Drug Interactions between dexamethasone ophthalmic and troleandomycin

Troleandomycin is primarily excreted by the liver and may accumulate in patients with impaired hepatic function. In addition, the use of troleandomycin has been associated with an allergic type of cholestatic hepatitis, particularly in patients receiving the drug for more than 2 weeks or given repeated courses. Therapy with troleandomycin should be administered cautiously in patients with liver and/or biliary disease. Liver function tests should be monitored during prolonged or repeated courses of therapy, and the drug discontinued if abnormalities develop.

Prolonged use of corticosteroids may cause posterior subcapsular cataracts and elevated intraocular pressure, the latter of which may lead to glaucoma and/or damage to the optic nerves. Therapy with ophthalmic corticosteroids should be administered cautiously in patients with a history of cataracts, glaucoma, or increased intraocular pressure. If these agents are used for more than 10 days, the manufacturers recommend that intraocular pressure be routinely monitored, including in children. The equatorial and posterior subcapsular portions of the lens should be examined for changes.

Clostridioides difficile-associated diarrhea (CDAD), formerly pseudomembranous colitis, has been reported with almost all antibacterial drugs and may range from mild diarrhea to fatal colitis. The most common culprits include clindamycin and lincomycin. Antibacterial therapy alters the normal flora of the colon, leading to overgrowth of C difficile, whose toxins A and B contribute to CDAD development. Morbidity and mortality are increased with hypertoxin-producing strains of C difficile; these infections can be resistant to antimicrobial therapy and may require colectomy. CDAD must be considered in all patients who present with diarrhea after antibacterial use. Since CDAD has been reported to occur more than 2 months after antibacterial use, careful medical history is necessary. Therapy with broad-spectrum antibacterials and other agents with significant antibacterial activity should be administered cautiously in patients with history of gastrointestinal disease, particularly colitis; pseudomembranous colitis (generally characterized by severe, persistent diarrhea and severe abdominal cramps, and sometimes associated with the passage of blood and mucus), if it occurs, may be more severe in these patients and may be associated with flares in underlying disease activity. Antibacterial drugs not directed against C difficile may need to be stopped if CDAD is suspected or confirmed. Appropriate fluid and electrolyte management, protein supplementation, antibacterial treatment of C difficile, and surgical evaluation should be started as clinically indicated.

Prolonged use of corticosteroids may cause posterior subcapsular cataracts and elevated intraocular pressure, the latter of which may lead to glaucoma and/or damage to the optic nerves. Therapy with ophthalmic corticosteroids should be administered cautiously in patients with a history of cataracts, glaucoma, or increased intraocular pressure. If these agents are used for more than 10 days, the manufacturers recommend that intraocular pressure be routinely monitored, including in children. The equatorial and posterior subcapsular portions of the lens should be examined for changes.

Troleandomycin is primarily excreted by the liver and may accumulate in patients with impaired hepatic function. In addition, the use of troleandomycin has been associated with an allergic type of cholestatic hepatitis, particularly in patients receiving the drug for more than 2 weeks or given repeated courses. Therapy with troleandomycin should be administered cautiously in patients with liver and/or biliary disease. Liver function tests should be monitored during prolonged or repeated courses of therapy, and the drug discontinued if abnormalities develop.

The use of ophthalmic corticosteroids is contraindicated in most viral diseases of the cornea and conjunctiva, including epithelial herpes simplex keratitis (dendritic keratitis), vaccinia, and varicella; fungal diseases of ocular structures; mycobacterial infections, including tuberculosis, of the eye; and any acute, purulent, untreated ocular infections. Corticosteroids may decrease host resistance to infectious agents, thus prolonging the course and/or exacerbating the severity of the infection while encouraging the development of new or secondary infection. In addition, administration of ophthalmic corticosteroids in severe ocular disease, especially acute herpes simplex keratitis, may lead to excessive corneal and scleral thinning, increasing the risk for perforation. In less serious ocular infections, therapy with ophthalmic corticosteroids may be administered but only with caution and accompanied by appropriate antimicrobial agents. Besides compromising host immune response, corticosteroids may also mask the symptoms of infection, thus hindering the recognition of potential ineffectiveness of the antibiotic therapy. If infection does not improve or becomes worse during administration of an ophthalmic corticosteroid, the drug should be discontinued and other appropriate therapy initiated.