Can you take Chloramphenicol / hydrocortisone / polymyxin b ophthalmic with Propylthiouracil?

Propylthiouracil has a major potential interaction with Alcoholism.

The use of thioamide antithyroid agents has been associated with hepatotoxic effects, including transient elevations of serum transaminases and, rarely, cholestatic jaundice, fulminant hepatitis, hepatic necrosis, encephalopathy and death. Therapy with thioamide derivatives should be administered cautiously in patients with preexisting liver disease, a history of alcohol abuse, or hepatitis. Treatment should be discontinued if deterioration in liver function or other signs of hepatic injury occur. The jaundice associated with methimazole-induced hepatitis may persist for several weeks after withdrawal of the medication.

Propylthiouracil has a major potential interaction with Bleeding Disorder.

Thioamide antithyroid agents may interfere with the action of vitamin K and have been reported in isolated cases to induce hypoprothombinemia and bleeding. Myelosuppression rarely resulting in thrombocytopenia has also been reported. Therapy with thioamide derivatives should be administered cautiously in patients with significant active bleeding or a hemorrhagic diathesis, including hemostatic and/or coagulation defects associated with hemophilia, vitamin K deficiency, hypoprothombinemia, thrombocytopenia, thrombocytopathy, or severe hepatic impairment. Clinical monitoring of prothrombin time or INR is recommended.

The chloramphenicol ophthalmic in chloramphenicol / hydrocortisone / polymyxin b ophthalmic has a major potential interaction with Bone Marrow Depression/Low Blood Counts.

Chloramphenicol may cause bone marrow depression and other hematologic toxicities, which can be irreversible or reversible. The former type is independent of dose and results in aplastic anemia with a high rate of mortality, generally from hemorrhage or infection. It has been reported following both systemic and topical administration of chloramphenicol and has an estimated incidence of 1 in 25,000 to 1 in 40,000 courses of therapy. Bone marrow aplasia or hypoplasia may occur after a single dose but more often develops weeks or months after the drug has been discontinued. A reversible myelosuppression occurs much more frequently and is characterized by anemia, vacuolation of red blood cells, decreased reticulocyte count, leukopenia, thrombocytopenia, increased serum iron concentrations, and increased serum iron-binding capacity. It is dose-dependent, occurring regularly at chloramphenicol dosages exceeding 4 g/day (in adults) or at plasma drug concentrations >= 25 mcg/mL, and usually responds to withdrawal of the drug. Therapy with chloramphenicol should be administered cautiously, if at all, in patients with preexisting blood dyscrasias and/or bone marrow depression. Complete blood counts and differential reticulocyte counts should be performed in all patients prior to initiating therapy and approximately every 2 days during therapy. Marked depression of blood counts and/or development of other hematologic abnormalities may be indication for withdrawal of chloramphenicol therapy.

The hydrocortisone ophthalmic in chloramphenicol / hydrocortisone / polymyxin b ophthalmic 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.

Propylthiouracil has a major potential interaction with Coagulation Defects and Disorders.

Thioamide antithyroid agents may interfere with the action of vitamin K and have been reported in isolated cases to induce hypoprothombinemia and bleeding. Myelosuppression rarely resulting in thrombocytopenia has also been reported. Therapy with thioamide derivatives should be administered cautiously in patients with significant active bleeding or a hemorrhagic diathesis, including hemostatic and/or coagulation defects associated with hemophilia, vitamin K deficiency, hypoprothombinemia, thrombocytopenia, thrombocytopathy, or severe hepatic impairment. Clinical monitoring of prothrombin time or INR is recommended.

The hydrocortisone ophthalmic in chloramphenicol / hydrocortisone / polymyxin b ophthalmic 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 hydrocortisone ophthalmic in chloramphenicol / hydrocortisone / polymyxin b ophthalmic 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.

Propylthiouracil has a major potential interaction with Liver Disease.

The use of thioamide antithyroid agents has been associated with hepatotoxic effects, including transient elevations of serum transaminases and, rarely, cholestatic jaundice, fulminant hepatitis, hepatic necrosis, encephalopathy and death. Therapy with thioamide derivatives should be administered cautiously in patients with preexisting liver disease, a history of alcohol abuse, or hepatitis. Treatment should be discontinued if deterioration in liver function or other signs of hepatic injury occur. The jaundice associated with methimazole-induced hepatitis may persist for several weeks after withdrawal of the medication.

Propylthiouracil has a major potential interaction with Neutropenia.

The use of thioamide antithyroid agents may infrequently be associated with the development of blood dyscrasias, primarily agranulocytosis but also leukopenia, thrombocytopenia, and aplastic anemia. Most cases of agranulocytosis occur within the first two months of therapy, with incidence declining gradually thereafter. Patients older than 40 years of age and those receiving more than 40 mg/day of methimazole appear to be at substantially increased risk (a dosage association has not been reported for propylthiouracil). Therapy with thioamide derivatives should be administered cautiously in patients with or predisposed to blood dyscrasias and/or bone marrow depression. Clinical monitoring of hematopoietic function is recommended, with particular focus on leukocyte and differential counts. Because leukopenia (i.e. leukocyte count < 4000/mm3) may also occur in 10% of patients with untreated hyperthyroidism and is often associated with relative granulocytopenia, baseline count should be determined prior to initiating antithyroid medication. Patients should be instructed to immediately report during therapy any signs or symptoms suggestive of myelosuppression such as fever, sore throat, local infection, easy bruising, or bleeding. Cessation of antithyroid drug and institution of appropriate supportive measures are necessary if agranulocytosis or aplastic anemia develops.

Propylthiouracil has a major potential interaction with Thrombocytopathy.

Thioamide antithyroid agents may interfere with the action of vitamin K and have been reported in isolated cases to induce hypoprothombinemia and bleeding. Myelosuppression rarely resulting in thrombocytopenia has also been reported. Therapy with thioamide derivatives should be administered cautiously in patients with significant active bleeding or a hemorrhagic diathesis, including hemostatic and/or coagulation defects associated with hemophilia, vitamin K deficiency, hypoprothombinemia, thrombocytopenia, thrombocytopathy, or severe hepatic impairment. Clinical monitoring of prothrombin time or INR is recommended.

Propylthiouracil has a major potential interaction with Thrombocytopenia.

The use of thioamide antithyroid agents may infrequently be associated with the development of blood dyscrasias, primarily agranulocytosis but also leukopenia, thrombocytopenia, and aplastic anemia. Most cases of agranulocytosis occur within the first two months of therapy, with incidence declining gradually thereafter. Patients older than 40 years of age and those receiving more than 40 mg/day of methimazole appear to be at substantially increased risk (a dosage association has not been reported for propylthiouracil). Therapy with thioamide derivatives should be administered cautiously in patients with or predisposed to blood dyscrasias and/or bone marrow depression. Clinical monitoring of hematopoietic function is recommended, with particular focus on leukocyte and differential counts. Because leukopenia (i.e. leukocyte count < 4000/mm3) may also occur in 10% of patients with untreated hyperthyroidism and is often associated with relative granulocytopenia, baseline count should be determined prior to initiating antithyroid medication. Patients should be instructed to immediately report during therapy any signs or symptoms suggestive of myelosuppression such as fever, sore throat, local infection, easy bruising, or bleeding. Cessation of antithyroid drug and institution of appropriate supportive measures are necessary if agranulocytosis or aplastic anemia develops.

Propylthiouracil has a moderate potential interaction with Thyroid Disease.

Propylthiouracil may cause hypothyroidism and it should be used with caution in patients with an impaired thyroid function. Routine monitoring of TSH and free T4 levels with adjustments in dosing to maintain a euthyroid state is recommended.

Propylthiouracil has a major potential interaction with Vitamin K Deficiency.

Thioamide antithyroid agents may interfere with the action of vitamin K and have been reported in isolated cases to induce hypoprothombinemia and bleeding. Myelosuppression rarely resulting in thrombocytopenia has also been reported. Therapy with thioamide derivatives should be administered cautiously in patients with significant active bleeding or a hemorrhagic diathesis, including hemostatic and/or coagulation defects associated with hemophilia, vitamin K deficiency, hypoprothombinemia, thrombocytopenia, thrombocytopathy, or severe hepatic impairment. Clinical monitoring of prothrombin time or INR is recommended.