M. Aragona et M. Inghilleri, INCREASED OCULAR PRESSURE IN 2 PATIENTS WITH NARROW-ANGLE GLAUCOMA TREATED WITH VENLAFAXINE, Clinical neuropharmacology, 21(2), 1998, pp. 130-131
Venlafaxine blocks the specific monoamine transporters and is devoid o
f significant action on muscarinic cholinergic receptors. To our knowl
edge, no cases of glaucoma have been reported so far. Because pain per
ception involves both serotonergic and noradrenergic mechanisms, venla
faxine also may be useful in neuropathic pain therapy. We report on tw
o patients with narrow angle glaucoma affected by chronic pain. When v
enlafaxine treatment was begun, their ocular pressure was steadily aro
und 17-18 mmHg. Venlafaxine was chosen (daily dose 75 mg) because this
drug is claimed not to bind on muscarinic cholinergic receptors. Howe
ver, 4 days later the ocular pressure of the first patient increased t
o 22 mmHg, which led to suspension of the drug. The ocular pressure of
the second patient was 18.5 mmHg after a week, 21 mmHg after 2 weeks,
and 23 mmHg after 16 days. One week after suspension, ocular pressure
of the patients was 17 and 18 mmHg, respectively. Possible explanatio
ns of this ocular effect are offered: pharmacokinetic interference on
the drugs used in glaucoma treatment, in vivo action on the muscarinic
receptor, indirect effect via dopaminergic receptors, or direct effec
t on the ocular sympathetic postganglionic neurones. In any case, from
a clinical viewpoint, caution should be used when giving venlafaxine
to patients with narrow-angle glaucoma, and ocular pressure must be mo
nitored.