Meibomian Gland Dysfunction: A Dermatological Perspective on Pathogenesis and Treatment Outlook

Gupta, Preeya K.; Periman, Laura M.; Lain, Edward; Donnenfeld, Eric D.; Hovanesian, John; Kim, Terry; Trattler, William; Yeu, Elizabeth; Holland, Edward J.

doi:10.2147/opth.s327407

Cited by 14 publications

(13 citation statements)

References 26 publications

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“…In another recent case report, MGD was observed in a patient with breast cancer who received HER-2-directed therapy (both trastuzumab and pertuzumab) and anastrozole (18). T h e p r i m a r y m e c h a n i s m o f M G D i n v o l v e s hyperkeratinization of the meibomian gland which leads to gland obstruction, reduced lipid-rich meibum output, and ultimately a tear film that is unstable and more prone to evaporation causing dry eyes (11,19). While the etiology of the keratinization process in MGD is not fully understood, reactive oxygen species and overexpression of heat shock protein HSP90-alpha and peroxiredoxins appear to be involved (19).…”

Section: Discussionmentioning

confidence: 99%

“…The primary mechanism of MGD involves hyperkeratinization of the meibomian gland which leads to gland obstruction, reduced lipid-rich meibum output, and ultimately a tear film that is unstable and more prone to evaporation causing dry eyes ( 11 , 19 ). While the etiology of the keratinization process in MGD is not fully understood, reactive oxygen species and overexpression of heat shock protein HSP90-alpha and peroxiredoxins appear to be involved ( 19 ). MGD may also be mediated by pro-inflammatory mechanisms.…”

Section: Discussionmentioning

confidence: 99%

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Case report: Immune-mediated meibomian gland dysfunction following pembrolizumab therapy for advanced urothelial carcinoma

Nguyen

Su²,

Morgan³

et al. 2022

Front. Oncol.

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Ocular immune-related adverse events are a relatively rare complication of immune checkpoint inhibitors. Common ocular toxicities range from dry eyes to inflammatory uveitis and ocular myasthenia gravis. Here, we present the case of a 55-year-old woman with recurrent urothelial carcinoma of the ureter after initially being managed with neoadjuvant cisplatin-based chemotherapy and surgical resection. She was treated with pembrolizumab which was complicated by immune-mediated pneumonitis after the eighth cycle, which was managed with a prolonged steroid course. The patient also developed red eyes along with recurrent styes. Eye examination revealed decreased tear breakup time, expression of thick and turbid meibum, and meibomian gland atrophy on infrared meibography. The patient was diagnosed with suspected immune-mediated meibomian gland dysfunction (MGD) as a result of pembrolizumab, a previously unreported complication of immunotherapy. The goal of MGD therapy is to stabilize the tear film and minimize evaporation with lipid-based lubricants and other conservative treatments.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Case report: Immune-mediated meibomian gland dysfunction following pembrolizumab therapy for advanced urothelial carcinoma

Nguyen

Su²,

Morgan³

et al. 2022

Front. Oncol.

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“…AZR-MD-001 is an ophthalmic ointment containing selenium sulfide, which has demonstrated keratolytic [170] and lipogenic [171] activity in preclinical studies. Hyperkeratinization may play a role in meibomian duct obstruction in MGD [172]. In a small randomized study (NCT04314362), patients with MGD (n = 22) were randomly assigned to receive AZR-MD-001 1% or vehicle control ointment administered to the lower eyelid margin [163].…”

Section: Emerging Pharmacologic Treatmentsmentioning

confidence: 99%

Dry Eye Disease Associated with Meibomian Gland Dysfunction: Focus on Tear Film Characteristics and the Therapeutic Landscape

Sheppard

Nichols

2023

Ophthalmol Ther

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Meibomian gland dysfunction (MGD) is highly prevalent and is the leading cause of evaporative dry eye disease (DED). MGD is characterized by a reduction in meibum secretion and/or a change in meibum composition that results in the disruption of the tear film lipid layer and an increase in the tear film evaporation rate. Excessive evaporation causes tear film instability, desiccation, tear hyperosmolarity, inflammation, and apoptosis of ocular surface cells, resulting in a continuous cycle of DED. The primary treatment goal for DED associated with MGD is to restore the tear film lipid layer and decrease evaporation, thereby reducing ocular signs and symptoms. The management of MGD includes home care options (eyelid hygiene, warming eye masks, ocular lubricants) and office-based treatments (manual expression, microblepharoexfoliation, thermal pulsation, intense pulsed light, intraductal probing).Topical ophthalmic prescription medications attempt to alter various factors that may contribute to DED (e.g., inflammation, bacterial growth, inadequate tear production). In this review, clinical evidence regarding available treatments and emerging therapies from randomized studies in patients with DED associated with MGD is summarized. Although some treatment modalities have been evaluated specifically for DED patients with MGD, largescale randomized controlled trials are needed to confirm efficacy and safety in this patient population. Currently, there are no approved prescription pharmacologic treatments specifically indicated for DED associated with MGD, and those medications approved for the treatment of DED do not target the key driver of the disease (i.e., excessive evaporation). NOV03 (perfluorohexyloctane; under review with the US Food and Drug Administration) is the most advanced emerging therapy for DED associated with MGD and has demonstrated statistically significant improvements in both signs and symptoms in randomized controlled trials. Development of novel pharmacotherapies will improve therapeutic options and allow for a more individualized approach for patients with DED associated with MGD.

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“…A noteworthy discovery was the overexpression of keratinization- related genes, including genes coding for small proline-rich proteins (SPRRs) and calcium binding proteins S100 (S100 A7, A8, and A9) [ 61 ]. Increased expression of genes involved in keratinization leads to the hyperkeratinization of the ductal system, which leads to altered meibum flow and plug formation [ 64 ]. According to the researchers, the gland orifice, central ducts, and meibum themselves exhibit abnormal keratinization in patients with MGD [ 64 ].…”

Section: Pathological Mechanism Of Mgdmentioning

confidence: 99%

Ductal Hyperkeratinization and Acinar Renewal Abnormality: New Concepts on Pathogenesis of Meibomian Gland Dysfunction

Peng

Liu

et al. 2023

CIMB

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Meibomian gland dysfunction (MGD) is a functional and morphological disorder of the meibomian glands which results in qualitative or quantitative alteration in meibum secretion and is the major cause of evaporative dry eye (EDE). EDE is often characterized by tear film instability, increased evaporation, hyperosmolarity, inflammation, and ocular surface disorder. The precise pathogenesis of MGD remains elusive. It has been widely considered that MGD develops as a result of ductal epithelial hyperkeratinization, which obstructs the meibomian orifice, halts meibum secretion, and causes secondary acinar atrophy and gland dropout. Abnormal self-renewal and differentiation of the acinar cells also play a significant role in MGD. This review summarizes the latest research findings regarding the possible pathogenesis of MGD and provides further treatment strategies for MGD-EDE patients.

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Meibomian Gland Dysfunction: A Dermatological Perspective on Pathogenesis and Treatment Outlook

Cited by 14 publications

References 26 publications

Case report: Immune-mediated meibomian gland dysfunction following pembrolizumab therapy for advanced urothelial carcinoma

Case report: Immune-mediated meibomian gland dysfunction following pembrolizumab therapy for advanced urothelial carcinoma

Dry Eye Disease Associated with Meibomian Gland Dysfunction: Focus on Tear Film Characteristics and the Therapeutic Landscape

Ductal Hyperkeratinization and Acinar Renewal Abnormality: New Concepts on Pathogenesis of Meibomian Gland Dysfunction

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