Meibomian Gland Dysfunction in Patients Receiving Long-Term Glaucoma Medications

Uzunosmanoglu, Enes; Mocan, Mehmet Cem; Kocabeyoğlu, Sibel; Karakaya, Jale; İrkeç, Murat

doi:10.1097/ico.0000000000000838

Cited by 36 publications

(38 citation statements)

References 26 publications

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“…Since lipid deficiency or abnormal lipids are characterized by an increased melting point, the secretions become thickened, mixing with biofilm, leading to a “toothpaste” quality, which eventually results in drastic decrease in functional lipids 83. Since the meibomian glands are just layered with biofilm, but not at capacity, expression may not elucidate the “toothpaste” secretions 84. Obvious MGD (Figure 7), on the other hand, is when inspissation and capping, or peaks over the gland openings, is noted on examination.…”

Section: The Four Stages Of Debsmentioning

confidence: 99%

“…A meibomian gland will become full of this “meibofilm”, and as production of biofilm continues, these secretions have nowhere to go except out of the ductule, and will appear as little domes trapped under the original lid margin biofilm. When these glands are expressed, one is much likely to be “rewarded” with copious amounts of meibomian sludge or inspissated secretions 84. Nonobvious MGD is a layering of the gland with these altered secretions, while obvious MGD is a gland that is full and distended with the secretions trying to escape out of the ductule 84,85.…”

Section: The Four Stages Of Debsmentioning

confidence: 99%

“…When these glands are expressed, one is much likely to be “rewarded” with copious amounts of meibomian sludge or inspissated secretions 84. Nonobvious MGD is a layering of the gland with these altered secretions, while obvious MGD is a gland that is full and distended with the secretions trying to escape out of the ductule 84,85. Hence, the difference is simply one of degree.…”

Section: The Four Stages Of Debsmentioning

confidence: 99%

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DEBS – a unification theory for dry eye and blepharitis

Rynerson¹,

Perry²

2016

OPTH

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For many years, blepharitis and dry eye disease have been thought to be two distinct diseases, and evaporative dry eye distinct from aqueous insufficiency. In this treatise, we propose a new way of looking at dry eye, both evaporative and insufficiency, as the natural sequelae of decades of chronic blepharitis. Dry eye is simply the late form and late manifestation of one disease, blepharitis. We suggest the use of a new term in describing this one chronic disease, namely dry eye blepharitis syndrome (DEBS). Bacteria colonize the lid margin within a structure known as a biofilm. The biofilm allows for population densities that initiate quorum-sensing gene activation. These newly activated gene products consist of inflammatory virulence factors, such as exotoxins, cytolytic toxins, and super-antigens, which are then present for the rest of the patient’s life. The biofilm never goes away; it only thickens with age, producing increasing quantities of bacterial virulence factors, and thus, increasing inflammation. These virulence factors are likely the culprits that first cause follicular inflammation, then meibomian gland dysfunction, aqueous insufficiency, and finally, after many decades, lid destruction. We suggest that there are four stages of DEBS which correlate with the clinical manifestations of folliculitis, meibomitis, lacrimalitis, and finally lid structure damage evidenced by entropion, ectropion, and floppy eyelid syndrome. When one fully understands the structure and location of the glands within the lid, it becomes easy to understand this staged disease process. The longer a gland can resist the relentless encroachment of the invading biofilm, the longer it can maintain normal function. The stages depend purely on anatomy and years of biofilm presence. Dry eye now becomes a very easy disease to understand. We feel that dry eye should be treated and prevented by early and routine biofilm removal through electromechanical lid margin debridement.

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Section: The Four Stages Of Debsmentioning

confidence: 99%

Section: The Four Stages Of Debsmentioning

confidence: 99%

Section: The Four Stages Of Debsmentioning

confidence: 99%

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DEBS – a unification theory for dry eye and blepharitis

Rynerson¹,

Perry²

2016

OPTH

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“…Further, this MGD reaction may help to explain why topical anti-glaucoma treatment often leads to, or worsens, DED in particular and ocular surface disease in general 8,17,20–23 . It is estimated that 40 to 59% of glaucoma patients suffer from ocular surface disease 20 .…”

Section: Introductionmentioning

confidence: 98%

“…Recently, investigators have discovered topical anti-glaucoma drugs induce meibomian gland dysfunction (MGD) 1–8 . This response is clearly a significant adverse effect.…”

Section: Introductionmentioning

confidence: 99%

Influence of Pilocarpine and Timolol on Human Meibomian Gland Epithelial Cells

Zhang

Kam

Liu

et al. 2017

Cornea

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Purpose Investigators have discovered that topical anti-glaucoma drugs may induce meibomian gland dysfunction. This response may contribute to the dry eye disease commonly found in glaucoma patients taking such medications. We hypothesize that drug action involves a direct effect on human meibomian gland epithelial cells (HMGECs). To test this hypothesis, we examined the influence of the antiglaucoma drugs, pilocarpine and timlolol, on the morphology, survival, proliferation and differentiation of HMGECs. Methods Immortalized (I) HMGECs (n = 2–3 wells/treatment/experiment) were cultured with multiple concentrations of pilocarpine or timolol for up to 7 days. Experiments included positive controls for proliferation (epidermal growth factor [EGF], and bovine pituitary extract, [BPE]) and differentiation (azithromycin; AZM). Cells were enumerated with a hemocytometer, and evaluated for morphology, neutral lipid staining and lysosome accumulation. Results Our results demonstrate that pilocarpine and timolol cause a dose-dependent decrease in the survival of IHMGECs. The clinically-used concentrations are toxic, and lead to cell atrophy, poor adherence or death. In contrast, drug levels that are known to accumulate within the conjunctiva, adjacent to meibomian glands, do not influence IHMGEC survival. These latter concentrations also have no effect on IHMGEC proliferation or differentiation, and do not interfere with the ability of AZM to stimulate cellular neutral lipid and lysosome accumulation. This dose of pilocarpine, though, did suppress the EGF+BPE-induced proliferation of IHMGECs. Conclusions Our results support our hypothesis and demonstrate that these antiglaucoma drugs, pilocarpine and timolol, have direct effects on HMGECs that may influence their morphology, survival and proliferative capacity.

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