Interactions between Inrebic and Thioridazine

Thioridazine has a major potential interaction with Abnormal Electrocardiogram.

The use of thioridazine is contraindicated in patients with congenital or acquired QT interval prolongation syndromes or a history of cardiac arrhythmias. Thioridazine can prolong the QT interval of the electrocardiogram in a dose-related manner. The risk of torsade de pointes is progressively increased as the degree of prolongation becomes greater. In a crossover study of nine patients, a single 50 mg dose of thioridazine increased the QTc interval by a mean maximum of 23 msec compared to placebo. During postmarketing experience, torsade de pointes and sudden death have been reported, although a causal relationship has not been determined. The manufacturer states that thioridazine should not be administered in patients with a baseline QTc interval greater than 450 msec, and that it should be discontinued in patients with QTc measurements exceeding 500 msec during therapy. Electrolyte disturbances such as hypokalemia and hypomagnesemia may augment the prolongation effect of thioridazine on the QT interval and should be corrected prior to institution of therapy. Patients who experience frequent, severe, or prolonged diarrhea may be subject to electrolyte losses and should be followed closely and managed accordingly during therapy with thioridazine.

Thioridazine has a major potential interaction with Acute Alcohol Intoxication.

Phenothiazines are contraindicated in the presence of large amounts of central nervous system depressants such as alcohol. The risk of suicide and the danger of overdose may be increased in patients who use alcohol excessively. Phenothiazines should be used with caution in patients experiencing alcohol withdrawal.

Thioridazine has a major potential interaction with Alcoholism.

Phenothiazines are contraindicated in the presence of large amounts of central nervous system depressants such as alcohol. The risk of suicide and the danger of overdose may be increased in patients who use alcohol excessively. Phenothiazines should be used with caution in patients experiencing alcohol withdrawal.

Thioridazine has a major potential interaction with Altered Consciousness.

The use of phenothiazines is contraindicated in comatose patients and patients with severe central nervous system depression. Phenothiazines may potentiate the CNS and respiratory depression in these patients.

The fedratinib in Inrebic 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.

Thioridazine has a major potential interaction with Arrhythmia.

The use of thioridazine is contraindicated in patients with congenital or acquired QT interval prolongation syndromes or a history of cardiac arrhythmias. Thioridazine can prolong the QT interval of the electrocardiogram in a dose-related manner. The risk of torsade de pointes is progressively increased as the degree of prolongation becomes greater. In a crossover study of nine patients, a single 50 mg dose of thioridazine increased the QTc interval by a mean maximum of 23 msec compared to placebo. During postmarketing experience, torsade de pointes and sudden death have been reported, although a causal relationship has not been determined. The manufacturer states that thioridazine should not be administered in patients with a baseline QTc interval greater than 450 msec, and that it should be discontinued in patients with QTc measurements exceeding 500 msec during therapy. Electrolyte disturbances such as hypokalemia and hypomagnesemia may augment the prolongation effect of thioridazine on the QT interval and should be corrected prior to institution of therapy. Patients who experience frequent, severe, or prolonged diarrhea may be subject to electrolyte losses and should be followed closely and managed accordingly during therapy with thioridazine.

Thioridazine has a major potential interaction with Arrhythmia.

Phenothiazines may cause hypotension. Patients with pheochromocytoma, cerebral vascular or renal insufficiency, cardiovascular disease, or a severe cardiac reserve deficiency (e.g., mitral insufficiency) may be more prone to hypotensive reactions. Close monitoring is recommended during treatment if used in at-risk patients; some products may be contraindicated (e.g., thioridazine). Large doses and parenteral administration should be used cautiously, or avoided, in patients with impaired cardiovascular systems.

The fedratinib in Inrebic 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.

The fedratinib in Inrebic 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.

Thioridazine has a major potential interaction with Bone Marrow Depression/Low Blood Counts.

Phenothiazines may cause hematologic toxicity. In patients with preexisting blood dyscrasias, bone marrow suppression, or a history of drug-induced leukopenia or neutropenia, phenothiazines should not be used or are contraindicated. Complete blood counts should be regularly monitored in patients with risk factors for blood dyscrasias. If white blood cell counts indicate cellular depression, discontinue treatment and institute appropriate therapy.

Thioridazine has a moderate potential interaction with Breast Cancer.

The chronic use of phenothiazines is associated with persistent elevations in prolactin levels. The clinical significance in patients with a history of breast cancer is unknown and should be considered prior to therapy; approximately one-third of human breast cancers are thought to be prolactin-dependent. Chronic administration of neuroleptic drugs has been associated with mammary tumorigenesis in animal studies; however, evidence is inconclusive in humans.

The fedratinib in Inrebic 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.

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

Phenothiazines may cause hypotension. Patients with pheochromocytoma, cerebral vascular or renal insufficiency, cardiovascular disease, or a severe cardiac reserve deficiency (e.g., mitral insufficiency) may be more prone to hypotensive reactions. Close monitoring is recommended during treatment if used in at-risk patients; some products may be contraindicated (e.g., thioridazine). Large doses and parenteral administration should be used cautiously, or avoided, in patients with impaired cardiovascular systems.

Thioridazine has a moderate potential interaction with Central Nervous System Disorders.

Phenothiazines can lower the seizure threshold. Caution is recommended during administration in patients with a history of convulsive disorders or EEG abnormalities. Anticonvulsant therapy should be maintained or adequately adjusted during phenothiazine treatment.

Thioridazine has a major potential interaction with Cerebrovascular Insufficiency.

Phenothiazines may cause hypotension. Patients with pheochromocytoma, cerebral vascular or renal insufficiency, cardiovascular disease, or a severe cardiac reserve deficiency (e.g., mitral insufficiency) may be more prone to hypotensive reactions. Close monitoring is recommended during treatment if used in at-risk patients; some products may be contraindicated (e.g., thioridazine). Large doses and parenteral administration should be used cautiously, or avoided, in patients with impaired cardiovascular systems.

Thioridazine has a major potential interaction with Dementia.

Antipsychotic drugs are not approved for the treatment of patients with dementia-related psychosis. Older patients with dementia-related psychosis treated with antipsychotic drugs are at an increased risk of death; although the causes were varied, most of the deaths appeared to be either cardiovascular (e.g., heart failure, sudden death) or infectious (e.g., pneumonia) in nature. A causal relationship with antipsychotic use has not been established. In controlled trials in older patients with dementia-related psychosis, patients randomized to risperidone, aripiprazole, and olanzapine had higher incidence of cerebrovascular adverse events (e.g., stroke, transient ischemic attack), including fatalities, compared to patients treated with placebo.

Thioridazine has a major potential interaction with Diarrhea.

The use of thioridazine is contraindicated in patients with congenital or acquired QT interval prolongation syndromes or a history of cardiac arrhythmias. Thioridazine can prolong the QT interval of the electrocardiogram in a dose-related manner. The risk of torsade de pointes is progressively increased as the degree of prolongation becomes greater. In a crossover study of nine patients, a single 50 mg dose of thioridazine increased the QTc interval by a mean maximum of 23 msec compared to placebo. During postmarketing experience, torsade de pointes and sudden death have been reported, although a causal relationship has not been determined. The manufacturer states that thioridazine should not be administered in patients with a baseline QTc interval greater than 450 msec, and that it should be discontinued in patients with QTc measurements exceeding 500 msec during therapy. Electrolyte disturbances such as hypokalemia and hypomagnesemia may augment the prolongation effect of thioridazine on the QT interval and should be corrected prior to institution of therapy. Patients who experience frequent, severe, or prolonged diarrhea may be subject to electrolyte losses and should be followed closely and managed accordingly during therapy with thioridazine.

Thioridazine has a major potential interaction with Electrolyte Abnormalities.

The use of thioridazine is contraindicated in patients with congenital or acquired QT interval prolongation syndromes or a history of cardiac arrhythmias. Thioridazine can prolong the QT interval of the electrocardiogram in a dose-related manner. The risk of torsade de pointes is progressively increased as the degree of prolongation becomes greater. In a crossover study of nine patients, a single 50 mg dose of thioridazine increased the QTc interval by a mean maximum of 23 msec compared to placebo. During postmarketing experience, torsade de pointes and sudden death have been reported, although a causal relationship has not been determined. The manufacturer states that thioridazine should not be administered in patients with a baseline QTc interval greater than 450 msec, and that it should be discontinued in patients with QTc measurements exceeding 500 msec during therapy. Electrolyte disturbances such as hypokalemia and hypomagnesemia may augment the prolongation effect of thioridazine on the QT interval and should be corrected prior to institution of therapy. Patients who experience frequent, severe, or prolonged diarrhea may be subject to electrolyte losses and should be followed closely and managed accordingly during therapy with thioridazine.

Thioridazine has a major potential interaction with High Blood Pressure.

Phenothiazines may cause hypotension. Patients with pheochromocytoma, cerebral vascular or renal insufficiency, cardiovascular disease, or a severe cardiac reserve deficiency (e.g., mitral insufficiency) may be more prone to hypotensive reactions. Close monitoring is recommended during treatment if used in at-risk patients; some products may be contraindicated (e.g., thioridazine). Large doses and parenteral administration should be used cautiously, or avoided, in patients with impaired cardiovascular systems.

Thioridazine has a major potential interaction with History - Cerebrovascular Disease.

Phenothiazines may cause hypotension. Patients with pheochromocytoma, cerebral vascular or renal insufficiency, cardiovascular disease, or a severe cardiac reserve deficiency (e.g., mitral insufficiency) may be more prone to hypotensive reactions. Close monitoring is recommended during treatment if used in at-risk patients; some products may be contraindicated (e.g., thioridazine). Large doses and parenteral administration should be used cautiously, or avoided, in patients with impaired cardiovascular systems.

Thioridazine has a major potential interaction with History - Myocardial Infarction.

Phenothiazines may cause hypotension. Patients with pheochromocytoma, cerebral vascular or renal insufficiency, cardiovascular disease, or a severe cardiac reserve deficiency (e.g., mitral insufficiency) may be more prone to hypotensive reactions. Close monitoring is recommended during treatment if used in at-risk patients; some products may be contraindicated (e.g., thioridazine). Large doses and parenteral administration should be used cautiously, or avoided, in patients with impaired cardiovascular systems.

Thioridazine has a major potential interaction with Hypokalemia.

The use of thioridazine is contraindicated in patients with congenital or acquired QT interval prolongation syndromes or a history of cardiac arrhythmias. Thioridazine can prolong the QT interval of the electrocardiogram in a dose-related manner. The risk of torsade de pointes is progressively increased as the degree of prolongation becomes greater. In a crossover study of nine patients, a single 50 mg dose of thioridazine increased the QTc interval by a mean maximum of 23 msec compared to placebo. During postmarketing experience, torsade de pointes and sudden death have been reported, although a causal relationship has not been determined. The manufacturer states that thioridazine should not be administered in patients with a baseline QTc interval greater than 450 msec, and that it should be discontinued in patients with QTc measurements exceeding 500 msec during therapy. Electrolyte disturbances such as hypokalemia and hypomagnesemia may augment the prolongation effect of thioridazine on the QT interval and should be corrected prior to institution of therapy. Patients who experience frequent, severe, or prolonged diarrhea may be subject to electrolyte losses and should be followed closely and managed accordingly during therapy with thioridazine.

Thioridazine has a major potential interaction with Hypotension.

Phenothiazines may cause hypotension. Patients with pheochromocytoma, cerebral vascular or renal insufficiency, cardiovascular disease, or a severe cardiac reserve deficiency (e.g., mitral insufficiency) may be more prone to hypotensive reactions. Close monitoring is recommended during treatment if used in at-risk patients; some products may be contraindicated (e.g., thioridazine). Large doses and parenteral administration should be used cautiously, or avoided, in patients with impaired cardiovascular systems.

Thioridazine has a major potential interaction with Liver Disease.

Therapy with phenothiazines should be administered cautiously or are contraindicated in patients with preexisting liver disease or with a history of jaundice due to phenothiazine hypersensitivity. Patients with a history of hepatic encephalopathy due to cirrhosis may have increased sensitivity to the central nervous system effects of some phenothiazines (e.g., chlorpromazine). Treatment should be discontinued if jaundice occurs.

Thioridazine has a major potential interaction with Magnesium Imbalance.

The use of thioridazine is contraindicated in patients with congenital or acquired QT interval prolongation syndromes or a history of cardiac arrhythmias. Thioridazine can prolong the QT interval of the electrocardiogram in a dose-related manner. The risk of torsade de pointes is progressively increased as the degree of prolongation becomes greater. In a crossover study of nine patients, a single 50 mg dose of thioridazine increased the QTc interval by a mean maximum of 23 msec compared to placebo. During postmarketing experience, torsade de pointes and sudden death have been reported, although a causal relationship has not been determined. The manufacturer states that thioridazine should not be administered in patients with a baseline QTc interval greater than 450 msec, and that it should be discontinued in patients with QTc measurements exceeding 500 msec during therapy. Electrolyte disturbances such as hypokalemia and hypomagnesemia may augment the prolongation effect of thioridazine on the QT interval and should be corrected prior to institution of therapy. Patients who experience frequent, severe, or prolonged diarrhea may be subject to electrolyte losses and should be followed closely and managed accordingly during therapy with thioridazine.

Thioridazine has a moderate potential interaction with Neuroleptic Malignant Syndrome.

Therapy with phenothiazines may precipitate or aggravate a potentially fatal symptom complex known as neuroleptic malignant syndrome (NMS). Treatment should not be initiated in patients with active NMS, and should be immediately discontinued if currently administered in such patients. In patients with a history of NMS, introduction or reintroduction of phenothiazines should be carefully considered, since NMS may recur.

Thioridazine has a major potential interaction with Pheochromocytoma.

Phenothiazines may cause hypotension. Patients with pheochromocytoma, cerebral vascular or renal insufficiency, cardiovascular disease, or a severe cardiac reserve deficiency (e.g., mitral insufficiency) may be more prone to hypotensive reactions. Close monitoring is recommended during treatment if used in at-risk patients; some products may be contraindicated (e.g., thioridazine). Large doses and parenteral administration should be used cautiously, or avoided, in patients with impaired cardiovascular systems.

The fedratinib in Inrebic 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).

Thioridazine has a major potential interaction with Respiratory Arrest.

The use of phenothiazines is contraindicated in comatose patients and patients with severe central nervous system depression. Phenothiazines may potentiate the CNS and respiratory depression in these patients.

Thioridazine has a moderate potential interaction with Seizures.

Phenothiazines can lower the seizure threshold. Caution is recommended during administration in patients with a history of convulsive disorders or EEG abnormalities. Anticonvulsant therapy should be maintained or adequately adjusted during phenothiazine treatment.

The fedratinib in Inrebic 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.

The fedratinib in Inrebic 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.

The fedratinib in Inrebic 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.

Thioridazine has a major potential interaction with Valvular Heart Disease.

Phenothiazines may cause hypotension. Patients with pheochromocytoma, cerebral vascular or renal insufficiency, cardiovascular disease, or a severe cardiac reserve deficiency (e.g., mitral insufficiency) may be more prone to hypotensive reactions. Close monitoring is recommended during treatment if used in at-risk patients; some products may be contraindicated (e.g., thioridazine). Large doses and parenteral administration should be used cautiously, or avoided, in patients with impaired cardiovascular systems.

The fedratinib in Inrebic 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.