The Effect of Long-term Antiglaucomatous Drug Administration on Central Corneal Thickness.
OBJECTIVE
To evaluate rates of changes per year of central corneal thickness after antiglaucomatous drug administration with β-blockers, prostaglandin analogs, and carbonic anhydrase inhibitors monotherapy and combined topical antiglaucomatous therapy, in a cohort of patients with ocular hypertension, glaucoma suspects, and patients with perimetric glaucoma as compared with normal controls.


METHODS
This retrospective single-center study included 130 eyes as healthy controls, 121 eyes of ocular hypertensive patients, 105 eyes of glaucoma suspects, and 49 eyes of perimetric glaucoma patients. All patients underwent standard automated perimetry, 24-hour intraocular pressure profile, optic disc photography, and optical coherence pachymetry (OCP; Heidelberg Engineering). The cohort was divided into 8 groups on the basis of topical antiglaucomatous medication. Linear regression analysis was conducted to analyze the relationship between central corneal thickness and exposure to antiglaucomatous medication during the follow-up.


RESULTS
Central corneal thickness did not change during the follow-up for investigated diagnostic subgroups. There was a statistically significant decrease in central corneal thickness for eyes treated with prostaglandin monotherapy (-3.1 μm/y for left eye), and a combined therapy with prostaglandins, carbonic anhydrase inhibitors, and β-blockers (-5.8 and -3.8 μm/y for right and left eye, respectively).


CONCLUSIONS
We recommend regular measurements before and during therapy with prostaglandin monotherapy and a combined therapy with prostaglandins, carbonic anhydrase inhibitors, and β-blockers. Follow-up intraocular pressure measurements may be underestimated for eyes treated with the aforementioned treatment regimens if central corneal thickness is not measured on a regular basis.
Department of Ophthalmology, University of Erlangen-Nuremberg, Erlangen, Germany.
Wolfgang A
WA
Schrems
Laura M
LM
Schrems-Hoesl
Christian Y
CY
Mardin
Folkert K
FK
Horn
Anselm G M
AG
Juenemann
Friedrich E
FE
Kruse
Joachim M
JM
Braun
Robert
R
Laemmer
D000319:Adrenergic beta-Antagonists / Q000008:administration & dosage / Q000009:adverse effects; D000328:Adult; D000368:Aged; D000959:Antihypertensive Agents / Q000008:administration & dosage / Q000009:adverse effects*; D002257:Carbonic Anhydrase Inhibitors / Q000008:administration & dosage / Q000009:adverse effects; D003315:Cornea / Q000187:drug effects* / Q000503:physiopathology; D003316:Corneal Diseases / Q000139:chemically induced* / Q000503:physiopathology; D063171:Corneal Pachymetry; D005260:Female; D005902:Glaucoma, Open-Angle / Q000188:drug therapy* / Q000503:physiopathology; D006801:Humans; D007368:Interferometry; D007429:Intraocular Pressure / Q000187:drug effects*; D008297:Male; D008875:Middle Aged; D009798:Ocular Hypertension / Q000188:drug therapy / Q000503:physiopathology; D011461:Prostaglandins F, Synthetic / Q000008:administration & dosage / Q000009:adverse effects; D012189:Retrospective Studies; D014065:Tonometry, Ocular; D058609:Visual Field Tests
D000319:Adrenergic beta-Antagonists; D000959:Antihypertensive Agents; D002257:Carbonic Anhydrase Inhibitors; D011461:Prostaglandins F, Synthetic