Can you take Anisindione with Marthritic?

The salsalate in Marthritic has a major potential interaction with Alcoholism.

Salicylates, particularly aspirin, can cause dose-related gastrointestinal bleeding and mucosal damage, which may occur independently of each other. Occult, often asymptomatic GI blood loss is quite common with usual dosages of aspirin and stems from the drug's local effect on the GI mucosa. During chronic therapy, this type of bleeding may occasionally produce iron deficiency anemia. In contrast, major upper GI bleeding rarely occurs except in patients with active peptic ulcers or recent GI bleeding. However, these patients generally do not experience greater occult blood loss than healthy patients following small doses of aspirin. Mucosal damage associated with the use of salicylates may lead to development of peptic ulcers with or without bleeding, reactivation of latent ulcers, and ulcer perforation. Therapy with salicylates and related agents such as salicylamide should be considered and administered cautiously in patients with a history of GI disease or alcoholism, particularly if they are elderly and/or debilitated, since such patients may be more susceptible to the GI toxicity of these drugs and seem to tolerate ulceration and bleeding less well than other individuals. Extreme caution and thorough assessment of risks and benefits are warranted in patients with active or recent GI bleeding or lesions. Whenever possible, especially if prolonged use is anticipated, treatment with non-ulcerogenic agents should be attempted first. If salicylates are used, close monitoring for toxicity is recommended. Some adverse GI effects may be minimized by administration with high dosages of antacids, use of enteric-coated or extended-release formulations, and/or concurrent use of a histamine H2-receptor antagonist or a cytoprotective agent such as misoprostol. Patients with active peptic ulceration or GI bleeding treated with salicylates should generally be administered a concomitant anti-ulcer regimen.

The salsalate in Marthritic has a moderate potential interaction with Anemia.

Occult, often asymptomatic GI blood loss occurs quite frequently with the use of normal dosages of aspirin and stems from the drug's local effect on the GI mucosa. During chronic therapy, this type of bleeding may occasionally produce iron deficiency anemia. Other salicylates reportedly cause little or no GI blood loss at usual dosages, but may do so at high dosages. Prolonged therapy with salicylates, particularly aspirin, should be administered cautiously in patients with or predisposed to anemia. Periodic monitoring of hematocrit is recommended. The same precautions should also be observed with the use of related agents such as salicylamide because of their structural and pharmacological similarities to salicylate.

Anisindione has a major potential interaction with Aortic Aneurysm.

In general, the use of oral anticoagulants is contraindicated in patients with active bleeding or a hemorrhagic diathesis or other significant risks for bleeding, including hemostatic and/or coagulation defects associated with hemophilia, hypoprothrombinemia, thrombocytopenia, thrombocytopathy, severe hepatic impairment, and myeloproliferative disorders such as leukemia or polycythemia vera. Additionally, oral anticoagulants are usually contraindicated in the presence of any active ulceration of the gastrointestinal, respiratory, or genitourinary tracts; cerebrovascular hemorrhage; aneurysms (cerebral, dissecting aortic); pericarditis and pericardial effusions; bacterial endocarditis; and eclampsia, preeclampsia, or threatened abortion. These patients may be at increased risk for uncontrollable hemorrhage or bleeding complications during therapy with oral anticoagulants. Other potential contraindications include diverticulitis, vasculitis, malnutrition, and vitamin C or vitamin K deficiency. The decision to administer anticoagulants must be based upon clinical judgment in which the risks are weighed against the benefits in each patient.

Anisindione has a major potential interaction with Bleeding Disorder.

In general, the use of oral anticoagulants is contraindicated in patients with active bleeding or a hemorrhagic diathesis or other significant risks for bleeding, including hemostatic and/or coagulation defects associated with hemophilia, hypoprothrombinemia, thrombocytopenia, thrombocytopathy, severe hepatic impairment, and myeloproliferative disorders such as leukemia or polycythemia vera. Additionally, oral anticoagulants are usually contraindicated in the presence of any active ulceration of the gastrointestinal, respiratory, or genitourinary tracts; cerebrovascular hemorrhage; aneurysms (cerebral, dissecting aortic); pericarditis and pericardial effusions; bacterial endocarditis; and eclampsia, preeclampsia, or threatened abortion. These patients may be at increased risk for uncontrollable hemorrhage or bleeding complications during therapy with oral anticoagulants. Other potential contraindications include diverticulitis, vasculitis, malnutrition, and vitamin C or vitamin K deficiency. The decision to administer anticoagulants must be based upon clinical judgment in which the risks are weighed against the benefits in each patient.

The salsalate in Marthritic has a moderate potential interaction with Bleeding Disorder.

All salicylates can interfere with the action of vitamin K and induce a dose-dependent alteration in hepatic synthesis of coagulation factors VII, IX and X. At usual recommended dosages, a slight increase in prothrombin time (PT) may occur. Therapy with salicylates, especially if given in high dosages, should be administered cautiously in patients with significant active bleeding or a hemorrhagic diathesis, including hemostatic and/or coagulation defects associated with hemophilia, vitamin K deficiency, hypoprothombinemia, thrombocytopenia, thrombocytopathy, or severe hepatic impairment. The same precaution should also be observed with the use of related agents such as salicylamide because of their structural and pharmacological similarities to salicylate.

Anisindione has a major potential interaction with Cerebral Aneurysm.

In general, the use of oral anticoagulants is contraindicated in patients with active bleeding or a hemorrhagic diathesis or other significant risks for bleeding, including hemostatic and/or coagulation defects associated with hemophilia, hypoprothrombinemia, thrombocytopenia, thrombocytopathy, severe hepatic impairment, and myeloproliferative disorders such as leukemia or polycythemia vera. Additionally, oral anticoagulants are usually contraindicated in the presence of any active ulceration of the gastrointestinal, respiratory, or genitourinary tracts; cerebrovascular hemorrhage; aneurysms (cerebral, dissecting aortic); pericarditis and pericardial effusions; bacterial endocarditis; and eclampsia, preeclampsia, or threatened abortion. These patients may be at increased risk for uncontrollable hemorrhage or bleeding complications during therapy with oral anticoagulants. Other potential contraindications include diverticulitis, vasculitis, malnutrition, and vitamin C or vitamin K deficiency. The decision to administer anticoagulants must be based upon clinical judgment in which the risks are weighed against the benefits in each patient.

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

In general, the use of oral anticoagulants is contraindicated in patients with active bleeding or a hemorrhagic diathesis or other significant risks for bleeding, including hemostatic and/or coagulation defects associated with hemophilia, hypoprothrombinemia, thrombocytopenia, thrombocytopathy, severe hepatic impairment, and myeloproliferative disorders such as leukemia or polycythemia vera. Additionally, oral anticoagulants are usually contraindicated in the presence of any active ulceration of the gastrointestinal, respiratory, or genitourinary tracts; cerebrovascular hemorrhage; aneurysms (cerebral, dissecting aortic); pericarditis and pericardial effusions; bacterial endocarditis; and eclampsia, preeclampsia, or threatened abortion. These patients may be at increased risk for uncontrollable hemorrhage or bleeding complications during therapy with oral anticoagulants. Other potential contraindications include diverticulitis, vasculitis, malnutrition, and vitamin C or vitamin K deficiency. The decision to administer anticoagulants must be based upon clinical judgment in which the risks are weighed against the benefits in each patient.

The salsalate in Marthritic has a moderate potential interaction with Coagulation Defects and Disorders.

All salicylates can interfere with the action of vitamin K and induce a dose-dependent alteration in hepatic synthesis of coagulation factors VII, IX and X. At usual recommended dosages, a slight increase in prothrombin time (PT) may occur. Therapy with salicylates, especially if given in high dosages, should be administered cautiously in patients with significant active bleeding or a hemorrhagic diathesis, including hemostatic and/or coagulation defects associated with hemophilia, vitamin K deficiency, hypoprothombinemia, thrombocytopenia, thrombocytopathy, or severe hepatic impairment. The same precaution should also be observed with the use of related agents such as salicylamide because of their structural and pharmacological similarities to salicylate.

Anisindione has a moderate potential interaction with Collagen Vascular Disease.

Patients with a collagen vascular disease (e.g., systemic lupus erythematosus, rheumatoid arthritis, scleroderma), congestive heart failure (especially decompensated disease), severe or prolonged diarrhea, fever, hyperthyroidism, malabsorption, or steatorrhea may exhibit greater than expected hypoprothrombinemic response to oral anticoagulants. Thus, more frequent laboratory (PT/INR) monitoring and dosage adjustment of anticoagulant may be required based on changes in the patient's condition. Patients should be advised to promptly report any signs of bleeding to their physician, including pain, swelling, headache, dizziness, weakness, prolonged bleeding from cuts, increased menstrual flow, vaginal bleeding, nosebleeds, bleeding of gums from brushing, unusual bleeding or bruising, red or brown urine, or red or black stools.

Anisindione has a major potential interaction with Colonic Ulceration.

In general, the use of oral anticoagulants is contraindicated in patients with active bleeding or a hemorrhagic diathesis or other significant risks for bleeding, including hemostatic and/or coagulation defects associated with hemophilia, hypoprothrombinemia, thrombocytopenia, thrombocytopathy, severe hepatic impairment, and myeloproliferative disorders such as leukemia or polycythemia vera. Additionally, oral anticoagulants are usually contraindicated in the presence of any active ulceration of the gastrointestinal, respiratory, or genitourinary tracts; cerebrovascular hemorrhage; aneurysms (cerebral, dissecting aortic); pericarditis and pericardial effusions; bacterial endocarditis; and eclampsia, preeclampsia, or threatened abortion. These patients may be at increased risk for uncontrollable hemorrhage or bleeding complications during therapy with oral anticoagulants. Other potential contraindications include diverticulitis, vasculitis, malnutrition, and vitamin C or vitamin K deficiency. The decision to administer anticoagulants must be based upon clinical judgment in which the risks are weighed against the benefits in each patient.

The salsalate in Marthritic has a major potential interaction with Colonic Ulceration.

Salicylates, particularly aspirin, can cause dose-related gastrointestinal bleeding and mucosal damage, which may occur independently of each other. Occult, often asymptomatic GI blood loss is quite common with usual dosages of aspirin and stems from the drug's local effect on the GI mucosa. During chronic therapy, this type of bleeding may occasionally produce iron deficiency anemia. In contrast, major upper GI bleeding rarely occurs except in patients with active peptic ulcers or recent GI bleeding. However, these patients generally do not experience greater occult blood loss than healthy patients following small doses of aspirin. Mucosal damage associated with the use of salicylates may lead to development of peptic ulcers with or without bleeding, reactivation of latent ulcers, and ulcer perforation. Therapy with salicylates and related agents such as salicylamide should be considered and administered cautiously in patients with a history of GI disease or alcoholism, particularly if they are elderly and/or debilitated, since such patients may be more susceptible to the GI toxicity of these drugs and seem to tolerate ulceration and bleeding less well than other individuals. Extreme caution and thorough assessment of risks and benefits are warranted in patients with active or recent GI bleeding or lesions. Whenever possible, especially if prolonged use is anticipated, treatment with non-ulcerogenic agents should be attempted first. If salicylates are used, close monitoring for toxicity is recommended. Some adverse GI effects may be minimized by administration with high dosages of antacids, use of enteric-coated or extended-release formulations, and/or concurrent use of a histamine H2-receptor antagonist or a cytoprotective agent such as misoprostol. Patients with active peptic ulceration or GI bleeding treated with salicylates should generally be administered a concomitant anti-ulcer regimen.

Anisindione has a major potential interaction with Diabetes Mellitus.

Therapy with oral anticoagulants should be administered cautiously in patients with severe diabetes because they may be at increased risk for hemorrhage. The INR should be monitored closely, and patients should be advised to promptly report any signs of bleeding to their physician, including pain, swelling, headache, dizziness, weakness, prolonged bleeding from cuts, increased menstrual flow, vaginal bleeding, nosebleeds, bleeding of gums from brushing, unusual bleeding or bruising, red or brown urine, or red or black stools.

Anisindione has a moderate potential interaction with Diarrhea.

Patients with a collagen vascular disease (e.g., systemic lupus erythematosus, rheumatoid arthritis, scleroderma), congestive heart failure (especially decompensated disease), severe or prolonged diarrhea, fever, hyperthyroidism, malabsorption, or steatorrhea may exhibit greater than expected hypoprothrombinemic response to oral anticoagulants. Thus, more frequent laboratory (PT/INR) monitoring and dosage adjustment of anticoagulant may be required based on changes in the patient's condition. Patients should be advised to promptly report any signs of bleeding to their physician, including pain, swelling, headache, dizziness, weakness, prolonged bleeding from cuts, increased menstrual flow, vaginal bleeding, nosebleeds, bleeding of gums from brushing, unusual bleeding or bruising, red or brown urine, or red or black stools.

Anisindione has a major potential interaction with Diverticulitis.

In general, the use of oral anticoagulants is contraindicated in patients with active bleeding or a hemorrhagic diathesis or other significant risks for bleeding, including hemostatic and/or coagulation defects associated with hemophilia, hypoprothrombinemia, thrombocytopenia, thrombocytopathy, severe hepatic impairment, and myeloproliferative disorders such as leukemia or polycythemia vera. Additionally, oral anticoagulants are usually contraindicated in the presence of any active ulceration of the gastrointestinal, respiratory, or genitourinary tracts; cerebrovascular hemorrhage; aneurysms (cerebral, dissecting aortic); pericarditis and pericardial effusions; bacterial endocarditis; and eclampsia, preeclampsia, or threatened abortion. These patients may be at increased risk for uncontrollable hemorrhage or bleeding complications during therapy with oral anticoagulants. Other potential contraindications include diverticulitis, vasculitis, malnutrition, and vitamin C or vitamin K deficiency. The decision to administer anticoagulants must be based upon clinical judgment in which the risks are weighed against the benefits in each patient.

Anisindione has a major potential interaction with Esophageal Ulceration.

In general, the use of oral anticoagulants is contraindicated in patients with active bleeding or a hemorrhagic diathesis or other significant risks for bleeding, including hemostatic and/or coagulation defects associated with hemophilia, hypoprothrombinemia, thrombocytopenia, thrombocytopathy, severe hepatic impairment, and myeloproliferative disorders such as leukemia or polycythemia vera. Additionally, oral anticoagulants are usually contraindicated in the presence of any active ulceration of the gastrointestinal, respiratory, or genitourinary tracts; cerebrovascular hemorrhage; aneurysms (cerebral, dissecting aortic); pericarditis and pericardial effusions; bacterial endocarditis; and eclampsia, preeclampsia, or threatened abortion. These patients may be at increased risk for uncontrollable hemorrhage or bleeding complications during therapy with oral anticoagulants. Other potential contraindications include diverticulitis, vasculitis, malnutrition, and vitamin C or vitamin K deficiency. The decision to administer anticoagulants must be based upon clinical judgment in which the risks are weighed against the benefits in each patient.

Anisindione has a moderate potential interaction with Fever.

Patients with a collagen vascular disease (e.g., systemic lupus erythematosus, rheumatoid arthritis, scleroderma), congestive heart failure (especially decompensated disease), severe or prolonged diarrhea, fever, hyperthyroidism, malabsorption, or steatorrhea may exhibit greater than expected hypoprothrombinemic response to oral anticoagulants. Thus, more frequent laboratory (PT/INR) monitoring and dosage adjustment of anticoagulant may be required based on changes in the patient's condition. Patients should be advised to promptly report any signs of bleeding to their physician, including pain, swelling, headache, dizziness, weakness, prolonged bleeding from cuts, increased menstrual flow, vaginal bleeding, nosebleeds, bleeding of gums from brushing, unusual bleeding or bruising, red or brown urine, or red or black stools.

Anisindione has a moderate potential interaction with Fluid Retention.

Patients with edema, hereditary coumarin resistance, hyperlipidemia, hypothyroidism, or nephrotic syndrome may exhibit lower than expected hypoprothrombinemic response to oral anticoagulants. Thus, more frequent laboratory (PT/INR) monitoring and dosage adjustment of anticoagulant may be required based on changes in the patient's condition.

The salsalate in Marthritic has a moderate potential interaction with G-6-PD Deficiency.

Salicylates, particularly aspirin, may cause or aggravate hemolysis in patients with pyruvate kinase or glucose-6-phosphate dehydrogenase (G-6-PD) deficiency. However, this effect has not been clearly established. Until more data are available, therapy with salicylates should be administered cautiously in patients with G-6-PD deficiency. The same precaution should also be observed with the use of related agents such as salicylamide because of their structural and pharmacological similarities to salicylate.

The salsalate in Marthritic has a major potential interaction with Gastritis/Duodenitis.

Salicylates, particularly aspirin, can cause dose-related gastrointestinal bleeding and mucosal damage, which may occur independently of each other. Occult, often asymptomatic GI blood loss is quite common with usual dosages of aspirin and stems from the drug's local effect on the GI mucosa. During chronic therapy, this type of bleeding may occasionally produce iron deficiency anemia. In contrast, major upper GI bleeding rarely occurs except in patients with active peptic ulcers or recent GI bleeding. However, these patients generally do not experience greater occult blood loss than healthy patients following small doses of aspirin. Mucosal damage associated with the use of salicylates may lead to development of peptic ulcers with or without bleeding, reactivation of latent ulcers, and ulcer perforation. Therapy with salicylates and related agents such as salicylamide should be considered and administered cautiously in patients with a history of GI disease or alcoholism, particularly if they are elderly and/or debilitated, since such patients may be more susceptible to the GI toxicity of these drugs and seem to tolerate ulceration and bleeding less well than other individuals. Extreme caution and thorough assessment of risks and benefits are warranted in patients with active or recent GI bleeding or lesions. Whenever possible, especially if prolonged use is anticipated, treatment with non-ulcerogenic agents should be attempted first. If salicylates are used, close monitoring for toxicity is recommended. Some adverse GI effects may be minimized by administration with high dosages of antacids, use of enteric-coated or extended-release formulations, and/or concurrent use of a histamine H2-receptor antagonist or a cytoprotective agent such as misoprostol. Patients with active peptic ulceration or GI bleeding treated with salicylates should generally be administered a concomitant anti-ulcer regimen.

The salsalate in Marthritic has a major potential interaction with Gastrointestinal Hemorrhage.

Salicylates, particularly aspirin, can cause dose-related gastrointestinal bleeding and mucosal damage, which may occur independently of each other. Occult, often asymptomatic GI blood loss is quite common with usual dosages of aspirin and stems from the drug's local effect on the GI mucosa. During chronic therapy, this type of bleeding may occasionally produce iron deficiency anemia. In contrast, major upper GI bleeding rarely occurs except in patients with active peptic ulcers or recent GI bleeding. However, these patients generally do not experience greater occult blood loss than healthy patients following small doses of aspirin. Mucosal damage associated with the use of salicylates may lead to development of peptic ulcers with or without bleeding, reactivation of latent ulcers, and ulcer perforation. Therapy with salicylates and related agents such as salicylamide should be considered and administered cautiously in patients with a history of GI disease or alcoholism, particularly if they are elderly and/or debilitated, since such patients may be more susceptible to the GI toxicity of these drugs and seem to tolerate ulceration and bleeding less well than other individuals. Extreme caution and thorough assessment of risks and benefits are warranted in patients with active or recent GI bleeding or lesions. Whenever possible, especially if prolonged use is anticipated, treatment with non-ulcerogenic agents should be attempted first. If salicylates are used, close monitoring for toxicity is recommended. Some adverse GI effects may be minimized by administration with high dosages of antacids, use of enteric-coated or extended-release formulations, and/or concurrent use of a histamine H2-receptor antagonist or a cytoprotective agent such as misoprostol. Patients with active peptic ulceration or GI bleeding treated with salicylates should generally be administered a concomitant anti-ulcer regimen.

The salsalate in Marthritic has a major potential interaction with Gastrointestinal Perforation.

Salicylates, particularly aspirin, can cause dose-related gastrointestinal bleeding and mucosal damage, which may occur independently of each other. Occult, often asymptomatic GI blood loss is quite common with usual dosages of aspirin and stems from the drug's local effect on the GI mucosa. During chronic therapy, this type of bleeding may occasionally produce iron deficiency anemia. In contrast, major upper GI bleeding rarely occurs except in patients with active peptic ulcers or recent GI bleeding. However, these patients generally do not experience greater occult blood loss than healthy patients following small doses of aspirin. Mucosal damage associated with the use of salicylates may lead to development of peptic ulcers with or without bleeding, reactivation of latent ulcers, and ulcer perforation. Therapy with salicylates and related agents such as salicylamide should be considered and administered cautiously in patients with a history of GI disease or alcoholism, particularly if they are elderly and/or debilitated, since such patients may be more susceptible to the GI toxicity of these drugs and seem to tolerate ulceration and bleeding less well than other individuals. Extreme caution and thorough assessment of risks and benefits are warranted in patients with active or recent GI bleeding or lesions. Whenever possible, especially if prolonged use is anticipated, treatment with non-ulcerogenic agents should be attempted first. If salicylates are used, close monitoring for toxicity is recommended. Some adverse GI effects may be minimized by administration with high dosages of antacids, use of enteric-coated or extended-release formulations, and/or concurrent use of a histamine H2-receptor antagonist or a cytoprotective agent such as misoprostol. Patients with active peptic ulceration or GI bleeding treated with salicylates should generally be administered a concomitant anti-ulcer regimen.

Anisindione has a moderate potential interaction with Heart Failure.

Patients with a collagen vascular disease (e.g., systemic lupus erythematosus, rheumatoid arthritis, scleroderma), congestive heart failure (especially decompensated disease), severe or prolonged diarrhea, fever, hyperthyroidism, malabsorption, or steatorrhea may exhibit greater than expected hypoprothrombinemic response to oral anticoagulants. Thus, more frequent laboratory (PT/INR) monitoring and dosage adjustment of anticoagulant may be required based on changes in the patient's condition. Patients should be advised to promptly report any signs of bleeding to their physician, including pain, swelling, headache, dizziness, weakness, prolonged bleeding from cuts, increased menstrual flow, vaginal bleeding, nosebleeds, bleeding of gums from brushing, unusual bleeding or bruising, red or brown urine, or red or black stools.

The salsalate in Marthritic has a moderate potential interaction with Hemodialysis.

Salicylate and its metabolites are readily removed by hemodialysis and, to a lesser extent, by peritoneal dialysis. Doses should either be scheduled for administration after dialysis or supplemental doses be given after dialysis.

Anisindione has a major potential interaction with High Blood Pressure.

In general, the use of oral anticoagulants is contraindicated in patients with malignant or severe, uncontrolled hypertension. These patients may be at increased risk for cerebral hemorrhage. Therapy with oral anticoagulants should be administered cautiously in patients with moderate hypertension.

Anisindione has a moderate potential interaction with High Cholesterol.

Patients with edema, hereditary coumarin resistance, hyperlipidemia, hypothyroidism, or nephrotic syndrome may exhibit lower than expected hypoprothrombinemic response to oral anticoagulants. Thus, more frequent laboratory (PT/INR) monitoring and dosage adjustment of anticoagulant may be required based on changes in the patient's condition.

The salsalate in Marthritic has a major potential interaction with History, Peptic Ulcer.

Salicylates, particularly aspirin, can cause dose-related gastrointestinal bleeding and mucosal damage, which may occur independently of each other. Occult, often asymptomatic GI blood loss is quite common with usual dosages of aspirin and stems from the drug's local effect on the GI mucosa. During chronic therapy, this type of bleeding may occasionally produce iron deficiency anemia. In contrast, major upper GI bleeding rarely occurs except in patients with active peptic ulcers or recent GI bleeding. However, these patients generally do not experience greater occult blood loss than healthy patients following small doses of aspirin. Mucosal damage associated with the use of salicylates may lead to development of peptic ulcers with or without bleeding, reactivation of latent ulcers, and ulcer perforation. Therapy with salicylates and related agents such as salicylamide should be considered and administered cautiously in patients with a history of GI disease or alcoholism, particularly if they are elderly and/or debilitated, since such patients may be more susceptible to the GI toxicity of these drugs and seem to tolerate ulceration and bleeding less well than other individuals. Extreme caution and thorough assessment of risks and benefits are warranted in patients with active or recent GI bleeding or lesions. Whenever possible, especially if prolonged use is anticipated, treatment with non-ulcerogenic agents should be attempted first. If salicylates are used, close monitoring for toxicity is recommended. Some adverse GI effects may be minimized by administration with high dosages of antacids, use of enteric-coated or extended-release formulations, and/or concurrent use of a histamine H2-receptor antagonist or a cytoprotective agent such as misoprostol. Patients with active peptic ulceration or GI bleeding treated with salicylates should generally be administered a concomitant anti-ulcer regimen.

Anisindione has a moderate potential interaction with Hyperthyroidism.

Patients with a collagen vascular disease (e.g., systemic lupus erythematosus, rheumatoid arthritis, scleroderma), congestive heart failure (especially decompensated disease), severe or prolonged diarrhea, fever, hyperthyroidism, malabsorption, or steatorrhea may exhibit greater than expected hypoprothrombinemic response to oral anticoagulants. Thus, more frequent laboratory (PT/INR) monitoring and dosage adjustment of anticoagulant may be required based on changes in the patient's condition. Patients should be advised to promptly report any signs of bleeding to their physician, including pain, swelling, headache, dizziness, weakness, prolonged bleeding from cuts, increased menstrual flow, vaginal bleeding, nosebleeds, bleeding of gums from brushing, unusual bleeding or bruising, red or brown urine, or red or black stools.

Anisindione has a major potential interaction with Infectious Endocarditis.

In general, the use of oral anticoagulants is contraindicated in patients with active bleeding or a hemorrhagic diathesis or other significant risks for bleeding, including hemostatic and/or coagulation defects associated with hemophilia, hypoprothrombinemia, thrombocytopenia, thrombocytopathy, severe hepatic impairment, and myeloproliferative disorders such as leukemia or polycythemia vera. Additionally, oral anticoagulants are usually contraindicated in the presence of any active ulceration of the gastrointestinal, respiratory, or genitourinary tracts; cerebrovascular hemorrhage; aneurysms (cerebral, dissecting aortic); pericarditis and pericardial effusions; bacterial endocarditis; and eclampsia, preeclampsia, or threatened abortion. These patients may be at increased risk for uncontrollable hemorrhage or bleeding complications during therapy with oral anticoagulants. Other potential contraindications include diverticulitis, vasculitis, malnutrition, and vitamin C or vitamin K deficiency. The decision to administer anticoagulants must be based upon clinical judgment in which the risks are weighed against the benefits in each patient.

The salsalate in Marthritic has a major potential interaction with Influenza.

The use of salicylates, primarily aspirin, in children with varicella infections or influenza-like illnesses has been associated with an increased risk of Reye's syndrome. Although a causal relationship has not been established, the majority of evidence to date seems to support the association. Most authorities, including the American Academy of Pediatrics Committee on Infectious Diseases, recommend avoiding the use of salicylates in children and teenagers with known or suspected varicella or influenza and during presumed outbreaks of influenza. If antipyretic or analgesic therapy is indicated under these circumstances, acetaminophen may be an appropriate alternative. The same precautions should also be observed with related agents such as salicylamide or diflunisal because of their structural and pharmacological similarities to salicylate.

Anisindione has a major potential interaction with Liver Disease.

Oral anticoagulants (coumarin and indandione derivatives) are primarily metabolized by the liver. Patients with hepatic impairment may have a heightened response to these agents due to decreased clearance of the drugs as well as defective hemostasis associated with impaired synthesis of clotting factors by the liver. Therapy with oral anticoagulants should be administered cautiously in patients with severe or moderate liver disease. The INR should be monitored closely, and patients should be advised to promptly report any signs of bleeding to their physician, including pain, swelling, headache, dizziness, weakness, prolonged bleeding from cuts, increased menstrual flow, vaginal bleeding, nosebleeds, bleeding of gums from brushing, unusual bleeding or bruising, red or brown urine, or red or black stools

The salsalate in Marthritic has a moderate potential interaction with Liver Disease.

The use of salicylates has occasionally been associated with acute, reversible hepatotoxicity, primarily manifested as elevations of serum transaminases, alkaline phosphatase and/or, rarely, bilirubin. Hepatic injury consistent with chronic active hepatitis has also been reported in a few patients, which resulted rarely in encephalopathy or death. Salicylate-induced hepatotoxicity appears to be dependent on serum salicylate concentration (> 25 mg/dL) and has occurred most frequently in patients with juvenile arthritis, active systemic lupus erythematosus, rheumatic fever, or preexisting hepatic impairment. Therapy with salicylates, particularly when given in high dosages, should be administered cautiously in these patients, and periodic monitoring of liver function is recommended. The same precautions should also be observed with the use of related agents such as salicylamide because of their structural and pharmacological similarities to salicylate. A dosage reduction may be necessary if liver function abnormalities develop and serum salicylate concentration exceeds 25 mg/dL, although serum transaminase elevations may sometimes be transient and return to pretreatment values despite continued therapy without dosage adjustment.

Anisindione has a moderate potential interaction with Malabsorption Syndrome.

Patients with a collagen vascular disease (e.g., systemic lupus erythematosus, rheumatoid arthritis, scleroderma), congestive heart failure (especially decompensated disease), severe or prolonged diarrhea, fever, hyperthyroidism, malabsorption, or steatorrhea may exhibit greater than expected hypoprothrombinemic response to oral anticoagulants. Thus, more frequent laboratory (PT/INR) monitoring and dosage adjustment of anticoagulant may be required based on changes in the patient's condition. Patients should be advised to promptly report any signs of bleeding to their physician, including pain, swelling, headache, dizziness, weakness, prolonged bleeding from cuts, increased menstrual flow, vaginal bleeding, nosebleeds, bleeding of gums from brushing, unusual bleeding or bruising, red or brown urine, or red or black stools.

Anisindione has a major potential interaction with Malnourishment.

In general, the use of oral anticoagulants is contraindicated in patients with active bleeding or a hemorrhagic diathesis or other significant risks for bleeding, including hemostatic and/or coagulation defects associated with hemophilia, hypoprothrombinemia, thrombocytopenia, thrombocytopathy, severe hepatic impairment, and myeloproliferative disorders such as leukemia or polycythemia vera. Additionally, oral anticoagulants are usually contraindicated in the presence of any active ulceration of the gastrointestinal, respiratory, or genitourinary tracts; cerebrovascular hemorrhage; aneurysms (cerebral, dissecting aortic); pericarditis and pericardial effusions; bacterial endocarditis; and eclampsia, preeclampsia, or threatened abortion. These patients may be at increased risk for uncontrollable hemorrhage or bleeding complications during therapy with oral anticoagulants. Other potential contraindications include diverticulitis, vasculitis, malnutrition, and vitamin C or vitamin K deficiency. The decision to administer anticoagulants must be based upon clinical judgment in which the risks are weighed against the benefits in each patient.

Anisindione has a major potential interaction with Myeloproliferative Disorders.

In general, the use of oral anticoagulants is contraindicated in patients with active bleeding or a hemorrhagic diathesis or other significant risks for bleeding, including hemostatic and/or coagulation defects associated with hemophilia, hypoprothrombinemia, thrombocytopenia, thrombocytopathy, severe hepatic impairment, and myeloproliferative disorders such as leukemia or polycythemia vera. Additionally, oral anticoagulants are usually contraindicated in the presence of any active ulceration of the gastrointestinal, respiratory, or genitourinary tracts; cerebrovascular hemorrhage; aneurysms (cerebral, dissecting aortic); pericarditis and pericardial effusions; bacterial endocarditis; and eclampsia, preeclampsia, or threatened abortion. These patients may be at increased risk for uncontrollable hemorrhage or bleeding complications during therapy with oral anticoagulants. Other potential contraindications include diverticulitis, vasculitis, malnutrition, and vitamin C or vitamin K deficiency. The decision to administer anticoagulants must be based upon clinical judgment in which the risks are weighed against the benefits in each patient.

The salsalate in Marthritic has a major potential interaction with Noninfectious Colitis.

Salicylates, particularly aspirin, can cause dose-related gastrointestinal bleeding and mucosal damage, which may occur independently of each other. Occult, often asymptomatic GI blood loss is quite common with usual dosages of aspirin and stems from the drug's local effect on the GI mucosa. During chronic therapy, this type of bleeding may occasionally produce iron deficiency anemia. In contrast, major upper GI bleeding rarely occurs except in patients with active peptic ulcers or recent GI bleeding. However, these patients generally do not experience greater occult blood loss than healthy patients following small doses of aspirin. Mucosal damage associated with the use of salicylates may lead to development of peptic ulcers with or without bleeding, reactivation of latent ulcers, and ulcer perforation. Therapy with salicylates and related agents such as salicylamide should be considered and administered cautiously in patients with a history of GI disease or alcoholism, particularly if they are elderly and/or debilitated, since such patients may be more susceptible to the GI toxicity of these drugs and seem to tolerate ulceration and bleeding less well than other individuals. Extreme caution and thorough assessment of risks and benefits are warranted in patients with active or recent GI bleeding or lesions. Whenever possible, especially if prolonged use is anticipated, treatment with non-ulcerogenic agents should be attempted first. If salicylates are used, close monitoring for toxicity is recommended. Some adverse GI effects may be minimized by administration with high dosages of antacids, use of enteric-coated or extended-release formulations, and/or concurrent use of a histamine H2-receptor antagonist or a cytoprotective agent such as misoprostol. Patients with active peptic ulceration or GI bleeding treated with salicylates should generally be administered a concomitant anti-ulcer regimen.

Anisindione has a major potential interaction with Peptic Ulcer.

In general, the use of oral anticoagulants is contraindicated in patients with active bleeding or a hemorrhagic diathesis or other significant risks for bleeding, including hemostatic and/or coagulation defects associated with hemophilia, hypoprothrombinemia, thrombocytopenia, thrombocytopathy, severe hepatic impairment, and myeloproliferative disorders such as leukemia or polycythemia vera. Additionally, oral anticoagulants are usually contraindicated in the presence of any active ulceration of the gastrointestinal, respiratory, or genitourinary tracts; cerebrovascular hemorrhage; aneurysms (cerebral, dissecting aortic); pericarditis and pericardial effusions; bacterial endocarditis; and eclampsia, preeclampsia, or threatened abortion. These patients may be at increased risk for uncontrollable hemorrhage or bleeding complications during therapy with oral anticoagulants. Other potential contraindications include diverticulitis, vasculitis, malnutrition, and vitamin C or vitamin K deficiency. The decision to administer anticoagulants must be based upon clinical judgment in which the risks are weighed against the benefits in each patient.

The salsalate in Marthritic has a major potential interaction with Peptic Ulcer.

Salicylates, particularly aspirin, can cause dose-related gastrointestinal bleeding and mucosal damage, which may occur independently of each other. Occult, often asymptomatic GI blood loss is quite common with usual dosages of aspirin and stems from the drug's local effect on the GI mucosa. During chronic therapy, this type of bleeding may occasionally produce iron deficiency anemia. In contrast, major upper GI bleeding rarely occurs except in patients with active peptic ulcers or recent GI bleeding. However, these patients generally do not experience greater occult blood loss than healthy patients following small doses of aspirin. Mucosal damage associated with the use of salicylates may lead to development of peptic ulcers with or without bleeding, reactivation of latent ulcers, and ulcer perforation. Therapy with salicylates and related agents such as salicylamide should be considered and administered cautiously in patients with a history of GI disease or alcoholism, particularly if they are elderly and/or debilitated, since such patients may be more susceptible to the GI toxicity of these drugs and seem to tolerate ulceration and bleeding less well than other individuals. Extreme caution and thorough assessment of risks and benefits are warranted in patients with active or recent GI bleeding or lesions. Whenever possible, especially if prolonged use is anticipated, treatment with non-ulcerogenic agents should be attempted first. If salicylates are used, close monitoring for toxicity is recommended. Some adverse GI effects may be minimized by administration with high dosages of antacids, use of enteric-coated or extended-release formulations, and/or concurrent use of a histamine H2-receptor antagonist or a cytoprotective agent such as misoprostol. Patients with active peptic ulceration or GI bleeding treated with salicylates should generally be administered a concomitant anti-ulcer regimen.

Anisindione has a major potential interaction with Pericarditis.

In general, the use of oral anticoagulants is contraindicated in patients with active bleeding or a hemorrhagic diathesis or other significant risks for bleeding, including hemostatic and/or coagulation defects associated with hemophilia, hypoprothrombinemia, thrombocytopenia, thrombocytopathy, severe hepatic impairment, and myeloproliferative disorders such as leukemia or polycythemia vera. Additionally, oral anticoagulants are usually contraindicated in the presence of any active ulceration of the gastrointestinal, respiratory, or genitourinary tracts; cerebrovascular hemorrhage; aneurysms (cerebral, dissecting aortic); pericarditis and pericardial effusions; bacterial endocarditis; and eclampsia, preeclampsia, or threatened abortion. These patients may be at increased risk for uncontrollable hemorrhage or bleeding complications during therapy with oral anticoagulants. Other potential contraindications include diverticulitis, vasculitis, malnutrition, and vitamin C or vitamin K deficiency. The decision to administer anticoagulants must be based upon clinical judgment in which the risks are weighed against the benefits in each patient.

Anisindione has a major potential interaction with Pheochromocytoma.

In general, the use of oral anticoagulants is contraindicated in patients with malignant or severe, uncontrolled hypertension. These patients may be at increased risk for cerebral hemorrhage. Therapy with oral anticoagulants should be administered cautiously in patients with moderate hypertension.

Anisindione has a major potential interaction with Protein C Deficiency.

Tissue necrosis is a rare complication that develops during the initiation of oral anticoagulant therapy due to thrombotic occlusion of venules in the dermis and subcutaneous tissues. Hereditary, familial, or clinical deficiencies of protein C or its cofactor, protein S, may be associated with a hypercoagulable state and an increased risk of the complication. Therapy with oral anticoagulants should be administered cautiously in patients with known or suspected deficiency in protein C-mediated anticoagulant response. Concomitant administration with heparin for the first 5 to 7 days of oral anticoagulant therapy may minimize the risk. If tissue necrosis develops, oral anticoagulant therapy should be discontinued promptly and vitamin K or frozen plasma administered at once. Heparin should then be considered for anticoagulation.

The salsalate in Marthritic has a major potential interaction with Renal Dysfunction.

Salicylate and its metabolites are eliminated almost entirely by the kidney. Therapy with salicylate drugs should be administered cautiously in patients with renal impairment, especially if it is severe. Reduced dosages may be necessary to avoid drug accumulation. Clinical monitoring of renal function is recommended during prolonged therapy, since the use of salicylate drugs has rarely been associated with renal toxicities, including elevations in serum creatinine, renal papillary necrosis, and acute tubular necrosis with renal failure. Most of the data have been derived from experience with aspirin but may apply to other salicylates as well. In patients with impaired renal function, aspirin has caused reversible and sometimes marked decreases in renal blood flow and glomerular filtration rate. Adverse renal effects have usually reversed rapidly following withdrawal of aspirin therapy.

Anisindione has a moderate potential interaction with Renal Dysfunction.

There is no evidence that hypoprothrombinemic response to oral anticoagulants (coumarin and indandione derivatives) is altered in renal impairment due to decreased plasma protein binding, thus dosage adjustments are generally not necessary. However, patients with renal impairment may demonstrate platelet defects and may be at increased risk for bleeding. Therapy with oral anticoagulants should be administered cautiously in patients with severe or moderate renal dysfunction. The INR should be monitored closely, and patients should be advised to promptly report any signs of bleeding to their physician, including pain, swelling, headache, dizziness, weakness, prolonged bleeding from cuts, increased menstrual flow, vaginal bleeding, nosebleeds, bleeding of gums from brushing, unusual bleeding or bruising, red or brown urine, or red or black stools.

Anisindione has a major potential interaction with Thrombocytopathy.

In general, the use of oral anticoagulants is contraindicated in patients with active bleeding or a hemorrhagic diathesis or other significant risks for bleeding, including hemostatic and/or coagulation defects associated with hemophilia, hypoprothrombinemia, thrombocytopenia, thrombocytopathy, severe hepatic impairment, and myeloproliferative disorders such as leukemia or polycythemia vera. Additionally, oral anticoagulants are usually contraindicated in the presence of any active ulceration of the gastrointestinal, respiratory, or genitourinary tracts; cerebrovascular hemorrhage; aneurysms (cerebral, dissecting aortic); pericarditis and pericardial effusions; bacterial endocarditis; and eclampsia, preeclampsia, or threatened abortion. These patients may be at increased risk for uncontrollable hemorrhage or bleeding complications during therapy with oral anticoagulants. Other potential contraindications include diverticulitis, vasculitis, malnutrition, and vitamin C or vitamin K deficiency. The decision to administer anticoagulants must be based upon clinical judgment in which the risks are weighed against the benefits in each patient.

The salsalate in Marthritic has a moderate potential interaction with Thrombocytopathy.

All salicylates can interfere with the action of vitamin K and induce a dose-dependent alteration in hepatic synthesis of coagulation factors VII, IX and X. At usual recommended dosages, a slight increase in prothrombin time (PT) may occur. Therapy with salicylates, especially if given in high dosages, should be administered cautiously in patients with significant active bleeding or a hemorrhagic diathesis, including hemostatic and/or coagulation defects associated with hemophilia, vitamin K deficiency, hypoprothombinemia, thrombocytopenia, thrombocytopathy, or severe hepatic impairment. The same precaution should also be observed with the use of related agents such as salicylamide because of their structural and pharmacological similarities to salicylate.

Anisindione has a major potential interaction with Thrombocytopenia.

In general, the use of oral anticoagulants is contraindicated in patients with active bleeding or a hemorrhagic diathesis or other significant risks for bleeding, including hemostatic and/or coagulation defects associated with hemophilia, hypoprothrombinemia, thrombocytopenia, thrombocytopathy, severe hepatic impairment, and myeloproliferative disorders such as leukemia or polycythemia vera. Additionally, oral anticoagulants are usually contraindicated in the presence of any active ulceration of the gastrointestinal, respiratory, or genitourinary tracts; cerebrovascular hemorrhage; aneurysms (cerebral, dissecting aortic); pericarditis and pericardial effusions; bacterial endocarditis; and eclampsia, preeclampsia, or threatened abortion. These patients may be at increased risk for uncontrollable hemorrhage or bleeding complications during therapy with oral anticoagulants. Other potential contraindications include diverticulitis, vasculitis, malnutrition, and vitamin C or vitamin K deficiency. The decision to administer anticoagulants must be based upon clinical judgment in which the risks are weighed against the benefits in each patient.

The salsalate in Marthritic has a moderate potential interaction with Thrombocytopenia.

All salicylates can interfere with the action of vitamin K and induce a dose-dependent alteration in hepatic synthesis of coagulation factors VII, IX and X. At usual recommended dosages, a slight increase in prothrombin time (PT) may occur. Therapy with salicylates, especially if given in high dosages, should be administered cautiously in patients with significant active bleeding or a hemorrhagic diathesis, including hemostatic and/or coagulation defects associated with hemophilia, vitamin K deficiency, hypoprothombinemia, thrombocytopenia, thrombocytopathy, or severe hepatic impairment. The same precaution should also be observed with the use of related agents such as salicylamide because of their structural and pharmacological similarities to salicylate.

Anisindione has a major potential interaction with Toxemia of pregnancy.

In general, the use of oral anticoagulants is contraindicated in patients with active bleeding or a hemorrhagic diathesis or other significant risks for bleeding, including hemostatic and/or coagulation defects associated with hemophilia, hypoprothrombinemia, thrombocytopenia, thrombocytopathy, severe hepatic impairment, and myeloproliferative disorders such as leukemia or polycythemia vera. Additionally, oral anticoagulants are usually contraindicated in the presence of any active ulceration of the gastrointestinal, respiratory, or genitourinary tracts; cerebrovascular hemorrhage; aneurysms (cerebral, dissecting aortic); pericarditis and pericardial effusions; bacterial endocarditis; and eclampsia, preeclampsia, or threatened abortion. These patients may be at increased risk for uncontrollable hemorrhage or bleeding complications during therapy with oral anticoagulants. Other potential contraindications include diverticulitis, vasculitis, malnutrition, and vitamin C or vitamin K deficiency. The decision to administer anticoagulants must be based upon clinical judgment in which the risks are weighed against the benefits in each patient.

Anisindione has a major potential interaction with Ulcerative Colitis.

In general, the use of oral anticoagulants is contraindicated in patients with active bleeding or a hemorrhagic diathesis or other significant risks for bleeding, including hemostatic and/or coagulation defects associated with hemophilia, hypoprothrombinemia, thrombocytopenia, thrombocytopathy, severe hepatic impairment, and myeloproliferative disorders such as leukemia or polycythemia vera. Additionally, oral anticoagulants are usually contraindicated in the presence of any active ulceration of the gastrointestinal, respiratory, or genitourinary tracts; cerebrovascular hemorrhage; aneurysms (cerebral, dissecting aortic); pericarditis and pericardial effusions; bacterial endocarditis; and eclampsia, preeclampsia, or threatened abortion. These patients may be at increased risk for uncontrollable hemorrhage or bleeding complications during therapy with oral anticoagulants. Other potential contraindications include diverticulitis, vasculitis, malnutrition, and vitamin C or vitamin K deficiency. The decision to administer anticoagulants must be based upon clinical judgment in which the risks are weighed against the benefits in each patient.

Anisindione has a moderate potential interaction with Underactive Thyroid.

Patients with edema, hereditary coumarin resistance, hyperlipidemia, hypothyroidism, or nephrotic syndrome may exhibit lower than expected hypoprothrombinemic response to oral anticoagulants. Thus, more frequent laboratory (PT/INR) monitoring and dosage adjustment of anticoagulant may be required based on changes in the patient's condition.

The salsalate in Marthritic has a major potential interaction with Varicella-Zoster.

The use of salicylates, primarily aspirin, in children with varicella infections or influenza-like illnesses has been associated with an increased risk of Reye's syndrome. Although a causal relationship has not been established, the majority of evidence to date seems to support the association. Most authorities, including the American Academy of Pediatrics Committee on Infectious Diseases, recommend avoiding the use of salicylates in children and teenagers with known or suspected varicella or influenza and during presumed outbreaks of influenza. If antipyretic or analgesic therapy is indicated under these circumstances, acetaminophen may be an appropriate alternative. The same precautions should also be observed with related agents such as salicylamide or diflunisal because of their structural and pharmacological similarities to salicylate.

Anisindione has a major potential interaction with Vasculitis.

In general, the use of oral anticoagulants is contraindicated in patients with active bleeding or a hemorrhagic diathesis or other significant risks for bleeding, including hemostatic and/or coagulation defects associated with hemophilia, hypoprothrombinemia, thrombocytopenia, thrombocytopathy, severe hepatic impairment, and myeloproliferative disorders such as leukemia or polycythemia vera. Additionally, oral anticoagulants are usually contraindicated in the presence of any active ulceration of the gastrointestinal, respiratory, or genitourinary tracts; cerebrovascular hemorrhage; aneurysms (cerebral, dissecting aortic); pericarditis and pericardial effusions; bacterial endocarditis; and eclampsia, preeclampsia, or threatened abortion. These patients may be at increased risk for uncontrollable hemorrhage or bleeding complications during therapy with oral anticoagulants. Other potential contraindications include diverticulitis, vasculitis, malnutrition, and vitamin C or vitamin K deficiency. The decision to administer anticoagulants must be based upon clinical judgment in which the risks are weighed against the benefits in each patient.

Anisindione has a major potential interaction with Vitamin C Deficiency.

In general, the use of oral anticoagulants is contraindicated in patients with active bleeding or a hemorrhagic diathesis or other significant risks for bleeding, including hemostatic and/or coagulation defects associated with hemophilia, hypoprothrombinemia, thrombocytopenia, thrombocytopathy, severe hepatic impairment, and myeloproliferative disorders such as leukemia or polycythemia vera. Additionally, oral anticoagulants are usually contraindicated in the presence of any active ulceration of the gastrointestinal, respiratory, or genitourinary tracts; cerebrovascular hemorrhage; aneurysms (cerebral, dissecting aortic); pericarditis and pericardial effusions; bacterial endocarditis; and eclampsia, preeclampsia, or threatened abortion. These patients may be at increased risk for uncontrollable hemorrhage or bleeding complications during therapy with oral anticoagulants. Other potential contraindications include diverticulitis, vasculitis, malnutrition, and vitamin C or vitamin K deficiency. The decision to administer anticoagulants must be based upon clinical judgment in which the risks are weighed against the benefits in each patient.

Anisindione has a major potential interaction with Vitamin K Deficiency.

In general, the use of oral anticoagulants is contraindicated in patients with active bleeding or a hemorrhagic diathesis or other significant risks for bleeding, including hemostatic and/or coagulation defects associated with hemophilia, hypoprothrombinemia, thrombocytopenia, thrombocytopathy, severe hepatic impairment, and myeloproliferative disorders such as leukemia or polycythemia vera. Additionally, oral anticoagulants are usually contraindicated in the presence of any active ulceration of the gastrointestinal, respiratory, or genitourinary tracts; cerebrovascular hemorrhage; aneurysms (cerebral, dissecting aortic); pericarditis and pericardial effusions; bacterial endocarditis; and eclampsia, preeclampsia, or threatened abortion. These patients may be at increased risk for uncontrollable hemorrhage or bleeding complications during therapy with oral anticoagulants. Other potential contraindications include diverticulitis, vasculitis, malnutrition, and vitamin C or vitamin K deficiency. The decision to administer anticoagulants must be based upon clinical judgment in which the risks are weighed against the benefits in each patient.

The salsalate in Marthritic has a moderate potential interaction with Vitamin K Deficiency.

All salicylates can interfere with the action of vitamin K and induce a dose-dependent alteration in hepatic synthesis of coagulation factors VII, IX and X. At usual recommended dosages, a slight increase in prothrombin time (PT) may occur. Therapy with salicylates, especially if given in high dosages, should be administered cautiously in patients with significant active bleeding or a hemorrhagic diathesis, including hemostatic and/or coagulation defects associated with hemophilia, vitamin K deficiency, hypoprothombinemia, thrombocytopenia, thrombocytopathy, or severe hepatic impairment. The same precaution should also be observed with the use of related agents such as salicylamide because of their structural and pharmacological similarities to salicylate.