脂分泌，使泪液蒸发过强，是蒸发过强型干眼症的最常见原因。目前对睑板腺和泪膜脂质层功能评价的认识尚不足。本就睑缘和睑板腺的功能特点和临床评价、睑缘炎和睑4板腺功能障碍与干眼症的关系以及治疗进展进行综述。     

中老年睑板腺功能障碍的临床分析

目的:探讨中老年患者睑板腺功能障碍(MGD)的临床特点及诊治要点。方法:通过问卷调查、泪膜破裂时间、ShimmerⅠ试验、角膜荧光素染色及睑板腺分泌物的检查,将74例145眼睑板腺功能障碍患者分为轻度、中度、重度三组,根据疾病程度,分别行睑缘清洁、疏通、按摩、人工泪液、或抗炎、抗感染等联合治疗。结果:睑板腺功能障碍患者74例145眼治疗1mo后,眼表疾病指数评分下降,睑腺分泌物评分下降,泪膜破裂时间延长,眼表活体染色评分下降。各型MGD的总治愈率34.5%,总有效率98.6%。结论:眼科医师应掌握中老年睑板腺功能障碍的临床特点,重视症状、病史的询问及眼表及睑板腺功能的检查。避免睑板腺功能障碍的误诊、误治。     

睑板腺功能障碍发病机制的研究进展

睑板腺功能障碍(meibomian gland dysfunction,MGD)是一种慢性、弥漫性的睑板腺病变,通常以睑板腺终末导管的阻塞或分泌的睑脂数量或质量发生改变为特征,临床上可以引起泪膜异常、角膜上皮损害、眼部刺激等干眼表现。MGD病因复杂且受多种因素影响,因此MGD发病机制的研究对于指导临床工作至关重要。本文对研究MGD的动物模型进行了介绍,并根据一些基础研究对MGD相关的细胞及分子机制等方面进行综述。     

放射科技师泪膜功能的研究

目的探讨放射科技师泪膜功能。方法前瞻性研究，放射科技师及对照组各34例，分别行干眼症状询问、泪膜破裂时间测定（BUT）、角膜荧光素染色（FIS）、基础泪液分泌实验（SIt）、睑板腺功能检查。结果病例组泪膜破裂时间、基础泪液分泌试验的结果及其异常的比率与对照组比较，差异有统计学意义（P〈0．05），病例组出现干眼症状的比率高于对照组（P〈0．05），角膜荧光素染色阳性、睑板腺功能障碍的比率与对照组比较，差异无统计学意义（P〉0．05），专业工作年限与眼干症状、泪膜破裂时间、角膜荧光素染色、睑板腺功能障碍、基础泪液分泌试验之间无相关性。结论放射科技师易发生泪膜功能及泪腺分泌异常，易出现干眼症状。     

睑板腺功能障碍研究进展

睑板腺功能障碍(meibomian gland dysfunction,MGD)以睑板腺终末导管阻塞和睑板腺分泌物的质量或数量改变为特征.睑板腺分泌的脂质成分发生相应改变,造成泪膜的稳定性下降和泪液蒸发量增加,从而导致干眼发生.目前MGD的发病原因尚不明确,临床上采取的治疗往往是对症治疗.本文主要对MGD的泪膜脂质变化及其国内外诊治进展进行总结.     

睑板腺功能异常

睑板腺功能异常是一种常见的眼表面疾病,可引起眼红,眼部痒、烧灼感、干燥感、刺激感,视力波动或流泪等眼部不适症状,可导致脂质缺乏性干眼症、睑缘炎、结膜炎、点状角膜炎及其他眼表面疾病.睑板腺开口阻塞是睑板腺功能障碍的最常见原因,阻塞可直接或间接引起睑板腺分泌物数量和质量改变,造成泪膜不稳定,脂质减少也可引起泪液蒸发加快,导致眼表面干燥.     

2型糖尿病患者睑板腺形态与功能的改变及其对泪膜功能的影响

目的：探究2型糖尿病患者睑板腺形态与功能的改变及其对泪膜功能的影响。

方法：选取2018-01/2020-01来我院就诊的2型糖尿病患者52例104眼,根据眼底改变分为无明显视网膜病变组(NDR组,31例62眼)、糖尿病视网膜病变组(DR组,21例 42眼)。选取同一时期就诊的无糖尿病的白内障患者38例76眼作为对照组。比较三组患者睑缘和睑板腺形态及功能评分、角膜荧光素染色评分、泪膜破裂时间(BUT)、泪膜脂质层厚度(LLT)、瞬目次数(BT)及不完全瞬目频率(PBR)的差异。

结果：DR组和NDR组睑缘和睑板腺形态及功能评分、角膜荧光素染色评分显著高于对照组,且DR组显著高于NDR组(均P<0.05)。DR组和NDR组BUT显著低于对照组,且DR组显著低于NDR组(均P<0.05)。三组间LLT、BT及PBR均有差异(P<0.05),且DR组和NDR组LLT、BT明显低于对照组,PBR显著高于对照组(均P<0.05),但DR组和NDR组间无显著差异(均P>0.05)。睑板腺形态异常的2型糖尿病患者泪膜功能异常的发生率更高。

结论：2型糖尿病患者易出现睑板腺短缩和缺失,睑板腺功能障碍,泪膜稳定性下降,而DR患者睑板腺形态异常与功能障碍更显著,泪膜稳定性更差。     

Effectiveness of pharmaceutical interventions for meibomian gland dysfunction: An evidence‐based review of clinical trials

Meibomian gland dysfunction is one of the most common ocular disorders encountered by ophthalmologists and is the leading cause of evaporative dry eye. The disease causes significant morbidity in the population such that patients seek treatment. Multiple clinical studies on pharmacological and mechanical interventions for the treatment of meibomian gland dysfunction have been evaluated. However, there is limited comparative clinical evidence for the effectiveness of these interventions. This review paper aims to report the clinical evidence for pharmaceutical interventions for meibomian gland dysfunction in order to guide clinicians in the management of the disease.     

A review of meibography

Meibomian gland dysfunction is one of the most common causes of dry eye resulting in morphology changes to the meibomian glands. Meibography provides an in vivo means to assess the structure of the meibomian gland. Over the past 40 years, meibography has undergone significant development regarding its application to research and clinical practice. This review describes the evolution of the various meibography techniques, grading methods, and their diagnostic relevance.     

提高对睑板腺功能障碍的认识 重视睑板腺功能障碍相关性干眼的药物治疗

睑板腺功能障碍（MGD）是临床常见的眼表疾病,以睑板腺终末导管的阻塞和／或睑板腺分泌物质或量的改变为特征,导致脂质向泪膜的排出减少,引起泪液蒸发过强。睑缘和睑板腺的炎症是引起睑板腺阻塞,进而导致MGD的直接原因,可引起眼表功能的异常。MGD的诊断主要依靠临床症状与体征,其症状与干眼的症状相似,因此无诊断特异性。体征主要包括睑缘形态的变化、睑板腺分泌异常和睑板腺缺失。MGD的治疗方法包括热敷、清洁睑缘、促进睑板腺的分泌、抗菌、抗炎治疗及润滑眼表,中度、重度MGD患者可给予必要的抗炎治疗,常用的抗炎药物有糖皮质激素、非甾体类抗炎药及免疫抑制剂。临床医师在进行眼部疾病的检查时应重视睑板腺的功能状态,尤其在角膜屈光手术及内眼手术前更应重视MGD的筛查,以免术后引起严重的眼表并发症,有效规避医疗风险。     

Intravitreally injected ranibizumab versus photodynamic therapy for CNV secondary to choroidal osteoma: a 7-year follow-up case report

Meibomian gland, the largest sebaceous gland of the body, is responsible for the biosynthesis of lipid layer of the tear film to prevent excessive evaporation. The loss of normal functions of meibomian gland, known as meibomian gland dysfunction (MGD), is a chronic disease and is the leading cause of dry eye symptoms in the clinics. Studies have found sex hormones, especially androgen, play vital roles in the regulation of the functions of meibomian gland. Recently, androgen has also been preliminarily applied in clinics for the treatment of MGD and showed promising results, especially in people with endogenous androgen deficiency. This review summarized the mechanisms of the function of androgen on meibomian gland based on molecular, animal, and clinical studies, and propose evidence-based views about its potential applications for the treatment of MGD.     

睑板腺功能障碍的相关危险因素

睑板腺功能障碍(meibomian gland dysfunction,MGD)是一种慢性、弥漫性睑板腺异常,它通常以睑板腺终末导管的阻塞和(或)睑板腺分泌物质或量改变为特征.MGD的危险因素错综复杂.任何影响睑板腺功能的原因如局部因素、药物因素、全身情况、先天性因素等均可导致MGD,有时可能为众多危险因素综合作用的结果.临床工作中眼科医生应关注MGD相关危险因素,以便针对性治疗.     

睑板腺功能障碍患者飞秒激光LASIK术后DLK发生率相关性研究

目的:通过对睑板腺功能障碍(meibomian gland dysfunction,MGD)患者行飞秒激光LASIK后弥漫性层间角膜炎(diffuse lamellar keratitis,DLK)发生情况的临床观察,分析睑板腺功能障碍与DLK发生的相关性.方法:收集2015-01/10就诊于我院近视治疗中心符合飞秒激光LASIK手术适应证,并进行手术者200例396眼,分成两组观察,A组为试验组(MGD组),有睑板腺功能障碍的患者100例197眼;B组为对照组(无MGD组),无睑板腺功能障碍的患者100例199眼.A组与B组之间年龄与性别差异无统计学意义.术前观察睑板腺开口阻塞情况、睑板腺分泌质和量、睑缘异常情况.观察术后1、3d,1wk DLK发生情况及严重程度.结果:MGD组100例197眼中发生DLK为15例18眼,发生率为9.1％;无MGD组100例199眼中发生DLK为3例3眼,发生率为1.5％;MGD组DLK的发生比率明显高于无MGD组.两组间DLK发生率存在明显的统计学差异(P＜0.05).结论:MGD可能是飞秒激光LASIK术后DLK发生的一种潜在危险因素.     

In vivo transillumination biomicroscopy and photography of meibomian gland dysfunction. A clinical study

Meibomian gland transillumination biomicroscopy and infrared photography were performed on 18 patients with clinically evident meibomian gland dysfunction (MGD) and dermatologic rosacea, 22 patients having MGD without evidence of dermatologic rosacea, and 15 unaffected individuals who served as controls. All patients having clinical signs of MGD demonstrated morphologic abnormalities of their meibomian glands by transilluminated biomicroscopy. Patients without dermatologic rosacea were noted to have varying degrees of gland distortion. Moreover, infrared photography documented a loss of the normal grape-like clusters of dark spots that represent the gland, suggesting a loss of glandular acini. Patients with dermatologic rosacea had more severe alterations, including marked distortion and loss of normal gland anatomy. There were no such abnormalities in clinically unaffected individuals. These data demonstrate that transilluminated biomicroscopy and infrared photography have the ability to identify a spectrum of morphologic alterations of the meibomian glands in MGD patients. The authors suggest that these techniques could be used to classify clinical MGD based upon the presence or absence of identifiable meibomian gland abnormalities.     

炎症在睑板腺功能障碍发病机制中的作用

Meibomian gland dysfunction(MGD) is the main cause of dry eye and is also a common disease in ophthalmology clinic. The main mechanism of MGD is terminal duct obstruction and/or qualitative/quantitative changes in the glandular secretion. The response of meibomian gland to inflammatory stimuli, the antibacterial and anti-inflammatory meibum, androgens and peroxisome proliferator-activated receptor gamma (PPAR-γ) involved in the regulation of inflammation may mediate the meibomian gland's resistance to inflammatory cell infiltration. Dysbacteriosis of meibomian gland and infection of demodex can induce inflammation and thus affect the pathogenesis and development of MGD. To clarify the role and mechanism of inflammation in MGD will provide new ideas and theoretical basis for the prevention and treatment of MGD. (Int Rev Ophthalmol, 2021, 45: 535-540)     

Age-related morphological changes in lid margin and meibomian gland anatomy.

Meibomian gland dysfunction (MGD) is responsible for recurrent irritative symptoms. Attempts to characterize MGD have largely concentrated on microbial and lipid abnormalities in meibomian gland secretions. Few reports describe histological abnormalities in this disease, and fewer still morphological changes. This article follows a previous study that established a classification for MGD. This was based on morphological changes in the meibomian gland and lid margin. Using this classification, we studied the age-related changes in 80 subjects, between 5 and 87 years of age without ocular disease. The lid margin became thicker after childhood. Lid margin vascularity and cutaneous hyperkeratinization increased with age in both lids, whereas, telangiectasia increased with age in the lower lid and squamous blepharitis and posterior lid margin rounding were more common after 50 years of age in the upper lid. Multiple rows of meibomian gland orifices occurred more frequently in the upper than lower lid, and orifice narrowing and pouting increased with age. No age-related changes in the shape or form of the mucocutaneous function, gland ducts, or acini were found. Meibomian gland secretions were less easily expressed in the elderly. We have attempted to define a normal range of lid morphology in healthy children and adults that we believe to be important for the subsequent definition of lid disease, and in particular, posterior blepharitis.