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See also Prostaglandins .
Latanoprost is an analogue of prostaglandin F 2α , used to treat glaucoma. The use of latanoprost and unoprostone in the treatment of open-angle glaucoma and ocular hypertension has been reviewed [ ]. More data on safety are needed to calculate its benefit-to-harm balance.
Latanoprost caused reduced intraocular pressure by 20–40% in adults with open-angle glaucoma or ocular hypertension, but its efficacy and safety in children have not been widely reported. Most children reported so far gained little benefit on intraocular pressure from latanoprost, but older children and those with juvenile-onset open-angle glaucoma do gain a significant ocular hypotensive effect. Systemic and ocular adverse reactions in children using latanoprost are infrequent [ ].
Two patients in their seventies developed hypertension during treatment with topical latanoprost (dosage not stated) for open-angle glaucoma; both were also taking tocopherol (vitamin E) supplements. Neither had a previous history of hypertension [ ]. The authors commented that it is likely that systemic absorption of topical latanoprost could cause hypertension. Self-medication with vitamin E has been reported to aggravate or precipitate hypertension.
Coronary spasm has been attributed to latanoprost [ ].
A 58-year-old man with stable angina pectoris started to use latanoprost eye drops and over the next few days his angina worsened and occurred at rest. After 15 days, he had syncope during physical exercise. Angiography showed coronary spasm.
Latanoprost aggravated respiratory symptoms in a patient with chronic bronchitis and emphysema, with improvement after latanoprost was withdrawn [ ].
Three cases of headache after latanoprost have been described [ ].
A 65-year-old man with primary open-angle glaucoma intolerant of dipivefrin and beta-blockers used latanoprost in both eyes at bedtime. He had no prior history of migraine, but he began to have headaches, the frequency and severity of which increased until they were occurring daily. The pain was not relieved by over-the-counter or narcotic analgesics, and he was virtually incapacitated. Latanoprost was discontinued and he had almost immediate relief, with only one migraine during the following week, and he was headache-free for the next 10 months. He then agreed to rechallenge. After the second night of latanoprost therapy his headache recurred, and therapy was withdrawn 2 days later when he had incapacitating pain. Headache did not recur within 4 months of follow-up.
A 65-year-old man with primary open-angle glaucoma, using levobunolol hydrochloride 0.5%, was given a nighttime dose of latanoprost. The next morning he awoke with a severe bifrontal throbbing headache, photophobia, and slight blurring of vision. The headache intensified, and 4 days later a CT scan was normal. On the sixth day he stopped using latanoprost. His headache disappeared within 24 hours and did not recur during follow-up for 1 year.
A 54-year-old woman with primary open-angle glaucoma, using betaxolol hydrochloride 0.5%, had mild progression of visual field loss in her left eye. Latanoprost was added nightly to her left eye. A few hours after the first dose she was awakened by a severe unilateral pounding headache extending from the left eye and brow to the left cranium. There were no associated neurological symptoms. The headache resolved spontaneously the next day, but recurred on three nights after instillation of latanoprost. On the fourth night the headache did not occur. She continued to use latanoprost, and the headache did not return.
Four patients treated with latanoprost developed dendritiform epitheliopathy, a sign of corneal toxicity; the lesions reversed in 1–4 weeks after latanoprost withdrawal [ ].
Three cases of Herpes simplex keratitis developed during latanoprost therapy [ ].
One patient, with a history of H. simplex keratitis, had recurrence with latanoprost (4 months); the infection resolved on withdrawal but recurred on rechallenge.
The second patient, with a history of H. simplex keratitis, had bilateral recurrence with latanoprost (1 month); antiviral therapy did not eradicate the infection until latanoprost was withdrawn.
The third patient developed the infection after 1 month; the keratitis cleared on withdrawal of latanoprost and antiviral therapy; reinstitution of latanoprost with prophylactic antiviral medication (valaciclovir) kept the cornea clear, but as soon as the antiviral drug was discontinued, H. simplex virus keratitis reappeared.
Although the mechanism is unclear, it is known that inhibitors of prostaglandin synthesis reduce recurrence of epithelial H. simplex infections and prostaglandins may stimulate their occurrence.
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