Meibomian Gland Inflammation Research Articles

Intense Pulsed Light Therapy to Inhibit Meibomian Gland Inflammation: Untargeted Metabolomics Analysis of Meibomian Gland Secretions.

Objective: To assess the inhibitory effects of intense pulsed light (IPL) on meibomian gland (MG) inflammation. Background: IPL treatment is effective for dry eye disease (DED) caused by meibomian gland dysfunction (MGD). However, the anti-inflammatory and regeneration stimulating effects of IPL on MGD remain unclear. Moreover, studies on inflammatory metabolites in MG secretions are lacking. Methods: Six patients with DED were administered two IPL treatments. Ocular surface disease index (OSDI) questionnaires were used to assess DED, MGD signs, including degree of obstruction, secretion, and atrophy of the MG, tear film break-up time (TBUT) was assessed before and after treatments. To determine IPL treatment-induced changes in metabolites, liquid chromatography tandem mass spectrometry (LC-MS/MS) was used to analyze MG secretions. Results: Data were gathered before the first treatment (time A) and 2 weeks after the second treatment (time B). Average OSDI score showed a significant decrease (time A and B measurements were 44.07 and 16.65, respectively). Besides, statistically significant differences were observed in MG signs before and after treatments: degree of obstruction improved and secretions became thinner. TBUT was significantly increased to the normal range. LC-MS/MS led to the identification of 53 differential metabolites: 23 were upregulated (e.g., estradiol, coenzyme Q, and azelaic acid) and 30 were downregulated (e.g., prostaglandins, 20-hydroxyeicosatetraenoic acid, and arachidonic acid). Kyoto Encyclopedia of Genes and Genomes pathway enrichment analysis showed that most differential metabolites were involved in steroid hormone biosynthesis. Conclusions: Periorbital IPL treatment can improve chronic inflammation of the MG and promote its normal secretion. The steroid hormone biosynthetic pathways may be activated to participate in this anti-inflammatory effect.

Comparable meibomian gland changes in patients with and without ocular graft-versus-host disease after hematopoietic stem cell transplantation

PurposeTo compare the presentation and severity of meibomian gland dysfunction (MGD) in patients with and without chronic ocular graft-versus-host disease (coGVHD) after allogeneic hematopoietic stem cell transplantation (allo-HSCT). MethodsThis prospective cross-sectional study included 79 patients (47 with coGVHD and 32 without) after allo-HSCT. All participants completed ocular surface disease index questionnaire, and received slit lamp, ocular surface interferometer, meibography and confocal microscopy examination. The prevalence and severity of MGD were compared between two groups and related factors were analyzed. Main outcome measures were lipid layer thickness (LLT) and meiboscore. ResultsSimilarly high prevalence of MGD was detected in coGVHD and non-coGVHD groups (87.2% vs 84.4%, P = 0.977). Among those with MGD, although patients without coGVHD had longer noninvasive break-up time [5.54 (2.87, 9.37) vs 2.29 (0.00, 3.82) s, P < 0.001], patients in two groups presented similarly decreased LLT (53.5 ± 22.3 vs 47.1 ± 25.2 nm, P = 0.286), increased meiboscore (2.7 ± 1.5 vs 3.5 ± 1.8, P = 0.060) and enlarged acinar unit area (1647.7 ± 942.9 vs 1808.8 ± 1211.5 μm2, P = 0.592). Meibomian gland inflammation and fibrosis were observed in both groups, but more predominant in coGVHD group. Results were consistent when patients within a comparable post-HSCT time interval were compared. Regression analysis revealed neither LLT nor meiboscore was associated with coGVHD severity. LLT was positively correlated with systemic immunosuppressant use (β = 12.0, P = 0.044), while meiboscore was positively correlated with lymphoma (β = 1.78, P = 0.040) and matched unrelated donor (β = 1.59,P = 0.008). ConclusionsMGD was common and evident in patients after allo-HSCT. MGD is not different between coGVHD and non-coGVHD patients except more inflammation and fibrosis in the former.

Inflamed Obstructive Meibomian Gland Dysfunction Causes Ocular Surface Inflammation.

Meibomian gland dysfunction (MGD) is one of the primary causes of evaporative dry eye. Stagnation of meibum induces an unstable tear film, thus resulting in shortened tear film breakup time and superficial punctate keratopathy (SPK) in the lower cornea and punctate staining of lower bulbar conjunctiva. MGD is sometimes accompanied with inflammation (termed "meibomitis") via the proliferation of bacteria in the meibomian gland and eyelash area. Meibomitis is strongly related to ocular surface inflammation such as corneal cellular infiltrates and neovascularization, SPK, and conjunctivitis. It is difficult to differentiate SPK caused by dry eye from that caused by meibomitis. When clinicians are unaware of the existence of meibomitis, and only aware of SPK on the cornea, they often try to treat SPK as it is caused by dry eye using dry eye-specific eyedrops or even using punctual plugs when conservative therapy is ineffective. However, even when intensive dry eye therapy is applied, it may be unsuccessful until SPK caused by meibomitis is recognized and treated with systemic antimicrobial agents. Hence, the tear secreting glands, including the meibomian glands, and the ocular surface should be clinically considered as one unit (i.e., the meibomian gland and ocular surface [MOS]) when considering the pathophysiology and treatment of ocular surface inflammatory diseases (i.e., corneal epithelial damage). Following this clinical pathway, a treatment focusing on meibomian gland inflammation may be a more reasonable approach for meibomitis-related or associated keratoconjunctivitis to more effectively treat this ocular surface disease.

Pediatric blepharokeratoconjunctivitis: is there a 'right' treatment?

This article highlights the importance of recognizing blepharokeratoconjunctivitis (BKC) in children and reviews the clinical characteristics and current therapeutic modalities. The mainstay of BKC treatment remains controlling the meibomian gland inflammation and treating cobormid conditions. BKC can occur in the setting of ocular rosacea and Demodex infestation. Small studies have shown treatment benefits of topical cyclosporine A as well as oral azithromycin in pediatric BKC. BKC is a cause for visual loss in children, and therefore pediatric ophthalmologists should be more vigilant about early diagnosis and long-term treatment. There is a lack of randomized controlled trials on this topic and no standardized outcome measures. Better ways to measure the clinical outcome of various treatment modalities need to be developed.

Meibomitis-Related Keratoconjunctivitis

Meibomian gland inflammation, "meibomitis," is associated with ocular surface inflammatory diseases. However, these diseases are poorly defined clinically, making effective treatment difficult. Herein, we propose a new disease subset, termed meibomitis-related keratoconjunctivitis (MRKC). The ocular surface features of MRKC include: meibomitis with redness and swelling of the eyelid margin and palpebral conjunctiva; superficial vascularization and granulomatous nodules in the cornea; and conjunctival hyperemia, similar or identical to that observed in phlyctenular keratitis. The characteristics of MRKC patients include a significantly higher prevalence in women, multiple history of chalazia, close association with meibomitis, the presence of specific human leukocyte antigen association, high Propionibacterium acnes detection rates in meibum culture, and the effectiveness of systemic antimicrobial therapy targeting P. acnes. MRKC may share many clinical features with ocular rosacea, especially during childhood. The clinical effectiveness of systemic antimicrobial agents in treating both diseases suggests the importance of focusing on the elimination of bacteria such as P. acnes.

Tear function changes of postmenopausal women in response to hormone replacement therapy

Objective: The goal of this study was to search the effect of hormone replacement therapy (HRT) on tear function changes in postmenopausal women. Methods: Following initial ophtalmic evaluation and tear sample collection, the subjects were given daily 0.625 mg conjugated estrogen, and either continuous combined or cyclic 5 mg medroxyprogesterone acetate was added. Eye examination included visual acuity, slit-lamp examination, fundus examination, tonometry, Schirmer's test, and break up time (BUT) evaluation. Six months later, control examination was done and repeat tear samples were obtained. Tear immune globulin A (IgA) and lysozyme levels were measured by gel electrophoresis. The pictures of the bands were evaluated by digital image analysis with Scion Image program. Results: Conjunctival vascular congestion, laxity and corneal desquamation did not change before and after HRT ( P>0.05). A significant improvement was noted in meibomian gland inflammation ( P=0.034). We have not observed any significant difference in burning, foreign body sensation, and tearing ( P>0.05). In addition, no significant difference was noted in BUT ( P=0.370) and Schirmer's test values ( P=0.271). Though both lysozyme and IgA levels were elevated following the therapy, only IgA levels increased significantly ( P=0.04) ( Fig. 2). Conclusion: HRT decreased meibomian gland inflammation and increased tear lysozyme and IgA levels in postmenopausal women.

Oral erythromycin treatment for childhood blepharokeratitis

Blepharokeratitis is a chronic external ocular and adnexal inflammatory condition marked by erythematous and edematous lid margins, lid margin crusting and scaling, meibomian gland inflammation and inspissation, and conjunctival hyperemia. The associated keratitis usually involves the inferior cornea and is characterized by punctate epithelial keratopathy and marginal stromal infiltrates. The inflammation sometimes leads to corneal thinning, scarring, and vascularization. The standard therapy for adult blepharokeratitis includes lid hygiene, topical cortico-steroid preparations, and topical antibiotics. Oral tetracycline and its analogues, doxycycline and minocycline, are used in adults to treat associated meibomian gland dysfunction. Whereas blepharitis is common in children, blepharokeratitis is rare and is often associated with severe ocular and psychosocial morbidity. Treatment of youths may be problematic because of poor compliance with lid hygiene and therapy that includes drops and ointment.1 Furthermore, the use of tetracycline and its analogues is contraindicated in children aged less than 8 years because it may cause dental enamel abnormalities. Isolated case reports have suggested that erythromycin may be a reasonable alternative to tetracycline in childhood blepharokeratitis.2,3 We report on the successful treatment of this condition with oral erythromycin in 5 children.J AAPOS 2000;4:379-80.

Acne Rosacea With Keratitis in Childhood

We present three cases of acne rosacea keratitis that developed in childhood. All three children were prepubescent and demonstrated characteristic dermatologic findings involving the nose, cheeks, and/or chin. The patients had complained of ocular irritation for at least 6 months, and in one case symptoms were reported by the family to have occurred intermittently since age 4 years. All three children showed evidence of meibomian gland inflammation; two patients demonstrated bilateral keratitis, the third had only unilateral involvement. In each case, oral tetracycline hydrochloride or doxycycline hyclate was necessary to relieve symptoms. Rosacea keratitis should be considered in the differential diagnosis of chronic keratoconjunctivitis during childhood.