Friday, June 1, 2012

A day in the life...

(deep breath)

A bad eye day.


I worked myself into such a foul mood over it that I finally went on to DryEyeTalk and started writing a "Need to vent" post. Never finished it.

Here's the draft:

I'm sitting here wearing one of my own stupid !@#$ products (single eye pressure patch), hating it, not just because of the stupid elastic strap sliding all over my hair and my eyebrows and because I don't even know which way the thing goes, but because I'm not sure whether it's helping the pain enough to make it worth the awful pressure it puts on my eye.
...I'm frustrated to pieces that I can't seem to get a dry eye bulletin out the door even after all this time. There's been so much interesting stuff published recently and I hate it when the bulletin gets pushed out from week to week because I'm either too tired or just don't have enough good eye time left at the end of the day. I used to do it after my daughter went to bed Thursday nights but my body staged a sit-in in favor of no more late nights working, so now I always think I'll squeeze it in by doing a bit of blogging early every morning but that never seems to happen. Finally a couple of nights ago - not listening to my left eye which was quietly murmuring "Please don't make me work to hard and for goodness' sakes don't overwear your PROSE this week or I might just throw a hissy fit" - I stayed up late to update my blog (only to realize afterwards that I only did the blogspot one and forgot to duplicate it on DryEyeTalk like I usually do). Took note of increased rumblings from the left eye yesterday but figured it would go away and went about my usual routine.
...So this morning my eyes were both in a state where I didn't dare put my lenses in. Started work, and it was all downhill from there. Eventually I put the right lens in because if there's anything worse than being in pain when you're trying to work, it's be in pain and not being able to !@#$ see when you're trying to work. Result, my left (normally by far the better) eye is just plain exploding in pain - and i honestly don't even know if it really is worse or if it's just the contrast now that I have PROSE in my right eye. I'd really like to just ignore the world and go sit outside with my sheep because I was away most of the day yesterday and as so often seems to happen am soooo behind on things.

At that point my daughter (who had done an admirable job of bearing with all my pain-and-stress-induced grouchiness all morning) walked in and placed a card on my desk and walked back out.

I opened it up and saw:

What's a doting mother to do but melt into a glob of grateful jelly. Yes, she turned my corners up. And I went over to my keyboard (the other kind of keyboard) and sang "Count your blessings" and "Redeemed" until they were fixed even more firmly in the upright position. And they really needed to be for what came next, because....

After she persuaded me to take out my right lens and go lie down, I went into the bathroom, took my prose case (which contained my left lens since I wasn't wearing it) out of the cupboard and... unaccountably dropped it on the floor.

Picked it up and it contained no left lens.

We scoured the bathroom over and over and over. No lens. Shook out my clothes, checked the drain, everything.

No lens.

Seems to have disappeared into thin air.

At that point we turned to comfort food. Hamburgers, mashed potatoes, and leftover cheesecake.

Tomorrow will be better :-) Meanwhile I'm grateful for what I have.

UPDATE (6/4). Later that day while we were preparing for company, my daughter was cleaning the bathroom and put her hand under the sink cabinet in search of a marble. Guess what was lodged just behind the marble. It apparently bounced there. We think the Lord was protecting it from being stepped on when it first flew out of the case because it took me a couple moments before I realized it was gone. I'm still not wearing the lenses though - right now both my lenses are on their way to Boston (they were overdue for a new plasma coating) and hopefully I will be back in business soon.

Wednesday, May 30, 2012

Abstract: CPAP nasal pillow & Jones tubes

I think this case report might be about someone I once spoke with. The situation was that the CPAP device was blowing air so forcefully up the Jones tubes that it was pushing up her lids and affecting her eyes.

Since then I have spoken with a few people who either believed, or suspected, or from their description I myself suspected, were suffering from the same effect but without the Jones tubes. I posted about it once before in my newsletter hoping to drum up more information but no such luck. When I saw this case report I emailed the author asking if this was a credible explanation (i.e. that CPAP pressure could force air the wrong way through the canaliculus) and he felt it might given sufficient pressure to bypass the valves in the lacrimal system. Anyway, just putting this out there for what it's worth. There are so many people using CPAP these days, surely we'll here more in the next few years.

A 49-year-old woman, who had previously undergone bilateral Jones tube placement, began nasal continuous positive airway pressure for obstructive sleep apnea. The patient's use of continuous positive airway pressure was limited by intolerance of the transfer of air through the Jones tube to her ocular surface resulting in irritation and discomfort. A change from nasal continuous positive airway pressure to a full face mask, including both Jones tubes in the pressure circuit, resolved the problem.

Ophthal Plast Reconstr Surg. 2012 May 21. [Epub ahead of print]
Servat JJBlack EHGladstone GJ.
*William Beaumont Hospital, Department of Ophthalmology, Royal Oak, Michigan, U.S.A. †Kresge Eye Institute/Wayne State University, St. Antoine Detroit, Michigan, U.S.A.

Abstract: Bleph, blech

When I was compiling a list of abstracts to look at and blog about recently, the note I made on this one was "Depressing bleph lit review". Musta been one of those days when I was talking to a lot of depressed people and I was thinking this would not be an appropriate one for them to read :-) You might want to skip it if you're not feeling good. Or at least keep in mind that the authors' conclusions are talking about cure as opposed to successful management.

Blepharitis, an inflammatory condition associated with itchiness, redness, flaking, and crusting of the eyelids, is a common eye condition that affects both children and adults. It is common in all ethnic groups and across all ages. Although infrequent, blepharitis can lead to permanent alterations to the eyelid margin or vision loss from superficial keratopathy (abnormality of the cornea), corneal neovascularization, and ulceration. Most importantly, blepharitis frequently causes significant ocular symptoms such as burning sensation, irritation, tearing, and red eyes as well as visual problems such as photophobia and blurred vision. The exact etiopathogenesis is unknown, but suspected to be multifactorial, including chronic low-grade infections of the ocular surface with bacteria, infestations with certain parasites such as demodex, and inflammatory skin conditions such as atopy and seborrhea. Blepharitis can be categorized in several different ways. First, categorization is based on the length of disease process: acute or chronic blepharitis. Second, categorization is based on the anatomical location of disease: anterior, or front of the eye (e.g. staphylococcal and seborrheic blepharitis), and posterior, or back of the eye (e.g. meibomian gland dysfunction (MGD)). This review focuses on chronic blepharitis and stratifies anterior and posterior blepharitis.
To examine the effectiveness of interventions in the treatment of chronic blepharitis.
We searched CENTRAL (which contains the Cochrane Eyes and Vision Group Trials Register) (The Cochrane Library 2012, Issue 1), MEDLINE (January 1950 to February 2012), EMBASE (January 1980 to February 2012), the metaRegister of Controlled Trials (mRCT) (, ( and the WHO International Clinical Trials Registry Platform (ICTRP) ( We searched the reference lists of included studies for any additional studies not identified by the electronic searches. There were no date or language restrictions in the electronic searches for trials. The electronic databases were last searched on 9 February 2012.
We included randomized controlled trials (RCTs) and quasi-randomized controlled trials (CCTs) in which participants were adults aged 16 years or older and clinically diagnosed with chronic blepharitis. We also included trials where participants with chronic blepharitis were a subset of the participants included in the study and data were reported separately for these participants. Interventions within the scope of this review included medical treatment and lid hygiene measures.
Two authors independently assessed search results, reviewed full-text copies for eligibility, examined risk of bias, and extracted data. Data were meta-analyzed for studies comparing similar interventions and reporting comparable outcomes with the same timing. Otherwise, results for included studies were summarized in the text.
There were 34 studies (2169 participants with blepharitis) included in this review: 20 studies (14 RCTs and 6 CCTs) included 1661 participants with anterior or mixed blepharitis and 14 studies (12 RCTs and 2 CCTs) included 508 participants with posterior blepharitis (MGD). Due to the heterogeneity of study characteristics among the included studies, with respect to follow-up periods and types of interventions, comparisons, and condition of participants, our ability to perform meta-analyses was limited. Topical antibiotics were shown to provide some symptomatic relief and were effective in eradicating bacteria from the eyelid margin for anterior blepharitis. Lid hygiene may provide symptomatic relief for anterior and posterior blepharitis. The effectiveness of other treatments for blepharitis, such as topical steroids and oral antibiotics, were inconclusive.
Despite identifying 34 trials related to treatments for blepharitis, there is no strong evidence for any of the treatments in terms of curing chronic blepharitis. Commercial products are marketed to consumers and prescribed to patients without substantial evidence of effectiveness. Further research is needed to evaluate the effectiveness of such treatments. Any RCT designed for this purpose should separate participants by type of condition (e.g. staphylococcal blepharitis or MGD) in order to minimize imbalances between groups (type I errors) and to achieve statistical power for analyses (prevent type II errors). Medical interventions and commercial products should be compared with conventional lid hygiene measures, such as warm compresses and eyelid margin washing, to determine effectiveness, as well as head-to-head to show comparative effectiveness between treatments. Outcomes of interest should be patient-centered and measured using validated questionnaires or scales. It is important that participants be followed long-term, at least one year, to assess chronic outcomes properly.

Cochrane Database Syst Rev. 2012 May 16;5:CD005556.
Center for Clinical Trials, Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, 615 North Wolfe Street, W5010, Baltimore, Maryland, USA, 21205.

Abstract: What serial aberrometry might tell or confirm

This one was surprisingly interesting. They performed serial wavefront aberrometry over a 10-second period after the patients blink. (For those who aren't familiar with that, aberrometry measures aspects of your vision such as reduced contrast sensitivity and poor vision quality, not just your vision in terms of what line you can read on the chart and what prescription you need to optimize it.) The pattern of how vision degraded in that time span correlated with what patients said about their vision and also with their clinical dry eye test results, so the authors suggest this test method be incorporated in dry eye evaluation.

Corneal and ocular wavefront aberrations were recorded together with clinical examination results and patient-reported vision-related quality-of-life evaluation results to define the relevance of dynamic optical analysis of the eye in dry eye disease (DED).
Prospective and comparative clinical study.
Forty DED patients and 40 age- and gender-matched control subjects.
Serial measurements of ocular and corneal higher-order aberrations (HOAs) after blink were performed for 10 seconds using the KR-1 aberrometer (Topcon, Clichy, France). Vision-related health-targeted quality of life was evaluated using the Ocular Surface Disease Index (OSDI) questionnaire. The clinical examination included tear film assessment (tear film break-up time and Schirmer I test), ocular surface damage assessment with the Oxford and van Bijsterveld indexes, and Meibomian dysfunction grading. Tear osmolarity also was measured.
The time course of HOAs and modulation transfer function (MTF) was compared between groups and was analyzed in comparison with the OSDI and clinical data in DED patients.
The root mean square of ocular and corneal total HOAs, particularly third-order aberrations, significantly increased over the 10-second period in DED patients, whereas no change occurred in controls. Analysis of MTF revealed progressive degradation of ocular optical quality resulting from loss of contrast at intermediate and high spatial frequencies in DED patients compared with controls. The progression index for corneal HOAs was correlated with the subjective index of patient-reported visual outcomes and with objective clinical findings of tear film and ocular surface damage.
Objective measurement of the time course of HOAs may constitute a new single instrument to evaluate and manage patients with DED because it reliably reflects the completeness of the disease.
The author(s) have no proprietary or commercial interest in any materials discussed in this article.

Ophthalmology. 2012 May 14. [Epub ahead of print]
Quinze-Vingts National Ophthalmology Hospital, Paris, France; INSERM, UPMC University Paris, Institut de la Vision, Paris, France.

Abstract: MGD

Kind of a nice blurb summarizing some barebones facts most of us know :-)

Meibomian gland dysfunction (MGD) is a chronic disease, usually caused by obstruction of the secretory Meibomian glands. The subsequent reduction of gland secretion results in a decreased amount of lipids in the tear film. This results in a faster evaporation of the tear film and thus an evaporative dry eye. MGD alone is responsible for about 60 % of all cases in combination with aqueous deficiency for a further 20 % of dry eyes. While in Europe up to 20 % of the population are suffering from MDD, this is true in Asia for over 60 % of the population. MGD is more common in women and it incidence increases with age. It is influenced by the hormonal status as well as chemical and mechanical noxious stimuli. Additional risk factors include various skin diseases such as rosacea, acne or atopy. To diagnose MGD, particular attention should be paid to changes in the lid margin such as plugging or pouting of the ducts, thickening and telangiectasia. However, most important is the diagnostic expression of the glands. At first it should be assessed whether secretion can be caused by pressure to the eyelid against the globe and secondly the quality of the expressed secretions should be evaluated. MGD should be treated according to the severity of the disease. While in mild stages instructions for lid margin hygiene, warming and massage in combination with artificial tears might be sufficient, in more severe stages oral tetracyclin derivatives and anti-inflammatory eye drops such as steroids or CSA are necessary for successful treatment.

Klin Monbl Augenheilkd. 2012 May;229(5):506-13. Epub 2012 May 16.
Abteilung für Augenheilkunde, Bundeswehrkrankenhaus Ulm.

Abstract: Corneal neovascularization and what tears can tell us about it

Corneal neovascularization results from the encroachment of blood vessels from the surrounding conjunctiva onto the normally avascular cornea. The aim of this study is to identify factors in human tears that are involved in development and/or maintenance of corneal neovascularization in humans. This could allow development of diagnostic tools for monitoring corneal neovascularization and combination monoclonal antibody therapies for its treatment. In an observational case-control study we enrolled a total of 12 patients with corneal neovascularization and 10 healthy volunteers. Basal tears along with reflex tears from the inferior fornix, superior fornix and using a corneal bath were collected along with blood serum samples. From all patients, ocular surface photographs were taken. Concentrations of the pro-angiogenic cytokines interleukin (IL)-6, IL-8, Vascular Endothelial Growth Factor (VEGF), Monocyte Chemoattractant Protein 1 (MCP-1) and Fas Ligand (FasL) were determined in blood and tear samples using a flow cytometric multiplex assay. Our results show that the concentration of pro-angiogenic cytokines in human tears are significantly higher compared to their concentrations in serum, with highest levels found in basal tears. Interestingly, we could detect a significantly higher concentration of IL- 6, IL-8 and VEGF in localized corneal tears of patients with neovascularized corneas when compared to the control group. This is the first study of its kind demonstrating a significant difference of defined factors in tears from patients with neovascularized corneas as compared to healthy controls. These results provide the basis for future research using animal models to further substantiate the role of these cytokines in the establishment and maintenance of corneal neovascularization.

PLoS One. 2012;7(5):e36451. Epub 2012 May 9.
Zakaria N, Van Grasdorff S, Wouters K, Rozema J, Koppen C, Lion E, Cools N, Berneman Z, Tassignon MJ.
Department of Ophthalmology, Antwerp University Hospital, Antwerp, Belgium.

Abstract: MGD & aging; retinoic acid and anti-aging skin products

Before you 20-somethings dismiss the study mentioned below as not relevant (after all, it's titled "Aging and dry eye disease") don't. This is another keeper that I had to get a copy of in its entirety.

First, this study zooms in on what we know, and don't, and need to find out, about how the meibomian glands change as we age. We know that there is an age-related increase in MGD (the leading cause of dry eye disease), but we don't know why, and this study looks at a number of possible mechanisms that might be gradually eroding their  healthy function. Of course, anything we can learn about the mechanism of natural change in the glands could conceivably be helpful for understanding MGD disease processes - and treatments - even where aging is not a factor. Anyway, the potential mechanisms of MGD suggested in the study are androgens, stem cells, growth hormone/IGF-1, insulin sensitivity, and converging signal FOXOs (don't ask me to explain what that means!)

Second, it identifies retinoic acid as a cause of MGD and dry eye disease and warns of the proliferation of anti-aging products that contain it:
Anti-aging skin care products, of which retinoids-based products are a major component, showed an annual growth rate of 11.8% from 2002 to 2007 and 9.7% from 2007 to 2012, far exceeding all the other skin care products combined…. Unfortunately one side effect of RA cream is dryness of the skin. In fact, retinoic acid (RA), also known as isotretinoin or Accutane, was initially used to treat acne before it found its way into the anti-aging cosmetics. It is highly effective in reducing sebaceous gland size by inhibiting sebocyte proliferation, differentiation and sebum production…. Not surprisingly, RA causes MGD and dry eye disease, given that meibomian gland is a sebaceous gland. 408 RA causes keratinization and thickening of the meibomian gland ducts…, degeneration and necrosis of the acinar cells, fibrosis of the periacinar tissue, and reduced lipid content in meibomian gland…. Further, isotretinoin exposure is associated with tear film instability and hyperosmolarity, dry eye symptoms and blepharitis…. In effect, RA promotes MGD and evaporative dry eye disease.
Anyway, here's the abstract:

Aging and dry eye disease.
Dry eye disease is a prevalent eye disorder that in particular affects the elderly population. One of the major causes of dry eye, meibomian gland dysfunction (MGD), shows increased prevalence with aging. MGD is caused by hyperkeratinization of the ductal epithelium of meibomian gland and reduced quantity and/or quality of meibum, the holocrine product that stabilizes and prevents the evaporation of the tear film. Of note, retinoids which are used in current anti-aging cosmetics may promote the development of MGD and dry eye disease. In this review, we will discuss the possible mechanisms of age-related MGD.

Exp Gerontol. 2012 Apr 28. [Epub ahead of print]
Ding J, Sullivan DA.

Abstract: More on booze and dry eye

Since the study authors failed to say what they meant by "heavy drinking", I looked up what CDC says: 

For men, heavy drinking is typically defined as consuming an average of more than 2 drinks per day. For women, heavy drinking is typically defined as consuming an average of more than 1 drink per day.

On the other hand, since the study doesn't talk about women, I guess we ladies don't have anything to worry about (LOL). 

To evaluate the tear film function and ocular surface changes in heavily drinking men.
This prospective case-control study involved 35 male subjects with heavy alcohol consumption (group 1) and 35 age- and sex-matched control subjects (group 2). Best-corrected visual acuity measurement, slit-lamp examination, Schirmer I test, tear film break-up time (BUT) measurement, and conjunctival impression cytology were performed in all subjects. The results were compared between the 2 groups.
The mean Schirmer I test results in group 1 and group 2 were 8.31 ± 3.56 mm and 13.17 ± 5.71 mm, respectively, and the mean BUT values were 9.22 ± 3.10 seconds and 13.20 ± 4.04 seconds, respectively. The mean Schirmer I and BUT results were statistically lower in group 1 than in group 2 (P < 0.0001). The mean impression cytology scores in group 1 and group 2 were 2.08 ± 0.78 and 1.37 ± 0.94, respectively. A statistically significant difference was noted between the study and control groups for the grading of cytological changes (P = 0.001).
Our data showed that heavily drinking men have decreased tear production, tear film instability, and significant degeneration of the ocular surface epithelium when compared with normal subjects.

Cornea. 2012 May 10. [Epub ahead of print]
Departments of *Ophthalmology †Psychiatry ‡Pathology, Inonu University School of Medicine, Malatya, Turkey.

Abstract: TearLab

To evaluate tear osmolarity with the recently introduced TearLab system (TearLab Corporation, San Diego, CA) in patients with non-Sjögren syndrome dry eye (NSSDE) and Sjögren syndrome dry eye (SSDE), and in healthy subjects, and to compare the results with those from classical dry eye tests.
Thirty-nine eyes of 21 patients with NSSDE, 39 eyes of 20 patients with SSDE, and 44 eyes of 22 healthy individuals were included in the study. Tear osmolarity was measured with the TearLab system, lid-parallel conjunctival folds score was examined with the slit lamp, and then the classical diagnostic tests such as Schirmer I test, tear film break-up time, and corneal staining were carried out, followed by the examination of meibomian glands and corneal transparency.
Mean tear osmolarity was 296.77 ± 16.48 mOsm/L in NSSDE (15% abnormal), 303.36 ± 17.22 mOsm/L in SSDE (23% abnormal), and 303.52 ± 12.92 mOsm/L in the control group (16% abnormal; P = 0.018, Kruskal-Wallis). Schirmer test, corneal staining, tear film break-up time, and meibomian gland status were significantly different in the 2 patient groups when compared with those in the control group (P < 0.0001). In the control and SSDE groups, no significant correlation was disclosed between tear osmolarity and any of the dry eye tests performed.
Tear hyperosmolarity is considered a key factor that leads to dry eye symptoms and to the progression of clinical signs. Osmolarity measurements with the TearLab system disclosed no ability to distinguish between healthy individuals and patients with dry eye. This suggests that the TearLab device should not be used alone but in combination with classical dry eye tests.

Cornea. 2012 May 10. [Epub ahead of print]
Szalai E, Berta A, Szekanecz Z, Szûcs G, Módis L Jr.
*Department of Ophthalmology, Medical and Health Science Center, University of Debrecen, Debrecen, Hungary †Department of Rheumatology, Institute of Medicine, Medical and Health Science Center, University of Debrecen, Debrecen, Hungary.

Abstract: Hylo-Comod vs preserved Optive


The stated purpose of this study is to compare unpreserved artificial tears to artificial tears preserved with Purite (one of the so-called dissipating or "preservative-free in the eye" preservatives). They induce epithelial defects in mice and then compare treating them with Hylo Comod (an unpreserved sodium hyaluronate drop) vs Optive (the version preserved with Purite). 

Both drops did their job as regards healing but the Optive caused superficial "stippling" of the cornea and as the authors point out, artificial tears are supposed to help dry eye, not cause it, so theres a strike against Optive.

However... seems to me that if you want to look at the effects of Purite y'oughtta be comparing preserved Optive to unpreserved Optive. 

Preservatives in artificial tears cause controversy. New developments such as the Purite® system have been introduced into the market, with the promise of little damage to the corneal surface. We wanted to give insight into the differences in the effect of preserved and unpreserved artifical tears on rabbit corneas cultured with the Ex Vivo Eye Irritation Test (EVEIT) system.
We compared the two artifical tears products Hylo Comod® and Optive® being dropped for 72 hours each hour one drop onto the corneal surface.
Each cornea was mechanically wounded with four epithelial defects on each cornea with a size of 3 to 4.5 mm(2). With n=4 corneas in the Hylo-Comod® and n=4 corneas in the Optive® group, we exposed the corneal surfaces to repeated doses of these artificial tears for 3 days. We observed healing of corneal erosions and surface epithelial integrity with sodium-fluoresceine staining under cobalt blue light illumination.
We found nearly complete healing of epithelial defects with both artificial tears. The Hylo-Comod® group healed significantly faster. After 72 hours, the vast majority of epithelial defects were closed. All corneas exposed to Purite® showed superficial stippling, whereas the HyloComod® group did not show any stippling of the cornea; this difference was significant.
Epithelial healing and recovery in the EVEIT system is observed in both groups, confirming the concept of artificial tears as a supporting factor of corneal health and healing. The superficial stippling of the corneal epithelium was observed only in the Optive® group. This effect is considered as a marker of dry eye syndrome, and should be prevented by the application of artificial tears. Preservative-free eye drops such as HyloComod® improve healing, and prevent symptoms of dry eye syndrome in the EVEITsystem. Compared to EVEIT results of former experiments with benzalconium chloride-preserved eye drops, Optive® promoted healing of corneal erosions.

Graefes Arch Clin Exp Ophthalmol. 2012 May 15. [Epub ahead of print]
ACTO e.V. An-Institut der medizinischen Fakultät RWTH Aachen, Karlsburgweg 9, 52070, Aachen, Germany,

Abstract: Topical cilomilast (mouse study)

PDE4 Inhibition Suppresses IL17-Associated Immunity in Dry Eye Disease.

I haven't updated the clinical trial roster in eons but I think this is what I once had listed as Alcon's AL-43546.

To determine the effect of phosphodiesterase type-4 (PDE4) inhibition on IL17- associated immunity in experimental dry eye disease (DED).
Murine DED was induced, after which a PDE4 inhibitor (cilomilast), dexamethasone, cyclosporine, or a relevant vehicle was administered topically. Real-time polymerase chain reaction, immunohistochemical staining, and flow cytometry were employed to evaluate the immuno-inflammatory parameters of DED with a focus on IL17-associated immunity. Corneal fluorescein staining (CFS) was performed to evaluate clinical disease progression.
DED induction increased proinflammatory cytokine expression, pathogenic immune cell infiltration, and CFS scores. Cilomilast significantly decreased the expression of TNF-α in the cornea (P ≤0.05) and IL-1α, IL-1β, and TNF-α in the conjunctiva (P ≤0.05) as compared to vehicle control. Cilomilast treatment markedly decreased the presence of CD11b+ antigen-presenting cells in the central and peripheral cornea (P ≤0.05), and led to decreased conjunctival expression of cytokines IL-6, IL-23, and IL-17 (P ≤ 0.05). Moreover, cilomilast decreased the expression of IL-17 and IL-23 in the draining lymph nodes (P ≤0.05). Topical cilomilast was significantly more effective than vehicle at reducing CFS scores (P ≤ 0.05). The therapeutic efficacy of cilomilast was comparable or superior to that of dexamethasone and cyclosporine in all tested measures.
Topical cilomilast suppresses the generation of IL17-associated immunity in experimental DED.

Invest Ophthalmol Vis Sci. 2012 May 10. [Epub ahead of print]
Sadrai Z, Stevenson W, Okanobo A, Chen Y, Dohlman TH, Hua J, Amparo F, Chauhan SK, Dana R.
Schepens Eye Research Institute and Massachusetts Eye & Ear Infirmary, Harvard Medical School, 20 Staniford Street, Boston, Massachusetts, 02114, United States.