Intraocular pressure adverse drug effects

The primary adverse effect of intravenous cidofovir is a dose-dependent nephrotoxicity. Concurrent administration of other potentially nephrotoxic agents (eg, amphotericin B, aminoglycosides, nonsteroidal anti-inflammatory drugs, pentamidine, foscarnet) should be avoided. Prior administration of foscarnet may increase the risk of nephrotoxicity. Other potential side effects include uveitis, decreased intraocular pressure, and probenecid-related hypersensitivity reactions. Neutropenia and metabolic acidosis are rare. The drug caused mammary adenocarcinomas in rats and is embryotoxic. 

The use of periocular steroids has several limitations and complications. The injections are usually somewhat uncomfortable, and thus patients prefer to avoid them. Adverse ocular effects have included retinal detachment, optic nerve atrophy, and preretinal membrane formation. Intraocular pressure (lOP) can rise, particularly because the drug may remain in the eye for several days to weeks. Some of the observed effects may result from the vehicle rather than from the steroid itself. 

Steroids may also be used in the treatment of GPC, with careftil monitoring for adverse effects. Loteprednol 0.5% is an effective and safe treatment option for GPC when used four times a day. Improvement in itching, lens tolerance, and papillae has been noted after 1 week of therapy and continued for 6 weeks after treatment.When intraocular pressure does rise with loteprednol use, it is usually transient, and pressure typically returns to normal within 7 days of drug discontinuation. 

Xylometazoline is contraindicated in patients with narrow-angle glaucoma, because the drug may increase intraocular pressure, and in patients receiving tricyclic antidepressants, because of the potential for adverse cardiovascular effects. 

These drugs are sedating, and have a variety of untoward effects. The most commonly seen major adverse effect is postural hypotension. Other adverse effects include anticholinergic effects (e.g., dry mouth, constipation, urinary retention, paralytic ileus, and tachycardia), blurred vision, increased intraocular pressure, gynecomastia, galactorrhea, and changes in libido. Glucose tolerance may also be affected. 

Other such enzyme deficiencies have been revealed through an individual s adverse reaction to drugs. More than 90% of Orientals are genetically rapid N-acetylators of isoniazid (6.12), whereas only 40% of black or white citizens of the United States showed this trait (Kalow, 1962). Rapid acetylators produce acetylhydrazine, which can cause liver damage. The same inheritance controls the acetylation (deactivation) of the sulphonamide antibacterials. The rise of intraocular pressure when glucocorticoids are placed in the eye is another pharmacogenetic effect. Low and high responses are shown by 66% and 5%, respectively, of a sample white population. 

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