Characteristics of meibomian gland dysfunction in patients with Stevens–Johnson syndrome

Abstract

To evaluate the characteristics of meibomian gland dysfunction (MGD) in patients with Stevens–Johnson Syndrome (SJS) and investigate the risk factors for severe MGD. Sixteen patients with a history of SJS were evaluated for MGD. To assess the SJS severity acute ocular involvement score (AOS), acute systemic involvement score (ASS), and chronic ocular manifestation score (COMS) were measured. Meibomian gland parameters were evaluated using meibomian gland dropout score (meiboscore - using a Keratograph 5 M), meibum expression score (MES), meibum quality score (MQS), and lid margin abnormality score (LMAS). Correlations between severity of meibomian gland parameters and degree of ocular and systemic involvement of SJS were analyzed. Risk factors for development of severe MGD were identified. The patients’ mean age was 32.0 ± 14.3 years. Four patients were men and 12 were women. MGD had developed in 14 patients (87.5%). The meibomian gland parameters were significantly correlated with ocular and systemic degree of SJS as evaluated using AOS ( P < .01), ASS ( P < .01), and COMS ( P < .01). Patients with severe MGD had a higher AOS ( P < .01) and COMS ( P = .02) values than those without severe MGD. On multivariate analysis, AOS higher than 2 was a significant risk factor for developing severe MGD ( P = .03). MGD was a common ocular manifestation with SJS patients. Severity of meibomian gland parameters was correlated with AOS, ASS, and COMS, and the presence of acute ocular complications was a risk factor for severe MGD in patients with SJS.

Clinical Characteristics of Patients With Chronic Stevens-Johnson Syndrome Treated at a Major Tertiary Eye Hospital Within the United Kingdom

“…SJS is a type IV hypersensitivity reaction and leads to a characteristic vesiculo-bullous reaction. Whilst the pathogenesis is unclear, it appears to be mediated by a cellmediated keratinocyte apoptosis via the Fas signaling cascade (3). In survivors of the disease, the unremitting chronic inflammation, dessication and scarring lead to blindness, with 20-79% of survivors experiencing chronic ocular surface disease (4)(5)(6).…”

A Retrospective Analysis of Tear Film and Blink Parameters in Patients With Ocular Surface Disease

“…This is consistent with the pathophysiology of SJS, in which squamous metaplasia results in meibomian gland inspissation and dropout. 24 Diffuse meibomian gland damage results in a higher meiboscore. The acute, severe ocular surface inflammation that occurs in SJS may also lead to chronic conjunctival scarring, loss of goblet cells with associated mucin deficiency, and obstruction of lacrimal gland ductules.…”

“…[19][20][21][22] Diagnosis of SJS was made in patients who had a history of biopsy-confirmed systemic SJS with ocular manifestations including aqueous tear deficiency, meibomian gland destruction, or cicatricial ocular changes. 23,24 The TearScience LipiView II Ocular Surface Interferometer ("LipiView Interferometer") (Johnson & Johnson Vision, Santa Ana, CA) noninvasively collects quantitative data about the lipid layer. The LipiView Interferometer also provides a detailed report including a graph describing the patient's blink pattern within the 20 sec testing period.…”

USA: Ophthalmologic Evaluation and Management of Acute Stevens-Johnson Syndrome

“…Damage to the eyelids in the acute phase can also be a significant source of longer term visual morbidity. Inflammation of the lid margins can cause occlusion of meibomian gland orifices and damage to the meibomian glands ( 11 , 12 ). Cicatricial changes may alter eyelid and eyelash anatomy, resulting in entropion, trichiasis, and distichiasis.…”