Can you take Tobradex ST with Vitamin D3?

The cholecalciferol in Vitamin D3 has a moderate potential interaction with Arrhythmia.

Vitamin D analogs function to increase serum calcium concentrations and can exacerbate arrhythmias, particularly in patients receiving cardiac glycosides. Therapy with vitamin D analogs should be administered cautiously in patients with or predisposed to cardiac arrhythmias. Clinical monitoring of serum electrolyte concentrations and cardiac function is recommended.

The cholecalciferol in Vitamin D3 has a moderate potential interaction with Biliary Obstruction.

Vitamin D analogs are fat soluble and oral formulations require bile for adequate intestinal absorption. Hepatic and/or biliary dysfunction decrease the absorption of vitamin D analogs. Metabolites of vitamin D analogs are primarily excreted in bile and feces. Ergocalciferol, cholecalciferol, and dihydrotachysterol undergo hepatic hydroxylation during metabolic activation. Hepatic impairment can alter the metabolic and therapeutic activity of certain vitamin D analogs. Alternative vitamin D analogs such as calcitriol (active form) may be considered in patients with compromised hepatic function.

The dexAMETHasone ophthalmic in Tobradex ST has a major potential interaction with Cataract.

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.

The dexAMETHasone ophthalmic in Tobradex ST has a major potential interaction with Eye Conditions.

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.

The dexAMETHasone ophthalmic in Tobradex ST has a major potential interaction with Glaucoma/Intraocular Hypertension.

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.

The cholecalciferol in Vitamin D3 has a major potential interaction with Hypercalcemia.

Vitamin D analogs such as calciferol and ergocalciferol should not be given to patients with hypercalcemia, malabsorption syndrome, or evidence of vitamin D toxicity.

The cholecalciferol in Vitamin D3 has a moderate potential interaction with Liver Disease.

Vitamin D analogs are fat soluble and oral formulations require bile for adequate intestinal absorption. Hepatic and/or biliary dysfunction decrease the absorption of vitamin D analogs. Metabolites of vitamin D analogs are primarily excreted in bile and feces. Ergocalciferol, cholecalciferol, and dihydrotachysterol undergo hepatic hydroxylation during metabolic activation. Hepatic impairment can alter the metabolic and therapeutic activity of certain vitamin D analogs. Alternative vitamin D analogs such as calcitriol (active form) may be considered in patients with compromised hepatic function.

The cholecalciferol in Vitamin D3 has a major potential interaction with Malabsorption Syndrome.

Vitamin D analogs such as calciferol and ergocalciferol should not be given to patients with hypercalcemia, malabsorption syndrome, or evidence of vitamin D toxicity.

The cholecalciferol in Vitamin D3 has a moderate potential interaction with Phosphate Imbalance.

Vitamin D analogs administered in the presence of hyperphosphatemia can result in precipitation of calcium-phosphate deposits within the vascular or renal systems or other soft tissue calcifications. A solubility product (Serum Calcium X Phosphate) should not exceed 70. Serum electrolyte concentrations should be corrected prior to vitamin D analog therapy and monitored during therapy.

The cholecalciferol in Vitamin D3 has a moderate potential interaction with Renal Dysfunction.

Ergocalciferol and cholecalciferol undergo renal biotransformation during metabolic activation. Renal impairment can alter metabolic and therapeutic activity of certain vitamin D analogs. Alternative vitamin D analogs such as dihydrotachysterol (hepatic activation) and calcitriol (active form) may be considered in patients with compromised renal function.