Average Scleral Lens Replacement Period at a Tertiary Care Hospital.

OBJECTIVE: To evaluate the average scleral lens replacement period at a tertiary care hospital. METHODS: Patients were identified retrospectively through electronic medical records. Inclusion criteria included scleral lens patients treated at the USC Department of Ophthalmology who had reordered a scleral lens at least once in one eye. Lens order histories were evaluated, and statistical analysis included a multivariable, mixed-methods, linear, regression model. RESULTS: Two hundred fifty-one patients (120 men and 131 women; average age 57.1±17.4 years, range 9-93 years) and a total of 445 eyes (227 OD, 218 OS; 199 irregular corneas, 246 ocular surface disease) were included. The average replacement period for a scleral lens was 23.9±14.3 months (range 5-2,617 days). Patients with greater scleral lens experience had a statistically significant increase in their average scleral lens replacement period; for every one year of additional experience wearing scleral lenses, average replacement period increased by 30.7 days ( P =0.001). There was no statistically significant correlation between average scleral lens replacement period and sex, diagnosis, prior outside scleral lens treatment, lens brand, or lens diameter. CONCLUSION: The average scleral lens replacement period in this patient cohort at a tertiary care hospital was 23.9±14.3 months (1.99±1.19 years). Further studies are needed to better understand the impact of scleral lens age on ocular health and vision. Certainly, proper scleral lens training and education are essential to ensure optimal lens condition and treatment outcomes.

The stimulatory G protein Gsα is required in melanocortin 4 receptor-expressing cells for normal energy balance, thermogenesis, and glucose metabolism.

Central melanocortin 4 receptors (MC4Rs) stimulate energy expenditure and inhibit food intake. MC4Rs activate the G protein Gsα, but whether Gsα mediates all MC4R actions has not been established. Individuals with Albright hereditary osteodystrophy (AHO), who have heterozygous Gsα-inactivating mutations, only develop obesity when the Gsα mutation is present on the maternal allele because of tissue-specific genomic imprinting. Furthermore, evidence in mice implicates Gsα imprinting within the central nervous system (CNS) in this disorder. In this study, we examined the effects of Gsα in MC4R-expressing cells on metabolic regulation. Mice with homozygous Gsα deficiency in MC4R-expressing cells (MC4RGsKO) developed significant obesity with increased food intake and decreased energy expenditure, along with impaired insulin sensitivity and cold-induced thermogenesis. Moreover, the ability of the MC4R agonist melanotan-II (MTII) to stimulate energy expenditure and to inhibit food intake was impaired in MC4RGsKO mice. MTII failed to stimulate the secretion of the anorexigenic hormone peptide YY (PYY) from enteroendocrine L cells, a physiological response mediated by MC4R-Gsα signaling, even though baseline PYY levels were elevated in these mice. In Gsα heterozygotes, mild obesity and reduced energy expenditure were present only in mice with a Gsα deletion on the maternal allele in MC4R-expressing cells, whereas food intake was unaffected. These results demonstrate that Gsα signaling in MC4R-expressing cells is required for controlling energy balance, thermogenesis, and peripheral glucose metabolism. They further indicate that Gsα imprinting in MC4R-expressing cells contributes to obesity in Gsα knockout mice and probably in individuals with Albright hereditary osteodystrophy as well.