Off the Cuff: 1-800 Contacts’ True Colors

Researchers wrote that benzalkonium chloride (BAK) is the most commonly used eye drop preservative. However, they added, BAK has been associated with toxic effects such as dry eye and trabecular meshwork degeneration, but the underlying biochemical mechanism of ocular toxicity by BAK is unclear. In their study, they suggested a mechanistic basis for BAK's adverse effects. Mitochondrial O2 consumption rates of human corneal epithelial primary cells (HCEP), osteosarcoma cybrid cells carrying healthy (control) or Leber’s hereditary optic neuropathy (LHON) mutant mtDNA [11778(G>A)], were measured before and after acute treatment with BAK. Mitochondrial adenosine triphosphate (ATP) synthesis and cell viability were also measured in the BAK-treated control including LHON mutant and human-derived trabecular meshwork cells (HTM3).

Benzalkonium chloride inhibited mitochondrial ATP (IC50, 5.3μm) and O2 consumption (IC50, 10.9μm) in a concentration-dependent manner, by directly targeting mitochondrial complex I. At its pharmaceutical concentrations (107μm to 667μm), BAK inhibited mitochondrial function >90%. In addition, BAK elicited concentration-dependent cytotoxicity to cybrid cells (IC50, 22.8μm) and induced apoptosis in HTM3 cells at similar concentrations. Furthermore, researchers showed that BAK directly inhibited mitochondrial O2 consumption in HCEP cells (IC50, 3.8 μM) at 50-fold lower concentrations than used in eye drops and that cells bearing mitochondrial blindness (LHON) mutations were further sensitized to BAK's mitotoxic effect.

In this study, BAK inhibited mitochondria of human corneal epithelial cells and cells bearing LHON mutations at pharmacologically relevant concentrations. Researchers suggested that this is the basis of BAK's ocular toxicity. They added that prescribing BAK-containing eye drops should be avoided in patients with mitochondrial deficiency, including LHON patients, LHON carriers and possibly primary open-angle glaucoma patients.

Recent studies have demonstrated that pterygium has a close relationship with dry eye disease. This study aimed to determine abnormalities in meibomian gland and tear function in patients with pterygium, and to assess the relationship between the variables. Forty eyes from 40 patients with primary nasal pterygium, and 40 eyes from 40 volunteers without ocular pathologies were enrolled. Ocular surface disease index scores, meibomian gland expression scores, lid margin abnormality scores, meiboscore, tear film breakup time (BUT), Schirmer test (SIT) value, lower tear meniscus height (TMH), tear meniscus depth (TMD) and tear meniscus area (TMA) using Fourier domain optical coherence were performed.

Ocular symptom scores, BUT scores, lid margin abnormality, meibomian gland expression and meiboscore were significantly higher in pterygium patients than in controls. However, SIT scores, lower TMH, TMD and TMA values did not reveal a significant difference between two groups. Multivariate regression analysis demonstrated that meiboscore significantly correlated with ocular symptom scores, BUT, lid margin abnormality scores and meibomian gland expression scores.

Investigators wrote that meibomian gland function may be altered in pterygium patients, a condition that is associated with uncomfortable ocular symptoms. They encouraged the need for clinician awareness of meibomian gland changes to understand the complex relationship between pterygium, tear film functions and ocular surface changes.

This study explored changes in the phenotypic features of Sjögren's syndrome (SS) and in SS status among participants in the Sjögren's International Collaborative Clinical Alliance (SICCA) registry over a two- to three-year interval. All participants in the SICCA registry who were found to have any objective measures of salivary hypofunction, dry eye, focal lymphocytic sialadenitis in minor salivary gland biopsy or anti-SSA/B antibodies were recalled over a window of two to three years after their baseline examinations to repeat clinical examinations and specimen collections. This goal was to determine whether there was any change in phenotypic features and in SS status.

As of September 15, 2013, 3,514 participants had enrolled in SICCA, and of the eligible 3,310, 771 presented for a follow-up visit. Among individuals found to have SS using the 2012 ACR classification criteria, 93% again met the criteria after two to three years, and this proportion was 89% when using the 2016 ACR-EULAR criteria. Those who did not meet ACR or ACR-EULAR criteria at baseline, 9% and 8%, respectively, progressed and met the criteria at follow-up. Those with hypergammaglobulinemia and hypocomplementemia at study entry were respectively four and six times more likely to progress to SS by ACR criteria than those without these characteristics (95% confidence interval: 1.5 to 10.1; and 1.8 to 20.4, respectively).

While there was stability of both individual phenotypic features with SS and of SS status over a two- to three-year period, hypergammaglobulinemia and hypocomplementemia at study entry were predictive of progression to SS.