Interactions between Fedratinib and Pseudogest-DM

Fedratinib has a moderate potential interaction with Anemia.

Adverse hematologic effects including neutropenia, thrombocytopenia, and anemia have been associated with the use of fedratinib. Therapy with fedratinib should only be initiated in patients with a baseline platelet count of at least 50 x 10(9)/L. CBC counts should be monitored at baseline and every 3 months thereafter; treatment should be modified based on platelet levels and active bleeding.

The pseudoephedrine in Pseudogest-DM has a moderate potential interaction with Benign Prostatic Hyperplasia.

Sympathomimetic agents may cause or worsen urinary difficulty in patients with prostate enlargement due to smooth muscle contraction in the bladder neck via stimulation of alpha-1 adrenergic receptors. Therapy with sympathomimetic agents should be administered cautiously in patients with hypertrophy or neoplasm of the prostate.

Fedratinib has a moderate potential interaction with Bleeding Associated with Coagulation Defect.

Adverse hematologic effects including neutropenia, thrombocytopenia, and anemia have been associated with the use of fedratinib. Therapy with fedratinib should only be initiated in patients with a baseline platelet count of at least 50 x 10(9)/L. CBC counts should be monitored at baseline and every 3 months thereafter; treatment should be modified based on platelet levels and active bleeding.

Fedratinib has a moderate potential interaction with Bleeding Disorder.

Adverse hematologic effects including neutropenia, thrombocytopenia, and anemia have been associated with the use of fedratinib. Therapy with fedratinib should only be initiated in patients with a baseline platelet count of at least 50 x 10(9)/L. CBC counts should be monitored at baseline and every 3 months thereafter; treatment should be modified based on platelet levels and active bleeding.

Fedratinib has a major potential interaction with Cardiovascular Conditions and Disorders.

In a major safety study of a Janus kinase (JAK) inhibitor, tofacitinib, in rheumatoid arthritis patients 50 years and older with at least 1 cardiovascular risk factor, higher rates of all-cause mortality (including sudden cardiovascular death) and major adverse cardiovascular events (MACE) (defined as cardiovascular death, myocardial infarction, and stroke) were observed with the JAK inhibitor when compared with tumor necrosis factor (TNF) blockers. Patients who were current or past smokers had an additional increased risk. Based on a shared mechanism of action, this risk should be considered for other JAK inhibitors, including baricitinib, upadacitinib, ruxolitinib, fedratinib, ritlecitinib, deuruxolitinib, and pacritinib. Consider the benefits and risks for each individual patient prior and during treatment with JAK inhibitors, especially in patients with other cardiovascular risk factors, history of cardiovascular events, and patients who are current or past smokers. Patients should be informed about the symptoms of serious cardiovascular events and what to do if they occur.

The pseudoephedrine in Pseudogest-DM has a major potential interaction with Cardiovascular Conditions and Disorders.

Sympathomimetic agents may cause adverse cardiovascular effects, particularly when used in high dosages and/or in susceptible patients. In cardiac tissues, these agents may produce positive chronotropic and inotropic effects via stimulation of beta- 1 adrenergic receptors. Cardiac output, oxygen consumption, and the work of the heart may be increased. In the peripheral vasculature, vasoconstriction may occur via stimulation of alpha-1 adrenergic receptors. Palpitations, tachycardia, arrhythmia, hypertension, reflex bradycardia, coronary occlusion, cerebral vasculitis, myocardial infarction, cardiac arrest, and death have been reported. Some of these agents, particularly ephedra alkaloids (ephedrine, ma huang, phenylpropanolamine), may also predispose patients to hemorrhagic and ischemic stroke. Therapy with sympathomimetic agents should generally be avoided or administered cautiously in patients with sensitivity to sympathomimetic amines, hyperthyroidism, or underlying cardiovascular or cerebrovascular disorders. These agents should not be used in patients with severe coronary artery disease or severe/uncontrolled hypertension.

The pseudoephedrine in Pseudogest-DM has a major potential interaction with Cerebrovascular Insufficiency.

Sympathomimetic agents may cause adverse cardiovascular effects, particularly when used in high dosages and/or in susceptible patients. In cardiac tissues, these agents may produce positive chronotropic and inotropic effects via stimulation of beta- 1 adrenergic receptors. Cardiac output, oxygen consumption, and the work of the heart may be increased. In the peripheral vasculature, vasoconstriction may occur via stimulation of alpha-1 adrenergic receptors. Palpitations, tachycardia, arrhythmia, hypertension, reflex bradycardia, coronary occlusion, cerebral vasculitis, myocardial infarction, cardiac arrest, and death have been reported. Some of these agents, particularly ephedra alkaloids (ephedrine, ma huang, phenylpropanolamine), may also predispose patients to hemorrhagic and ischemic stroke. Therapy with sympathomimetic agents should generally be avoided or administered cautiously in patients with sensitivity to sympathomimetic amines, hyperthyroidism, or underlying cardiovascular or cerebrovascular disorders. These agents should not be used in patients with severe coronary artery disease or severe/uncontrolled hypertension.

The pseudoephedrine in Pseudogest-DM has a moderate potential interaction with Diabetes Mellitus.

Sympathomimetic agents may cause increases in blood glucose concentrations. These effects are usually transient and slight but may be significant with dosages higher than those normally recommended. Therapy with sympathomimetic agents should be administered cautiously in patients with diabetes mellitus. Closer monitoring of blood glucose concentrations may be appropriate.

The pseudoephedrine in Pseudogest-DM has a moderate potential interaction with Gastrointestinal Obstruction.

The extended-release formulation of pseudoephedrine (Sudafed 24 Hour) contains a non-deformable material. There have been rare reports of obstructive symptoms in patients with known strictures following the ingestion of similar sustained-release products. Therapy with the extended-release formulation of pseudoephedrine should be administered cautiously in patients with preexisting severe gastrointestinal narrowing or obstruction, whether pathologic or iatrogenic.

The pseudoephedrine in Pseudogest-DM has a moderate potential interaction with Glaucoma/Intraocular Hypertension.

Sympathomimetic agents can induce transient mydriasis via stimulation of alpha-1 adrenergic receptors. In patients with anatomically narrow angles or narrow-angle glaucoma, pupillary dilation can provoke an acute attack. In patients with other forms of glaucoma, mydriasis may occasionally increase intraocular pressure. Therapy with sympathomimetic agents should be administered cautiously in patients with or predisposed to glaucoma, particularly narrow-angle glaucoma.

The pseudoephedrine in Pseudogest-DM has a major potential interaction with Hyperthyroidism.

Sympathomimetic agents may cause adverse cardiovascular effects, particularly when used in high dosages and/or in susceptible patients. In cardiac tissues, these agents may produce positive chronotropic and inotropic effects via stimulation of beta- 1 adrenergic receptors. Cardiac output, oxygen consumption, and the work of the heart may be increased. In the peripheral vasculature, vasoconstriction may occur via stimulation of alpha-1 adrenergic receptors. Palpitations, tachycardia, arrhythmia, hypertension, reflex bradycardia, coronary occlusion, cerebral vasculitis, myocardial infarction, cardiac arrest, and death have been reported. Some of these agents, particularly ephedra alkaloids (ephedrine, ma huang, phenylpropanolamine), may also predispose patients to hemorrhagic and ischemic stroke. Therapy with sympathomimetic agents should generally be avoided or administered cautiously in patients with sensitivity to sympathomimetic amines, hyperthyroidism, or underlying cardiovascular or cerebrovascular disorders. These agents should not be used in patients with severe coronary artery disease or severe/uncontrolled hypertension.

The pseudoephedrine in Pseudogest-DM has a moderate potential interaction with Phenylketonuria.

Chewable products frequently may contain aspartame, which is metabolized in the gastrointestinal tract to phenylalanine. Sudafed (brand of pseudoephedrine) chewable 15 mg tablets provide the equivalent of 0.78 mg of phenylalanine per each tablet. The aspartame/phenylalanine content should be considered when this and similar products are used in patients who must restrict their intake of phenylalanine (i.e. phenylketonurics).

The pseudoephedrine in Pseudogest-DM has a major potential interaction with Pheochromocytoma.

Sympathomimetic agents may cause adverse cardiovascular effects, particularly when used in high dosages and/or in susceptible patients. In cardiac tissues, these agents may produce positive chronotropic and inotropic effects via stimulation of beta- 1 adrenergic receptors. Cardiac output, oxygen consumption, and the work of the heart may be increased. In the peripheral vasculature, vasoconstriction may occur via stimulation of alpha-1 adrenergic receptors. Palpitations, tachycardia, arrhythmia, hypertension, reflex bradycardia, coronary occlusion, cerebral vasculitis, myocardial infarction, cardiac arrest, and death have been reported. Some of these agents, particularly ephedra alkaloids (ephedrine, ma huang, phenylpropanolamine), may also predispose patients to hemorrhagic and ischemic stroke. Therapy with sympathomimetic agents should generally be avoided or administered cautiously in patients with sensitivity to sympathomimetic amines, hyperthyroidism, or underlying cardiovascular or cerebrovascular disorders. These agents should not be used in patients with severe coronary artery disease or severe/uncontrolled hypertension.

The pseudoephedrine in Pseudogest-DM has a moderate potential interaction with Prostate Tumor, Benign.

Sympathomimetic agents may cause or worsen urinary difficulty in patients with prostate enlargement due to smooth muscle contraction in the bladder neck via stimulation of alpha-1 adrenergic receptors. Therapy with sympathomimetic agents should be administered cautiously in patients with hypertrophy or neoplasm of the prostate.

Fedratinib has a moderate potential interaction with Renal Dysfunction.

Due to potential increase of exposure, patients with preexisting-existing moderate renal impairment require more intensive safety monitoring, and if necessary, dose modifications based on adverse reactions when treated with fedratinib. Reduce fedratinib dose when administered to patients with severe renal impairment (CrCl 15 mL/min to 29 mL/min by Cockcroft-Gault). No modification of the starting dose is recommended for patients with mild to moderate renal impairment (CrCl 30 mL/min to 89 mL/min by Cockcroft-Gault).

Fedratinib has a major potential interaction with Smoking.

In a major safety study of a Janus kinase (JAK) inhibitor, tofacitinib, in rheumatoid arthritis patients 50 years and older with at least 1 cardiovascular risk factor, higher rates of all-cause mortality (including sudden cardiovascular death) and major adverse cardiovascular events (MACE) (defined as cardiovascular death, myocardial infarction, and stroke) were observed with the JAK inhibitor when compared with tumor necrosis factor (TNF) blockers. Patients who were current or past smokers had an additional increased risk. Based on a shared mechanism of action, this risk should be considered for other JAK inhibitors, including baricitinib, upadacitinib, ruxolitinib, fedratinib, ritlecitinib, deuruxolitinib, and pacritinib. Consider the benefits and risks for each individual patient prior and during treatment with JAK inhibitors, especially in patients with other cardiovascular risk factors, history of cardiovascular events, and patients who are current or past smokers. Patients should be informed about the symptoms of serious cardiovascular events and what to do if they occur.

Fedratinib has a major potential interaction with Smoking.

Malignancies (including lymphomas and solid tumors) have been reported in patients treated with tofacitinib, baricitinib, upadacitinib, deuruxolitinib and other Janus kinase (JAK) inhibitors used to treat inflammatory conditions. Patients who are current or past smokers are at additional increased risk of malignancies. Based on a shared mechanism of action, this risk should be considered for other JAK inhibitors, including ruxolitinib, pacritinib, and fedratinib. Before starting or continuing therapy, the benefits and risks for the individual patient should be considered, especially in patients with a known malignancy (other than successfully treated nonmelanoma skin cancer), patients who develop a malignancy during therapy, and patients who are current or past smokers. Periodic skin examination is recommended for patients who are at increased risk for skin cancer.

Fedratinib has a major potential interaction with Thrombotic/Thromboembolic Disorder.

Thrombosis (including deep venous thrombosis, pulmonary embolism, cerebral venous sinus thrombosis, and arterial thrombosis) has occurred in patients treated for inflammatory conditions with Janus kinase (JAK) inhibitors, including baricitinib, tofacitinib, deuruxolitinib and upadacitinib. Many of these adverse events were serious and some resulted in death. Based on a shared mechanism of action, this risk should be considered for other JAK inhibitors, including ruxolitinib, fedratinib, and pacritinib. In general, JAK inhibitors should be avoided in patients who may be at increased risk of thrombosis. Tofacitinib should be used at the lowest effective dose and for the shortest duration needed to achieve/maintain therapeutic response when treating ulcerative colitis. If symptoms of thrombosis occur in any patients receiving JAK inhibitors, treatment should be discontinued and patients should be evaluated promptly and treated appropriately.

Fedratinib has a major potential interaction with Vitamin B1 Deficiency.

Serious and fatal encephalopathy, including Wernicke's disease, has occurred in patients treated with fedratinib. Wernicke's encephalopathy is a neurologic emergency. Assess thiamine levels in all patients prior to starting treatment, periodically during treatment, and as clinically indicated. Do not start fedratinib in patients with thiamine deficiency; replete thiamine prior to treatment initiation. If encephalopathy is suspected, immediately discontinue fedratinib and initiate parenteral thiamine. Patients who develop any change in their mental status during treatment, including confusion or memory impairment, should be evaluated for potential encephalopathy (e.g., neurologic examination, thiamine level assessment, imaging). Monitor until symptoms resolve or improve and thiamine levels normalize.