VISUAL FIELD PATTERNS IN GLAUCOMA: A SYSTEMIC REVIEW

INTRODUCTION:

Retinal nerve fiber bundles are arranged in a specific distribution. As the greater part is located in the central 30° area, most early glaucomatous visual field defects (VFDs) are detected within this region. 

Typical glaucomatous visual field patterns include nasal step, paracentral scotoma, arcuate-like defects, diffuse loss, and altitudinal defects. 

Footnote: The blind spot is located at 15° temporally, where the optic nerve leaves the eye.

PRIMARY OPEN ANGLE GLAUCOMA (POAG):

The nasal step is described as the most frequent and earliest VFD, followed by paracentral scotomas and arcuate-like defects. 

The superior hemifield is more affected than the inferior hemifield.

Repeatable diffuse visual field loss was seen in 4.4% of patients, the only sign of early glaucomatous visual field loss. 

Diffuse visual field loss is nonspecific and can be caused by various other factors such as cataract, extreme miosis, and unreliable performance of the perimetry.

Early diffuse visual field loss usually converts into well-defined pattern defects at later stages. 

INFLUENCING FACTORS FOR VFDs IN POAG:

Initial VFDs located in the superior hemifield were associated with greater disc ovality (maximum diameter of an ellipse fitted to disc contour/minimum diameter of an ellipse fitted to disc contour), β-peripapillary atrophy and thinner central corneal thickness.

VFD in the inferior hemifield was more frequently found in both insulin-dependent as noninsulin-dependent diabetic patients (odds ratio [OR] =1.8).

The presence of systemic risk factors for glaucoma (especially NTG) such as hypotension, migraine, Raynaud’s phenomenon, and sleep apnea was significantly higher in POAG as well as NTG patients with an initial parafoveal scotoma than in patients with initial nasal step.

In NTG, these above-mentioned systemic risk factors for glaucoma were more prevalent in patients exhibiting initial central scotoma than in patients with initial peripheral scotoma. These findings suggest that systemic vascular risk factors in POAG and NTG patients are associated with central VFDs.

Body mass index and smoking (measured in pack-years) were more strongly associated with a lower risk of paracentral VFDs (HR [hazard ratio] Body mass index [BMI] =0.67; HR smoking = 0.92) than with peripheral VFDs (HR BMI = 0.93; HR smoking = 0.98). The relation between cigarette smoking and POAG overall has been conflicting. Nicotine has been mentioned to have a neuroprotective role. 

NORMAL TENSION GLAUCOMA:

NTG patients show more localized VFDs and are characterized by deeper, more central, and more depressed VFDs compared to POAG patients. 

PRIMARY ANGLE CLOSURE GLAUCOMA:

In early disease stages, the VFDs are most common in the nasal area.

Jiang et al. and Sim et al. observed that (partial) arcuate defects were the most common types of VFDs in PACG eyes. Atalay et al. showed that the superior hemifield was more impaired than the inferior hemifield across the whole severity spectrum. In contrast, Lau et al. found no significant difference in visual field loss between the superior and inferior hemifield.

Following an acute episode of angle-closure, a hemifield defect was the most common VFD.

PROGRESSION OF VFDs:

Primary-open angle glaucoma:

The most common pattern of progression is the deepening of an existing scotoma, followed by expansion, rather than the development of new scotomas, emphasizing the importance of reliable baseline VF testing.

With increasing severity, the VFD showed progression to the center and progression toward a connection with the blind spot.

The initial parafoveal scotoma showed a characteristic pattern of progression in a retrospective study conducted by Su et al. The parafoveal scotoma in the superior hemifield initially had an arcuate pattern that first deepened 3° to 5° above fixation, then elongated toward the physiologic blind spot, and spread towards the nasal periphery, sparing the area corresponding to the papillomacular bundle. The inferior parafoveal scotoma, showed similar characteristics, but tended to be further away from fixation. POAG patients progress faster in the superior hemifield defects compared to the inferior counterparts. This difference is more pronounced in the central, paracentral, and nasal area.

Patients with initial damage in both hemifields had higher chances of glaucomatous progression.

Normal-tension glaucoma:

NTG patients progress more often in the paracentral area. NTG patients with lower heart-rate variability had faster central visual field progression than those with higher heart-rate variability. Other vascular factors, such as migraine and orthostatic dysfunction were also related to increased central visual field progression.

REFERENCE:

Vandersnickt MF, van Eijgen J, Lemmens S, Stalmans I, Pinto LA, Vandewalle EM. Visual field patterns in glaucoma: A systematic review. Saudi J Ophthalmol. 2024 Dec 26;38(4):306-315. doi: 10.4103/sjopt.sjopt_143_24. Erratum in: Saudi J Ophthalmol. 2025 Oct 13;39(3):286. doi: 10.4103/sjopt.sjopt_374_25. PMID: 39943959; PMCID: PMC11811403.

SCHWARTZ-MATSUO SYNDROME

Introduction:

Schwartz-Matsuo syndrome is a rare condition characterized by the triad of rhegmatogenous retinal detachment (RRD) (usually with peripheral breaks or oral dialysis), elevated intraocular pressure (IOP) with marked fluctuation, and cells in the anterior chamber. In cases of retinal detachments not associated with Schwartz-Matsuo syndrome, there is usually low IOP secondary to increased outflow by active pumping of aqueous humor through the exposed retinal pigment epithelium. However, IOP in Schwartz-Matsuo syndrome is elevated.

The syndrome was first described by Schwartz in 1973. He described the classic findings of elevated IOP and apparent iridocyclitis associated with RRD and open AC angles. In 1986 Matsuo et al. discovered photoreceptor outer segments on electron microscopy of the aqueous humor and theorized that the free photoreceptor outer segments blocked the trabecular outflow leading to elevated IOP.

Electron microscopy of aqueous humor in such patients has demonstrated photoreceptors outer segments. The photoreceptor outer segments and/or retinal pigment epithelium (RPE) pigment pass through a retinal break, leading to outflow obstruction in the trabecular meshwork. 

The syndrome presents with, or mimics, severe open-angle glaucoma. It can be mistaken for uveitis or uveitic glaucoma, but it does not respond to corticosteroids. There are no features of inflammation such as pain, redness or ciliary flush.

Following retinal detachment repair, IOP typically normalizes and prognosis is favorable.

Symptoms:

Patients typically present with complaints of unilateral blurry vision, eye pain, and nausea associated with the elevated IOP, as well as floaters, photopsia, and scotoma secondary to the retinal detachment. 

Risk Factors:

Shallow RRD involving the vitreous base (a shallow detachment allows for constant sloughing of dying photoreceptor outer segments and involvement of the vitreous base allows for the photoreceptor outer segments to gain access to the anterior chamber. An intact hyaloid would not allow them to reach the anterior segment).

Other risk factors include:

• Retinal dialysis or retinal tears at the ora serrata. 
• History of ocular trauma or surgery.
• Myopia, or lattice degeneration.

Diagnosis:

On examination, IOP is elevated, with marked fluctuation in pressures. Pigmented aqueous cells are present in varying number, but there are usually no other signs of uveitis. On gonioscopy, the anterior chamber angles are typically open; however, angle recession may indicate prior ocular trauma. Finally, there is retinal detachment with tears most commonly located at the ora serrata or non-pigmented epithelium of the pars plana or pars plicata. The retinal detachment is often shallow and involves a wide area, including the macula.

Identification of photoreceptor outer segments in the aqueous humor by electron microscopy assists in the diagnosis. OCT will demonstrate the presence of subretinal fluid indicative of retinal detachment.

Systemic examination (Marfan's syndrome or atopic dermatitis may help identify patients who are at risk of a retinal break around the ora serrata).

Routine assessment of the visual acuity and monitoring of IOP should be done.

Gonioscopy will show an open angle and can rule out other etiologies of increased IOP: angle recession, angle closure, peripheral anterior synechiae, neovascularization, and others.

Differential diagnosis:

1. Iritis: The anterior chamber findings in Schwartz-Matsuo syndrome are not inflammatory. The presence of anterior synechiae and keratic precipitates indicates an inflammatory condition which would rule out this condition. It should also be noted that the aqueous cells in Schwartz-Matsuo syndrome are unresponsive to corticosteroid treatment.
2. Open-angle or other secondary glaucomas should be considered, especially if it occurs in a patient with a history of blunt trauma.
3. Posner-Schlossman syndrome shows very mild anterior chamber inflammation with few cells and little flare, few fine keratic precipitates, and responds to steroid treatment.

Management:

Schwartz-Matsuo syndrome should be managed as a secondary cause of glaucoma, with first line treatment including repair of the retinal detachment and washout of the AC cellular debris. Typically, IOP returns to normal following retinal detachment repair. 

Immediate glaucoma management includes maximizing medical therapy before retinal surgery with oral carbonic anhydrase inhibitors with or without pilocarpine. Pilocarpine may help to open the trabecular meshwork pores but is associated with miosis and increased risk of retinal detachments.

Similar to the treatment of pigmented cells seen in pigment dispersion syndrome, laser trabeculoplasty should lower the IOP, but may not achieve satisfactory results. Additionally, laser trabeculoplasty may place patients at higher risk for post-operative IOP spikes given their compromised trabecular function. 

A tube shunt is preferred over trabeculectomy given the possible conjunctival scaring following retinal surgery and the risk of hypotony maculopathy with the use of antifibrotic agents in young, highly myopic patients. Tube shunts may induce diplopia via restrictive strabismus when combined with sclera buckle. An additional consideration is the timing of the tube shunt implantation, whether at the time of retinal surgery or not.

Prognosis:

Is usually good, with IOP returning to normal following successful RRD surgery.

HIGH PILLOW POSITION & IOP

Intraocular pressure (IOP) fluctuates significantly in response to body position. The IOP is lowest in the sitting posture and increases in the order of supine and lateral decubitus positions.

These changes are attributed to the increase in episcleral venous pressure and choroidal vascular volume. The uveal tissues also develop congestion and expansion from increased venous and arterial pressures in the orbit, contributing to the increased IOP.

Therefore, postural modification may serve as a potential adjunctive strategy for IOP management in glaucoma patients.

In a study by Liu et al, involving 144 glaucoma patients, IOP was measured and compared between the high-pillow position (head elevated by 20–35° using two pillows) and the supine position. Additionally, changes in jugular venous lumen in response to postural variation were evaluated via ultrasonography in 20 healthy volunteers.

The authors reported that, compared with the supine position, the high-pillow position was associated with significantly elevated IOP, increased 24-hour IOP fluctuation and reduced ocular perfusion pressure (OPP) (all p<0.001). 

Greater postural IOP fluctuation (ΔIOP) was observed in younger individuals (p=0.027) and patients with primary open-angle glaucoma (POAG) (p<0.001). 

Multiple regression analysis identified thicker central corneal thickness and the presence of POAG (vs normal-tension glaucoma) as positive predictors of larger ΔIOP changes (both p<0.05). 

Ultrasonography in healthy volunteers revealed significant constriction of both internal and external jugular venous lumen in the high-pillow position (all p<0.001), accompanied by an increase in maximum blood flow velocity of the internal jugular vein (p=0.013).

Therefore, compared with the supine position, the high-pillow position is associated with increased IOP and decreased OPP in patients with glaucoma, which may be linked to jugular venous compression. 

ADVICE: 

Patients with glaucoma may benefit from avoiding sleeping postures that induce jugular venous compression to mitigate postural IOP elevation.

REFERENCE:

Liu T, Hu M, Liu X, et al. Association of high-pillow sleeping posture with intraocular pressure in patients with glaucoma. British Journal of Ophthalmology. Published Online First: 27 January 2026. doi: 10.1136/bjo-2025-328037.

Key morphological determinants of optic nerve head biomechanics

 

Glaucoma is closely linked to optic nerve head (ONH) damage, particularly within the lamina cribrosa (LC).

Recent advances in optical coherence tomography (OCT) imaging and deep learning-based segmentation enable accurate reconstruction of patient-specific ONH geometries.

OCT-based approaches can directly quantify ONH biomechanics and LC strain, providing critical insights into the mechanical behaviour of ocular tissues.

Li and associates have developed an automated pipeline that converts routine OCT into patient‑specific finite element (FE) models and quantifies biomechanical and morphological determinants based on the unique individual ONH structures.

This study used OCT images of the ONH from a large cohort of healthy individuals and glaucoma subjects. The overall workflow followed a sequential pipeline.

Collectively, these results demonstrate the capability of the automated pipeline to (1) robustly segment ONH tissues from routine OCT images, (2) extract a comprehensive set of morphological parameters, (3) quantify LC strain across a large cohort, and (4) identify key determinants of biomechanical response through both statistical and machine learning approaches.

In the study, LC depth showed the strongest linear association with LC strain (r = −0.31). Other parameters with smaller associations included BMO radius (r = 0.17), pre-lamina volume (r =  −0.14) and mean choroidal thickness (r = −0.12). 

After adjusting for age and gender, glaucomatous eyes exhibited significantly lower LC strain than healthy eyes (coefficient = 0.0018, p = 0.011), suggesting potential tissue remodelling. 

The pre-lamina depth, LC curvature, BMO radius, and LC depth were also found to be influential predictors for ONH morphological changes, despite modest explained variance.

REFERENCE:

Li, Q., Zhan, B., Liu, T. et al. An automated optical coherence tomography to finite element analysis pipeline reveals key morphological determinants of optic nerve head biomechanics in glaucoma. Eye 40, 238–244 (2026).

MEDIEVAL ARABIC CONTRIBUTION TO GLAUCOMA

Arab medieval physicians/philosophers have contributed immensely to our early knowledge of glaucoma. 

They introduced the term zarqaa (derived from azraq, the word for blue in Arabic) to the condition which we now call glaucoma, a Greek term, which means greenish. The disease is even now called maa' (water)- or nuzool-azraq or nuzool aswad (black) in Arabian populations.

The origin of the term zarqaa is not entirely clear. The nonspecific word zarqaa was translated by some as viriditate oculi (green). Did this translation result from the blue-green ambiguity present in many languages, or was the translation influenced by observations by oculists and physicians? The answer remains unknown. However, there are a few theories which point towards a possible explanation.

It was observed that patients suffering from glaucoma had dilated pupils which caused the lens to become more prominent. This greenish blue hue of the lens could have led to the condition being diagnosed as zarqaa. It could also imply the color of the iris seen in some populations. According to some accounts the Arab and European (specially Roman) conflicts led to the antagonism of Arabs for the blue green eyes of the Europeans. This could have led to using their eye color with a negative perception in their writings.

Al-tabbari (916-986) was one of the first to diagnose glaucoma based on the raised eye pressure in those patients. See link for post on Tabari: 

https://ourgsc.blogspot.com/2019/05/abu-al-hasan-ali-ibn-sahl-rabbani-al.html

Abu Ali al-Husain Ibn Sina (c. 980–1037 AD), a Persian also known as Avicenna, believed the zarqaa pupillary hue could be associated with anterior prominence of the lens (or a forward displacement of the lens) and could occur in an acquired (pathologic) manner. It is amazing that the modern pathophysiology of closed angle glaucoma has been described based on the position of the lens. Ibn Sina explained hardening of the eye in zarqaa due to the intraocular humor thickening or coagulating, leading to the lenses being more difficult to displace. He and other authors diagnosed eye hardness through palpation. Ibn Sina mentioned a grave prognosis when the lens could not be moved around in the eye. According to him surgery in such a case has poor visual outcomes.

Some authors have mentioned that the Quranic verses also point to blue eyed people being sent to the hell fire during Qayamat (Day of judgement). Allah knows best. 

https://www.dovepress.com/article/supplementary_file/77471/77471.pdf

Jacques Guillemeau (1550–1613) of France cited Ibn Sina and wrote that glaucoma, or viriditas oculi, was incurable, and involved a dry, thick, and green lens.

SITAGLIPTIN

The underlying molecular mechanisms involved in retinal ganglion cell (RGC) apoptosis in glaucoma remain to be fully elucidated, but inflammation plays an important role. 

Studies have shown neuroprotective properties with Glucagon-Like Peptide (GLP-1) and GLP-1 receptor agonists (GLP-1RA).

GLP-1/GLP-1R are produced by the human retina and mRNA levels and protein content of GLP-1 were significantly lower in retinas from subjects with diabetes in comparison with normal individuals.

GLP-1 levels in the retina can be increased by two mechanisms. One, by topical administration of GLP-1, so that the agent reaches the retina. And two, by reducing the degradation of GLP-1. 

Degradation of GLP-1 occurs by catalytic activity of the enzyme dipeptidyl peptidase IV (DPP-IV). This enzyme is found in higher concentration in diabetic retinas.

Sitagliptin an inhibitor of DPP-IV, reduces the degradation of GLP-1 and thereby, increases its levels in the retina.

The main function of mature oligodendrocytes in the central nervous system is to generate myelin sheaths, which accelerate the conduction of nerve impulses and provide metabolic support for neuronal axons. In a dexamethasone induced glaucoma model, researchers found a significant loss of positive Oligo-2 cells compared to untreated controls (p < 0.05). However, Sitagliptin treatment prevented RGC and oligodendrocyte (OL) loss in the retina and optic nerve head (ONH).

In glaucomatous retina, three types of glial cells, astrocytes, microglia, and Müller cells, can become activated. Microglia and macroglia are the cell types involved in inflammatory responses within the retina. Under pathological conditions, these glial cells become reactive, lose their homeostatic functions of trophic and metabolic support, and gain neurotoxic properties that trigger inflammatory-mediated neurodegeneration. Sitagliptin is neuroprotective by reducing astroglial activation in the ONH and the retina. It also reduces microglial activation in the ONH.

Gamma-synuclein can be considered a member of the Bcl-2 apoptosis family, and its overexpression and accumulation in glaucomatous eyes has a role in the pathogenesis of glaucomatous neurodegeneration by facilitating the disintegration of neurofilament networks such as Neurofilament heavy subunit (NFH) by activating astrocyte phagocytosis in the ONH and inhibiting optic nerve regeneration. The loss and dephosphorylation of neurofilament deprives metabolic routes of essential substrates for axonal energetics, thereby increasing the susceptibility of axons to injury. 

The authors found that topical administration of sitagliptin inhibits the overexpression of both macro and microglial activation that occurs in the neuroretina and in the ONH. In glaucoma there is significant loss of NFH, which is prevented by topical administration of sitagliptin.

REFERENCE:

Bogdanov P, Duarri A, Sabater D, Canz MJ, Isla-Magrané H, Ramos H, Deàs-Just A, Simó R, Hernández C. Topical Administration of Sitagliptin Prevents Retinal Neurodegeneration in a Model of Glaucoma Induced by Dexamethasone. Int J Mol Sci. 2025 Dec 20;27(1):48. doi: 10.3390/ijms27010048. PMID: 41515932; PMCID: PMC12785737.

HYPOTONIC MACULOPATHY

Ocular hypotony may occur after ocular inflammation, trauma or surgery, especially glaucoma filtration surgery (GFS) with antifibrosis drugs. Postoperative hypotony may develop following retina, cataract, cornea and strabismus surgeries in addition to filtering surgery. 

Several definitions are used for describing ocular hypotony. A statistical or numerical definition is IOP below 6.5 mmHg, which is more than three standard deviations below the mean. An alternative clinical definition is IOP low enough to result in vision loss, although low IOP alone may not result in vision loss. Vision loss associated with low IOP is commonly caused by corneal edema, astigmatism, cystoid macular edema or maculopathy. The World Glaucoma Association considers hypotonic IOP one which causes clinical complications with a potential of visual disturbance. This is regarded as IOP ≤5 mmHg.

Hypotony maculopathy is characterized by a low IOP with associated fundus changes, including chorioretinal folds, optic nerve swelling and vascular tortuosity. The chorioretinal folds are most likely secondary to the collapse of the scleral wall. Wrinkling in the retina or thickening in the choroid may cause axial shortening of the eye, leading to hyperopia.

Disc swelling results from restricted axoplasmic flow, presumably from anterior bowing of the lamina cribrosa in the optic nerve. These findings may be less pronounced in eyes with advanced glaucoma because these eyes have fewer remaining axons that can swell. Clinically, patients may experience metamorphopsia or central vision loss, or they may be asymptomatic.

Hypotony maculopathy can occur with increased outflow of aqueous humor or, less often, with decreased aqueous production. Outflow can increase because of wound leak, scleral rupture, cyclodialysis cleft, retinal detachment or an overfiltering bleb—or, rarely, from ciliochoroidal detachment. Decreased aqueous humor production may be secondary to uveitis, hypoperfusion of the ciliary body in ocular ischemia, or a ciliochoroidal detachment.

One of the most important risk factors for hypotony maculopathy is the use of antifibrosis drugs, especially mitomycin C, during GFS. Intraoperative use of MMC can lead to overfiltration or bleb leaks in the late postoperative period which may be associated with hypotony maculopathy. Higher concentrations and increased application times of antifibrosis agents not only may lead to excessive filtration but also may have a toxic effect on the ciliary body, thus leading to decreased aqueous humor production.

A retrospective study of other risk factors for hypotony maculopathy showed that young age, male gender and myopia increased the risk, whereas a history of diabetes and the presence of choroidal effusions decreased the risk.

Diagnosis of the condition is made by performing a Seidel's test which demonstrates aqueous leak from the bleb. Fundus examination reveals the characteristic retino-choroidal changes. Investigations such as B-scan and OCT will demonstrate other findings associated with hypotonic maculopathy such as thickening of the posterior sclera or choroid, and choroidal detachments or macular changes. Ultrasound biomicroscopy and intravenous fluorescein angiography help in identifying choroidal folds.

In treating hypotony maculopathy, the goal is to normalize IOP as soon as possible to prevent permanent retinal dysfunction and associated vision loss. However, IOP correction is not guaranteed to improved visual acuity, especially in cases of long-standing hypotony maculopathy.

Treatment of hypotonic maculopathy is aimed at the cause. Bleb leaks can be managed by scleral or bandage contact lenses, symblepheron ring, aqueous suppression, topical antibiotics like gentamicin which facilitates fibrosis and broad spectrum antibiotics to prevent infection, or suturing if conservative approach fails. Other options are autologous blood injection into the bleb, fibrin tissue glue, cyanoacrylate glue, argon laser application or direct suturing of the bleb, although these treatments seldom produce a longlasting solution. 

Late-onset bleb leaks that do not resolve spontaneously or with conservative measures often require surgical intervention. Amniotic membrane or autologous conjunctival grafts can be considered.

Hypotony maculopathy secondary to overfiltration may be managed by adding compression sutures to the elevated, overfiltering bleb. Autologous blood injection, in or around the bleb, may be helpful in some patients. During the early postop period, with an overfiltering bleb, anti-inflammatory medications may be rapidly tapered to facilitate episcleral scarring.

Preventive measures can be taken intraoperatively during GFS to reduce the risk of post-op hypotony maculopathy. There are three critical areas created during GFS that ensure smooth passage of aqueous humor. These are:

1) sclerostomy; 

2) scleral flap; and 

3) subepiscleral/subconjunctival areas. 

The above-mentioned intraoperative areas should be controlled meticulously to prevent the development of post-op hypotony. 

Multiple flap sutures should be placed, with additional sutures if aqueous flow is excessive. The conjunctiva should be closed with the use of tapered (vascular) needles to reduce suture track leaks. If possible, the conjunctival closure should incorporate Tenon’s capsule, whether by a two-layer or a one-layer method. Postoperatively, properly timed removal of releasable sutures or laser lysis of other sutures can decrease the precipitous reduction of IOP and the potential for hypotony maculopathy.

In cases of glaucoma drainage devices, intraoperative tube ligation is performed using absorbable sutures. These sutures usually absorb after 5 weeks and controlled IOP is seen. However, early absorption or opening of the suture causes over-filtration. Techniques such as blocking the tube ab interno or ligating the tube have been described.

Some authors recommend viscoelastic substance or perfluoropropane gas injection into the anterior chamber in conjunction with tube ligation. In case of failure, ab interno stent, tube shunt plate truncation and implant 

explantation are other surgical methods that can be considered.

PLURIPOTENT EPIGENETIC REGULATOR OBP-801

 

OBP-801 (also known as YM753) is a novel histone deacetylase (HDAC) inhibitor developed by Oncolys BioPharma for potential anticancer treatment, demonstrating effects like inducing cell death (apoptosis) and halting cancer cell growth in various cancers, including lung, breast, and brain tumors, often synergistically with other drugs, by interfering with HDAC enzymes crucial for cancer progression. It works by inhibiting HDACs, leading to gene expression changes that trigger cancer cell death.

OBP-801 has been studied in animal glaucoma models and found to improve the survival of filtering blebs.

Koga and colleagues have demonstrated the anti-fibrotic effect of OBP-801 (OBP) on filtering blebs in a rabbit glaucoma filtration surgery (GFS) model, as well as rabbit eyes which underwent PRESERFLO microshunt implantation surgery (PMS).

The second study involved 19 Japanese white rabbits that underwent PMS in the right eye, with those eyes divided into 3 groups: (1) intraoperative subconjunctival injection of 0.02% mitomycin-C (MMC) (n = 6), (2) postoperative instillation of 100 nM OBP eye drops (n = 7), or (3) a balanced salt solution (BSS) control (n = 6). 

Bleb morphology and IOP were monitored for 12 weeks postoperative, with the bleb tissues then undergoing evaluation of fibrosis and Western blot analysis. 

A lower postoperative IOP was maintained in the OBP-group eyes, and at 12 weeks postoperative, the IOP was significantly lower in that group than in the BSS and MMC groups (p < 0.01). 

OBP-treated eyes showed no adverse effects and reduced levels of alpha-smooth muscle actin and collagen deposition, thus suggesting that OBP is a promising candidate for improving surgical outcomes post PMS.

Yamamoto et al have also studied the effect of OBP in rabbit eyes with GFS. They found OBP treatment involving subconjunctival injection or eye drops showed no adverse effects, and reduced levels of α-SMA and collagen deposition at the surgical wound site. OBP maintained the long-lived bleb without scar formation, and IOP was lower at 30 postoperative days compared with the vehicle control group. These findings suggest that OBP is an effective and useful candidate low-molecular-weight agent for improving wound healing and surgical outcomes in a rabbit model of GFS.

REFERENCES:

1. Koga, Y., Ikushima, T., Hiramoto, N. et al. Pluripotent epigenetic regulator OBP-801 attenuates fibrosis and maintains lower intraocular pressure in a rabbit PRESERFLO MicroShunt surgery model. Sci Rep (2025). https://doi.org/10.1038/s41598-025-34244-4.
2. Yamamoto Y, Mukai A, Ikushima T, Urata Y, Kinoshita S, Hamuro J, Ueno M, Sotozono C. Pluripotent epigenetic regulator OBP-801 maintains filtering blebs in glaucoma filtration surgery model. Sci Rep. 2020 Dec 1;10(1):20936. doi: 10.1038/s41598-020-77811-7. PMID: 33262357; PMCID: PMC7708845.