scholarly journals Correlation of Chronic Smoking with Meibomian Gland Dysfunction – A Study at Wardha, Maharashtra, India

2021 ◽  
Vol 10 (19) ◽  
pp. 1382-1386
Author(s):  
Swapneel Mathurkar ◽  
Sachin Daigavane ◽  
Madhumita Prasad ◽  
Kervi Mehta

BACKGROUND Meibomian gland dysfunction (MGD) is one of the causes of evaporative dry eye disease. It is the terminal duct obstruction of the Meibomian gland and is associated with glandular secretion changes. These changes lead to decreased amount of lipids secretion which accounts for instability of tear film leading to evaporative dry eye disease. Chronic smoking also causes irritative, burning eyes along with unstable tear film. We wanted to study the corelation of chronic smoking with Meibomian gland dysfunction. METHODS This is a hospital based observational cross-sectional study that enrolled a total of 100 subjects having Meibomian gland disease (MGD), out of whom 61 were smokers and 39 were non-smokers. All enrolled subjects underwent tear film breakup time (TBUT), Schirmer I test (SIT) and slit-lamp microscope examination of lid margin abnormalities, Meibomian gland expression as well as meibum. RESULTS Our study found that the patients with Meibomian gland dysfunction with the history of chronic smoking had a remarkably decreased value of tear film break up time (TBUT), Schirmer’s 1 Test which explains the dry eye symptoms as compared to MGD patients without smoking. No significant differences were seen in lid margin irregularity and meibum secretion. Meibomitis is found in 29 smokers with MGD and 5 non-smokers with MGD which is not significant. CONCLUSIONS Chronic smoking is associated with MGD. KEY WORDS Cigarette Smoking, Meibomian Gland Dysfunction, Tear Film Tests

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Ricaurte Ramiro Crespo-Treviño ◽  
Anna Karen Salinas-Sánchez ◽  
Francisco Amparo ◽  
Manuel Garza-Leon

AbstractMany recent studies have showed that morphological changes are one of the key signs of meibomian gland disease (MGD). These changes can be seen even before symptom onset, potentially underestimating the prevalence of MGD; however, until now, there is no conclusive information about the impact of meibomian gland (MG) morphology in tear film physiology and disease. This study aimed to investigate the prevalence of anatomical and morphological MG alterations between patients with evaporative dry eye disease (DED) and healthy controls. Retrospective chart review of seventy-five patients with evaporative DED and healthy individuals who had dry eye assessments included Ocular Surface Disease Index questionnaire, meibum quality, meibum expressibility, lid margin abnormality, ocular staining, non-invasive tear film break-up time, and meibography. We did not find significant differences in MG alterations in the upper lid between healthy and DED subjects. Patients with evaporative DED presented MG alterations in the lower lid more frequently than healthy subjects (54.8 vs. 30.3%; p = 0.03). The presence of shortened glands was the only MG alteration that was more prevalent in the lower lid in dry-eye patients than in healthy subjects (p < 0.05). Subjects with evaporative DED presented more alterations in the lower lid than healthy subjects.


2019 ◽  
Vol 35 (1) ◽  
Author(s):  
Sameera Irfan

Dry eyes is a common, chronic condition that has a prevalence of about 5- 50%.1 According to the Dry Eye Workshop II report (DEWS II report), published in 2017, the updated definition of Dry Eye Disease is, “a multifactorial disease of the ocular surface characterised by a loss of homeostasis of the tear film, and accompanied by ocular symptoms, in which tear film instability and hyper-osmolarity, ocular surface inflammation and damage, and neurosensory abnormalities play etiological roles.” The Tear Film & Ocular Surface Society (TFOS) released their report on the international work on Meibomian Gland Dysfunction (MGD)2 in 2011, which defined MGD, classified it and considered it as the primary cause of dry eye disease worldwide. Previously dry eye disease was considered as an aqueous deficiency problem, but after this report by TFOS, there is a paradigm shift towards “not producing enough lipids to retain the tears that are being produced”. This has led to a huge impact on the treatment protocols which were previously focused on managing the sequelae and symptoms of dry eyes rather than targeting directly on the underlying cause, the MGD. It has now been accepted worldwide that dry eye occurs when the ocular surface system cannot adequately protect itself from the desiccating stress due to the lack of a healthy meibomian gland secretion. This article is mainly focussed on the Meibomian Gland Dysfunction, discussing the normal anatomy of the glands, how they are affected by disease, its implications on the ocular surface and finally, the various treatment strategies. Key words: Blepharitis, Dry eyes, Meibomian gland dysfunction, blepharospasm.


Author(s):  
Maria Vincent ◽  
Jose Quintero ◽  
Henry D. Perry ◽  
James M. Rynerson

Blepharitis and dry eye disease have long been viewed as two distinct diseases with overlapping presentations and separate etiologies. Evaporative dry eye, although frequently associated with aqueous deficiency, is also considered a separate entity. We propose viewing dry eye, both evaporative and insufficiency, as the natural sequelae of chronic blepharitis induced by biofilm. We suggest describing this one chronic disease as dry eye blepharitis syndrome (DEBS). The disease process begins when normal flora bacteria colonize the lid margin beginning shortly after birth. This colonization accompanies the development of a biofilm on the lid margin. As years pass, the biofilm matures, and the increased bacterial population initiates the production of inflammatory virulence factors, such as exotoxins, cytolytic toxins, and super-antigens, which persist on the lid margin for the rest of the patient’s life. These virulence factors cause early follicular inflammation and later, meibomian gland dysfunction followed by aqueous insufficiency, and finally, after many decades, loss of the dense collagen in the tarsal plate. We proposed four stages of DEBS, which correlate with the clinical manifestations of folliculitis (anterior blepharitis), meibomitis (meibomian gland dysfunction), lacrimalitis (aqueous deficiency), and lid structure damage evidenced by increased lid laxity resulting in entropion, ectropion, and floppy eyelid syndrome.


2018 ◽  
Vol 1 (1) ◽  
pp. e28-e31
Author(s):  
Liem Hieu Nguyen ◽  
Edward H. Jaccoma

Background and Objectives A chalazion, also known as a stye, is a common and chronic inflammatory problem of the eyelids where one or more Meibomian glands are blocked. Previous studies have shown that a chalazion is a sign of Meibomian Gland Dysfunction (MGD) and evaporative dry eye disease. The prevalence of chalazia in the pediatric population has recently been noted. In this report, we will describe two pediatric cases of chalazion that are associated with MGD and related dry eye disease.  Methods This is a case report of non-genetically related 7-year-old and 16-year-old patients as they were each seen for newly developed chalazia. Results External exam in both patients showed chalazia, waxy plugs and poor Meibomian gland expression. Meibography showed shorten, truncated, and dilated Meibomian glands with rapid tear break-up times leading to the diagnosis of evaporative dry eye disease due to MGD. Conclusion These cases serve to confirm an increase in the prevalence of MGD in the pediatric population and to emphasize the need for early screening for dry eye disease.  Key Words: Chalazion - Meibomian gland dysfunction - Pediatric Dry Eye Disease


2020 ◽  
Vol 17 (10) ◽  
pp. 1385-1392
Author(s):  
Abhishek Suwal ◽  
Ji-long Hao ◽  
Dan-dan Zhou ◽  
Xiu-fen Liu ◽  
Raja Suwal ◽  
...  

2019 ◽  
Vol 103 (10) ◽  
pp. 1475-1480 ◽  
Author(s):  
Marc Labetoulle ◽  
Tristan Bourcier ◽  
Serge Doan

Background/aimsDry eye disease (DED) is categorised by pathophysiology as aqueous deficient dry eye (ADDE), evaporative dry eye (EDE) or mixed. Treatment should be tailored to DED pathophysiology, but this is challenging to determine. This Delphi consultation aimed to categorise and weight signs and symptoms to help identify the evaporative or aqueous deficient DED origin.MethodsA panel of French DED experts created an initial list of 77 DED signs and symptoms. In a Delphi consultation, experts categorised items by DED pathophysiology. Likert scoring was used to indicate whether items were strongly or moderately indicative of ADDE or EDE. Items could also be judged non-applicable to DED, with the opportunity to suggest alternative diagnoses.ResultsExperts attributed 19 items (of which 11 were strongly indicative) to a pathophysiology of EDE and 12 items (of which four were strongly indicative) to ADDE. Items scored strongly indicative with agreement >90% for EDE were previous chalazia, rosacea/rhinophyma, telangiectasias of eyelid margin and thick non-expressible meibomian gland secretions, and for ADDE were Sjögren syndrome or associated disease, and Schirmer <5 mm after 5 min (without anaesthesia). Seventeen items indicated neither pathophysiology and 18 items were found to be suggestive of alternative diagnoses.ConclusionsThis Delphi consultation categorised signs and symptoms, using an innovative weighting system to identify DED pathophysiology. An algorithm integrating the weighting of each sign and symptom of an individual patient would be valuable to help general ophthalmologists to classify the DED subtype and tailor treatment to DED underlying mechanism.


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