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Review
. 2022 Oct 12:13:1015338.
doi: 10.3389/fphar.2022.1015338. eCollection 2022.

Clinical pharmacology and pharmacogenetics of prostaglandin analogues in glaucoma

Lin Zhou  1 , Wenyi Zhan  2 , Xin Wei  1
Affiliations
Review

Clinical pharmacology and pharmacogenetics of prostaglandin analogues in glaucoma

Lin Zhou et al. Front Pharmacol. .

Abstract

Glaucoma is the main cause of irreversible visual loss worldwide, and comprises a group of progressive, age-related, and chronic optic neuropathies. Prostaglandin analogs are considered a first-line treatment in the management of glaucoma and have the best efficacy in reducing intraocular pressure. When comparing these therapeutic agents between them, long-term therapy with 0.03% bimatoprost is the most effective followed by treatment with 0.005% latanoprost and 0.004% travoprost. The prevalence of adverse events is lower for latanoprost than for other prostaglandin analogs. However, some patients do not respond to the treatment with prostaglandin analogs (non-responders). Intraocular pressure-lowering efficacy differs significantly between individuals partly owing to genetic factors. Rs1045642 in ABCB1, rs4241366 in SLCO2A1, rs9503012 in GMDS, rs10306114 in PTGS1, rs11568658 in MRP4, rs10786455 and rs6686438 in PTGFR were reported to be positive with the response to prostaglandin analogs in patients with glaucoma. A negative association was found between single nucleotide polymorphisms of PTGFR (rs11578155 and rs6672484) and the response to prostaglandin analogs in patients with glaucoma. The current review is an analysis of the information relevant to prostaglandin analog treatments based on previous literatures. It describes in detail the clinical pharmacology and pharmacogenetics of drugs belonging to this therapeutical class to provide a sound pharmacological basis for their proper use in ophthalmological clinical practice.

Keywords: efficiency; glaucoma; neuropathy; pharmacogenetics; prostaglandin analogues; safety; visual loss.

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Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

FIGURE 1
FIGURE 1
The distribution of IOP-lowering efficacy of PGAs at different time points of therapy and the distribution of ocular side events of PGAs in previous RCTs. (A) The distribution of the IOP-lowering efficacy of PGAs at 1M, 3M, and 6M. The abscissa represents the mean IOP reduction from baseline to the endpoint. The ordinate represents the data from different reported literatures. (A1): The distribution of IOP-lowering efficacy of PGAs at 1 month. (A2): The distribution of IOP-lowering efficacy of PGAs at 3 months. (A3): The distribution of IOP-lowering efficacy of PGAs at 6 months. Red circle: Latanoprost; Green square: Bimatoprost; Dark triangle: Travoprost. (B) The distribution of ocular side events of PGAs in previous RCTs. The horizontal axis represents the incidence of ocular side effects. The pale green columns in the top represent the ocular side effects in Bimatoprost. The faint yellow columns in the middle represent the ocular side effects in Travoprost. The pale blue columns in the bottom represent the ocular side effects in Latanoprost. Green square: conjunctival hyperemia; yellow circle: growth of eyelashes; blue circle: other discomfort.
FIGURE 2
FIGURE 2
Genetic variants that influence latanoprost therapy outcomes. Blue circular cylinder: negative association; gray circular cylinder: no association; orange circular cylinder: positive association.
See this image and copyright information in PMC

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