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Antidote preparations, Immunosuppressant

Methotrexate inhibits dihydrofolic acid reductase. Dihydrofolates must be reduced to tetrahydrofolates by this enzyme before they can be utilized as carriers of one-carbon groups in the synthesis of p.r.n. nucleotides and thymidylate. Therefore, methotrexate interferes with DNA synthesis, repair, and cellular replication. Actively proliferating tissues such as malignant cells, bone marrow, fetal cells, buccal and intestinal mucosa, and cells of the urinary bladder are in general more sensitive to this effect of methotrexate. When cellular proliferation in malignant tissues is greater than in most normal tissues, methotrexate may impair malignant growth without irreversible damage to normal tissues

Oral-

• Choriocarcinoma: 15-30 mg daily for 5 days, repeat after an interval of ≥1 wk for 3-5 courses.
• Acute lymphoblastic leukaemia: Maintenance: 15 mg/m2 once or twice wkly, with other agents.
• Burkitt's lymphoma: 10-25 mg daily for 4-8 days, repeated after 7-10 days.
• Psoriasis: 10-25 mg wkly as a single dose, adjust subsequent doses based on response.
• Rheumatoid arthritis: 7.5 mg once wkly, adjust by response. Not more than 20 mg/wk.
• Mycosis fungoides: 2.5-10 mg daily to induce remission.
• Crohn's disease: 12.5-22.5 mg once wkly for up to 1 yr.

Parenteral-

• Psoriasis: 10-25 mg wkly as a single dose. Adjust subsequent doses based on response. May be given via IV/IM admin.

Intramuscular-

• Choriocarcinoma: 15-30 mg daily for 5 days. Repeat after at least 1 wk for 3-5 courses. Alternatively, 0.25-1 mg/kg (max: 60 mg) every 48 hr for 4 doses followed by folinic acid rescue, repeat at intervals of 7 days for 4 or more courses.
• Mycosis fungoides: 50 mg wkly as a single dose or 2 divided doses.
• Acute lymphoblastic leukaemia: Maintenance: 15 mg/m² once or twice wkly, with other agents.
• Crohn's disease: 25 mg once wkly for 16 wk. Maintenance: 15 mg wkly.

Intrathecal-

• Meningeal leukaemia: 12 mg/m² (max 15 mg) once wkly for 2-3 wk, then once mthly. Alternatively, 200-500 mcg/kg every 2-5 day until CSF cell count is normalised.

Intravenous-

• Osteosarcoma: Initial recommended dose: 12 g/m² as a 4-hr infusion, followed by folinic acid, as part of combined therapy. May increase dose to 15 g/m² in subsequent treatments if initial dosage is insufficient to achieve peak serum methotrexate levels of 454 mcg/mL at the end of the infusion. Methotrexate infusion is administered on postoperative wk 4, 5, 6, 7, 11, 12, 15, 16, 29, 30, 44 and 45; in combination with other chemotherapy agents. Folinic acid can be given orally, IM or IV inj starting 24 hr after the beginning of the methotrexate infusion. Give via parenteral routes If patient experiences GI toxicity (e.g., nausea, vomiting). Usual dosage of folinic acid: 15 mg every 6 hr for a total of 60 hr or a total of 10 doses.
• Breast cancer: 10-60 mg/m² often with cyclophosphamide and fluorouracil.
• Advanced lymphosarcoma: Up to 30 mg/kg, followed by folinic acid rescue.
• Acute lymphoblastic leukaemia: Maintenance: 2.5 mg/kg every 14 days.

Should be taken on an empty stomach. Best taken on an empty stomach. May be taken with meals to reduce GI discomfort. Avoid taking with milk-rich products.

Ulceration of the mouth and GI disturbances (e.g. stomatitis and diarrhoea), bone marrow depression, hepatotoxicity, renal failure, skin reactions, alopecia, ocular irritation, arachnoiditis in intrathecal use, megaloblastic anaemia, osteoporosis, precipitation of diabetes, arthralgias, necrosis of soft tissue and bone, anaphylaxis, impaired fertility.

Severe renal or hepatic impairment, pre-existing profound bone marrow suppression in patients with psoriasis or rheumatoid arthritis, alcoholic liver disease, AIDS, pre-existing blood dyscrasias, pregnancy (in patients with psoriasis or rheumatoid arthritis), breast-feeding.

Hepatic or renal impairment, bone marrow depression, elderly, neonates. Ulcerative disorders of the GI tract. Monitor haematological, renal and hepatic function, and GI toxicity regularly.

Decreased effectiveness with folic acid and its derivatives.

Pregnancy category X. Studies in animals or human beings have demonstrated fetal abnormalities or there is evidence of fetal risk based on human experience or both, and the risk of the use of the drug in pregnant women clearly outweighs any possible benefit. The drug is contraindicated in women who are or may become pregnant.

Nausea, vomiting, alopecia, melena, and renal failure.

Intramuscular: Dilute powder with D5W or normal saline to a concentration ≤25 mg/ml (20 mg and 50 mg vials) and 50 mg/ml (1 g vial).

Intrathecal: Reconstitute to 2.5-5 mg/ml with normal saline, D5W, lactated Ringer's, or Elliott's B solution. Use preservative-free preparations.

Intravenous: Dilute powder with D5W or normal saline to a concentration ≤25 mg/ml (20 mg and 50 mg vials) and 50 mg/ml (1 g vial).

Parenteral: Dilute powder with D5W or normal saline to a concentration ≤25 mg/ml (20 mg and 50 mg vials) and 50 mg/ml (1 g vial).

Store at room temperature (15-25°C).

Anti-fibrinolytic drugs, Haemostatic drugs

This is a preparation of tranexamic acid (trans-4 aminomethyl-cyclohexanecarboxylic acid). Tranexamic acid is a substance endowed with a strong antifibrinolytic action and both in vivo and in vitro it has proved to be 10 times more active than conventional hemostatics, depending on the test. The antihemorrhagic action of tranexamic acid is essentially due to an inhibition of the plasminogen activation of both exogenous activators like streptokinase and endogenous ones like urokinase and the plasminogen tissue activator. This fact is particularly important for the clinical use of Tranexamic Acid, because it ensures an antihemorrhagic activity with an antifibrinolytic mechanism under a variety of conditions.

The acute toxicity of Tranexamic Acid is extremely low and chronic toxicity almost non-existent. Tranexamic Acid is well absorbed by oral route and the effect is already seen 15-30 minutes after administration. It is excreted mainly by renal route but more slowly than conventional hemostatics. These features make the Tranexamic Acid effect more lasting than those conventional hemostatics. Considerably lower single doses of Tranexamic Acid can thus be administered at greater intervals without the drug plasma levels dropping to inefficient levels of antifibrinolytic activity between one dose and the other.

Tranexamic Acid at therapeutic doses does not interfere with clotting processes and even a prolonged administration has not been seen to be accompanied by any tendency to thrombophilia.

Adults-

• The usual dose: 500-1000 mg 3 times daily.
• For prophylaxis: The mean recommended daily doses are 0.5-1 gm orally, 500 mg by the parenteral (intravenous or intramuscular) route.
• For therapy of hemorrhagic manifestations: the oral dose increases to 1-3 gm given in divided doses: in cases of particular seriousness and urgency, begin by injecting an ampoule (500 mg) slowly by intravenous route and administer the necessary subsequent oral doses.

Children-

• For prophylaxis: For every kg of body weight from 5-10 mg are orally administered daily in divided doses.
• For therapeutic purposes: The oral doses are doubled (from 10 to 20 mg/kg), while the intravenous and intramuscular treatment is begun with 10 mg/kg (=0.5 ml every 5 kg) by the slow intravenous route, continuing the oral administration up to the required dose. Where it is more convenient (e.g. in small babies) the ampoules, diluted in a little sweetened water, maybe orally administered instead of the Capsules.

Elderly patients: No reduction in dosage is necessary unless there is evidence of renal failure.

Known individual hypersensitivity to the product. Thromboembolic disease, arterial and venous thrombosis, endocavitary hemorrhages, serious kidney failure.

Tranexamic Acid is a synthetic Amino Acid that is incompatible with solutions containing penicillins (eg: Benzyl penicillin). Thrombolytic drugs like Streptokinase & Urokinase antagonise the antifibrinolytic action of Tranexamic Acid. The potential for thrombus formation may be increased by concomitant administration of estrogen containing drugs, like oral contraceptives. Direct admixture of Tranexamic Acid with whole blood should be avoided during Transfusion.

Since the transplacental passage of the drug and its possible effects on the fetus are unknown, Tranexamic Acid should not be administered during known and presumed pregnancy. Tranexamic Acid passes into breast milk to a concentration of approximately one hundredth of the concentration in the maternal blood. An antifibrinolytic effect in the infant is unlikely.

Store in a dry place at 15-30°C, away from light and keep out of children's reach.

Anti-fibrinolytic drugs, Haemostatic drugs

This is a preparation of tranexamic acid (trans-4 aminomethyl-cyclohexanecarboxylic acid). Tranexamic acid is a substance endowed with a strong antifibrinolytic action and both in vivo and in vitro it has proved to be 10 times more active than conventional hemostatics, depending on the test. The antihemorrhagic action of tranexamic acid is essentially due to an inhibition of the plasminogen activation of both exogenous activators like streptokinase and endogenous ones like urokinase and the plasminogen tissue activator. This fact is particularly important for the clinical use of Tranexamic Acid, because it ensures an antihemorrhagic activity with an antifibrinolytic mechanism under a variety of conditions.

The acute toxicity of Tranexamic Acid is extremely low and chronic toxicity almost non-existent. Tranexamic Acid is well absorbed by oral route and the effect is already seen 15-30 minutes after administration. It is excreted mainly by renal route but more slowly than conventional hemostatics. These features make the Tranexamic Acid effect more lasting than those conventional hemostatics. Considerably lower single doses of Tranexamic Acid can thus be administered at greater intervals without the drug plasma levels dropping to inefficient levels of antifibrinolytic activity between one dose and the other.

Tranexamic Acid at therapeutic doses does not interfere with clotting processes and even a prolonged administration has not been seen to be accompanied by any tendency to thrombophilia.

Adults-

• The usual dose: 500-1000 mg 3 times daily.
• For prophylaxis: The mean recommended daily doses are 0.5-1 gm orally, 500 mg by the parenteral (intravenous or intramuscular) route.
• For therapy of hemorrhagic manifestations: the oral dose increases to 1-3 gm given in divided doses: in cases of particular seriousness and urgency, begin by injecting an ampoule (500 mg) slowly by intravenous route and administer the necessary subsequent oral doses.

Children-

• For prophylaxis: For every kg of body weight from 5-10 mg are orally administered daily in divided doses.
• For therapeutic purposes: The oral doses are doubled (from 10 to 20 mg/kg), while the intravenous and intramuscular treatment is begun with 10 mg/kg (=0.5 ml every 5 kg) by the slow intravenous route, continuing the oral administration up to the required dose. Where it is more convenient (e.g. in small babies) the ampoules, diluted in a little sweetened water, maybe orally administered instead of the Capsules.

Elderly patients: No reduction in dosage is necessary unless there is evidence of renal failure.

Known individual hypersensitivity to the product. Thromboembolic disease, arterial and venous thrombosis, endocavitary hemorrhages, serious kidney failure.

Tranexamic Acid is a synthetic Amino Acid that is incompatible with solutions containing penicillins (eg: Benzyl penicillin). Thrombolytic drugs like Streptokinase & Urokinase antagonise the antifibrinolytic action of Tranexamic Acid. The potential for thrombus formation may be increased by concomitant administration of estrogen containing drugs, like oral contraceptives. Direct admixture of Tranexamic Acid with whole blood should be avoided during Transfusion.

Since the transplacental passage of the drug and its possible effects on the fetus are unknown, Tranexamic Acid should not be administered during known and presumed pregnancy. Tranexamic Acid passes into breast milk to a concentration of approximately one hundredth of the concentration in the maternal blood. An antifibrinolytic effect in the infant is unlikely.

Store in a dry place at 15-30°C, away from light and keep out of children's reach.

Anti-fibrinolytic drugs, Haemostatic drugs

This is a preparation of tranexamic acid (trans-4 aminomethyl-cyclohexanecarboxylic acid). Tranexamic acid is a substance endowed with a strong antifibrinolytic action and both in vivo and in vitro it has proved to be 10 times more active than conventional hemostatics, depending on the test. The antihemorrhagic action of tranexamic acid is essentially due to an inhibition of the plasminogen activation of both exogenous activators like streptokinase and endogenous ones like urokinase and the plasminogen tissue activator. This fact is particularly important for the clinical use of Tranexamic Acid, because it ensures an antihemorrhagic activity with an antifibrinolytic mechanism under a variety of conditions.

The acute toxicity of Tranexamic Acid is extremely low and chronic toxicity almost non-existent. Tranexamic Acid is well absorbed by oral route and the effect is already seen 15-30 minutes after administration. It is excreted mainly by renal route but more slowly than conventional hemostatics. These features make the Tranexamic Acid effect more lasting than those conventional hemostatics. Considerably lower single doses of Tranexamic Acid can thus be administered at greater intervals without the drug plasma levels dropping to inefficient levels of antifibrinolytic activity between one dose and the other.

Tranexamic Acid at therapeutic doses does not interfere with clotting processes and even a prolonged administration has not been seen to be accompanied by any tendency to thrombophilia.

Adults-

• The usual dose: 500-1000 mg 3 times daily.
• For prophylaxis: The mean recommended daily doses are 0.5-1 gm orally, 500 mg by the parenteral (intravenous or intramuscular) route.
• For therapy of hemorrhagic manifestations: the oral dose increases to 1-3 gm given in divided doses: in cases of particular seriousness and urgency, begin by injecting an ampoule (500 mg) slowly by intravenous route and administer the necessary subsequent oral doses.

Children-

• For prophylaxis: For every kg of body weight from 5-10 mg are orally administered daily in divided doses.
• For therapeutic purposes: The oral doses are doubled (from 10 to 20 mg/kg), while the intravenous and intramuscular treatment is begun with 10 mg/kg (=0.5 ml every 5 kg) by the slow intravenous route, continuing the oral administration up to the required dose. Where it is more convenient (e.g. in small babies) the ampoules, diluted in a little sweetened water, maybe orally administered instead of the Capsules.

Elderly patients: No reduction in dosage is necessary unless there is evidence of renal failure.

Known individual hypersensitivity to the product. Thromboembolic disease, arterial and venous thrombosis, endocavitary hemorrhages, serious kidney failure.

Tranexamic Acid is a synthetic Amino Acid that is incompatible with solutions containing penicillins (eg: Benzyl penicillin). Thrombolytic drugs like Streptokinase & Urokinase antagonise the antifibrinolytic action of Tranexamic Acid. The potential for thrombus formation may be increased by concomitant administration of estrogen containing drugs, like oral contraceptives. Direct admixture of Tranexamic Acid with whole blood should be avoided during Transfusion.

Since the transplacental passage of the drug and its possible effects on the fetus are unknown, Tranexamic Acid should not be administered during known and presumed pregnancy. Tranexamic Acid passes into breast milk to a concentration of approximately one hundredth of the concentration in the maternal blood. An antifibrinolytic effect in the infant is unlikely.

Store in a dry place at 15-30°C, away from light and keep out of children's reach.

Antidote preparations, Immunosuppressant

Methotrexate inhibits dihydrofolic acid reductase. Dihydrofolates must be reduced to tetrahydrofolates by this enzyme before they can be utilized as carriers of one-carbon groups in the synthesis of p.r.n. nucleotides and thymidylate. Therefore, methotrexate interferes with DNA synthesis, repair, and cellular replication. Actively proliferating tissues such as malignant cells, bone marrow, fetal cells, buccal and intestinal mucosa, and cells of the urinary bladder are in general more sensitive to this effect of methotrexate. When cellular proliferation in malignant tissues is greater than in most normal tissues, methotrexate may impair malignant growth without irreversible damage to normal tissues

Oral-

• Choriocarcinoma: 15-30 mg daily for 5 days, repeat after an interval of ≥1 wk for 3-5 courses.
• Acute lymphoblastic leukaemia: Maintenance: 15 mg/m2 once or twice wkly, with other agents.
• Burkitt's lymphoma: 10-25 mg daily for 4-8 days, repeated after 7-10 days.
• Psoriasis: 10-25 mg wkly as a single dose, adjust subsequent doses based on response.
• Rheumatoid arthritis: 7.5 mg once wkly, adjust by response. Not more than 20 mg/wk.
• Mycosis fungoides: 2.5-10 mg daily to induce remission.
• Crohn's disease: 12.5-22.5 mg once wkly for up to 1 yr.

Parenteral-

• Psoriasis: 10-25 mg wkly as a single dose. Adjust subsequent doses based on response. May be given via IV/IM admin.

Intramuscular-

• Choriocarcinoma: 15-30 mg daily for 5 days. Repeat after at least 1 wk for 3-5 courses. Alternatively, 0.25-1 mg/kg (max: 60 mg) every 48 hr for 4 doses followed by folinic acid rescue, repeat at intervals of 7 days for 4 or more courses.
• Mycosis fungoides: 50 mg wkly as a single dose or 2 divided doses.
• Acute lymphoblastic leukaemia: Maintenance: 15 mg/m² once or twice wkly, with other agents.
• Crohn's disease: 25 mg once wkly for 16 wk. Maintenance: 15 mg wkly.

Intrathecal-

• Meningeal leukaemia: 12 mg/m² (max 15 mg) once wkly for 2-3 wk, then once mthly. Alternatively, 200-500 mcg/kg every 2-5 day until CSF cell count is normalised.

Intravenous-

• Osteosarcoma: Initial recommended dose: 12 g/m² as a 4-hr infusion, followed by folinic acid, as part of combined therapy. May increase dose to 15 g/m² in subsequent treatments if initial dosage is insufficient to achieve peak serum methotrexate levels of 454 mcg/mL at the end of the infusion. Methotrexate infusion is administered on postoperative wk 4, 5, 6, 7, 11, 12, 15, 16, 29, 30, 44 and 45; in combination with other chemotherapy agents. Folinic acid can be given orally, IM or IV inj starting 24 hr after the beginning of the methotrexate infusion. Give via parenteral routes If patient experiences GI toxicity (e.g., nausea, vomiting). Usual dosage of folinic acid: 15 mg every 6 hr for a total of 60 hr or a total of 10 doses.
• Breast cancer: 10-60 mg/m² often with cyclophosphamide and fluorouracil.
• Advanced lymphosarcoma: Up to 30 mg/kg, followed by folinic acid rescue.
• Acute lymphoblastic leukaemia: Maintenance: 2.5 mg/kg every 14 days.

Should be taken on an empty stomach. Best taken on an empty stomach. May be taken with meals to reduce GI discomfort. Avoid taking with milk-rich products.

Ulceration of the mouth and GI disturbances (e.g. stomatitis and diarrhoea), bone marrow depression, hepatotoxicity, renal failure, skin reactions, alopecia, ocular irritation, arachnoiditis in intrathecal use, megaloblastic anaemia, osteoporosis, precipitation of diabetes, arthralgias, necrosis of soft tissue and bone, anaphylaxis, impaired fertility.

Severe renal or hepatic impairment, pre-existing profound bone marrow suppression in patients with psoriasis or rheumatoid arthritis, alcoholic liver disease, AIDS, pre-existing blood dyscrasias, pregnancy (in patients with psoriasis or rheumatoid arthritis), breast-feeding.

Hepatic or renal impairment, bone marrow depression, elderly, neonates. Ulcerative disorders of the GI tract. Monitor haematological, renal and hepatic function, and GI toxicity regularly.

Decreased effectiveness with folic acid and its derivatives.

Pregnancy category X. Studies in animals or human beings have demonstrated fetal abnormalities or there is evidence of fetal risk based on human experience or both, and the risk of the use of the drug in pregnant women clearly outweighs any possible benefit. The drug is contraindicated in women who are or may become pregnant.

Nausea, vomiting, alopecia, melena, and renal failure.

Intramuscular: Dilute powder with D5W or normal saline to a concentration ≤25 mg/ml (20 mg and 50 mg vials) and 50 mg/ml (1 g vial).

Intrathecal: Reconstitute to 2.5-5 mg/ml with normal saline, D5W, lactated Ringer's, or Elliott's B solution. Use preservative-free preparations.

Intravenous: Dilute powder with D5W or normal saline to a concentration ≤25 mg/ml (20 mg and 50 mg vials) and 50 mg/ml (1 g vial).

Parenteral: Dilute powder with D5W or normal saline to a concentration ≤25 mg/ml (20 mg and 50 mg vials) and 50 mg/ml (1 g vial).

Store at room temperature (15-25°C).

Antidote preparations, Immunosuppressant

Methotrexate inhibits dihydrofolic acid reductase. Dihydrofolates must be reduced to tetrahydrofolates by this enzyme before they can be utilized as carriers of one-carbon groups in the synthesis of p.r.n. nucleotides and thymidylate. Therefore, methotrexate interferes with DNA synthesis, repair, and cellular replication. Actively proliferating tissues such as malignant cells, bone marrow, fetal cells, buccal and intestinal mucosa, and cells of the urinary bladder are in general more sensitive to this effect of methotrexate. When cellular proliferation in malignant tissues is greater than in most normal tissues, methotrexate may impair malignant growth without irreversible damage to normal tissues

Oral-

• Choriocarcinoma: 15-30 mg daily for 5 days, repeat after an interval of ≥1 wk for 3-5 courses.
• Acute lymphoblastic leukaemia: Maintenance: 15 mg/m2 once or twice wkly, with other agents.
• Burkitt's lymphoma: 10-25 mg daily for 4-8 days, repeated after 7-10 days.
• Psoriasis: 10-25 mg wkly as a single dose, adjust subsequent doses based on response.
• Rheumatoid arthritis: 7.5 mg once wkly, adjust by response. Not more than 20 mg/wk.
• Mycosis fungoides: 2.5-10 mg daily to induce remission.
• Crohn's disease: 12.5-22.5 mg once wkly for up to 1 yr.

Parenteral-

• Psoriasis: 10-25 mg wkly as a single dose. Adjust subsequent doses based on response. May be given via IV/IM admin.

Intramuscular-

• Choriocarcinoma: 15-30 mg daily for 5 days. Repeat after at least 1 wk for 3-5 courses. Alternatively, 0.25-1 mg/kg (max: 60 mg) every 48 hr for 4 doses followed by folinic acid rescue, repeat at intervals of 7 days for 4 or more courses.
• Mycosis fungoides: 50 mg wkly as a single dose or 2 divided doses.
• Acute lymphoblastic leukaemia: Maintenance: 15 mg/m² once or twice wkly, with other agents.
• Crohn's disease: 25 mg once wkly for 16 wk. Maintenance: 15 mg wkly.

Intrathecal-

• Meningeal leukaemia: 12 mg/m² (max 15 mg) once wkly for 2-3 wk, then once mthly. Alternatively, 200-500 mcg/kg every 2-5 day until CSF cell count is normalised.

Intravenous-

• Osteosarcoma: Initial recommended dose: 12 g/m² as a 4-hr infusion, followed by folinic acid, as part of combined therapy. May increase dose to 15 g/m² in subsequent treatments if initial dosage is insufficient to achieve peak serum methotrexate levels of 454 mcg/mL at the end of the infusion. Methotrexate infusion is administered on postoperative wk 4, 5, 6, 7, 11, 12, 15, 16, 29, 30, 44 and 45; in combination with other chemotherapy agents. Folinic acid can be given orally, IM or IV inj starting 24 hr after the beginning of the methotrexate infusion. Give via parenteral routes If patient experiences GI toxicity (e.g., nausea, vomiting). Usual dosage of folinic acid: 15 mg every 6 hr for a total of 60 hr or a total of 10 doses.
• Breast cancer: 10-60 mg/m² often with cyclophosphamide and fluorouracil.
• Advanced lymphosarcoma: Up to 30 mg/kg, followed by folinic acid rescue.
• Acute lymphoblastic leukaemia: Maintenance: 2.5 mg/kg every 14 days.

Should be taken on an empty stomach. Best taken on an empty stomach. May be taken with meals to reduce GI discomfort. Avoid taking with milk-rich products.

Ulceration of the mouth and GI disturbances (e.g. stomatitis and diarrhoea), bone marrow depression, hepatotoxicity, renal failure, skin reactions, alopecia, ocular irritation, arachnoiditis in intrathecal use, megaloblastic anaemia, osteoporosis, precipitation of diabetes, arthralgias, necrosis of soft tissue and bone, anaphylaxis, impaired fertility.

Severe renal or hepatic impairment, pre-existing profound bone marrow suppression in patients with psoriasis or rheumatoid arthritis, alcoholic liver disease, AIDS, pre-existing blood dyscrasias, pregnancy (in patients with psoriasis or rheumatoid arthritis), breast-feeding.

Hepatic or renal impairment, bone marrow depression, elderly, neonates. Ulcerative disorders of the GI tract. Monitor haematological, renal and hepatic function, and GI toxicity regularly.

Decreased effectiveness with folic acid and its derivatives.

Pregnancy category X. Studies in animals or human beings have demonstrated fetal abnormalities or there is evidence of fetal risk based on human experience or both, and the risk of the use of the drug in pregnant women clearly outweighs any possible benefit. The drug is contraindicated in women who are or may become pregnant.

Nausea, vomiting, alopecia, melena, and renal failure.

Intramuscular: Dilute powder with D5W or normal saline to a concentration ≤25 mg/ml (20 mg and 50 mg vials) and 50 mg/ml (1 g vial).

Intrathecal: Reconstitute to 2.5-5 mg/ml with normal saline, D5W, lactated Ringer's, or Elliott's B solution. Use preservative-free preparations.

Intravenous: Dilute powder with D5W or normal saline to a concentration ≤25 mg/ml (20 mg and 50 mg vials) and 50 mg/ml (1 g vial).

Parenteral: Dilute powder with D5W or normal saline to a concentration ≤25 mg/ml (20 mg and 50 mg vials) and 50 mg/ml (1 g vial).

Store at room temperature (15-25°C).

Antidote preparations, Immunosuppressant

Methotrexate inhibits dihydrofolic acid reductase. Dihydrofolates must be reduced to tetrahydrofolates by this enzyme before they can be utilized as carriers of one-carbon groups in the synthesis of p.r.n. nucleotides and thymidylate. Therefore, methotrexate interferes with DNA synthesis, repair, and cellular replication. Actively proliferating tissues such as malignant cells, bone marrow, fetal cells, buccal and intestinal mucosa, and cells of the urinary bladder are in general more sensitive to this effect of methotrexate. When cellular proliferation in malignant tissues is greater than in most normal tissues, methotrexate may impair malignant growth without irreversible damage to normal tissues

Oral-

• Choriocarcinoma: 15-30 mg daily for 5 days, repeat after an interval of ≥1 wk for 3-5 courses.
• Acute lymphoblastic leukaemia: Maintenance: 15 mg/m2 once or twice wkly, with other agents.
• Burkitt's lymphoma: 10-25 mg daily for 4-8 days, repeated after 7-10 days.
• Psoriasis: 10-25 mg wkly as a single dose, adjust subsequent doses based on response.
• Rheumatoid arthritis: 7.5 mg once wkly, adjust by response. Not more than 20 mg/wk.
• Mycosis fungoides: 2.5-10 mg daily to induce remission.
• Crohn's disease: 12.5-22.5 mg once wkly for up to 1 yr.

Parenteral-

• Psoriasis: 10-25 mg wkly as a single dose. Adjust subsequent doses based on response. May be given via IV/IM admin.

Intramuscular-

• Choriocarcinoma: 15-30 mg daily for 5 days. Repeat after at least 1 wk for 3-5 courses. Alternatively, 0.25-1 mg/kg (max: 60 mg) every 48 hr for 4 doses followed by folinic acid rescue, repeat at intervals of 7 days for 4 or more courses.
• Mycosis fungoides: 50 mg wkly as a single dose or 2 divided doses.
• Acute lymphoblastic leukaemia: Maintenance: 15 mg/m² once or twice wkly, with other agents.
• Crohn's disease: 25 mg once wkly for 16 wk. Maintenance: 15 mg wkly.

Intrathecal-

• Meningeal leukaemia: 12 mg/m² (max 15 mg) once wkly for 2-3 wk, then once mthly. Alternatively, 200-500 mcg/kg every 2-5 day until CSF cell count is normalised.

Intravenous-

• Osteosarcoma: Initial recommended dose: 12 g/m² as a 4-hr infusion, followed by folinic acid, as part of combined therapy. May increase dose to 15 g/m² in subsequent treatments if initial dosage is insufficient to achieve peak serum methotrexate levels of 454 mcg/mL at the end of the infusion. Methotrexate infusion is administered on postoperative wk 4, 5, 6, 7, 11, 12, 15, 16, 29, 30, 44 and 45; in combination with other chemotherapy agents. Folinic acid can be given orally, IM or IV inj starting 24 hr after the beginning of the methotrexate infusion. Give via parenteral routes If patient experiences GI toxicity (e.g., nausea, vomiting). Usual dosage of folinic acid: 15 mg every 6 hr for a total of 60 hr or a total of 10 doses.
• Breast cancer: 10-60 mg/m² often with cyclophosphamide and fluorouracil.
• Advanced lymphosarcoma: Up to 30 mg/kg, followed by folinic acid rescue.
• Acute lymphoblastic leukaemia: Maintenance: 2.5 mg/kg every 14 days.

Should be taken on an empty stomach. Best taken on an empty stomach. May be taken with meals to reduce GI discomfort. Avoid taking with milk-rich products.

Ulceration of the mouth and GI disturbances (e.g. stomatitis and diarrhoea), bone marrow depression, hepatotoxicity, renal failure, skin reactions, alopecia, ocular irritation, arachnoiditis in intrathecal use, megaloblastic anaemia, osteoporosis, precipitation of diabetes, arthralgias, necrosis of soft tissue and bone, anaphylaxis, impaired fertility.

Severe renal or hepatic impairment, pre-existing profound bone marrow suppression in patients with psoriasis or rheumatoid arthritis, alcoholic liver disease, AIDS, pre-existing blood dyscrasias, pregnancy (in patients with psoriasis or rheumatoid arthritis), breast-feeding.

Hepatic or renal impairment, bone marrow depression, elderly, neonates. Ulcerative disorders of the GI tract. Monitor haematological, renal and hepatic function, and GI toxicity regularly.

Decreased effectiveness with folic acid and its derivatives.

Pregnancy category X. Studies in animals or human beings have demonstrated fetal abnormalities or there is evidence of fetal risk based on human experience or both, and the risk of the use of the drug in pregnant women clearly outweighs any possible benefit. The drug is contraindicated in women who are or may become pregnant.

Nausea, vomiting, alopecia, melena, and renal failure.

Intramuscular: Dilute powder with D5W or normal saline to a concentration ≤25 mg/ml (20 mg and 50 mg vials) and 50 mg/ml (1 g vial).

Intrathecal: Reconstitute to 2.5-5 mg/ml with normal saline, D5W, lactated Ringer's, or Elliott's B solution. Use preservative-free preparations.

Intravenous: Dilute powder with D5W or normal saline to a concentration ≤25 mg/ml (20 mg and 50 mg vials) and 50 mg/ml (1 g vial).

Parenteral: Dilute powder with D5W or normal saline to a concentration ≤25 mg/ml (20 mg and 50 mg vials) and 50 mg/ml (1 g vial).

Store at room temperature (15-25°C).

Vitamin B1, B6 & B12 is indicated for the treatment of vitamin B1, B6 & B12 deficiency syndrome. It is also indicated for the supportive treatment of neuritis & non-inflammatory diseases of the nerves, e.g.- Diabetic neuropathy, Peripheral neuralgin, Lumbago, Myalgia, Optic neuritis, Sciatica, Facial neuralgia, Intercostal neuralgia, Spinal pain.

Specific combined vitamin preparations

Vitamin B1 converts carbohydrates, fatty acids and amino acids into energy, promotes healthy nerves, improves mood, strengthens the heart. Vitamin B6 forms RBCs, helps cells to make proteins, manufactures neurotransmitters e.g. serotonin and releases stored forms of energy, helps to prevent CVS diseases and stroke, helps to lift depression and eases insomnia. Vitamin B12 is essential for cell replication and important for RBC production, prevents anemia, helps to prevent depression, reduces nerve pain, numbness, tingling and lowers the risk of heart diseases.

The vitamin ingredients are absorbed well in per oral reception. It is widely distributed to most tissues and appears in breast milk. Within the cell, thiamine is mostly present as diphosphate. Thiamine is not stored to any appreciable extent in the body and amounts in excess of the body’s requirements are excreted in the urine as unchanged thiamine or as metabolites. Pyridoxine, pyridoxal and pyridoxamine are readily absorbed from the GIT following oral administration and are converted to the active forms of pyridoxal phosphate an pyridoxamine phosphate. They are stored mainly in liver where there is oxidation to 4-pyridoxic acid and other inactive metabolites, which are excreted in urine. As the dose increases, proportionally greater amounts are excreted unchanged in the urine.

Tablet: 1-3 Tablets per day or as advised by the physician.

Injection:

• In severe (acute) cases: 1 injection daily until the acute symptoms subside or taken as advised by the physician.
• In mild cases: 1 injection 2-3 times per week. Ampoules are preferably injected intramuscularly.

Use in children: There is no information on the use of this drug in children.

Generally well tolerated but allergic reactions may be observed in few cases.

Vitamin B1, Vitamin B6 and Vitamin B12 is contraindicated in patients on levodopa therapy, and in patients with hypersensitivity to any of the ingredients of the preparation.

Cyanocobalamin should not be given in patients with subacute degeneration of the spinal cord. Cyanocobalamin is not suitable form of vitamin B12 for the treatment of optic neuropathies associated with raised plasma concentrations of cyanocobalamin.

No drug interaction has been reported yet.

Oral tablet form is recommended but due to the presence of benzyl alcohol, injection is not recommended during pregnancy & lactation.

No overdosage symptoms are to be expected in the recommended dosage. If there is known overdose then treatment is symptomatic & supportive.

Keep out of reach of children. Store in a cool (below 25°C temperature) and dry place, protected from light.

Corticosteroid, Glucocorticoids, Triamcinolone & Combined preparations

The antiinflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition of arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Firstly, however, these glucocorticoids bind to the glucocorticoid receptors which translocate into the nucleus and bind DNA (GRE) and change genetic expression both positively and negatively. The immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.

Adults and children over 12 years of age: Initial dose is 60 mg. Dosage is usually adjusted within the range of 40 to 80 mg. For local areas, dose for adults is up to 10 mg for smaller areas and up to 40 mg for larger areas.

Children 6 to 12 years: Initial dose is 40 mg

Cushingoid syndrome, weakness, bruising or purpura, aggravation of infections, peptic ulcer, activation of latent or aggravation of existing diabetes, altered menstrual cycle, hirsutism.

Triamcinolone Acetonide injection is contraindicated in patients with a sensitivity to the active or inactive ingredients.

Triamcinolone Acetonide injection should be used cautiously in patients with ocular herpes simplex, nonspecific ulcerative colitis, active or latent peptic ulcer, renal insufficiency, hypertension, osteoporosis, Cushing's syndrome, diabetes mellitus, congestive heart failure, chronic nephritis.

Aminoglutethimide: Aminoglutethimide may lead to a loss of corticosteroid-induced adrenal suppression. 

Amphotericin B injection and potassium-depleting agents: When corticosteroids are administered concomitantly with potassium-depleting agents (ie, amphotericin B, diuretics), patients should be observed closely for development of hypokalemia. There have been cases reported in which concomitant use of amphotericin B and hydrocortisone was followed by cardiac enlargement and congestive heart failure. 

Antibiotics: Macrolide antibiotics have been reported to cause a significant decrease in corticosteroid clearance. 

Anticholinesterases: Concomitant use of anticholinesterase agents and corticosteroids may produce severe weakness in patients with myasthenia gravis. If possible, anticholinesterase agents should be withdrawn at least 24 hours before initiating corticosteroid therapy.
 
Anticoagulants, oral: Coadministration of corticosteroids and warfarin usually results in inhibition of response to warfarin, although there have been some conflicting reports. Therefore, coagulation indices should be monitored frequently to maintain the desired anticoagulant effect.
 
Antidiabetics: Because corticosteroids may increase blood glucose concentrations, dosage adjustments of antidiabetic agents may be required. 

Antitubercular drugs: Serum concentrations of isoniazid may be decreased. 

Cholestyramine: Cholestyramine may increase the clearance of corticosteroids. 

Cyclosporine: Increased activity of both cyclosporine and corticosteroids may occur when the two are used concurrently. Convulsions have been reported with this concurrent use. 

Digitalis glycosides: Patients on digitalis glycosides may be at increased risk of arrhythmias due to hypokalemia. 
Estrogens, including oral contraceptives: Estrogens may decrease the hepatic metabolism of certain corticosteroids, thereby increasing their effect. 

Hepatic enzyme inducers (eg, barbiturates, phenytoin, carbamazepine, rifampin): Drugs which induce hepatic microsomal drug metabolizing enzyme activity may enhance the metabolism of corticosteroids and require that the dosage of the corticosteroid be increased. 

Ketoconazole: Ketoconazole has been reported to decrease the metabolism of certain corticosteroids by up to 60%, leading to an increased risk of corticosteroid side effects. 

Nonsteroidal anti-inflammatory drugs (NSAIDs): Concomitant use of aspirin (or other nonsteroidal anti-inflammatory drugs) and corticosteroids increases the risk of gastrointestinal side effects. Aspirin should be used cautiously in conjunction with corticosteroids in hypoprothrombinemia. The clearance of salicylates may be increased with concurrent use of corticosteroids. 

Skin tests: Corticosteroids may suppress reactions to skin tests. 

Vaccines: Patients on prolonged corticosteroid therapy may exhibit a diminished response to toxoids and live or inactivated vaccines due to inhibition of antibody response. Corticosteroids may also potentiate the replication of some organisms contained in live attenuated vaccines. Routine administration of vaccines or toxoids should be deferred until corticosteroid therapy is discontinued if possible.

Triamcinolone Acetonide injection should be used during pregnancy, nursing mothers if the possible benefits of the medication justify the potential hazards to the fetus or nursing infant.

Use in the elderly: The common adverse effects of systemic corticosteroids such as osteoporosis or hypertension may be associated with more serious consequences in old age. Close clinical supervision is recommended.

Use in children: As corticosteroids can suppress growth, the development of infants and children on prolonged corticosteroid therapy should be carefully observed. Caution should be taken in the event of exposure to chicken pox, measles or other communicable diseases. Children should not be vaccinated or immunized while on corticosteroid therapy. Corticosteroids may also affect endogenous steroid production.

Treatment of acute overdosage is by supportive and symptomatic therapy. For chronic overdosage in the face of severe disease requiring continuous steroid therapy, the dosage of the corticosteroid may be reduced only temporarily, or alternate day treatment may be introduced.

Store at controlled room temperature, 20-25°C, avoid freezing and protect from light.

Corticosteroid, Glucocorticoids, Triamcinolone & Combined preparations

The antiinflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition of arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Firstly, however, these glucocorticoids bind to the glucocorticoid receptors which translocate into the nucleus and bind DNA (GRE) and change genetic expression both positively and negatively. The immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.

Adults and children over 12 years of age: Initial dose is 60 mg. Dosage is usually adjusted within the range of 40 to 80 mg. For local areas, dose for adults is up to 10 mg for smaller areas and up to 40 mg for larger areas.

Children 6 to 12 years: Initial dose is 40 mg

Cushingoid syndrome, weakness, bruising or purpura, aggravation of infections, peptic ulcer, activation of latent or aggravation of existing diabetes, altered menstrual cycle, hirsutism.

Triamcinolone Acetonide injection is contraindicated in patients with a sensitivity to the active or inactive ingredients.

Triamcinolone Acetonide injection should be used cautiously in patients with ocular herpes simplex, nonspecific ulcerative colitis, active or latent peptic ulcer, renal insufficiency, hypertension, osteoporosis, Cushing's syndrome, diabetes mellitus, congestive heart failure, chronic nephritis.

Aminoglutethimide: Aminoglutethimide may lead to a loss of corticosteroid-induced adrenal suppression. 

Amphotericin B injection and potassium-depleting agents: When corticosteroids are administered concomitantly with potassium-depleting agents (ie, amphotericin B, diuretics), patients should be observed closely for development of hypokalemia. There have been cases reported in which concomitant use of amphotericin B and hydrocortisone was followed by cardiac enlargement and congestive heart failure. 

Antibiotics: Macrolide antibiotics have been reported to cause a significant decrease in corticosteroid clearance. 

Anticholinesterases: Concomitant use of anticholinesterase agents and corticosteroids may produce severe weakness in patients with myasthenia gravis. If possible, anticholinesterase agents should be withdrawn at least 24 hours before initiating corticosteroid therapy.
 
Anticoagulants, oral: Coadministration of corticosteroids and warfarin usually results in inhibition of response to warfarin, although there have been some conflicting reports. Therefore, coagulation indices should be monitored frequently to maintain the desired anticoagulant effect.
 
Antidiabetics: Because corticosteroids may increase blood glucose concentrations, dosage adjustments of antidiabetic agents may be required. 

Antitubercular drugs: Serum concentrations of isoniazid may be decreased. 

Cholestyramine: Cholestyramine may increase the clearance of corticosteroids. 

Cyclosporine: Increased activity of both cyclosporine and corticosteroids may occur when the two are used concurrently. Convulsions have been reported with this concurrent use. 

Digitalis glycosides: Patients on digitalis glycosides may be at increased risk of arrhythmias due to hypokalemia. 
Estrogens, including oral contraceptives: Estrogens may decrease the hepatic metabolism of certain corticosteroids, thereby increasing their effect. 

Hepatic enzyme inducers (eg, barbiturates, phenytoin, carbamazepine, rifampin): Drugs which induce hepatic microsomal drug metabolizing enzyme activity may enhance the metabolism of corticosteroids and require that the dosage of the corticosteroid be increased. 

Ketoconazole: Ketoconazole has been reported to decrease the metabolism of certain corticosteroids by up to 60%, leading to an increased risk of corticosteroid side effects. 

Nonsteroidal anti-inflammatory drugs (NSAIDs): Concomitant use of aspirin (or other nonsteroidal anti-inflammatory drugs) and corticosteroids increases the risk of gastrointestinal side effects. Aspirin should be used cautiously in conjunction with corticosteroids in hypoprothrombinemia. The clearance of salicylates may be increased with concurrent use of corticosteroids. 

Skin tests: Corticosteroids may suppress reactions to skin tests. 

Vaccines: Patients on prolonged corticosteroid therapy may exhibit a diminished response to toxoids and live or inactivated vaccines due to inhibition of antibody response. Corticosteroids may also potentiate the replication of some organisms contained in live attenuated vaccines. Routine administration of vaccines or toxoids should be deferred until corticosteroid therapy is discontinued if possible.

Triamcinolone Acetonide injection should be used during pregnancy, nursing mothers if the possible benefits of the medication justify the potential hazards to the fetus or nursing infant.

Use in the elderly: The common adverse effects of systemic corticosteroids such as osteoporosis or hypertension may be associated with more serious consequences in old age. Close clinical supervision is recommended.

Use in children: As corticosteroids can suppress growth, the development of infants and children on prolonged corticosteroid therapy should be carefully observed. Caution should be taken in the event of exposure to chicken pox, measles or other communicable diseases. Children should not be vaccinated or immunized while on corticosteroid therapy. Corticosteroids may also affect endogenous steroid production.

Treatment of acute overdosage is by supportive and symptomatic therapy. For chronic overdosage in the face of severe disease requiring continuous steroid therapy, the dosage of the corticosteroid may be reduced only temporarily, or alternate day treatment may be introduced.

Store at controlled room temperature, 20-25°C, avoid freezing and protect from light.

is indicated for the relief of the inflammatory and pruritic manifestations of corticosteroid responsive dermatoses including atopic dermatitis, contact dermatitis, eczematous dermatitis, neurodermatitis, seborrheic dermatitis, insect bites, lichen simplex chronicus, exfoliative dermatitis, stasis dermatitis, nummular eczema, psoriasis and pruritus ani and vulvae.

Corticosteroid, Glucocorticoids, Triamcinolone & Combined preparations

Triamcinolone Acetonide (a derivative of Triamcinolone) in a compatible base. Topical steroids are primarily effective because of their anti-inflammatory, antipruritic & vasoconstrictive actions.

A small amount of Triamcinolone is gently rub to the affected area 1-2 times daily. Some cases of eczematised psoriasis may be treated more effectively by the application of Triamcinolone under an occlusive dressing.

Occlusive dressing technique: Gently rub a small amount of Triamcinolone on the lesion until it disappears. Then reapply, leaving a thin coating and cover with a pliable non porous film. For convenience apply Triamcinolone intermittently (12 hour occlusion during the night) followed by reapplication without occlusion, during the day.

Pediatric use: Triamcinolone should not be used in children under 8 years. Administration of topical corticosteroids to children should be limited to the least amount compatible with an effective therapeutic regimen. Chronic corticosteroid therapy may interfere with the growth and development of children. As children are more likely to get side effects, they should not normally be treated for longer than 5 days.

The following local side effects have been reported with topical corticosteroids, either with or without occlusive dressings: burning, itching, irritation, dryness, folliculitis, hypertrichosis, acneiform eruptions, hypopigmentation, perioral dermatitis and allergic contact dermatitis, maceration of the skin, secondary infection, skin atrophy, striae and miliaria.

Triamcinolone Acetonide is contraindicated in those patients with a history of hypersensitivity to any of the components of the preparation. It is also contraindicated in tuberculosis of the skin, fungus infections and viral diseases of the skin (Herpes simplex, chickenpox and vaccinia), perioral dermatitis, rosacea and ulcerative conditions.

If reactions or idiosyncrasies are encountered, Triamcinolone Acetonide should be discontinued. The use of topical steroids on infected areas should be attended with caution and careful observation, bearing in mind the potential spreading of infections by anti-inflammatory steroids and the possible advisability of discontinuing steroid therapy and/or initiating antibacterial measures.

Triamcinolone Acetonide should not be used on healthy skin or over large areas of skin and not to be used in the eye as there is potential risk of glaucoma and cataract. When steroids are applied for long periods of time (more than 4 weeks) the occurrence of atrophic striae is likely. Prolonged use on flexures and intertriginous areas is undesirable. Children may absorb proportionately larger amounts of topical corticosteroids and thus may be more susceptible to systemic toxicity. In infants, long term continuous topical steroid therapy should be avoided. Adrenal suppression can occur even without occlusion.

There are no adequate and well-controlled studies in pregnant women on teratogenic effects from topically applied corticosteroids. Therefore, topical corticosteroid should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus. It is not known whether topical administration of corticosteroid could result in sufficient systemic absorption to produce detectable quantities in breast milk. Systemically administered corticosteroids are secreted into breast milk in quantities not likely to have a deleterious effect on the infant. Nevertheless, caution should be exercised when topical corticosteroids are administered to a nursing woman.

Topically applied corticosteroids can be absorbed in sufficient amounts to produce systemic effects e.g., mild, reversible suppression of adrenal function, ecchymoses of the skin, peptic ulceration, hypertension, aggravation of infection, hirsutism, acne, edema and muscle weakness

Store in a cool & dry place. Protect from light.

Triamcinolone is indicated for the treatment and prophylaxis of the nasal symptoms of seasonal and perennial allergic rhinitis in adults and children 6 years of age and older.

Corticosteroid, Glucocorticoids, Nasal Steroid Preparations

The antiinflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition of arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Firstly, however, these glucocorticoids bind to the glucocorticoid receptors which translocate into the nucleus and bind DNA (GRE) and change genetic expression both positively and negatively. The immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.

Triamcinolone Acetonide is a more potent derivative of Triamcinolone and is approximately 8 times more potent than prednisone. Corticosteroids are very effective in the treatment of allergic diseases in man. When given by intranasal spray, Triamcinolone Acetonide provides relief from allergy-induced watery nasal discharge (rhinorrhea), nasal congestion, postnasal drip, sneezing, and itching of the back of the throat.

Adults and children 12 years of age and older: The recommended dose is 220 µgm as 2 sprays in each nostril once daily. Once symptoms are controlled patients can be maintained on 110 µgm (1 spray in each nostril once daily). The minimum effective dose should be used to ensure continued control of symptoms.

Pediatric Patients aged 6 to 12 years: The recommended dose is 110 µgm as 1 spray in each nostril once daily. Triamcinolone spray is not recommended for children under 6 years of age.

How to use the Nasal Spray-

• Shake the bottle gently and remove the dust cover.
• Hold the spray with your forefinger and middle finger on either side of the nozzle and your thumb underneath the bottle. Press down until a fine spray appears. If using for the first time or if you have not used it for a week or more, press the nasal applicator several times until a fine moist comes out from the container.
• Gently blow the nose to clear the nostrils.
• Close one nostril and carefully insert the nasal applicator into the open nostril. Tilt your head forward slightly and keep the spray upright. Breathe in through your nose and while breathing in, press the white-collar of nasal applicator firmly down once to release a spray.
• Breathe out through your mouth.
• Repeat the above steps in the same/ other nostril for consecutive doses.

Cleaning: The nasal spray should be cleaned at least once a week. The procedures are as follows-

• Remove the dust cover.
• Gently pull off the nasal applicator.
• Wash the applicator and dust cover in warm water.
• Shake off the excess water and leave to dry in a normal place. Avoid to apply additional heat.
• Gently push the applicator back on the top of the bottle and re-fix the dust cover.

The most commonly reported adverse reactions in clinical trials with Triamcinolone included those involving mucous membranes of the nose & throat. The most prevalent adverse reactions considered are rhinitis, headache, & pharyngitis. The nasopharyngeal adverse effects included epistaxis, nasal irritation, dry mucous membrane, naso-sinus congestion and sneezing although these are seen as frequently with placebo. As with other nasally inhaled corticosteroids, nasal septal perforation has been reported.

No specific contraindications but caution is required in patients with hypersensitivity to any constituents of the formulation.

If there is any reason to suppose that adrenal function is impaired, care must be taken while transferring patients from systemic steroid treatment to Triamcinolone. In clinical studies with Triamcinolone administered intranasally, the development of localized infections, on the nose, and pharynx with Candida albicans, has rarely occurred. When such an infection develops it may require treatment with appropriate local therapy and discontinuance of treatment with Triamcinolone. Because of the inhibitory effect of corticosteroids on wound healing in patients who have experienced recent nasal septal ulcers, nasal surgery of trauma, Triamcinolone should be used with caution until healing has occurred.

There are no adequate and well controlled studies in pregnant women with Triamcinolone. Because animal studies indicate a teratogenic effect, Triamcinolone should be used during pregnancy if the potential benefit justifies the potential benefit to fetus. It is not known whether Triamcinolone is excreted in human breast milk.

Like any other nasally administered corticosteroid, acute overdosing with Triamcinolone is unlikely in view of the total amount of active ingredient present

Store at a temperature not exceeding 25˚C. Protect from light and moisture. Keep out of the reach of children.

is indicated for the relief of the inflammatory and pruritic manifestations of corticosteroid responsive dermatoses including atopic dermatitis, contact dermatitis, eczematous dermatitis, neurodermatitis, seborrheic dermatitis, insect bites, lichen simplex chronicus, exfoliative dermatitis, stasis dermatitis, nummular eczema, psoriasis and pruritus ani and vulvae.

Corticosteroid, Glucocorticoids, Triamcinolone & Combined preparations

Triamcinolone Acetonide (a derivative of Triamcinolone) in a compatible base. Topical steroids are primarily effective because of their anti-inflammatory, antipruritic & vasoconstrictive actions.

A small amount of Triamcinolone is gently rub to the affected area 1-2 times daily. Some cases of eczematised psoriasis may be treated more effectively by the application of Triamcinolone under an occlusive dressing.

Occlusive dressing technique: Gently rub a small amount of Triamcinolone on the lesion until it disappears. Then reapply, leaving a thin coating and cover with a pliable non porous film. For convenience apply Triamcinolone intermittently (12 hour occlusion during the night) followed by reapplication without occlusion, during the day.

Pediatric use: Triamcinolone should not be used in children under 8 years. Administration of topical corticosteroids to children should be limited to the least amount compatible with an effective therapeutic regimen. Chronic corticosteroid therapy may interfere with the growth and development of children. As children are more likely to get side effects, they should not normally be treated for longer than 5 days.

The following local side effects have been reported with topical corticosteroids, either with or without occlusive dressings: burning, itching, irritation, dryness, folliculitis, hypertrichosis, acneiform eruptions, hypopigmentation, perioral dermatitis and allergic contact dermatitis, maceration of the skin, secondary infection, skin atrophy, striae and miliaria.

Triamcinolone Acetonide is contraindicated in those patients with a history of hypersensitivity to any of the components of the preparation. It is also contraindicated in tuberculosis of the skin, fungus infections and viral diseases of the skin (Herpes simplex, chickenpox and vaccinia), perioral dermatitis, rosacea and ulcerative conditions.

If reactions or idiosyncrasies are encountered, Triamcinolone Acetonide should be discontinued. The use of topical steroids on infected areas should be attended with caution and careful observation, bearing in mind the potential spreading of infections by anti-inflammatory steroids and the possible advisability of discontinuing steroid therapy and/or initiating antibacterial measures.

Triamcinolone Acetonide should not be used on healthy skin or over large areas of skin and not to be used in the eye as there is potential risk of glaucoma and cataract. When steroids are applied for long periods of time (more than 4 weeks) the occurrence of atrophic striae is likely. Prolonged use on flexures and intertriginous areas is undesirable. Children may absorb proportionately larger amounts of topical corticosteroids and thus may be more susceptible to systemic toxicity. In infants, long term continuous topical steroid therapy should be avoided. Adrenal suppression can occur even without occlusion.

There are no adequate and well-controlled studies in pregnant women on teratogenic effects from topically applied corticosteroids. Therefore, topical corticosteroid should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus. It is not known whether topical administration of corticosteroid could result in sufficient systemic absorption to produce detectable quantities in breast milk. Systemically administered corticosteroids are secreted into breast milk in quantities not likely to have a deleterious effect on the infant. Nevertheless, caution should be exercised when topical corticosteroids are administered to a nursing woman.

Topically applied corticosteroids can be absorbed in sufficient amounts to produce systemic effects e.g., mild, reversible suppression of adrenal function, ecchymoses of the skin, peptic ulceration, hypertension, aggravation of infection, hirsutism, acne, edema and muscle weakness

Store in a cool & dry place. Protect from light.

Aluminium Hydroxide and Magnesium Hydroxide is indicated for Hyperacidity, peptic ulcer, gastritis, heartburn, sour stomach & dyspepsia.

Antacids

This drug is well-balanced combination of essential non-systemic antacids which excel in efficacy and palatability. These are dependable antacid preparations without acid rebound, constipating or cathertic effects. Both the preparations provide symptomatic relief of hyperacidity associated with heartburn, acid ingestion or sour stomach.

Aluminium hydroxide gel, a slow acting antacid and an adsorbent with prolonged effect, has high neutralizing power. Magnesium Hydroxide possesses a slow but sustained acid neutralizing property. Antacids of both tablet and suspension possess adsorbent property. They form a protecting coating over the ulcer surface facilitating its healing; thus protecting the sensitive mucosa of stomach and duodenum from further irritation.

Tablet: Two tablets 1-3 hours after meal and at bed time or as directed by the physician.

Suspension: 2 tea spoonful 1-3 hours after meal and at bed time or as directed by the physician.

Long term use of any antacid results in alkaluria, which may predispose to nephrolithiasis by forming precipitation of calcium phosphate.

This is contraindicated in hypophosphataemia. It is also contraindicated in alkalosis and hypermagnesaemia where abdominal distention may be due to partial or complete intestinal obstruction.

Antacids reduce the absorption of tetracycline when given concomitantly. These should not be used concomitantly

This drug inhibits the absorption of following drugs: Azithromycin, cefpodoxime, ciprofloxacin, isoniazid, rifampicin, norfloxacin, ofloxacin, pivampicillin, tetracyclines, Gabapentin and phenytoin, Itraconazole, ketoconazole, Chloroquine, hydroxychloroquine and Phenothiazines.

It is advised to avoid antacid preparations in the first trimester of pregnancy.

Keep below 30°C temperature, away from light & moisture. Keep out of the reach of children.

Triamcinolone & Combined preparations

Adults: This cream should be applied sparingly to the skin lesion no more than 2 times daily, preferably once in the morning and once in the evening. This cream should not be applied with an occlusive dressing, or to large areas of skin on the body. The duration of treatment with this cream should continue until the inflammatory symptoms subside but not longer than 2 weeks; after 2 weeks of therapy with this cream, continue therapy as needed with a preparation containing econazole or econazole nitrate alone.

Pediatric Use: Pediatric patients may demonstrate greater susceptibility to topical corticosteroid-induced HPA axis suppression and Cushing's syndrome than mature patients because of a larger skin surface area to body weight. Caution should be exercised.

Rarely, transient local mild irritation, itching & redness may occur immediately after application. Econazole has the minimal allergenic effect and is well tolerated, even by delicate skin. Adrenal suppression on long term continuous topical steroid therapy may occur, particularly in infants or children, or when occlusive dressings are applied. It should be noted that an infant's napkin may act as an occlusive dressing.

This Cream is contraindicated-

• In individuals who have shown hypersensitivity to any of its ingredients.
• Like any other dermatological preparation containing corticosteroids, this Cream is contraindicated in specific skin conditions such as tuberculous, varicella, herpes simplex or other viral infections of the skin, or fresh vaccination sites.
• Decubitus ulcers: Viral, bacterial or fungal skin infections (e.g. tuberculosis of the skin, syphilis of the skin, herpes simplex, herpes zoster, chickenpox).
• Rosacea and rosacea-like dermatitis.

• For external use only. This Cream is not for ophthalmic or oral use.
• If a reaction suggesting hypersensitivity or chemical irritation should occur, use of the medication should be discontinued.
• Corticosteroids applied to the skin can be absorbed in sufficient amounts to produce systemic effects, including adrenal suppression. Systemic absorption may be increased by various factors such as application over a large skin surface area, application to damaged skin, application under occlusive skin dressings and prolonged duration of therapy.
• Topical corticosteroids are associated with skin thinning and atrophy, striae, telangiectasis and purpura.
• Topical corticosteroids may lead to increased risk of dermatological superinfection or opportunistic infection.

Children: Increased caution is required when treating children. Compared to adults, the nature of a child's skin and the larger skin surface area relative to body weight may lead to an increased absorption of the corticosteroid via the child's skin. This cream should be used in children only for short periods of time (less than 2 weeks) and on small areas (less than 10% of body surface area).

Visual disturbance may be associated with systemic and topical corticosteroid use. If a patient presents with symptoms such as blurred vision or other visual disturbances, the patient should be considered for referral to an ophthalmologist for evaluation of possible causes which may include cataract, glaucoma or rare diseases such as central serous chorioretinopathy (CSCR).

Econazole: compound metabolized by CYP3A4/2C9 oral anticoagulants (warfarin & acenocoumarol).

Triamcinolone: lowering of plasma salicylates levels. Increased risk of Gl bleeding and ulceration with NSAIDs. Antagonised blood glucose-lowering effects of the antidiabetics. Increased risk of Hyperkalemia with amphotericin B, beta-blockers, potassium-depleting diuretics, theophylline. Increased clearance of the triamcinolone with ciclosporin, carbamazepine, phenytoin, barbiturate, rifampicin.

Pregnancy: Not the Econazole but the Triamcinolone Acetonide crosses the placenta and topical administration of corticosteroids during pregnancy can cause abnormalities of foetal development. The relevance of this finding to human beings has not been established. However, topical steroids in large amounts or for prolonged periods
should not be used in pregnancy.

Lactation: Negligible amount of econazole and to some extent Triamcinolone may be excreted in small amounts in breast milk. So this cream should not be prescribed to the lactating mother or if prescribed lactation should be withheld during treatment.

This Cream is for cutaneous application only. Corticosteroids applied to the skin, including triamcinolone, can be absorbed in sufficient amounts to produce systemic effects. In the event of accidental ingestion, treat symptomatically. If this cream is accidentally applied to the eyes, wash with clean water or saline and seek medical attention if symptoms persist.

Store in a cool (below 30°C) and dry place, away from light. Keep out of the reach of children.

Corticosteroid, Glucocorticoids, Triamcinolone & Combined preparations

The antiinflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition of arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Firstly, however, these glucocorticoids bind to the glucocorticoid receptors which translocate into the nucleus and bind DNA (GRE) and change genetic expression both positively and negatively. The immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.

Adults and children over 12 years of age: Initial dose is 60 mg. Dosage is usually adjusted within the range of 40 to 80 mg. For local areas, dose for adults is up to 10 mg for smaller areas and up to 40 mg for larger areas.

Children 6 to 12 years: Initial dose is 40 mg

Cushingoid syndrome, weakness, bruising or purpura, aggravation of infections, peptic ulcer, activation of latent or aggravation of existing diabetes, altered menstrual cycle, hirsutism.

Triamcinolone Acetonide injection is contraindicated in patients with a sensitivity to the active or inactive ingredients.

Triamcinolone Acetonide injection should be used cautiously in patients with ocular herpes simplex, nonspecific ulcerative colitis, active or latent peptic ulcer, renal insufficiency, hypertension, osteoporosis, Cushing's syndrome, diabetes mellitus, congestive heart failure, chronic nephritis.

Aminoglutethimide: Aminoglutethimide may lead to a loss of corticosteroid-induced adrenal suppression. 

Amphotericin B injection and potassium-depleting agents: When corticosteroids are administered concomitantly with potassium-depleting agents (ie, amphotericin B, diuretics), patients should be observed closely for development of hypokalemia. There have been cases reported in which concomitant use of amphotericin B and hydrocortisone was followed by cardiac enlargement and congestive heart failure. 

Antibiotics: Macrolide antibiotics have been reported to cause a significant decrease in corticosteroid clearance. 

Anticholinesterases: Concomitant use of anticholinesterase agents and corticosteroids may produce severe weakness in patients with myasthenia gravis. If possible, anticholinesterase agents should be withdrawn at least 24 hours before initiating corticosteroid therapy.
 
Anticoagulants, oral: Coadministration of corticosteroids and warfarin usually results in inhibition of response to warfarin, although there have been some conflicting reports. Therefore, coagulation indices should be monitored frequently to maintain the desired anticoagulant effect.
 
Antidiabetics: Because corticosteroids may increase blood glucose concentrations, dosage adjustments of antidiabetic agents may be required. 

Antitubercular drugs: Serum concentrations of isoniazid may be decreased. 

Cholestyramine: Cholestyramine may increase the clearance of corticosteroids. 

Cyclosporine: Increased activity of both cyclosporine and corticosteroids may occur when the two are used concurrently. Convulsions have been reported with this concurrent use. 

Digitalis glycosides: Patients on digitalis glycosides may be at increased risk of arrhythmias due to hypokalemia. 
Estrogens, including oral contraceptives: Estrogens may decrease the hepatic metabolism of certain corticosteroids, thereby increasing their effect. 

Hepatic enzyme inducers (eg, barbiturates, phenytoin, carbamazepine, rifampin): Drugs which induce hepatic microsomal drug metabolizing enzyme activity may enhance the metabolism of corticosteroids and require that the dosage of the corticosteroid be increased. 

Ketoconazole: Ketoconazole has been reported to decrease the metabolism of certain corticosteroids by up to 60%, leading to an increased risk of corticosteroid side effects. 

Nonsteroidal anti-inflammatory drugs (NSAIDs): Concomitant use of aspirin (or other nonsteroidal anti-inflammatory drugs) and corticosteroids increases the risk of gastrointestinal side effects. Aspirin should be used cautiously in conjunction with corticosteroids in hypoprothrombinemia. The clearance of salicylates may be increased with concurrent use of corticosteroids. 

Skin tests: Corticosteroids may suppress reactions to skin tests. 

Vaccines: Patients on prolonged corticosteroid therapy may exhibit a diminished response to toxoids and live or inactivated vaccines due to inhibition of antibody response. Corticosteroids may also potentiate the replication of some organisms contained in live attenuated vaccines. Routine administration of vaccines or toxoids should be deferred until corticosteroid therapy is discontinued if possible.

Triamcinolone Acetonide injection should be used during pregnancy, nursing mothers if the possible benefits of the medication justify the potential hazards to the fetus or nursing infant.

Use in the elderly: The common adverse effects of systemic corticosteroids such as osteoporosis or hypertension may be associated with more serious consequences in old age. Close clinical supervision is recommended.

Use in children: As corticosteroids can suppress growth, the development of infants and children on prolonged corticosteroid therapy should be carefully observed. Caution should be taken in the event of exposure to chicken pox, measles or other communicable diseases. Children should not be vaccinated or immunized while on corticosteroid therapy. Corticosteroids may also affect endogenous steroid production.

Treatment of acute overdosage is by supportive and symptomatic therapy. For chronic overdosage in the face of severe disease requiring continuous steroid therapy, the dosage of the corticosteroid may be reduced only temporarily, or alternate day treatment may be introduced.

Store at controlled room temperature, 20-25°C, avoid freezing and protect from light.

Third generation Cephalosporins

Ceftriaxone is a 3rd generation broad-spectrum parenteral cephalosporin antibiotic. It has potent bactericidal activity against a wide range of Gram-positive and Gram-negative organisms. Like other cephalosporins and penicillins, Ceftriaxone kills bacteria by interfering with the synthesis of the bacterial cell wall. Ceftriaxone has a high degree of stability in the presence of beta lactamases. A remarkable feature of Ceftriaxone is its relatively long plasma elimination half-life of about 6 to 9 hours, which makes single or once-daily dosage of the drug appropriate for most patients. Ceftriaxone is not metabolized in the body. About 40-65% of a dose of Ceftriaxone is excreted unchanged in the urine; the remainder is excreted in the bile and ultimately found in the feces as unchanged drug and microbiologically inactive compound. The drug is highly protein bound (95%).

Adult: The usual dose is 1 to 2 gm by intravenous or intramuscular administration once a day (or in equally divided doses twice a day).

• Pneumonia, Bronchitis, Acute bacterial otitis media, Skin and skin structure infection, Urinary tract infections, Bacterial Septicemia, Bone and joint infections, Meningitis: 1 to 2 g IV or IM once a day (or in equally divided doses twice a day); Maximum dose: 4 gm/day
• Uncomplicated gonococcal infections: 250 mg IM as a single dose
• Surgical prophylaxis: 1 g IV as a single dose 30 to 120 minutes before surgery

Infants and Children (01 month or older): The usual dose is 50 to 75 mg/kg intravenous or intramuscular administration once a day (or in equally divided doses twice a day).

• Pneumonia, Bronchitis, Skin and skin structure infection, Urinary tract infections, Bacterial Septicemia, Bone and joint infections: 50 to 75 mg/kg IV or IM once a day (or in equally divided doses twice a day); Maximum dose: 2 gm/day
• Acute bacterial otitis media: 50 mg/kg IM in single dose; Maximum dose: 1 gm/day
• Meningitis: 100 mg/kg IV or IM in single daily dose or (or in equally divided doses twice a day); Maximum dose: 4 gm/day

Duration of therapy: Continue for more than 2 days after signs and symptoms of infection have disappeared. Usual duration is 4 to 14 days; in complicated infections, longer therapy may be required.

Preparation of Solutions for Intramuscular / Intravenous Injections:

• For Intramuscular Injection: 250 mg or 500 mg Ceftriaxone should be dissolved in 2 ml Lidocaine HCI 1% injection or 1 g Ceftriaxone in 3.5 ml of Lidocaine HCI 1% injection.
• For Intravenous Injection: 250 mg or 500 mg Ceftriaxone should be dissolved in 5 ml of Water for injection or 1 g Ceftriaxone in 10 ml of Water for injection USP or 2 g Ceftriaxone in 20 ml of Water for injection.

The injection should be administered over 2-4 minutes, by Intramuscular or Intravenous injection or by tubing infusion over a period of 30 minutes at concentration between 10 mg/mL and 40 mg/mL. Before starting treatment through Ceftriaxone injection, patient tolerance test should be checked by administration of a test dose. (The use of freshly reconstituted solution is recommended. However, it maintains potency for at least 6 hours at room temperature or 24 hours at 5°C).

Ceftriaxone is generally well tolerated. A few side effects such as gastro-intestinal effects including diarrhea, nausea and vomiting, stomatitis and glossitis; cutaneous reactions including rash, pruritus, urticaria, edema and erythema multiforme; hematologic reactions including eosinophilia, thrombocytopenia, leucopenia, anemia and neutropenia; hepatic reactions including elevations of SGOT or SGPT, bilirubinemia; CNS reactions including nervousness, confusion, sleep disturbances, headache, hyperactivity, convulsion, hypertonia and dizziness were reported. Local phlebitis occurs rarely following intravenous administration but can be minimized by slow injections over 2-4 minutes.

Ceftriaxone should not be given to patients with a history of hypersensitivity to cephalosporin antibiotics.

As with other cephalosporins, anaphylactic shock cannot be ruled out even if a thorough patient history is taken. Anaphylactic shock requires immediate countermeasures such as intravenous epinephrine followed by a glucocorticoid. In rare cases, shadows suggesting sludge have been detected by sonograms of the gallbladder. This condition was reversible on discontinuation or completion of Ceftriaxone therapy. Even if such findings are associated with pain, conservative, nonsurgical management is recommended. During prolonged treatment the blood picture should be checked at regular intervals.

No drug interactions have been reported.

Its safety in human pregnancy has not been established. Therefore, it should not be used in pregnancy unless absolutely indicated. Low concentrations of Ceftriaxone are excreted in human milk. Caution should be exercised when Ceftriaxone is administered to a lactating mother.

Ceftriaxone must not be given to neonates if the neonates is premature and newborn (up to 28 days of age).

There is no specific antidote. Treatment of overdosage should be symptomatic.

Vial store in a cool, dry place (below 30° C), away from light & moisture. Keep out of the reach of children.

Third generation Cephalosporins

Ceftriaxone is a 3rd generation broad-spectrum parenteral cephalosporin antibiotic. It has potent bactericidal activity against a wide range of Gram-positive and Gram-negative organisms. Like other cephalosporins and penicillins, Ceftriaxone kills bacteria by interfering with the synthesis of the bacterial cell wall. Ceftriaxone has a high degree of stability in the presence of beta lactamases. A remarkable feature of Ceftriaxone is its relatively long plasma elimination half-life of about 6 to 9 hours, which makes single or once-daily dosage of the drug appropriate for most patients. Ceftriaxone is not metabolized in the body. About 40-65% of a dose of Ceftriaxone is excreted unchanged in the urine; the remainder is excreted in the bile and ultimately found in the feces as unchanged drug and microbiologically inactive compound. The drug is highly protein bound (95%).

Adult: The usual dose is 1 to 2 gm by intravenous or intramuscular administration once a day (or in equally divided doses twice a day).

• Pneumonia, Bronchitis, Acute bacterial otitis media, Skin and skin structure infection, Urinary tract infections, Bacterial Septicemia, Bone and joint infections, Meningitis: 1 to 2 g IV or IM once a day (or in equally divided doses twice a day); Maximum dose: 4 gm/day
• Uncomplicated gonococcal infections: 250 mg IM as a single dose
• Surgical prophylaxis: 1 g IV as a single dose 30 to 120 minutes before surgery

Infants and Children (01 month or older): The usual dose is 50 to 75 mg/kg intravenous or intramuscular administration once a day (or in equally divided doses twice a day).

• Pneumonia, Bronchitis, Skin and skin structure infection, Urinary tract infections, Bacterial Septicemia, Bone and joint infections: 50 to 75 mg/kg IV or IM once a day (or in equally divided doses twice a day); Maximum dose: 2 gm/day
• Acute bacterial otitis media: 50 mg/kg IM in single dose; Maximum dose: 1 gm/day
• Meningitis: 100 mg/kg IV or IM in single daily dose or (or in equally divided doses twice a day); Maximum dose: 4 gm/day

Duration of therapy: Continue for more than 2 days after signs and symptoms of infection have disappeared. Usual duration is 4 to 14 days; in complicated infections, longer therapy may be required.

Preparation of Solutions for Intramuscular / Intravenous Injections:

• For Intramuscular Injection: 250 mg or 500 mg Ceftriaxone should be dissolved in 2 ml Lidocaine HCI 1% injection or 1 g Ceftriaxone in 3.5 ml of Lidocaine HCI 1% injection.
• For Intravenous Injection: 250 mg or 500 mg Ceftriaxone should be dissolved in 5 ml of Water for injection or 1 g Ceftriaxone in 10 ml of Water for injection USP or 2 g Ceftriaxone in 20 ml of Water for injection.

The injection should be administered over 2-4 minutes, by Intramuscular or Intravenous injection or by tubing infusion over a period of 30 minutes at concentration between 10 mg/mL and 40 mg/mL. Before starting treatment through Ceftriaxone injection, patient tolerance test should be checked by administration of a test dose. (The use of freshly reconstituted solution is recommended. However, it maintains potency for at least 6 hours at room temperature or 24 hours at 5°C).

Ceftriaxone is generally well tolerated. A few side effects such as gastro-intestinal effects including diarrhea, nausea and vomiting, stomatitis and glossitis; cutaneous reactions including rash, pruritus, urticaria, edema and erythema multiforme; hematologic reactions including eosinophilia, thrombocytopenia, leucopenia, anemia and neutropenia; hepatic reactions including elevations of SGOT or SGPT, bilirubinemia; CNS reactions including nervousness, confusion, sleep disturbances, headache, hyperactivity, convulsion, hypertonia and dizziness were reported. Local phlebitis occurs rarely following intravenous administration but can be minimized by slow injections over 2-4 minutes.

Ceftriaxone should not be given to patients with a history of hypersensitivity to cephalosporin antibiotics.

As with other cephalosporins, anaphylactic shock cannot be ruled out even if a thorough patient history is taken. Anaphylactic shock requires immediate countermeasures such as intravenous epinephrine followed by a glucocorticoid. In rare cases, shadows suggesting sludge have been detected by sonograms of the gallbladder. This condition was reversible on discontinuation or completion of Ceftriaxone therapy. Even if such findings are associated with pain, conservative, nonsurgical management is recommended. During prolonged treatment the blood picture should be checked at regular intervals.

No drug interactions have been reported.

Its safety in human pregnancy has not been established. Therefore, it should not be used in pregnancy unless absolutely indicated. Low concentrations of Ceftriaxone are excreted in human milk. Caution should be exercised when Ceftriaxone is administered to a lactating mother.

Ceftriaxone must not be given to neonates if the neonates is premature and newborn (up to 28 days of age).

There is no specific antidote. Treatment of overdosage should be symptomatic.

Vial store in a cool, dry place (below 30° C), away from light & moisture. Keep out of the reach of children.

Third generation Cephalosporins

Ceftriaxone is a 3rd generation broad-spectrum parenteral cephalosporin antibiotic. It has potent bactericidal activity against a wide range of Gram-positive and Gram-negative organisms. Like other cephalosporins and penicillins, Ceftriaxone kills bacteria by interfering with the synthesis of the bacterial cell wall. Ceftriaxone has a high degree of stability in the presence of beta lactamases. A remarkable feature of Ceftriaxone is its relatively long plasma elimination half-life of about 6 to 9 hours, which makes single or once-daily dosage of the drug appropriate for most patients. Ceftriaxone is not metabolized in the body. About 40-65% of a dose of Ceftriaxone is excreted unchanged in the urine; the remainder is excreted in the bile and ultimately found in the feces as unchanged drug and microbiologically inactive compound. The drug is highly protein bound (95%).

Adult: The usual dose is 1 to 2 gm by intravenous or intramuscular administration once a day (or in equally divided doses twice a day).

• Pneumonia, Bronchitis, Acute bacterial otitis media, Skin and skin structure infection, Urinary tract infections, Bacterial Septicemia, Bone and joint infections, Meningitis: 1 to 2 g IV or IM once a day (or in equally divided doses twice a day); Maximum dose: 4 gm/day
• Uncomplicated gonococcal infections: 250 mg IM as a single dose
• Surgical prophylaxis: 1 g IV as a single dose 30 to 120 minutes before surgery

Infants and Children (01 month or older): The usual dose is 50 to 75 mg/kg intravenous or intramuscular administration once a day (or in equally divided doses twice a day).

• Pneumonia, Bronchitis, Skin and skin structure infection, Urinary tract infections, Bacterial Septicemia, Bone and joint infections: 50 to 75 mg/kg IV or IM once a day (or in equally divided doses twice a day); Maximum dose: 2 gm/day
• Acute bacterial otitis media: 50 mg/kg IM in single dose; Maximum dose: 1 gm/day
• Meningitis: 100 mg/kg IV or IM in single daily dose or (or in equally divided doses twice a day); Maximum dose: 4 gm/day

Duration of therapy: Continue for more than 2 days after signs and symptoms of infection have disappeared. Usual duration is 4 to 14 days; in complicated infections, longer therapy may be required.

Preparation of Solutions for Intramuscular / Intravenous Injections:

• For Intramuscular Injection: 250 mg or 500 mg Ceftriaxone should be dissolved in 2 ml Lidocaine HCI 1% injection or 1 g Ceftriaxone in 3.5 ml of Lidocaine HCI 1% injection.
• For Intravenous Injection: 250 mg or 500 mg Ceftriaxone should be dissolved in 5 ml of Water for injection or 1 g Ceftriaxone in 10 ml of Water for injection USP or 2 g Ceftriaxone in 20 ml of Water for injection.

The injection should be administered over 2-4 minutes, by Intramuscular or Intravenous injection or by tubing infusion over a period of 30 minutes at concentration between 10 mg/mL and 40 mg/mL. Before starting treatment through Ceftriaxone injection, patient tolerance test should be checked by administration of a test dose. (The use of freshly reconstituted solution is recommended. However, it maintains potency for at least 6 hours at room temperature or 24 hours at 5°C).

Ceftriaxone is generally well tolerated. A few side effects such as gastro-intestinal effects including diarrhea, nausea and vomiting, stomatitis and glossitis; cutaneous reactions including rash, pruritus, urticaria, edema and erythema multiforme; hematologic reactions including eosinophilia, thrombocytopenia, leucopenia, anemia and neutropenia; hepatic reactions including elevations of SGOT or SGPT, bilirubinemia; CNS reactions including nervousness, confusion, sleep disturbances, headache, hyperactivity, convulsion, hypertonia and dizziness were reported. Local phlebitis occurs rarely following intravenous administration but can be minimized by slow injections over 2-4 minutes.

Ceftriaxone should not be given to patients with a history of hypersensitivity to cephalosporin antibiotics.

As with other cephalosporins, anaphylactic shock cannot be ruled out even if a thorough patient history is taken. Anaphylactic shock requires immediate countermeasures such as intravenous epinephrine followed by a glucocorticoid. In rare cases, shadows suggesting sludge have been detected by sonograms of the gallbladder. This condition was reversible on discontinuation or completion of Ceftriaxone therapy. Even if such findings are associated with pain, conservative, nonsurgical management is recommended. During prolonged treatment the blood picture should be checked at regular intervals.

No drug interactions have been reported.

Its safety in human pregnancy has not been established. Therefore, it should not be used in pregnancy unless absolutely indicated. Low concentrations of Ceftriaxone are excreted in human milk. Caution should be exercised when Ceftriaxone is administered to a lactating mother.

Ceftriaxone must not be given to neonates if the neonates is premature and newborn (up to 28 days of age).

There is no specific antidote. Treatment of overdosage should be symptomatic.

Vial store in a cool, dry place (below 30° C), away from light & moisture. Keep out of the reach of children.

Third generation Cephalosporins

Ceftriaxone is a 3rd generation broad-spectrum parenteral cephalosporin antibiotic. It has potent bactericidal activity against a wide range of Gram-positive and Gram-negative organisms. Like other cephalosporins and penicillins, Ceftriaxone kills bacteria by interfering with the synthesis of the bacterial cell wall. Ceftriaxone has a high degree of stability in the presence of beta lactamases. A remarkable feature of Ceftriaxone is its relatively long plasma elimination half-life of about 6 to 9 hours, which makes single or once-daily dosage of the drug appropriate for most patients. Ceftriaxone is not metabolized in the body. About 40-65% of a dose of Ceftriaxone is excreted unchanged in the urine; the remainder is excreted in the bile and ultimately found in the feces as unchanged drug and microbiologically inactive compound. The drug is highly protein bound (95%).

Adult: The usual dose is 1 to 2 gm by intravenous or intramuscular administration once a day (or in equally divided doses twice a day).

• Pneumonia, Bronchitis, Acute bacterial otitis media, Skin and skin structure infection, Urinary tract infections, Bacterial Septicemia, Bone and joint infections, Meningitis: 1 to 2 g IV or IM once a day (or in equally divided doses twice a day); Maximum dose: 4 gm/day
• Uncomplicated gonococcal infections: 250 mg IM as a single dose
• Surgical prophylaxis: 1 g IV as a single dose 30 to 120 minutes before surgery

Infants and Children (01 month or older): The usual dose is 50 to 75 mg/kg intravenous or intramuscular administration once a day (or in equally divided doses twice a day).

• Pneumonia, Bronchitis, Skin and skin structure infection, Urinary tract infections, Bacterial Septicemia, Bone and joint infections: 50 to 75 mg/kg IV or IM once a day (or in equally divided doses twice a day); Maximum dose: 2 gm/day
• Acute bacterial otitis media: 50 mg/kg IM in single dose; Maximum dose: 1 gm/day
• Meningitis: 100 mg/kg IV or IM in single daily dose or (or in equally divided doses twice a day); Maximum dose: 4 gm/day

Duration of therapy: Continue for more than 2 days after signs and symptoms of infection have disappeared. Usual duration is 4 to 14 days; in complicated infections, longer therapy may be required.

Preparation of Solutions for Intramuscular / Intravenous Injections:

• For Intramuscular Injection: 250 mg or 500 mg Ceftriaxone should be dissolved in 2 ml Lidocaine HCI 1% injection or 1 g Ceftriaxone in 3.5 ml of Lidocaine HCI 1% injection.
• For Intravenous Injection: 250 mg or 500 mg Ceftriaxone should be dissolved in 5 ml of Water for injection or 1 g Ceftriaxone in 10 ml of Water for injection USP or 2 g Ceftriaxone in 20 ml of Water for injection.

The injection should be administered over 2-4 minutes, by Intramuscular or Intravenous injection or by tubing infusion over a period of 30 minutes at concentration between 10 mg/mL and 40 mg/mL. Before starting treatment through Ceftriaxone injection, patient tolerance test should be checked by administration of a test dose. (The use of freshly reconstituted solution is recommended. However, it maintains potency for at least 6 hours at room temperature or 24 hours at 5°C).

Ceftriaxone is generally well tolerated. A few side effects such as gastro-intestinal effects including diarrhea, nausea and vomiting, stomatitis and glossitis; cutaneous reactions including rash, pruritus, urticaria, edema and erythema multiforme; hematologic reactions including eosinophilia, thrombocytopenia, leucopenia, anemia and neutropenia; hepatic reactions including elevations of SGOT or SGPT, bilirubinemia; CNS reactions including nervousness, confusion, sleep disturbances, headache, hyperactivity, convulsion, hypertonia and dizziness were reported. Local phlebitis occurs rarely following intravenous administration but can be minimized by slow injections over 2-4 minutes.

Ceftriaxone should not be given to patients with a history of hypersensitivity to cephalosporin antibiotics.

As with other cephalosporins, anaphylactic shock cannot be ruled out even if a thorough patient history is taken. Anaphylactic shock requires immediate countermeasures such as intravenous epinephrine followed by a glucocorticoid. In rare cases, shadows suggesting sludge have been detected by sonograms of the gallbladder. This condition was reversible on discontinuation or completion of Ceftriaxone therapy. Even if such findings are associated with pain, conservative, nonsurgical management is recommended. During prolonged treatment the blood picture should be checked at regular intervals.

No drug interactions have been reported.

Its safety in human pregnancy has not been established. Therefore, it should not be used in pregnancy unless absolutely indicated. Low concentrations of Ceftriaxone are excreted in human milk. Caution should be exercised when Ceftriaxone is administered to a lactating mother.

Ceftriaxone must not be given to neonates if the neonates is premature and newborn (up to 28 days of age).

There is no specific antidote. Treatment of overdosage should be symptomatic.

Vial store in a cool, dry place (below 30° C), away from light & moisture. Keep out of the reach of children.