Factors Predetermining Increased Aqueous Humour Flare in Long-Term Glaucoma Treatment.

Glaucoma patients often require long-term or even lifelong medical antiglaucomatous treatment. Benzalkonium chloride (BAK) is the most frequently used preservative in medical glaucoma treatment. Laser flare photometry is the noninvasive quantitative measurement of anterior chamber protein level and helps tracking intraocular inflammation. The purpose of our study was to evaluate the ocular aqueous humour flare in glaucoma patients, scheduled for cataract surgery without any other ocular diseases, and the association with pseudoexfoliation (PEX) syndrome, number of medications used, and BAK. A prospective case-control age- and gender-matched study, including open-angle glaucoma patients (>2 years of treatment) with cataract, matched with cataract patients with no other ocular pathology (control group). We found that the aqueous humour flare was higher in the glaucoma group than in the control group. PEX syndrome increased the aqueous humour flare independently from glaucoma diagnosis. The number of used antiglaucomatous medications correlated moderately with the aqueous humour flare. The BAK index showed weak positive correlation with aqueous humour flare. A variety of factors can affect aqueous humour flare increase, including PEX syndrome, medical substance used to treat glaucoma, number of different medications, and presence of BAK. The combination of these factors is of key importance to long-term glaucoma treatment.

Literature review and meta-analysis of translaminar pressure difference in open-angle glaucoma.

There is increasing evidence in the literature regarding translaminar pressure difference's (TPD) role in the pathophysiology of glaucoma. The optic nerve is exposed not only to intraocular pressure in the eye, but also to intracranial pressure (ICP), as it is surrounded by cerebrospinal fluid in the subarachnoid space. Although pilot studies have identified the potential importance of TPD in glaucoma, limited available data currently prevent a comprehensive description of the role that TPD may have in glaucomatous pathophysiology. In this review, we present all available qualified data from a systematic review of the literature of the role of TPD in open-angle glaucoma (OAG). PubMed (Medline), OVID Medline, ScienceDirect, SpringerLink, and all available library databases were reviewed and subsequent meta-analysis of pooled mean differences are presented where appropriate. Five papers including 396 patients met criteria for inclusion to the analysis. Importantly, we included all observational studies despite differences in ICP measurement methods, as there is no consensus regarding best-practice ICP measurements in glaucoma. Our results show that not only TPD is higher in glaucoma patients compared with healthy subjects, it is related to structural glaucomatous changes of the optic disc. Our analysis suggests further longitudinal prospective studies are needed to investigate the influence of TPD in OAG, with a goal of overcoming methodological weaknesses of previous studies.

The response of retrobulbar vasculature to hypercapnia in primary open-angle glaucoma and ocular hypertension.

PURPOSE: To evaluate the physiological effects of hypercapnia on the retrobulbar vasculature in ocular hypertension (OH) and open-angle glaucoma (OAG). METHODS: Peak systolic velocity (PSV), end-diastolic velocity (EDV) and resistive index (RI) of the ophthalmic (OA) and central retinal arteries (CRA) were evaluated in 12 eyes with OH and 8 eyes with OAG using color Doppler imaging. Measurements were taken before and during hypercapnia. RESULTS: Patients with OAG were found to have increased EDV (p < 0.035) of the CRA, and decreased PSV (p < 0.097) and EDV (p < 0.098) of the OA, during hypercapnia. Patients with OH had increased PSV (p < 0.062) and EDV (p < 0.072) of the CRA during hypercapnia. Patients with OH also demonstrated a greater percent change in the calculated RI (p < 0.065) of the CRA in response to hypercapnia when compared to OAG. The mean RI of the CRA decreased during hypercapnia. DISCUSSION: Patients with OH were found to have a normal vasodilatory response within the retrobulbar vasculature during hypercapnia resulting in increased volumetric blood flow to the retina while patients with OAG did not, suggesting there is vasospasm at or downstream from the CRA resulting in decreased volumetric blood flow to the retina.

A comparison of the effects of dorzolamide/timolol fixed combination versus latanoprost on intraocular pressure and pulsatile ocular blood flow in primary open-angle glaucoma patients.

PURPOSE: To evaluate the effects of dorzolamide/timolol fixed combination (D/T) compared to latanoprost on intraocular pressure (IOP) and pulsatile ocular blood flow (POBF) in primary open-angle glaucoma (POAG) patients. METHODS: Thirty patients with POAG were randomized in an open-label, cross-over study. Intraocular pressure reduction was achieved by 4 weeks medical therapy with D/T twice daily or latanoprost 0.005% dosed once in the evening. During a 4-week run-in and a 4-week wash-out period between study arms, patients ceased use of all other glaucoma medications and used timolol maleate 0.5% twice daily. Primary efficacy variables were IOP and POBF. RESULTS: There was no difference in baseline IOP and POBF parameters between the two study arms. Both D/T and latanoprost statistically significantly reduced IOP by 4.6 mmHg (p < 0.0001) and 3.75 mmHg (p < 0.0001) and increased POBF by 2.048 microl/second (p = 0.0030) and 2.147 microl/second (p = 0.0009), respectively. Repeated measures anova detected significant changes in POBF with treatment (p = 0.0361). Dorzolamide/timolol fixed combination statistically significantly increased pulse volume by 0.767 microl (p = 0.0087), while latanoprost therapy had no significant effect (p = 0.2407). CONCLUSIONS: Both drugs had similar effects in terms of IOP reduction. Dorzolamide/timolol significantly increased pulse volume while latanoprost had no effect. Further studies are necessary to establish whether the enhancement of choroidal blood flow can prevent glaucoma progression.