Si Yoon Park

Analysis of Factors Associated With the Tear Film Lipid Layer Thickness in Normal Eyes and Patients With Dry Eye Syndrome

PURPOSE To determine the effects of clinical variables, including age, sex, history of refractive or cataract surgery, contact lens use, and ocular surface and meibomian gland parameters on the lipid layer thickness (LLT) in normal subjects and patients with dry eye syndrome (DES). METHODS A total of 64 normal subjects and 326 patients with DES were enrolled, and they underwent measurements of LLT with a LipiView interferometer and tear meniscus height using optical coherence tomography, tear film break-up time (TBUT) determination, ocular surface staining, Schirmers test, examination of the lid margins and meibomian glands, and assessment using the Ocular Surface Disease Index (OSDI). RESULTS In normal subjects, the median (range) LLT was 67 (33-100) nm, and age was the only factor that was significantly associated with LLT (β = 0.678, P = 0.028). In patients with DES, the median (range) LLT was 84 (20-100) nm, and 79.0% of the participants fulfilled the diagnostic criteria for meibomian gland dysfunction (MGD). In a multivariate analysis, increased age and female sex were significantly related to increased LLT (β = 0.282, P = 0.005 and β = 11.493, P < 0.001), and hypersecretory MGD and lid margin inflammation were independently associated with increased LLT (β = 11.299, P = 0.001 and β = 12.747, P = 0.001). CONCLUSIONS Lipid layer thickness measurements using a new interferometer are significantly affected by demographic factors such as age, sex, ocular surgical history, and MGD type. Therefore, all of these factors must be considered in the diagnosis of ocular surface diseases.

Photorefractive keratectomy combined with corneal wavefront-guided and hyperaspheric ablation profiles to correct myopia.

Purpose To evaluate the effects of photorefractive keratectomy (PRK) combined with corneal wavefront–guided ablation profiles and hyperaspheric ablation profiles on changes in higher‐order aberrations (HOAs). Setting Yonsei University College of Medicine and Eyereum Clinic, Seoul, South Korea. Design Comparative observational case series. Methods Medical records of patients who had corneal wavefront–guided hyperaspheric PRK, corneal wavefront–guided mild‐aspheric PRK, or non‐corneal wavefront–guided mild‐aspheric PRK were analyzed. The logMAR uncorrected distance visual acuity (UDVA), manifest refraction spherical equivalent (MRSE), and changes in corneal aberrations (root‐mean‐square [RMS] HOAs, spherical aberration, coma) were evaluated 1, 3, and 6 months postoperatively. Results The records of 61 patients (96 eyes) were reviewed. There was no statistically significant difference in logMAR UDVA or MRSE between the 3 groups at any timepoint. Corneal RMS HOAs were significantly smaller in the corneal wavefront–guided hyperaspheric group and the corneal wavefront–guided mild‐aspheric group than in the noncorneal wavefront–guided mild‐aspheric group at each timepoint. Corneal spherical aberration was significantly smaller for corneal wavefront–guided hyperaspheric PRK than for noncorneal wavefront–guided mild‐aspheric PRK 6 months postoperatively. Changes in corneal spherical aberration (preoperatively and 6 months postoperatively) in corneal wavefront–guided hyperaspheric PRK were significantly smaller than in corneal wavefront–guided mild‐aspheric PRK (P = .046). Corneal coma was significantly smaller with corneal wavefront–guided hyperaspheric PRK and corneal wavefront–guided mild‐aspheric PRK than with noncorneal wavefront–guided mild‐aspheric PRK 3 months and 6 months postoperatively. Conclusion Corneal wavefront–guided hyperaspheric PRK induced less corneal spherical aberration 6 months postoperatively than corneal wavefront–guided mild‐aspheric PRK and noncorneal wavefront–guided mild‐aspheric PRK. Financial Disclosure None of the authors has a financial or proprietary interest in any material or method mentioned.

Effects of Pigment Location in Tinted Contact Lenses on the Ocular Surface.

Purpose To evaluate the effects of the location of pigments in decorative tinted soft contact lenses on the ocular surface. Methods Thirty test subjects were enrolled in this study. All subjects wore the following types of contact lenses, classified according to the location of the pigment layer, in one eye in three different testing sessions: conventional clear lenses, tinted lenses with a pigment layer embedded in the lens matrix, and tinted lenses with an exposed pigment layer on the surface. Tear samples were collected, the ocular surface status was evaluated, and subjective symptoms were surveyed after lens wear for 8 hours. Results The tinted lenses with surface pigments resulted in a greater increase in epidermal growth factor and interleukin-8 levels compared with the clear lenses and tinted lenses with embedded pigments (p < 0.050). Ocular surface parameters and subjective symptom scores were significantly different among three lens types (p < 0.050), with the clear lenses showing superior results compared with the two tinted lenses (p < 0.050). The tinted lenses with exposed pigments resulted in a greater degree of conjunctival redness and ocular surface staining and poorer symptom scores compared with the tinted lens with embedded pigments (p < 0.050). Conclusions Our results suggest that the presence of surface pigments in tinted contact lenses increases ocular inflammation and results in a poorer ocular surface status and greater discomfort compared with clear lenses and tinted lenses with an embedded pigment layer.

Delayed Onset of Lattice Corneal Dystrophy Type IIIA Due to a Novel T621P Mutation in TGFBI

To the Editor: We recently identified a family with lattice corneal dystrophy type IIIA (LCD IIIA) associated with a novel threonine-to-proline (T621P) mutation in the transforming growth factor-beta induced (TGFBI) gene. The 50-year-old female proband (II-2) visited our clinic because of decreased visual acuity. Slit-lamp examination disclosed thick, branching, refractile, ropy lattice lines located in both stromal corneas, which extended to the limbus radially (Figures AA-AC, available in the online version of this article). The right cornea showed a higher number of lattice lines than the left cornea. Molecular analysis involving bidirectional complete sequencing demonstrated a novel T621P mutation in exon 14 of TGFBI. After we identified this new mutation, we performed genetic and clinical examinations on 10 other family members (Severance Hospital Institutional Review Board [No. 4-2014-1046]). The corneas of elderly affected members (I-1, II-1, and II-2) showed the LCD IIIA phenotype with asymmetry between both corneas, as reported for LCD IIIA. Three family members in their mid-twenties (III-1, III2, and III-4) had clear corneas despite having the mutated TGFBI gene (Figure AD). This suggests that the family had a late-onset form of LCD IIIA. The 26-year-old son of the proband (III-3), who had undergone LASIK 5 years earlier at a different facility, maintains clear corneas and showed no mutation in the recent genetic test. He was aware that his grandmother and mother had visual problems but was not aware of the genetic basis of the condition. Therefore, he did not notify the surgeon of any visual problems of the family before the LASIK procedure because he was not asked about them. The relatively late onset of LCD IIIA is favorable for young affected individuals in that visual acuity is well preserved until advanced age. However, the III-3 family member, who is the only one having the normal gene among the four genetically examined cousins, highlights the worrying possibility of young adults harboring the mutation but having clear corneas and undergoing LASIK.

Mechanical meibomian gland squeezing combined with eyelid scrubs and warm compresses for the treatment of meibomian gland dysfunction

The aim was to investigate the efficacy of mechanical meibomian gland squeezing combined with eyelid scrubs and warm compresses in participants with moderate and severe meibomian gland dysfunction (MGD).

The value of reliable genetic testing in refractive surgery candidates

To the Editor: The corneal deposits seen in heterozygote granular corneal dystrophy type 2 (GCD2) can be observed in individuals with variable appearances.1 When the deposits are small and at times undetectable, only genetic analysis is effective for the confirmative diagnosis. Many refractive surgeons have adopted genetic testing prior to refractive surgery to verify that their patients are free from the risk of exacerbation of GCD2 following LASIK, LASEK, or photorefractive keratectomy.2-4 As an example, a 30-year-old Korean woman visited the Corneal Dystrophy Clinic of Severance Hospital, Seoul, Korea in April 2016 with decreased visual acuity and fine central corneal deposits in both eyes (Figures 1A-1B). The corneal findings were representative of the typical appearance of exacerbated GCD2 after LASEK, as previously reported.2 She had received uneventful bilateral LASEK in September 2009 at a local Korean clinic. On presentation, her corrected distance visual acuity was 20/32 in the right eye and 20/63 in the left eye. Preoperative manifest refraction was -4.50 -2.50 × 175 in the right eye and -6.75 -1.50 × 175 in the left eye, yielding 20/20 in both eyes. One year after LASEK, the patient began to notice decreased visual acuity. Her preoperative medical record from the local clinic described four small subepithelial opacities on her right cornea with no deposits on the left cornea (Figure 1C). A preoperative gene test report for GCD2 from a local commercial company for detecting GCD2 mutation reported the patient as negative for the mutation. This company used a patented adhesive tape technique,5 applying the tape to the forearm for 20 seconds and then peeling it off to obtain the epidermal keratinocytes for DNA extraction, followed by polymerase chain reaction (PCR) and DNA sequencing. The additional collection of three hair follicles was used to ensure sufficient quantity of DNA. The company offered GCD2 gene testing services in 2009 and subsequently stopped testing in 2010. The surgeon performed LASEK after receipt of the negative GCD2 report. The patient was retested for GCD2 mutation after informed consent in our hospital using PCR and sequencing of DNA from peripheral blood with two different primers, which identified the patient to be a GCD2 heterozygote. In addition, the Avellino Universal Test (performed by Avellino Lab Korea using Avellino Lab USA’s proprietary technology), which uses buccal epithelial cells collected with a cotton swab, reported the patient to be a GCD2 heterozygote. These new tests demonstrate that the genetic test system performed in 2009 was inaccurate at notifying the surgeon of the patient’s GCD2 condition. The patient was not able to confirm whether she provided the three additional hair follicles for the test performed in 2009, which may have contributed to the test error. This case report shows the importance of reliable genetic testing before certain refractive surgical procedures. Tests performed by genetic testing laboratories using methods validated with clinical trials and the Clinical Laboratory Improvement Amendments certification or equivalent validation would provide the refractive surgeon with high confidence in the reported test results. Genetic testing that can detect all TGFBI mutations would certainly be welcome in the future.