Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022568 (keratitis)
 5,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We reviewed records from 428 consecutive patients with severe Graves' ophthalmopathy to determine early and late results after transantral orbital decompression. Optic neuropathy was present in 217 (50.7%) patients. Post-operatively, 402 (89%) of 453 eyes with preoperative visual acuity worse than 20/20 improved or remained the same. Visual field scotomas improved or resolved in 245 (91%) of 269 eyes tested pre- and postoperatively. Preoperative papilledema resolved or improved in 99 (94%) of 105 eyes, and preoperative exposure keratitis improved or resolved in 178 (92%) of 195 eyes. Average proptosis reduction was 4.7 mm. Postoperatively, new diplopia developed in 74 (64%) of 116 patients who had no diplopia before orbital decompression, although 300 patients ultimately had strabismus surgery. At late follow-up (N = 293 patients), 226 (77%) had single vision and 44 (15%) had correction with prism. Complications included sinusitis (18 patients), lower eyelid entropion (38 patients), numb lip (23 patients), cerebrospinal fluid leaks (15 patients), and one frontal lobe hematoma (one patient). The average duration of follow-up was 8.7 years. Transantral orbital decompression effectively reduces proptosis and usually corrects optic neuropathy. In other circumstances, the benefits achieved and the side effects incurred must be carefully balanced for each patient before transantral orbital decompression is considered.
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PMID:Results of transantral orbital decompression in 428 patients with severe Graves' ophthalmopathy. 823 12

Treatments used for several neurological conditions may adversely affect the eye. Vigabatrin-related retinal toxicity leads to a visual field defect. Optic neuropathy may result from ethambutol and isoniazid, and from radiation therapy. Posterior subcapsular cataract is associated with systemic corticosteroids. Transient refractive error changes may follow treatment with acetazolamide or topiramate, and corneal deposits and keratitis with amandatine. Intraocular pressure can be elevated in susceptible individuals by anticholinergic drugs, including oxybutynin, tolterodine, benzhexol, propantheline, atropine and amitriptyline, and also by systemic corticosteroids and by topiramate. Nystagmus, diplopia and extraocular muscle palsies can occur with antiepileptic drugs, particularly phenytoin and carbamazepine. Ocular neuromyotonia can follow parasellar radiation. Congenital ocular malformations can result from in utero exposure to maternally prescribed sodium valproate, phenytoin and carbamazepine. Neurologists must be aware of potential ocular toxicity of these drugs, and appropriately monitor for potential adverse events.
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PMID:Ocular complications of neurological therapy. 1595 88