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Drug overview for PACLITAXEL (paclitaxel):
Generic name: PACLITAXEL (pack-lih-TAX-el)
Drug class: Antineoplastic - Taxanes
Therapeutic class: Antineoplastics
Paclitaxel is a natural or semisynthetic diterpene antineoplastic agent extracted from the bark of the Western (Pacific) yew (Taxus brevifolia) or the needles and twigs of Taxus baccata.
Paclitaxel is commercially available in 2 types of formulations: conventional paclitaxel (in a nonaqueous solution) and albumin-bound paclitaxel. The efficacy and safety of paclitaxel for each indication is based on research and clinical experience using a specific formulation. Albumin-bound paclitaxel currently is labeled for use only in the second-line therapy of metastatic breast cancer, first-line therapy of non-small cell lung cancer in combination with carboplatin, and first-line therapy of metastatic adenocarcinoma of the pancreas in combination with gemcitabine. The functional properties of paclitaxel may differ substantially according to formulation; therefore, albumin-bound paclitaxel may not be substituted for or used in combination with other formulations of paclitaxel.
Generic name: PACLITAXEL (pack-lih-TAX-el)
Drug class: Antineoplastic - Taxanes
Therapeutic class: Antineoplastics
Paclitaxel is a natural or semisynthetic diterpene antineoplastic agent extracted from the bark of the Western (Pacific) yew (Taxus brevifolia) or the needles and twigs of Taxus baccata.
Paclitaxel is commercially available in 2 types of formulations: conventional paclitaxel (in a nonaqueous solution) and albumin-bound paclitaxel. The efficacy and safety of paclitaxel for each indication is based on research and clinical experience using a specific formulation. Albumin-bound paclitaxel currently is labeled for use only in the second-line therapy of metastatic breast cancer, first-line therapy of non-small cell lung cancer in combination with carboplatin, and first-line therapy of metastatic adenocarcinoma of the pancreas in combination with gemcitabine. The functional properties of paclitaxel may differ substantially according to formulation; therefore, albumin-bound paclitaxel may not be substituted for or used in combination with other formulations of paclitaxel.
DRUG IMAGES
PACLITAXEL 300 MG/50 ML VIAL
PACLITAXEL 100 MG/16.7 ML VIAL
The following indications for PACLITAXEL (paclitaxel) have been approved by the FDA:
Indications:
Epithelial ovarian cancer
Kaposi's sarcoma
Locally advanced breast carcinoma
Malignant neoplasm of the ovary
Metastatic breast carcinoma
Non-small cell lung cancer
Professional Synonyms:
Advanced breast carcinoma
Carcinoma of ovary
Endotheliosarcoma
Epithelial carcinoma of ovary
Epithelial ovarian carcinoma
Malignant epithelial neoplasm of ovary
Malignant neoplasm of ovary
Malignant tumor of the ovary
Metastatic breast cancer
Metastatic malignancy of breast
Metastatic malignant neoplasm of breast
Metastatic malignant tumor of breast
Multiple idiopathic hemorrhagic sarcoma
Ovarian cancer
Ovarian carcinoma
Ovarian malignancy
Indications:
Epithelial ovarian cancer
Kaposi's sarcoma
Locally advanced breast carcinoma
Malignant neoplasm of the ovary
Metastatic breast carcinoma
Non-small cell lung cancer
Professional Synonyms:
Advanced breast carcinoma
Carcinoma of ovary
Endotheliosarcoma
Epithelial carcinoma of ovary
Epithelial ovarian carcinoma
Malignant epithelial neoplasm of ovary
Malignant neoplasm of ovary
Malignant tumor of the ovary
Metastatic breast cancer
Metastatic malignancy of breast
Metastatic malignant neoplasm of breast
Metastatic malignant tumor of breast
Multiple idiopathic hemorrhagic sarcoma
Ovarian cancer
Ovarian carcinoma
Ovarian malignancy
The following dosing information is available for PACLITAXEL (paclitaxel):
Response rates for paclitaxel therapy vary with tumor histology, volume of residual tumor, and development of resistance to previous platinum-based chemotherapy.
Current evidence suggests that increased dose intensity (amount of paclitaxel per unit time) may affect response to paclitaxel but that paclitaxel doses exceeding 175 mg/m2 are more toxic and do not improve survival in patients with advanced ovarian cancer. In addition to dose effect, the effect of duration of infusion of paclitaxel has been studied in patients with ovarian cancer. Efficacy was similar but toxicity, particularly myelosuppression, was greater when paclitaxel alone was administered by 24-hour versus 3-hour infusion for the subsequent therapy of advanced ovarian cancer.
Limited evidence suggests that subsequent therapy with prolonged infusion of paclitaxel (96-hour IV infusion) does not produce response in patients with advanced ovarian cancer that was resistant to previous therapy with the drug administered by 3-hour or 24-hour IV infusion.
The effect of duration of infusion on the efficacy and toxicity of paclitaxel administered as a component of combination therapy also has not been fully established. Increased incidence and severity of neurotoxicity is associated with administration of paclitaxel by 3-hour IV infusion in combination therapy with cisplatin in patients with gynecologic cancers. In a large randomized trial, patients with advanced ovarian cancer receiving paclitaxel (175 mg/m2 administered as a 3-hour IV infusion) and cisplatin had an increased incidence of severe neurosensory toxicity compared with those receiving cyclophosphamide and cisplatin.
Prolonged paclitaxel infusions do not appear to offer benefit in the treatment of ovarian cancer. In a randomized trial comparing 96-hour infusion of paclitaxel 120 mg/m2 with 24-hour infusion of paclitaxel 135 mg/m2 (each in a combination regimen of paclitaxel and cisplatin) for suboptimal stage III or IV ovarian epithelial cancer, median survival rates were similar between the groups but the relative death rate was approximately 5% greater among patients receiving the prolonged infusion of paclitaxel.
Maintenance therapy with paclitaxel for advanced ovarian cancer+ is being investigated. In a randomized trial, patients receiving 12 months of single-agent paclitaxel therapy following complete response to induction therapy with platinum/paclitaxel therapy for advanced ovarian cancer experienced longer progression-free survival but greater neurotoxicity than those receiving 3 months of such therapy. Because the trial was terminated according to study design following a planned interim analysis that detected the difference in progression-free survival, and cross-over treatment was allowed, overall survival data may be unavailable.
Whether maintenance therapy with paclitaxel is superior to treatment upon progression of disease is unclear, and a confirmatory randomized trial is needed. Until further evidence is available, clinicians should discuss maintenance paclitaxel therapy and offer it as an option for patients with advanced ovarian cancer that has a complete response to induction therapy.
Paclitaxel is commercially available in 2 types of formulations: conventional paclitaxel (in a nonaqueous solution) and albumin-bound paclitaxel. The functional properties of paclitaxel may differ according to formulation, and the dosage instructions for paclitaxel are specific to formulation. Albumin-bound paclitaxel may not be substituted for or used in combination with other formulations of paclitaxel.
Clinicians should consult the respective manufacturer's labeling and published protocols for formulation-specific regimens and specific dosages, methods of administration, and administration sequence of other antineoplastic agents used in combination regimens.
Dosage of albumin-bound paclitaxel is expressed in terms of paclitaxel.
Conventional or albumin-bound paclitaxel should not be administered to patients with baseline neutrophil counts less than 1500/mm3. In patients with HIV infection, conventional paclitaxel should not be administered if baseline neutrophil counts are less than 1000/mm3. To monitor the occurrence of paclitaxel-induced bone marrow suppression, mainly neutropenia, which may be severe and result in infection, it is recommended that frequent peripheral blood cell counts be performed in all patients receiving paclitaxel.
When dosage modification is necessary for patients receiving albumin-bound paclitaxel and gemcitabine for pancreatic cancer, dosage of albumin-bound paclitaxel should be reduced in decrements of 25 mg/m2 (i.e., 1 dose level) and dosage of gemcitabine should be reduced in decrements of 200 mg/m2 (i.e., 1 dose level); however, if a dose of albumin-bound paclitaxel 75 mg/m2 or gemcitabine 600 mg/m2 requires further reduction, both drugs should be discontinued.
The effect of renal impairment on the disposition of paclitaxel has not been fully established. Reduction of paclitaxel dosage in patients with impaired renal function does not appear to be necessary.
Paclitaxel is metabolized mainly in the liver, and increased toxicity may occur in patients with hepatic impairment.
Toxicity associated with paclitaxel, particularly grade 3 or 4 myelosuppression, may be exacerbated in patients with serum total bilirubin concentrations greater than 2 times the upper limit of normal. Paclitaxel should be used with extreme caution in patients with hepatic impairment, and dosage reduction is recommended depending on the degree of hepatic impairment. Such patients should be monitored closely for the development of profound myelosuppression.
For patients receiving conventional paclitaxel as a 24-hour IV infusion for ovarian or non-small cell lung cancer, the usual dose of 135 mg/m2 may be administered for the first course of therapy in those who have serum transaminase concentrations less than 2 times the upper limit of normal and serum bilirubin concentrations up to 1.5 mg/dL; for patients with elevated serum transaminase concentrations less than 10 times the upper limit of normal and serum bilirubin concentrations up to 1.5 mg/dL, a reduced dose of paclitaxel 100 mg/m2 is recommended; for patients with elevated serum transaminase concentrations less than 10 times the upper limit of normal and serum bilirubin concentrations of 1.6-7.5
mg/dL, a reduced dose of paclitaxel 50 mg/m2 is recommended. For patients with elevated serum transaminase concentrations at least 10 times the upper limit of normal or serum bilirubin concentrations exceeding 7.5 mg/dL, paclitaxel therapy is not recommended.
For patients receiving conventional paclitaxel as a 3-hour IV infusion for ovarian or breast cancer, the usual dose of 175 mg/m2 may be administered for the first course of therapy in those who have serum transaminase concentrations less than 10 times the upper limit of normal and serum bilirubin concentrations up to 1.25 times the upper limit of normal; for patients with serum transaminase concentrations less than 10 times the upper limit of normal and serum bilirubin concentrations of 1.26-2 times the upper limit of normal, a reduced dose of paclitaxel 135 mg/m2 is recommended; for patients with serum transaminase concentrations less than 10 times the upper limit of normal and serum bilirubin concentrations of 2.01-5
times the upper limit of normal, a reduced dose of paclitaxel 90 mg/m2 is recommended. For patients with elevated serum transaminase concentrations at least 10 times the upper limit of normal or serum bilirubin concentrations exceeding 5 times the upper limit of normal, paclitaxel therapy is not recommended.
Further reduction of paclitaxel dosage for subsequent courses of therapy should be based on patient tolerance.
Patients should be monitored closely since toxicity associated with paclitaxel may be exacerbated in patients with hepatic impairment. Paclitaxel should be used with caution in patients with hepatic impairment, and dosage reduction is recommended depending on the degree of hepatic impairment. No adjustment of the initial dosage is required in patients with mild hepatic impairment.
Current evidence suggests that increased dose intensity (amount of paclitaxel per unit time) may affect response to paclitaxel but that paclitaxel doses exceeding 175 mg/m2 are more toxic and do not improve survival in patients with advanced ovarian cancer. In addition to dose effect, the effect of duration of infusion of paclitaxel has been studied in patients with ovarian cancer. Efficacy was similar but toxicity, particularly myelosuppression, was greater when paclitaxel alone was administered by 24-hour versus 3-hour infusion for the subsequent therapy of advanced ovarian cancer.
Limited evidence suggests that subsequent therapy with prolonged infusion of paclitaxel (96-hour IV infusion) does not produce response in patients with advanced ovarian cancer that was resistant to previous therapy with the drug administered by 3-hour or 24-hour IV infusion.
The effect of duration of infusion on the efficacy and toxicity of paclitaxel administered as a component of combination therapy also has not been fully established. Increased incidence and severity of neurotoxicity is associated with administration of paclitaxel by 3-hour IV infusion in combination therapy with cisplatin in patients with gynecologic cancers. In a large randomized trial, patients with advanced ovarian cancer receiving paclitaxel (175 mg/m2 administered as a 3-hour IV infusion) and cisplatin had an increased incidence of severe neurosensory toxicity compared with those receiving cyclophosphamide and cisplatin.
Prolonged paclitaxel infusions do not appear to offer benefit in the treatment of ovarian cancer. In a randomized trial comparing 96-hour infusion of paclitaxel 120 mg/m2 with 24-hour infusion of paclitaxel 135 mg/m2 (each in a combination regimen of paclitaxel and cisplatin) for suboptimal stage III or IV ovarian epithelial cancer, median survival rates were similar between the groups but the relative death rate was approximately 5% greater among patients receiving the prolonged infusion of paclitaxel.
Maintenance therapy with paclitaxel for advanced ovarian cancer+ is being investigated. In a randomized trial, patients receiving 12 months of single-agent paclitaxel therapy following complete response to induction therapy with platinum/paclitaxel therapy for advanced ovarian cancer experienced longer progression-free survival but greater neurotoxicity than those receiving 3 months of such therapy. Because the trial was terminated according to study design following a planned interim analysis that detected the difference in progression-free survival, and cross-over treatment was allowed, overall survival data may be unavailable.
Whether maintenance therapy with paclitaxel is superior to treatment upon progression of disease is unclear, and a confirmatory randomized trial is needed. Until further evidence is available, clinicians should discuss maintenance paclitaxel therapy and offer it as an option for patients with advanced ovarian cancer that has a complete response to induction therapy.
Paclitaxel is commercially available in 2 types of formulations: conventional paclitaxel (in a nonaqueous solution) and albumin-bound paclitaxel. The functional properties of paclitaxel may differ according to formulation, and the dosage instructions for paclitaxel are specific to formulation. Albumin-bound paclitaxel may not be substituted for or used in combination with other formulations of paclitaxel.
Clinicians should consult the respective manufacturer's labeling and published protocols for formulation-specific regimens and specific dosages, methods of administration, and administration sequence of other antineoplastic agents used in combination regimens.
Dosage of albumin-bound paclitaxel is expressed in terms of paclitaxel.
Conventional or albumin-bound paclitaxel should not be administered to patients with baseline neutrophil counts less than 1500/mm3. In patients with HIV infection, conventional paclitaxel should not be administered if baseline neutrophil counts are less than 1000/mm3. To monitor the occurrence of paclitaxel-induced bone marrow suppression, mainly neutropenia, which may be severe and result in infection, it is recommended that frequent peripheral blood cell counts be performed in all patients receiving paclitaxel.
When dosage modification is necessary for patients receiving albumin-bound paclitaxel and gemcitabine for pancreatic cancer, dosage of albumin-bound paclitaxel should be reduced in decrements of 25 mg/m2 (i.e., 1 dose level) and dosage of gemcitabine should be reduced in decrements of 200 mg/m2 (i.e., 1 dose level); however, if a dose of albumin-bound paclitaxel 75 mg/m2 or gemcitabine 600 mg/m2 requires further reduction, both drugs should be discontinued.
The effect of renal impairment on the disposition of paclitaxel has not been fully established. Reduction of paclitaxel dosage in patients with impaired renal function does not appear to be necessary.
Paclitaxel is metabolized mainly in the liver, and increased toxicity may occur in patients with hepatic impairment.
Toxicity associated with paclitaxel, particularly grade 3 or 4 myelosuppression, may be exacerbated in patients with serum total bilirubin concentrations greater than 2 times the upper limit of normal. Paclitaxel should be used with extreme caution in patients with hepatic impairment, and dosage reduction is recommended depending on the degree of hepatic impairment. Such patients should be monitored closely for the development of profound myelosuppression.
For patients receiving conventional paclitaxel as a 24-hour IV infusion for ovarian or non-small cell lung cancer, the usual dose of 135 mg/m2 may be administered for the first course of therapy in those who have serum transaminase concentrations less than 2 times the upper limit of normal and serum bilirubin concentrations up to 1.5 mg/dL; for patients with elevated serum transaminase concentrations less than 10 times the upper limit of normal and serum bilirubin concentrations up to 1.5 mg/dL, a reduced dose of paclitaxel 100 mg/m2 is recommended; for patients with elevated serum transaminase concentrations less than 10 times the upper limit of normal and serum bilirubin concentrations of 1.6-7.5
mg/dL, a reduced dose of paclitaxel 50 mg/m2 is recommended. For patients with elevated serum transaminase concentrations at least 10 times the upper limit of normal or serum bilirubin concentrations exceeding 7.5 mg/dL, paclitaxel therapy is not recommended.
For patients receiving conventional paclitaxel as a 3-hour IV infusion for ovarian or breast cancer, the usual dose of 175 mg/m2 may be administered for the first course of therapy in those who have serum transaminase concentrations less than 10 times the upper limit of normal and serum bilirubin concentrations up to 1.25 times the upper limit of normal; for patients with serum transaminase concentrations less than 10 times the upper limit of normal and serum bilirubin concentrations of 1.26-2 times the upper limit of normal, a reduced dose of paclitaxel 135 mg/m2 is recommended; for patients with serum transaminase concentrations less than 10 times the upper limit of normal and serum bilirubin concentrations of 2.01-5
times the upper limit of normal, a reduced dose of paclitaxel 90 mg/m2 is recommended. For patients with elevated serum transaminase concentrations at least 10 times the upper limit of normal or serum bilirubin concentrations exceeding 5 times the upper limit of normal, paclitaxel therapy is not recommended.
Further reduction of paclitaxel dosage for subsequent courses of therapy should be based on patient tolerance.
Patients should be monitored closely since toxicity associated with paclitaxel may be exacerbated in patients with hepatic impairment. Paclitaxel should be used with caution in patients with hepatic impairment, and dosage reduction is recommended depending on the degree of hepatic impairment. No adjustment of the initial dosage is required in patients with mild hepatic impairment.
No enhanced Administration information available for this drug.
No dosing information available.
No generic dosing information available.
The following drug interaction information is available for PACLITAXEL (paclitaxel):
There are 4 contraindications.
These drug combinations generally should not be dispensed or administered to the same patient. A manufacturer label warning that indicates the contraindication warrants inclusion of a drug combination in this category, regardless of clinical evidence or lack of clinical evidence to support the contraindication.
| Drug Interaction | Drug Names |
|---|---|
| Efalizumab; Natalizumab/Immunosuppressives; Immunomodulators SEVERITY LEVEL: 1-Contraindicated Drug Combination: This drug combination is contraindicated and generally should not be dispensed or administered to the same patient. MECHANISM OF ACTION: Natalizumab,(1-3) efalizumab,(4) immunosuppressives, and immunomodulators all suppress the immune system. CLINICAL EFFECTS: Concurrent use of natalizumab(1-3) or efalizumab(4) with immunosuppressives or immunomodulators may result in an increased risk of infections, including progressive multifocal leukoencephalopathy (PML), an opportunistic infection caused by the JC virus (JCV). PREDISPOSING FACTORS: Previous JCV infection, longer duration of natalizumab treatment - especially if greater than 2 years, and prior or concomitant treatment with immunosuppressant medication are all independent risk factors which increase the risk for PML.(1,5) The FDA has estimated PML incidence stratified by risk factors: If anti-JCV antibody positive, no prior immunosuppressant use and natalizumab treatment less than 25 months, incidence <1/1,000. If anti-JCV antibody positive, history of prior immunosuppressant use and natalizumab treatment less than 25 months, incidence 2/1,000 If anti-JCV antibody positive, no prior immunosuppressant use and natalizumab treatment 25-48 months, incidence 4/1,000 If anti-JCV antibody positive, history of prior immunosuppressant use and natalizumab treatment 25-48 months, incidence 11/1,000. PATIENT MANAGEMENT: The US manufacturer of natalizumab states patients with Crohn's disease should not receive concurrent immunosuppressants, with the exception of limited overlap of corticosteroids, due to the increased risk for PML. For new natalizumab patients currently receiving chronic oral corticosteroids for Crohn's Disease, begin corticosteroid taper when therapeutic response to natalizumab has occurred. If corticosteroids cannot be discontinued within six months of starting natalizumab, discontinue natalizumab.(3) The US manufacturer of natalizumab states that natalizumab should not ordinarily be used in multiple sclerosis patients receiving immunosuppressants or immunomodulators due to the increased risk for PML. Immunosuppressives include, but are not limited to azathioprine, cyclophosphamide, cyclosporine, mercaptopurine, methotrexate, mitoxantrone, mycophenolate, and corticosteroids.(3,6) The UK manufacturer of natalizumab states that concurrent use with immunosuppressives or antineoplastic agents is contraindicated.(1) The Canadian manufacturer of natalizumab states that natalizumab should not be used with immunosuppressive or immunomodulatory agents.(2) The US manufacturer of certolizumab states that concurrent therapy with natalizumab is not recommended.(7) DISCUSSION: Progressive multifocal leukoencephalopathy has been reported in patients receiving concurrent natalizumab were recently or concomitantly taking immunomodulators or immunosuppressants.(1-5,8,9) In a retrospective cohort study of multiple sclerosis patients newly initiated on a disease-modifying therapy, use of high-efficacy agents (alemtuzumab, natalizumab, or ocrelizumab) resulted in the same risk of overall infections as moderate-efficacy agents, but there was an elevated risk of serious infections (adjusted hazard ratio [aHR] = 1.24, 95% confidence interval (CI) = 1.06-1.44) and UTIs (aHR = 1.21, 95% CI = 1.14-1.30).(10) |
TYSABRI |
| Live Vaccines; Live BCG/Selected Immunosuppressive Agents SEVERITY LEVEL: 1-Contraindicated Drug Combination: This drug combination is contraindicated and generally should not be dispensed or administered to the same patient. MECHANISM OF ACTION: A variety of disease modifying agents suppress the immune system. Immunocompromised patients may be at increased risk for uninhibited replication after administration of live, attenuated vaccines or intravesicular BCG. Immune response to vaccines may be decreased during periods of immunocompromise.(1) CLINICAL EFFECTS: The expected serum antibody response may not be obtained and/or the vaccine may result in illness.(1) After instillation of intravesicular BCG, immunosuppression may interfere with local immune response, or increase the severity of mycobacterial infection following inadvertent systemic exposure.(2) PREDISPOSING FACTORS: Immunosuppressive diseases (e.g. hematologic malignancies, HIV disease), treatments (e.g. radiation) and drugs may all increase the magnitude of immunodeficiency. PATIENT MANAGEMENT: The Centers for Disease Control(CDC) Advisory Committee on Immunization Practices (ACIP) states that live-virus and live, attenuated vaccines should not be administered to patients who are immunocompromised. The magnitude of immunocompromise and associated risks should be determined by a physician.(1) For patients scheduled to receive chemotherapy, vaccination should ideally precede the initiation of chemotherapy by 14 days. Patients vaccinated while on immunosuppressive therapy or in the 2 weeks prior to starting therapy should be considered unimmunized and should be revaccinated at least 3 months after discontinuation of therapy.(1) Patients who receive anti-B cell therapies should not receive live vaccines for at least 6 months after such therapies due to a prolonged duration of immunosuppression. An exception is the Zoster vaccine, which can be given at least 1 month after receipt of anti-B cell therapies.(1) The US manufacturer of abatacept states live vaccines should not be given during or for up to 3 months after discontinuation of abatacept.(2) The US manufacturer of live BCG for intravesicular treatment of bladder cancer states use is contraindicated in immunosuppressed patients.(3) The US manufacturer of daclizumab states live vaccines are not recommended during and for up to 4 months after discontinuation of treatment.(4) The US manufacturer of guselkumab states that live vaccines should be avoided during treatment with guselkumab.(5) The US manufacturer of inebilizumab-cdon states that live vaccines are not recommended during treatment and after discontinuation until B-cell repletion. Administer all live vaccinations at least 4 weeks prior to initiation of inebilizumab-cdon.(6) The US manufacturer of ocrelizumab states that live vaccines are not recommended during treatment and until B-cell repletion occurs after discontinuation of therapy. Administer all live vaccines at least 4 weeks prior to initiation of ocrelizumab.(7) The US manufacturer of ozanimod states that live vaccines should be avoided during and for up to 3 months after discontinuation of ozanimod.(8) The US manufacturer of siponimod states that live vaccines are not recommended during treatment and for up to 4 weeks after discontinuation of treatment.(9) The US manufacturer of ustekinumab states BCG vaccines should not be given in the year prior to, during, or the year after ustekinumab therapy.(10) The US manufacturer of satralizumab-mwge states that live vaccines are not recommended during treatment and should be administered at least four weeks prior to initiation of satralizumab-mwge.(11) The US manufacturer of ublituximab-xiiy states that live vaccines are not recommended during treatment and until B-cell recovery. Live vaccines should be administered at least 4 weeks prior to initiation of ublituximab-xiiy.(12) The US manufacturer of etrasimod states that live vaccines should be avoided during and for 5 weeks after treatment. Live vaccines should be administered at least 4 weeks prior to initiation of etrasimod.(13) The US manufacturer of emapalumab-lzsg states that live vaccines should not be administered to patients receiving emapalumab-lzsg and for at least 4 weeks after the last dose of emapalumab-lzsg. The safety of immunization with live vaccines during or following emapalumab-lzsg therapy has not been studied.(14) DISCUSSION: Killed or inactivated vaccines do not pose a danger to immunocompromised patients.(1) Patients with a history of leukemia who are in remission and have not received chemotherapy for at least 3 months are not considered to be immunocompromised.(1) |
ACAM2000 (NATIONAL STOCKPILE), ADENOVIRUS TYPE 4, ADENOVIRUS TYPE 4 AND TYPE 7, ADENOVIRUS TYPE 7, BCG (TICE STRAIN), BCG VACCINE (TICE STRAIN), DENGVAXIA, ERVEBO (NATIONAL STOCKPILE), FLUMIST TRIVALENT 2024-2025, IXCHIQ, M-M-R II VACCINE, PRIORIX, PROQUAD, ROTARIX, ROTATEQ, STAMARIL, VARIVAX VACCINE, VAXCHORA ACTIVE COMPONENT, VAXCHORA VACCINE, VIVOTIF, YF-VAX |
| Talimogene laherparepvec/Selected Immunosuppressants SEVERITY LEVEL: 1-Contraindicated Drug Combination: This drug combination is contraindicated and generally should not be dispensed or administered to the same patient. MECHANISM OF ACTION: Talimogene laherparepvec is a live, attenuated herpes simplex virus.(1) CLINICAL EFFECTS: Concurrent use of talimogene laherparepvec in patients receiving immunosuppressive therapy may cause a life-threatening disseminated herpetic infection.(1) PREDISPOSING FACTORS: None determined. PATIENT MANAGEMENT: Talimogene laherparepvec is contraindicated in immunosuppressed patients.(1) The magnitude of immunocompromise and associated risks due to immunosuppressant drugs should be determined by a physician. DISCUSSION: Concurrent use of talimogene laherparepvec in patients receiving immunosuppressive therapy may cause a life-threatening disseminated herpetic infection.(1) |
IMLYGIC |
| Nadofaragene Firadenovec/Selected Immunosuppressants SEVERITY LEVEL: 1-Contraindicated Drug Combination: This drug combination is contraindicated and generally should not be dispensed or administered to the same patient. MECHANISM OF ACTION: Nadofaragene firadenovec may contain low levels of replication-competent adenovirus.(1) CLINICAL EFFECTS: Concurrent use of nadofaragene firadenovec in patients receiving immunosuppressive therapy may cause disseminated adenovirus infection.(1) PREDISPOSING FACTORS: None determined. PATIENT MANAGEMENT: Individuals who are immunosuppressed or immune-deficient should not receive nadofaragene firadenovec.(1) DISCUSSION: Nadofaragene firadenovec is a non-replicating adenoviral vector-based gene therapy but may contain low levels of replication-competent adenovirus. Immunocompromised persons, including those receiving immunosuppressant therapy, may be at risk for disseminated adenovirus infection.(1) |
ADSTILADRIN |
There are 19 severe interactions.
These drug interactions can produce serious consequences in most patients. Actions required for severe interactions include, but are not limited to, discontinuing one or both agents, adjusting dosage, altering administration scheduling, and providing additional patient monitoring. Review the full interaction monograph for more information.
| Drug Interaction | Drug Names |
|---|---|
| Deferiprone/Selected Myelosuppressive Agents SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction. MECHANISM OF ACTION: Concurrent use of deferiprone with other drugs known to be associated with neutropenia or agranulocytosis may increase the frequency or risk for severe toxicity.(1) CLINICAL EFFECTS: Concurrent use of deferiprone and myelosuppressive agents may result in severe neutropenia or agranulocytosis, which may be fatal. PREDISPOSING FACTORS: Agranulocytosis may be less common in patients receiving deferiprone for thalassemia, and more common in patients treated for other systemic iron overload conditions (e.g. myelodysplastic syndromes, sickle cell disease).(2,3) Inadequate monitoring appears to increase the risk for severe outcomes. Manufacturer post market surveillance found that in all fatal cases of agranulocytosis reported between 1999 and 2005, data on weekly white blood count (WBC) monitoring was missing. In three fatal cases, deferiprone was continued for two to seven days after the detection of neutropenia or agranulocytosis.(2) PATIENT MANAGEMENT: If possible, discontinue one of the drugs associated with risk for neutropenia or agranulocytosis. If alternative therapy is not available, documentation and adherence to the deferiprone monitoring protocol is essential. Baseline absolute neutrophil count (ANC) must be at least 1,500/uL prior to starting deferiprone. Monitor ANC weekly during therapy. If infection develops, interrupt deferiprone therapy and monitor ANC more frequently. If ANC is less than 1,500/uL but greater than 500/uL, discontinue deferiprone and any other drugs possibly associated with neutropenia. Initiate ANC and platelet counts daily until recovery (i.e. ANC at least 1,500/uL). If ANC is less than 500/uL, discontinue deferiprone, evaluate patient and hospitalize if appropriate. Do not resume deferiprone unless potential benefits outweigh potential risks.(1) DISCUSSION: Drugs linked to this monograph have an FDA Boxed Warning for risk of neutropenia, agranulocytosis, or pancytopenia, or have > 5% risk for neutropenia and/or warnings describing risk for myelosuppression in manufacturer prescribing information.(1-25) In pooled clinical studies submitted to the FDA, 6.1% of deferiprone patients met criteria for neutropenia and 1.7% of patients developed agranulocytosis.(1) The time to onset of agranulocytosis was highly variable with a range of 65 days to 9.2 years (median, 161 days).(3) |
DEFERIPRONE, DEFERIPRONE (3 TIMES A DAY), FERRIPROX, FERRIPROX (2 TIMES A DAY), FERRIPROX (3 TIMES A DAY) |
| Tofacitinib/Immunosuppressives; Immunomodulators SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction. MECHANISM OF ACTION: Concurrent use of tofacitinib and azathioprine, other biologic disease-modifying antirheumatic drugs (DMARDs), or potent immunosuppressants may result in additive or synergistic effects on the immune system.(1) CLINICAL EFFECTS: Concurrent use of tofacitinib and azathioprine, other biologic DMARDs, or potent immunosuppressants use may increase the risk of serious infections.(1) PREDISPOSING FACTORS: None determined. PATIENT MANAGEMENT: Tofacitinib should not be used concurrently with azathioprine, other biologic DMARDs, or cyclosporine.(1) Patient should be monitored for decreases in lymphocytes and neutrophils. Therapy should be adjusted based on the indication. - For all indications: If absolute neutrophil count (ANC) or lymphocyte count is less than 500 cells/mm3, discontinue tofacitinib. - For rheumatoid arthritis or psoriatic arthritis and absolute neutrophil count (ANC) 500 to 1000 cells/mm3: interrupt dosing. When ANC is greater than 1000 cells/mm3, resume Xeljanz 5 mg twice daily or Xeljanz XR 11 mg once daily. - For ulcerative colitis and ANC 500 to 1000 cells/mm3: -If taking Xeljanz 10 mg twice daily, decrease to 5 mg twice daily. When ANC is greater than 1000 cells/mm3, increase to 10 mg twice daily based on clinical response. -If taking Xeljanz 5 mg twice daily, interrupt dosing. When ANC is greater than 1000 cells/mm3, resume 5 mg twice daily. -If taking Xeljanz XR 22 mg once daily, decrease to 11 mg once daily. When ANC is greater than 1000 cells/mm3, increase to 22 mg once daily based on clinical response. -If taking Xeljanz XR 11 mg once daily, interrupt dosing. When ANC is greater than 1000 cells/mm3, resume 11 mg once daily. - For polyarticular course juvenile idiopathic arthritis (pcJIA) and ANC 500 to 1000 cells/mm3: interrupt dosing until ANC is greater than 1000 cells/mm3.(1) DISCUSSION: Concurrent use of tofacitinib and azathioprine, other biologic DMARDs, or potent immunosuppressants may increase the risk of infection.(1) |
TOFACITINIB CITRATE, XELJANZ, XELJANZ XR |
| Clozapine/Selected Myelosuppressive Agents SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction. MECHANISM OF ACTION: Clozapine and other myelosuppressive agents may be associated with neutropenia or agranulocytosis.(2) CLINICAL EFFECTS: Moderate neutropenia, even if due to combination therapy, may require abrupt discontinuation of clozapine resulting in decompensation of the patient's psychiatric disorder (e.g. schizophrenia). The disease treated by the myelosuppressive agent may be compromised if myelosuppression requires dose reduction, delay, or discontinuation of the myelosuppressive agent. Undetected severe neutropenia or agranulocytosis may be fatal. PREDISPOSING FACTORS: Low white blood counts prior to initiation of the myelosuppressive agent may increase risk for clinically significant neutropenia. PATIENT MANAGEMENT: If a patient stabilized on clozapine therapy requires treatment with a myelosuppressive agent, the clozapine prescriber should consult with prescriber of the myelosuppressive agent (e.g. oncologist) to discuss treatment and monitoring options.(2) More frequent ANC monitoring or treatment alternatives secondary to neutropenic episodes may need to be considered. Clozapine is only available through a restricted distribution system which requires documentation of the absolute neutrophil count (ANC) prior to dispensing.(1-2) For most clozapine patients, clozapine treatment must be interrupted for a suspected clozapine-induced ANC < 1000 cells/microliter. For patients with benign ethnic neutropenia (BEN), treatment must be interrupted for suspected clozapine-induced neutropenia < 500 cells/microliter.(2) DISCUSSION: Clozapine is only available through a restricted distribution system which requires documentation of the ANC prior to dispensing.(1) Agents linked to this interaction generally have > 5% risk for neutropenia and/or warnings describing risk for myelosuppression in manufacturer prescribing information.(3-26) |
CLOZAPINE, CLOZAPINE ODT, CLOZARIL, VERSACLOZ |
| Selected Multiple Sclerosis Agents/Immunosuppressants; Immunomodulators SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction. MECHANISM OF ACTION: Ocrelizumab or ofatumumab in combination with immunosuppressives and immune-modulators all suppress the immune system.(1,2) CLINICAL EFFECTS: Concurrent use of ocrelizumab or ofatumumab with immunosuppressive or immune-modulating agents may result in an increased risk of serious infections, such as disseminated herpetic infection or progressive multifocal leukoencephalopathy (PML), an opportunistic infection caused by the JC virus (JCV).(1,2) PREDISPOSING FACTORS: Incomplete washout of previously prescribed immunosuppressive or immune-modulating medications. PATIENT MANAGEMENT: The ocrelizumab US prescribing information states: - Ocrelizumab and other immune-modulating or immunosuppressive therapies, (including immunosuppressant doses of corticosteroids) are expected to increase the risk of immunosuppression, and the risk of additive immune system effects must be considered if these therapies are coadministered with ocrelizumab. When switching from drugs with prolonged immune effects, such as daclizumab, fingolimod, natalizumab, teriflunomide, or mitoxantrone, the duration and mode of action of these drugs must be considered to avoid unintended additive immunosuppressive effects when initiating ocrelizumab.(1) The ofatumumab US prescribing information states: - Ofatumumab and other immunosuppressive therapies (including systemic corticosteroids) may have the potential for increased immunosuppressive effects and increase the risk of infection. When switching between therapies, the duration and mechanism of action of each therapy should be considered due to the potential for additive immunosuppressive effects. Ofatumumab for MS therapy has not been studied in combination with other MS agents that suppress the immune system.(2) DISCUSSION: Fatal disseminated herpes zoster and herpes simplex infections and cases of progressive multifocal leukoencephalopathy (PML) have been reported in patients who previously received immunomodulators or immunosuppressants.(1,2) In a retrospective cohort study of multiple sclerosis patients newly initiated on a disease-modifying therapy, use of high-efficacy agents (alemtuzumab, natalizumab, or ocrelizumab) resulted in the same risk of overall infections as moderate-efficacy agents, but there was an elevated risk of serious infections (adjusted hazard ratio [aHR] = 1.24, 95% confidence interval (CI) = 1.06-1.44) and UTIs (aHR = 1.21, 95% CI = 1.14-1.30).(3) |
KESIMPTA PEN, OCREVUS, OCREVUS ZUNOVO |
| Upadacitinib/Immunosuppressives; Immunomodulators SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction. MECHANISM OF ACTION: Upadacitinib, immunosuppressives, and immunomodulators all suppress the immune system. CLINICAL EFFECTS: Concurrent use of upadacitinib with immunosuppressives or immunomodulators may result in an increased risk of serious infections. PREDISPOSING FACTORS: None determined. PATIENT MANAGEMENT: The US manufacturer of upadacitinib states that concurrent use of upadacitinib with immunosuppressives or immunomodulators is not recommended. DISCUSSION: Serious infections have been reported in patients receiving upadacitinib. Reported infections included pneumonia, cellulitis, tuberculosis, multidermatomal herpes zoster, oral/esophageal candidiasis, cryptococcosis. Reports of viral reactivation, including herpes virus reactivation and hepatitis B reactivation, were reported in clinical studies with upadacitinib.(1) |
RINVOQ, RINVOQ LQ |
| Inebilizumab/Immunosuppressives; Immunomodulators SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction. MECHANISM OF ACTION: Inebilizumab, immunosuppressives, and immunomodulators all suppress the immune system.(1) CLINICAL EFFECTS: Concurrent use of inebilizumab with immunosuppressive or immunomodulating agents may result in myelosuppression including neutropenia resulting in an increased risk for serious infections.(1) PREDISPOSING FACTORS: None determined. PATIENT MANAGEMENT: The US manufacturer of inebilizumab states that the concurrent use of inebilizumab with immunosuppressive agents, including systemic corticosteroids, may increase the risk of infection. If concurrent therapy is warranted, consider the risk of additive immune suppression and monitor based on prescribing information for both agents.(1) DISCUSSION: Inebilizumab has not been studied in combination with other immunosuppressants. If concurrent therapy is warranted, consider the potential for increased immunosuppressive risks from both agents. The most common infections reported by inebilizumab treated patients in the randomized and open-label clinical trial periods included urinary tract infections (20%), nasopharyngitis (13%), upper respiratory tract infections (8%), and influenza (7%). Although there been no cases of Hepatitis B virus reactivation or progressive multifocal leukoencephalopathy reported in patients taking inebilizumab, these infections have been observed in patients taking other B-cell-depleting antibodies.(1) |
UPLIZNA |
| Baricitinib/Immunosuppressives; Immunomodulators SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction. MECHANISM OF ACTION: Concurrent use of baricitinib with other biologic disease-modifying antirheumatic drugs (DMARDs) or potent immunosuppressants such as azathioprine or cyclosporine may result in additive or synergistic effects on the immune system. CLINICAL EFFECTS: Concurrent use of baricitinib with other biologic DMARDs or potent immunosuppressants such as azathioprine or cyclosporine may increase the risk of serious infections.(1) PREDISPOSING FACTORS: None determined. PATIENT MANAGEMENT: The US manufacturer of baricitinib states that concurrent use of baricitinib with biologic DMARDs or potent immunosuppressants is not recommended.(1) DISCUSSION: Most patients who developed serious infections while being treated with baricitinib were on concomitant immunosuppressants like methotrexate and corticosteroids. The combination of baricitinib with other biologic DMARDs has not been studied.(1) |
OLUMIANT |
| Paclitaxel/Strong CYP3A4 Inhibitors SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction. MECHANISM OF ACTION: Agents that inhibit the CYP3A4 isoenzyme may inhibit the metabolism of paclitaxel.(1) CLINICAL EFFECTS: Concurrent use of strong CYP3A4 inhibitors may increase levels of and effects from paclitaxel, including myelosuppression, neutropenia, sensory neuropathy, pneumonitis, anemia, or thrombocytopenia.(1) PREDISPOSING FACTORS: None determined. PATIENT MANAGEMENT: Avoid the use of strong CYP3A4 inhibitors in patients undergoing therapy with paclitaxel.(1) Consider alternatives with no or minimal enzyme inhibition. DISCUSSION: In vitro studies indicate CYP3A4 may be the secondary pathway for two minor metabolites of paclitaxel.(1) Strong inhibitors of CYP3A4 include: adagrasib, boceprevir, ceritinib, clarithromycin, cobicistat, idelalisib, indinavir, itraconazole, josamycin, ketoconazole, lonafarnib, lopinavir, mibefradil, mifepristone, nefazodone, nelfinavir, nirmatrelvir/ritonavir, paritaprevir, posaconazole, ribociclib, saquinavir, telaprevir, telithromycin, tipranavir, troleandomycin, tucatinib, or voriconazole.(2,3) |
APTIVUS, CLARITHROMYCIN, CLARITHROMYCIN ER, EVOTAZ, GENVOYA, ITRACONAZOLE, ITRACONAZOLE MICRONIZED, KALETRA, KETOCONAZOLE, KISQALI, KORLYM, KRAZATI, LANSOPRAZOL-AMOXICIL-CLARITHRO, LOPINAVIR-RITONAVIR, MIFEPREX, MIFEPRISTONE, NEFAZODONE HCL, NOXAFIL, OMECLAMOX-PAK, PAXLOVID, POSACONAZOLE, PREZCOBIX, RECORLEV, SPORANOX, STRIBILD, SYMTUZA, TOLSURA, TUKYSA, TYBOST, VFEND, VFEND IV, VIRACEPT, VOQUEZNA TRIPLE PAK, VORICONAZOLE, ZOKINVY, ZYDELIG, ZYKADIA |
| Ponesimod/Immunosuppressives; Immunomodulators SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction. MECHANISM OF ACTION: Ponesimod in combination with immunosuppressives and immune-modulators all suppress the immune system.(1) CLINICAL EFFECTS: Concurrent use of ponesimod with immunosuppressive or immune-modulating agents may result in an increased risk of serious infections, such as disseminated herpetic infection, cryptococcal infection, or progressive multifocal leukoencephalopathy (PML), an opportunistic infection caused by the JC virus (JCV).(1) PREDISPOSING FACTORS: Incomplete washout of previously prescribed immunosuppressive or immune-modulating medications. PATIENT MANAGEMENT: The ponesimod US prescribing information states ponesimod has not been studied in combination with anti-neoplastic, immune-modulating, or immunosuppressive therapies. Caution should be used during concomitant administration because of the risk of additive immune effects during therapy and in the weeks following administration. When switching from drugs with prolonged immune effects, the half-life and mode of action of these drugs must be considered in order to avoid unintended additive immunosuppressive effects. Initiating treatment with ponesimod after alemtuzumab is not recommended. However, ponesimod can generally be started immediately after discontinuation of beta interferon or glatiramer acetate.(1) DISCUSSION: Fatal disseminated herpes zoster and herpes simplex infections, cryptococcal meningitis, disseminated cryptococcal infections, and cases of progressive multifocal leukoencephalopathy (PML) have been reported in patients who previously received immunomodulators or immunosuppressants.(1) |
PONVORY |
| Sodium Iodide I 131/Myelosuppressives; Immunomodulators SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction. MECHANISM OF ACTION: Sodium iodide I 131 can cause depression of the hematopoetic system. Myelosuppressives and immunomodulators also suppress the immune system.(1) CLINICAL EFFECTS: Concurrent use of sodium iodide I 131 with agents that cause bone marrow depression, including myelosuppressives or immunomodulators, may result in an enhanced risk of hematologic disorders, including anemia, blood dyscrasias, bone marrow depression, leukopenia, and thrombocytopenia. Bone marrow depression may increase the risk of serious infections and bleeding.(1) PREDISPOSING FACTORS: None determined. PATIENT MANAGEMENT: The US manufacturer of sodium iodide I 131 states that concurrent use with bone marrow depressants may enhance the depression of the hematopoetic system caused by large doses of sodium iodide I 131.(1) Sodium iodide I 131 causes a dose-dependent bone marrow suppression, including neutropenia or thrombocytopenia, in the 3 to 5 weeks following administration. Patients may be at increased risk of infections or bleeding during this time. Monitor complete blood counts within one month of therapy. If results indicate leukopenia or thrombocytopenia, dosimetry should be used to determine a safe sodium iodide I 131 activity.(1) DISCUSSION: Hematologic disorders including death have been reported with sodium iodide I 131. The most common hematologic disorders reported include anemia, blood dyscrasias, bone marrow depression, leukopenia, and thrombocytopenia.(1) |
HICON, SODIUM IODIDE I-131 |
| Fingolimod/Immunosuppressives; Immunomodulators SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction. MECHANISM OF ACTION: Fingolimod in combination with immunosuppressives and immune-modulators all suppress the immune system.(1-3) CLINICAL EFFECTS: Concurrent use of fingolimod with immunosuppressive or immune-modulating agents may result in an increased risk of serious infections, such as disseminated herpetic infection or progressive multifocal leukoencephalopathy (PML), an opportunistic infection caused by the JC virus (JCV).(1-3) PREDISPOSING FACTORS: Incomplete washout of previously prescribed immunosuppressive or immune-modulating medications. PATIENT MANAGEMENT: Recommendations for fingolimod regarding this interaction differ between regulatory approving agencies. The fingolimod US prescribing information states: - Antineoplastic, immune-modulating, or immunosuppressive therapies, (including corticosteroids) are expected to increase the risk of immunosuppression, and the risk of additive immune system effects must be considered if these therapies are coadministered with fingolimod. When switching from drugs with prolonged immune effects, such as natalizumab, teriflunomide or mitoxantrone, the duration and mode of action of these drugs must be considered to avoid unintended additive immunosuppressive effects when initiating fingolimod.(1) The fingolimod Canadian prescribing information states: - Concurrent use with immunosuppressive or immunomodulatory agents is contraindicated due to the risk of additive immune system effects. However, co-administration of a short course of corticosteroids (up to 5 days) did not increase the overall rate of infection in patients participating Phase III clinical trials.(2) The fingolimod UK specific product characteristics states: - Fingolimod is contraindicated in patients currently receiving immunosuppressive therapies or those immunocompromised by prior therapies. When switching patients from another disease modifying therapy to Gilenya, the half-life and mode of action of the other therapy must be considered in order to avoid an additive immune effect whilst at the same time minimizing the risk of disease activation.(3) DISCUSSION: Fatal disseminated herpes zoster and herpes simplex infections and cases of progressive multifocal leukoencephalopathy (PML) have been reported in patients who previously received immunomodulators or immunosuppressants.(1-3) |
FINGOLIMOD, GILENYA, TASCENSO ODT |
| Ozanimod/Immunosuppressives; Immunomodulators SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction. MECHANISM OF ACTION: Ozanimod in combination with immunosuppressives and immune-modulators all suppress the immune system.(1) CLINICAL EFFECTS: Concurrent use of ozanimod with immunosuppressive or immune-modulating agents may result in an increased risk of serious infections, such as disseminated herpetic infection or progressive multifocal leukoencephalopathy (PML), an opportunistic infection caused by the JC virus (JCV).(1) PREDISPOSING FACTORS: Incomplete washout of previously prescribed immunosuppressive or immune-modulating medications. PATIENT MANAGEMENT: The ozanimod US prescribing information state this information regarding this interaction: -Ozanimod has not been studied in combination with anti-neoplastic, immune-modulating, or immunosuppressive therapies. Caution should be used during concomitant administration because of the risk of additive immune effects during therapy and in the week following administration. When switching from drugs with prolonged immune effects, the half-life and mode of action of these drugs must be considered in order to avoid unintended additive immunosuppressive effects. Initiating treatment with ozanimod after alemtuzumab is not recommended. However, ozanimod can generally be started immediately after discontinuation of beta interferon or glatiramer acetate.(1) DISCUSSION: Fatal disseminated herpes zoster and herpes simplex infections and cases of progressive multifocal leukoencephalopathy (PML) have been reported in patients who previously received immunomodulators or immunosuppressants.(1) |
ZEPOSIA |
| Siponimod/Immunosuppressives; Immunomodulators SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction. MECHANISM OF ACTION: Siponimod in combination with immunosuppressives and immune-modulators all suppress the immune system.(1) CLINICAL EFFECTS: Concurrent use of siponimod with immunosuppressive or immune-modulating agents may result in an increased risk of serious infections, such as disseminated herpetic infection or progressive multifocal leukoencephalopathy (PML), an opportunistic infection caused by the JC virus (JCV).(1) PREDISPOSING FACTORS: Incomplete washout of previously prescribed immunosuppressive or immune-modulating medications. PATIENT MANAGEMENT: The siponimod US prescribing information state this information regarding this interaction: -Siponimod has not been studied in combination with anti-neoplastic, immune-modulating, or immunosuppressive therapies. Caution should be used during concomitant administration because of the risk of additive immune effects during therapy and in the week following administration. When switching from drugs with prolonged immune effects, the half-life and mode of action of these drugs must be considered in order to avoid unintended additive immunosuppressive effects. Initiating treatment with siponimod after alemtuzumab is not recommended. However, siponimod can generally be started immediately after discontinuation of beta interferon or glatiramer acetate.(1) DISCUSSION: Fatal disseminated herpes zoster and herpes simplex infections and cases of progressive multifocal leukoencephalopathy (PML) have been reported in patients who previously received immunomodulators or immunosuppressants.(1) |
MAYZENT |
| Cladribine/Immunosuppressives; Immunomodulators SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction. MECHANISM OF ACTION: Cladribine in combination with immunosuppressives and immune-modulators all suppress the immune system.(1-2) CLINICAL EFFECTS: Concurrent use of cladribine with immunosuppressive or immune-modulating agents may result in an increased risk of serious infections, such as disseminated herpetic infection or progressive multifocal leukoencephalopathy (PML), an opportunistic infection caused by the JC virus (JCV).(1-2) PREDISPOSING FACTORS: Incomplete washout of previously prescribed immunosuppressive or immune-modulating medications. PATIENT MANAGEMENT: Recommendations for cladribine regarding this interaction differ between regulatory approving agencies. The cladribine US prescribing information states: -Concomitant use with myelosuppressive or other immunosuppressive drugs is not recommended. Acute short-term therapy with corticosteroids can be administered. In patients who have previously been treated with immunomodulatory or immunosuppressive drugs, consider potential additive effect, the mode of action, and duration of effect of the other drugs prior to initiation of cladribine.(1) The cladribine Canadian prescribing information states: -Use of cladribine in immunocompromised patients is contraindicated because of a risk of additive effects on the immune system. Acute short-term therapy with corticosteroids can be administered during cladribine treatment.(2) DISCUSSION: Fatal disseminated herpes zoster and herpes simplex infections and cases of progressive multifocal leukoencephalopathy (PML) have been reported in patients who previously received immunomodulators or immunosuppressants.(1-2) |
CLADRIBINE, MAVENCLAD |
| Ritlecitinib/Immunosuppressives; Immunomodulators SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction. MECHANISM OF ACTION: Ritlecitinib, immunosuppressives, and immunomodulators all suppress the immune system. CLINICAL EFFECTS: Concurrent use of ritlecitinib with immunosuppressives or immunomodulators may result in an increased risk of serious infections. PREDISPOSING FACTORS: None determined. PATIENT MANAGEMENT: The US manufacturer of ritlecitinib states that concurrent use of ritlecitinib with other JAK inhibitors, biologic immunomodulators, cyclosporine or other potent immunosuppressants is not recommended.(1) DISCUSSION: Serious infections have been reported in patients receiving ritlecitinib. Reported infections included appendicitis, COVID-19 infection (including pneumonia), and sepsis. Reports of viral reactivation, including herpes virus reactivation was reported in clinical studies with ritlecitinib.(1) |
LITFULO |
| Paclitaxel/Strong CYP3A4 Inducers SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction. MECHANISM OF ACTION: Strong inducers of CYP3A4 may induce the metabolism of paclitaxel.(1) CLINICAL EFFECTS: Concurrent or recent use of a strong inducer of CYP3A4 may result in decreased levels and effectiveness of paclitaxel.(1) PREDISPOSING FACTORS: Induction effects may be more likely with regular use of the inducer for longer than 1-2 weeks. PATIENT MANAGEMENT: Avoid concurrent use of strong inducers of CYP3A4 with paclitaxel.(1) Consider the use of agents with no or minimal induction potential if possible. Monitor patients for decreased response to therapy. DISCUSSION: Paclitaxel is metabolized by CYP3A4 and strong inducers of this isoenzyme are expected to decrease levels of paclitaxel.(1) In a Phase 2 study of paclitaxel, none of the subjects taking phenytoin experienced a partial or complete response to paclitaxel. Paclitaxel levels were 70% lower in these patients than in patients not receiving phenytoin.(2) Strong inducers of CYP3A4 include: apalutamide, barbiturates, carbamazepine, encorafenib, enzalutamide, fosphenytoin, ivosidenib, lumacaftor, mitotane, phenobarbital, phenytoin, primidone, rifampin, rifapentine, and St. John's wort.(3,4) |
ASA-BUTALB-CAFFEINE-CODEINE, ASCOMP WITH CODEINE, BRAFTOVI, BUTALB-ACETAMINOPH-CAFF-CODEIN, BUTALBITAL, BUTALBITAL-ACETAMINOPHEN, BUTALBITAL-ACETAMINOPHEN-CAFFE, BUTALBITAL-ASPIRIN-CAFFEINE, CARBAMAZEPINE, CARBAMAZEPINE ER, CARBATROL, CEREBYX, DILANTIN, DILANTIN-125, DONNATAL, EPITOL, EQUETRO, ERLEADA, FIORICET, FIORICET WITH CODEINE, FOSPHENYTOIN SODIUM, LYSODREN, MITOTANE, MYSOLINE, ORKAMBI, PENTOBARBITAL SODIUM, PHENOBARBITAL, PHENOBARBITAL SODIUM, PHENOBARBITAL-BELLADONNA, PHENOBARBITAL-HYOSC-ATROP-SCOP, PHENOHYTRO, PHENYTEK, PHENYTOIN, PHENYTOIN SODIUM, PHENYTOIN SODIUM EXTENDED, PRIFTIN, PRIMIDONE, RIFADIN, RIFAMPIN, SEZABY, TEGRETOL, TEGRETOL XR, TENCON, TIBSOVO, XTANDI |
| Etrasimod/Immunosuppressives; Immunomodulators SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction. MECHANISM OF ACTION: Etrasimod causes reversible sequestration of lymphocytes in lymphoid tissues, resulting in a mean 55% decrease in peripheral blood lymphocyte count at 52 weeks.(1) Other immunosuppressives and immune-modulators also suppress the immune system. CLINICAL EFFECTS: Concurrent use of etrasimod with immunosuppressive or immune-modulating agents may result in an increased risk of serious and fatal infections, such as disseminated herpetic infection, cryptococcal infection, or progressive multifocal leukoencephalopathy (PML).(1) PREDISPOSING FACTORS: Incomplete washout of previously prescribed immunosuppressive or immune-modulating medications increases the risk of adverse effects. PATIENT MANAGEMENT: The etrasimod US prescribing information states etrasimod has not been studied in combination with anti-neoplastic, immune-modulating, or immunosuppressive therapies. Concomitant administration of these therapies with etrasimod should be avoided because of the risk of additive immune effects during therapy and in the weeks following administration. Etrasimod's effect on peripheral lymphocytes may persist for up to 5 weeks after discontinuation.(1) When switching from drugs with prolonged immune effects, the half-life and mode of action of these drugs must be considered in order to avoid unintended additive immunosuppressive effects.(1) DISCUSSION: Fatal disseminated herpes zoster and herpes simplex infections, cryptococcal meningitis, disseminated cryptococcal infections, and cases of progressive multifocal leukoencephalopathy (PML) have been reported in patients treated with other sphingosine-1 phosphate receptor modulators.(1) |
VELSIPITY |
| Paclitaxel/Immunosuppressive CYP2C8 Inhibitors SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction. MECHANISM OF ACTION: Immunosuppressive inhibitors of CYP2C8 may inhibit the metabolism of paclitaxel and increase the risk of additive immunosuppression.(1) Leflunomide and teriflunomide are moderate CYP2C8 inhibitors.(3) CLINICAL EFFECTS: Concurrent use of immunosuppressive CYP2C8 inhibitors and paclitaxel may result in elevated levels and clinical effects of paclitaxel, including immunosuppression.(1,2) PREDISPOSING FACTORS: None determined. PATIENT MANAGEMENT: The US manufacturers of paclitaxel recommend combination use CYP2C8 inhibitors with caution. If concomitant use is necessary, paclitaxel dose reduction may be required.(1,2) DISCUSSION: The US manufacturer of paclitaxel recommends use with CYP2C8 inhibitors with caution.(1,2) |
ARAVA, AUBAGIO, LEFLUNICLO, LEFLUNOMIDE, TERIFLUNOMIDE |
| Ropeginterferon alfa-2b/Slt Immunosuppress; Immunomodulator SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction. MECHANISM OF ACTION: Ropeginterferon alfa-2b and immunosuppressives both suppress the immune system. CLINICAL EFFECTS: Concurrent use of ropeginterferon alfa-2b with immunosuppressives may result in an increased risk of serious infections. PREDISPOSING FACTORS: None determined. PATIENT MANAGEMENT: Avoid concurrent use of myelosuppressive agents.(1-2) If concurrent use cannot be avoided, monitor for effects of excessive immunosuppression. DISCUSSION: In clinical trials, 20% of patients experienced leukopenia. Interferon alfa products may cause fatal or life-threatening infections.(1-2) |
BESREMI |
There are 9 moderate interactions.
The clinician should assess the patient’s characteristics and take action as needed. Actions required for moderate interactions include, but are not limited to, discontinuing one or both agents, adjusting dosage, altering administration.
| Drug Interaction | Drug Names |
|---|---|
| Erlotinib/Docetaxel; Paclitaxel SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed. MECHANISM OF ACTION: The exact mechanism is unknown. CLINICAL EFFECTS: Concurrent use of docetaxel or paclitaxel may increase the risk of gastrointestinal perforation in patients receiving erlotinib. Fatalities have been reported.(1) PREDISPOSING FACTORS: Patients with a history of peptic ulceration or diverticular disease or who are receiving concomitant anti-angiogenic, corticosteroids, and/or NSAIDs may be an increased risk of gastrointestinal perforation.(1) PATIENT MANAGEMENT: Monitor patients receiving concurrent therapy for signs of gastrointestinal perforation. Discontinue erlotinib in patients who develop gastrointestinal perforation.(1) DISCUSSION: In a phase II trial of concurrent bevacizumab plus erlotinib, 2 of 13 patients suffered fatal gastrointestinal perforations.(2) In another phase II trial of concurrent bevacizumab with erlotinib, 1 of 104 patients died of gastrointestinal perforation.(3) Two trials showed no benefit from combination therapy with erlotinib and paclitaxel in first-line patients with locally advanced or metastatic NSCLC.(1) |
ERLOTINIB HCL, TARCEVA |
| Doxorubicin/Paclitaxel SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed. MECHANISM OF ACTION: Paclitaxel and Cremophor, a vehicle of paclitaxel, may interfere with the pharmacokinetics of doxorubicin, which may cause an increase in the exposure of doxorubicin and its metabolites.(2)(3) CLINICAL EFFECTS: Concurrent use of doxorubicin and paclitaxel may increase the doxorubicin exposure. This may increase the risk of doxorubicin associated adverse effects.(1) PREDISPOSING FACTORS: None determined. PATIENT MANAGEMENT: Monitor patients receiving concurrent therapy for signs of cardiotoxicity, heart failure, or other adverse effects associated with doxorubicin.(1) Avoid coadministration within a short interval.(2) DISCUSSION: An open-label drug interaction study, as part of two parallel clinical phase I trials, studied 19 oncology patients receiving doxorubicin combined with either paclitaxel or docetaxel. When administered with paclitaxel the mean increase in doxorubicin area-under-curve(AUC) was 80% (p=0.002, 95%CI: 23%-136%) and the mean doxorubicin clearance was decreased by 71% (p=0/013, 95%CI: 8%-133%).(1) In a study of 28 female breast cancer patients receiving concurrent administration of doxorubicin and paclitaxel, the mean AUC0-24 ratio was 1.59 (p <0.0001) when doxorubicin was administered 30 minutes before paclitaxel versus 24 hours before paclitaxel. Even when paclitaxel was given 24 hours after doxorubicin, there was a rebound 240% increase in the plasma concentration of doxorubicinol.(2) Cremophor, a vehicle of paclitaxel, has been demonstrated to inhibit p-glycoprotein (P-gp) in a noncompetitive manner.(3) Paclitaxel is a substrate of P-gp and therefore metabolism may be inhibited if Cremophor is co-administered.(2) |
ADRIAMYCIN, CAELYX, DOXIL, DOXORUBICIN HCL, DOXORUBICIN HCL LIPOSOME |
| Paclitaxel/Selected Strong and Moderate CYP2C8 Inhibitors SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed. MECHANISM OF ACTION: Inhibitors of CYP2C8 may inhibit paclitaxel metabolism by this pathway. Clopidogrel and gemfibrozil are strong inhibitors of CYP2C8. Deferasirox is a moderate inhibitor of CYP2C8.(1-3) CLINICAL EFFECTS: Concurrent use of CYP2C8 inhibitors and paclitaxel may result in elevated levels and clinical effects of paclitaxel.(1,2) PREDISPOSING FACTORS: None determined. PATIENT MANAGEMENT: The US manufacturers of paclitaxel recommend combination use CYP2C8 inhibitors with caution. If concomitant use is necessary, paclitaxel dose reduction may be required.(1,2) DISCUSSION: The US manufacturer of paclitaxel recommends use with CYP2C8 inhibitors with caution.(1,2) |
CLOPIDOGREL, CLOPIDOGREL BISULFATE, DEFERASIROX, EXJADE, GEMFIBROZIL, JADENU, JADENU SPRINKLE, LOPID, PLAVIX, PREVYMIS, RETEVMO |
| Selected CYP2C9 Substrates/Lorlatinib SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed. MECHANISM OF ACTION: Lorlatinib is a moderate inducer of CYP2C9 and may increase the metabolism of drugs metabolized by the CYP2C9 enzyme.(1) CLINICAL EFFECTS: Concurrent use of lorlatinib may lead to decreased serum levels and effectiveness of drugs metabolized by the CYP2C9 pathway.(1) PREDISPOSING FACTORS: None determined. PATIENT MANAGEMENT: Patients maintained on a CYP2C9 substrate who start therapy with lorlatinib may require closer monitoring and dose adjustment of the CYP2C9 substrate. DISCUSSION: In a study, lorlatinib 100 mg daily for 15 days decreased the area-under-curve (AUC) and maximum concentration (Cmax) of single-dose tolbutamide 100 mg (a sensitive CYP2C9 substrate) by 43% and 15%, respectively.(1) CYP2C9 substrates with a narrow therapeutic index linked to this monograph include: dasabuvir, paclitaxel, and warfarin.(2,3) |
LORBRENA |
| Ustekinumab/Immunosuppressives; Immunomodulators SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed. MECHANISM OF ACTION: Ustekinumab, immunosuppressives, and immunomodulators all suppress the immune system.(1) CLINICAL EFFECTS: Concurrent use of ustekinumab with immunosuppressive or immunomodulating agents may result in an increased risk for serious infections.(1) PREDISPOSING FACTORS: None determined. PATIENT MANAGEMENT: The US manufacturer of ustekinumab recommends caution because the concurrent use of ustekinumab with immunosuppressive agents may increase the risk of infection. If concurrent therapy is warranted, consider the risk of additive immune suppression and monitor based on prescribing information for both agents.(1) DISCUSSION: Ustekinumab has not been studied in combination with other immunosuppressants in psoriasis studies. In psoriatic arthritis studies, concomitant methotrexate use did not appear to influence the safety or efficacy of ustekinumab. In Crohn's disease and ulcerative colitis studies, concomitant use of immunosuppressants or corticosteroids did not appear to influence the safety or efficacy of ustekinumab. If concurrent therapy is warranted, consider the potential for increased immunosuppressive risks from both agents.(1) The most common infections reported by ustekinumab treated patients in the clinical trial periods included nasopharyngitis(8%) and upper respiratory tract infection(5%). Serious bacterial, mycobacterial, fungal, and viral infections were observed in patients receiving ustekinumab. Cases of interstitial pneumonia, eosinophilic pneumonia, and cryptogenic organizing pneumonia resulting in respiratory failure or prolonged hospitalization have been reported in patients receiving ustekinumab.(1) |
OTULFI, PYZCHIVA, SELARSDI, STELARA, STEQEYMA, USTEKINUMAB, USTEKINUMAB-AEKN, USTEKINUMAB-TTWE, WEZLANA, YESINTEK |
| COVID-19 Vaccines/Immunosuppressives; Immunomodulators SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed. MECHANISM OF ACTION: Immunosuppressants and immunomodulators may prevent the immune system from properly responding to the COVID-19 vaccine.(1,2) CLINICAL EFFECTS: Administration of a COVID-19 vaccine with immunosuppressants or immunomodulators may interfere with vaccine-induced immune response and impair the efficacy of the vaccine. However, patients should be offered and given a COVID-19 vaccine even if the use and timing of immunosuppressive agents cannot be adjusted.(1,2) PREDISPOSING FACTORS: None determined. PATIENT MANAGEMENT: In an effort to optimize COVID-19 vaccine response, the American College of Rheumatology (ACR) published conditional recommendations for administration of COVID-19 vaccines with immunosuppressants and immunomodulators.(1) The CDC also provides clinical considerations for COVID-19 vaccination in patients on immunosuppressants.(2) The CDC states that all immunocompromised patients over 6 months of age should receive at least 1 dose of COVID-19 vaccine if eligible. See the CDC's Interim Clinical Considerations for Use of COVID-19 Vaccines for specific recommendations based on age, vaccination history, and vaccine manufacturer.(2) The ACR states that in general, immunosuppressants and immunomodulators should be held for 1-2 weeks after each vaccine dose. See below for specific recommendations for certain agents.(1) The CDC advises planning for vaccination at least 2 weeks before starting or resuming immunosuppressive therapy.(2) Patients should be offered and given a COVID-19 vaccine even if the use and timing of immunosuppressive agents cannot be adjusted.(1,2) B-cell depleting agents, including rituximab: The ACR recommends consulting with the rheumatologist to determine optimal timing of COVID-19 vaccination. Measuring CD19 B cells may be considered to determine need for a booster vaccine dose. If B cell levels are not measured, a supplemental vaccine dose 2-4 weeks before the next scheduled dose of rituximab is recommended.(1) The CDC states that the utility of B-cell quantification to guide clinical care is not known and is not recommended. Patients who receive B-cell depleting therapy should receive COVID-19 vaccines about 4 weeks before the next scheduled dose. For patients who received 1 or more doses of COVID-19 vaccine during treatment with B-cell-depleting therapies that were administered over a limited period (e.g., as part of a treatment regimen for certain malignancies), revaccination may be considered. The suggested interval to start revaccination is about 6 months after completion of the B-cell-depleting therapy.(2) Abatacept: - Subcutaneous abatacept should be withheld for 1-2 weeks after each vaccine dose, as disease activity allows. - For intravenous abatacept, time administration so that vaccination will occur 1 week before the next abatacept infusion.(1) Cyclophosphamide: When feasible, administer cyclophosphamide one week after each COVID-19 vaccine dose.(1) Recipients of hematopoietic cell transplant or CAR-T-cell therapy who received one or more doses of COVID-19 vaccine prior to or during treatment should undergo revaccination following the current CDC recommendations for unvaccinated patients. Revaccination should start at least 3 months (12 weeks) after transplant or CAR-T-cell therapy.(2) TNF-alpha inhibitors and cytokine inhibitors: The ACR was not able to reach consensus on whether to modify dosing or timing of these agents with COVID-19 vaccination.(1) The CDC includes these agents in their general recommendation to hold therapy for at least 2 weeks following vaccination.(2) DISCUSSION: The ACR convened a COVID-19 Vaccine Guidance Task Force to provide guidance on optimal use of COVID-19 vaccines in rheumatology patients. These recommendations are based on limited clinical evidence of COVID-19 vaccines in patients without rheumatic and musculoskeletal disorders and evidence of other vaccines in this patient population.(1) The ACR recommendation for rituximab is based on studies of humoral immunity following receipt of other vaccines. These studies have uncertain generalizability to vaccination against COVID-19, as it is unknown if efficacy is attributable to induction of host T cells versus B cell (antibody-based) immunity.(1) The ACR recommendation for mycophenolate is based on preexisting data of mycophenolate on non-COVID-19 vaccine immunogenicity. Emerging data suggests that mycophenolate may impair SARS-CoV-2 vaccine response in rheumatic and musculoskeletal disease and transplant patients.(1) The ACR recommendation for methotrexate is based on data from influenza vaccines and pneumococcal vaccines with methotrexate.(1) The ACR recommendation for JAK inhibitors is based on concerns related to the effects of JAK inhibitors on interferon signaling that may result in a diminished vaccine response.(1) The ACR recommendation for subcutaneous abatacept is based on several studies suggesting a negative effect of abatacept on vaccine immunogenicity. The first vaccine dose primes naive T cells, naive T cell priming is inhibited by CTLA-4, and abatacept is a CTLA-4Ig construct. CTLA-4 should not inhibit boosts of already primed T cells at the time of the second vaccine dose.(1) |
COMIRNATY 2024-2025, MODERNA COVID 24-25(6M-11Y)EUA, NOVAVAX COVID 2024-2025 (EUA), PFIZER COVID 2024-25(5-11Y)EUA, PFIZER COVID 2024-25(6M-4Y)EUA, SPIKEVAX 2024-2025 |
| Sarilumab/Immunosuppressives; Immunomodulators SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed. MECHANISM OF ACTION: Sarilumab, immunosuppressives, and immunomodulators all suppress the immune system.(1) CLINICAL EFFECTS: Concurrent use of sarilumab with immunosuppressive or immunomodulating agents may result in an increased risk for serious infections.(1) PREDISPOSING FACTORS: None determined. PATIENT MANAGEMENT: The US manufacturer of sarilumab recommends caution because the concurrent use of sarilumab with immunosuppressive agents may increase the risk of infection. If concurrent therapy is warranted, consider the risk of additive immune suppression and monitor based on prescribing information for both agents.(1) DISCUSSION: Sarilumab was studied as monotherapy and in combination with methotrexate or conventional disease modifying antirheumatic drugs (DMARDs) in rheumatoid arthritis studies. Sarilumab has not been studied with biological DMARDs and concurrent use should be avoided. If concurrent therapy is warranted, consider the potential for increased immunosuppressive risks from both agents.(1) The most common infections reported by sarilumab treated patients in the clinical trial periods included pneumonia and cellulitis. Serious bacterial, mycobacterial, fungal, and viral infections were observed in patients receiving sarilumab. Cases of tuberculosis, candidiasis, and pneumocystis with sarilumab have been reported.(1) |
KEVZARA |
| Ublituximab/Immunosuppressives; Immunomodulators SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed. MECHANISM OF ACTION: Ublituximab, immunosuppressives, and immunomodulators all suppress the immune system.(1) CLINICAL EFFECTS: Concurrent use of ublituximab with immunosuppressive or immunomodulating agents may result in an increased risk for serious infections.(1) PREDISPOSING FACTORS: Incomplete washout of previously prescribed immunosuppressive or immune-modulating medications. PATIENT MANAGEMENT: The US manufacturer of ublituximab recommends caution because the concurrent use of ublituximab with immunomodulating or immunosuppressive agents, including immunosuppressant doses of corticosteroids, may increase the risk of infection.(1) If concurrent therapy is warranted, consider the risk of additive immune suppression and monitor based on prescribing information for both agents. When switching from agents with immune effects, the half-life and mechanism of action of these drugs must be taken into consideration in order to prevent additive immunosuppressive effects.(1) DISCUSSION: The most common infections reported by ublituximab-treated patients in the clinical trial periods included upper respiratory tract infections and urinary tract infections. Serious, including life-threatening or fatal, bacterial and viral infections were observed in patients receiving ublituximab.(1) Serious and/or fatal bacterial, fungal, and new or reactivated viral infections have been associated with other anti-CD20 B-cell depleting therapies. There were no cases of progressive multifocal leukoencephalopathy (PML) reported during the clinical trials; however, there have been reports of PML during or following completion of other anti-CD20 B-cell depleting therapies.(1) |
BRIUMVI |
| Tocilizumab/Immunosuppressives; Immunomodulators SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed. MECHANISM OF ACTION: Tocilizumab, immunosuppressives, and immunomodulators all suppress the immune system.(1) CLINICAL EFFECTS: Concurrent use of tocilizumab with immunosuppressive or immunomodulating agents may result in an increased risk for serious infections.(1) PREDISPOSING FACTORS: None determined. PATIENT MANAGEMENT: The US manufacturer of tocilizumab recommends caution because the concurrent use of tocilizumab with immunosuppressive agents may increase the risk of infection. If concurrent therapy is warranted, consider the risk of additive immune suppression and monitor based on prescribing information for both agents.(1) DISCUSSION: Tocilizumab was studied as monotherapy and in combination with methotrexate, non-biologic DMARDs or corticosteroids, depending on the indication. Tocilizumab has not been studied with biological DMARDs and concurrent use should be avoided. If concurrent therapy is warranted, consider the potential for increased immunosuppressive risks from both agents.(1) The most common infections reported by tocilizumab treated patients in the clinical trial periods included pneumonia, urinary tract infection, cellulitis, herpes zoster, gastroenteritis, diverticulitis, sepsis and bacterial arthritis. Serious bacterial, mycobacterial, fungal, and viral infections were observed in patients receiving tocilizumab. Cases of tuberculosis, cryptococcus, aspergillosis, candidiasis, and pneumocystosis have been reported.(1) |
ACTEMRA, ACTEMRA ACTPEN, TOFIDENCE, TYENNE, TYENNE AUTOINJECTOR |
The following contraindication information is available for PACLITAXEL (paclitaxel):
Drug contraindication overview.
No enhanced Contraindications information available for this drug.
No enhanced Contraindications information available for this drug.
There are 1 contraindications.
Absolute contraindication.
| Contraindication List |
|---|
| Lactation |
There are 10 severe contraindications.
Adequate patient monitoring is recommended for safer drug use.
| Severe List |
|---|
| Anemia |
| Child-pugh class B hepatic impairment |
| Child-pugh class C hepatic impairment |
| Disease of liver |
| Hyperbilirubinemia |
| Neutropenic disorder |
| Peripheral neuropathy |
| Pregnancy |
| Severe infection |
| Thrombocytopenic disorder |
There are 1 moderate contraindications.
Clinically significant contraindication, where the condition can be managed or treated before the drug may be given safely.
| Moderate List |
|---|
| Hypotension |
The following adverse reaction information is available for PACLITAXEL (paclitaxel):
Adverse reaction overview.
No enhanced Common Adverse Effects information available for this drug.
No enhanced Common Adverse Effects information available for this drug.
There are 31 severe adverse reactions.
| More Frequent | Less Frequent |
|---|---|
|
Anemia Dyspnea Erythema Leukopenia Neutropenic disorder Skin rash Thrombocytopenic disorder |
Abnormal hepatic function tests Anaphylaxis Angioedema Bradycardia Hypersensitivity drug reaction Hypotension Severe neutropenic disorder Urticaria |
| Rare/Very Rare |
|---|
|
Ascites Dehydration Dermal necrosis Exfoliative dermatitis Gastrointestinal obstruction Hypertension Injection site sequelae Intestinal perforation Ischemic colitis Pancreatitis Paralytic ileus Phlebitis after infusion Radiation recall syndrome Stevens-johnson syndrome Stomatitis Toxic epidermal necrolysis |
There are 15 less severe adverse reactions.
| More Frequent | Less Frequent |
|---|---|
|
Alopecia Arthralgia Diarrhea Edema Myalgia Nausea Paresthesia Peripheral neuropathy Vomiting |
None. |
| Rare/Very Rare |
|---|
|
Cellulitis Constipation Esophagitis General weakness Induration of skin Pruritus of skin |
The following precautions are available for PACLITAXEL (paclitaxel):
No enhanced Pediatric Use information available for this drug.
Contraindicated
Severe Precaution
Management or Monitoring Precaution
Contraindicated
| None |
Severe Precaution
| None |
Management or Monitoring Precaution
| None |
Paclitaxel can cause fetal toxicity when administered to pregnant women, but potential benefits may be acceptable in certain conditions despite the possible risks to the fetus. Reproduction studies in rabbits receiving IV conventional paclitaxel doses of 3 mg/kg daily (approximately 0.2 times the maximum recommended human dose on a mg/m2 basis) during organogenesis revealed evidence of maternal toxicity, embryotoxicity, and fetotoxicity. The drug caused intrauterine mortality, increased resorptions, and increased fetal deaths.
Reproduction studies in rats receiving IV paclitaxel doses of 1 mg/kg daily (approximately 0.04 times the maximum recommended human dose on a mg/m2 basis) during organogenesis resulted in embryotoxicity and fetotoxicity. No teratogenic effects were observed in the offspring of rats receiving daily IV paclitaxel doses of 1 mg/kg; however, the teratogenic potential of higher paclitaxel doses could not be assessed because of extensive fetal mortality. Reproduction studies in rats receiving albumin-bound paclitaxel at IV doses of 6 mg/m2 (approximately 2% of the maximum recommended human dose on a mg/m2 basis) on gestation days 7 to 17 resulted in embryotoxicity and fetotoxicity.
The drug caused intrauterine mortality, increased resorptions, reduced numbers of litters, increased fetal deaths, reduction in fetal body weight, and increased fetal anomalies including soft tissue and skeletal malformations, such as eye bulge, folded retina, microphthalmia, and dilation of brain ventricles. Fetal anomalies also occurred in the offspring of rats receiving lower doses of albumin-bound paclitaxel (IV doses of 3 mg/m2 or approximately 1% of the maximum recommended human dose on a mg/m2 basis). There are no adequate and well-controlled studies to date using paclitaxel in pregnant women.
Paclitaxel should be used during pregnancy only in life-threatening situations or for severe disease for which safer drugs cannot be used or are ineffective. When paclitaxel is used during pregnancy or if the patient becomes pregnant while receiving the drug, the patient should be informed of the potential hazard to the fetus. Women of childbearing potential should be advised to avoid becoming pregnant during therapy with paclitaxel. Men receiving albumin-bound paclitaxel should be advised to avoid fathering a child.
Reproduction studies in rats receiving IV paclitaxel doses of 1 mg/kg daily (approximately 0.04 times the maximum recommended human dose on a mg/m2 basis) during organogenesis resulted in embryotoxicity and fetotoxicity. No teratogenic effects were observed in the offspring of rats receiving daily IV paclitaxel doses of 1 mg/kg; however, the teratogenic potential of higher paclitaxel doses could not be assessed because of extensive fetal mortality. Reproduction studies in rats receiving albumin-bound paclitaxel at IV doses of 6 mg/m2 (approximately 2% of the maximum recommended human dose on a mg/m2 basis) on gestation days 7 to 17 resulted in embryotoxicity and fetotoxicity.
The drug caused intrauterine mortality, increased resorptions, reduced numbers of litters, increased fetal deaths, reduction in fetal body weight, and increased fetal anomalies including soft tissue and skeletal malformations, such as eye bulge, folded retina, microphthalmia, and dilation of brain ventricles. Fetal anomalies also occurred in the offspring of rats receiving lower doses of albumin-bound paclitaxel (IV doses of 3 mg/m2 or approximately 1% of the maximum recommended human dose on a mg/m2 basis). There are no adequate and well-controlled studies to date using paclitaxel in pregnant women.
Paclitaxel should be used during pregnancy only in life-threatening situations or for severe disease for which safer drugs cannot be used or are ineffective. When paclitaxel is used during pregnancy or if the patient becomes pregnant while receiving the drug, the patient should be informed of the potential hazard to the fetus. Women of childbearing potential should be advised to avoid becoming pregnant during therapy with paclitaxel. Men receiving albumin-bound paclitaxel should be advised to avoid fathering a child.
It is not known whether paclitaxel is distributed into human milk. However, in lactating rats given radiolabeled paclitaxel, concentrations of radioactivity in milk were higher than those in plasma and declined in parallel with plasma concentrations of the drug. Because of the potential for serious adverse reactions to paclitaxel in nursing infants, a decision should be made whether to discontinue nursing or the drug, taking into account the importance of the drug to the woman.
No enhanced Geriatric Use information available for this drug.
The following prioritized warning is available for PACLITAXEL (paclitaxel):
WARNING: Paclitaxel may rarely cause serious (rarely fatal) allergic reactions. Patients who experience a severe allergic reaction with this drug must never use it again. Your doctor may prescribe other medications (such as antihistamines, corticosteroids) to help prevent an allergic reaction.
However, severe allergic reactions may still occur in a few patients. Get medical help right away if you develop any signs of an allergic reaction such as rash, itching, swelling, severe dizziness, trouble breathing, or chest pain. This medication may often cause a serious blood disorder (decreased bone marrow function leading to a low number of white blood cells).
This effect can lower your body's ability to fight an infection. Your doctor will monitor you closely and check your blood often during treatment. If your white blood cell count is too low, you should not receive this medication. Tell your doctor right away if you develop any signs of infection (such as sore throat that doesn't go away, fever, chills, painful/difficult urination).
WARNING: Paclitaxel may rarely cause serious (rarely fatal) allergic reactions. Patients who experience a severe allergic reaction with this drug must never use it again. Your doctor may prescribe other medications (such as antihistamines, corticosteroids) to help prevent an allergic reaction.
However, severe allergic reactions may still occur in a few patients. Get medical help right away if you develop any signs of an allergic reaction such as rash, itching, swelling, severe dizziness, trouble breathing, or chest pain. This medication may often cause a serious blood disorder (decreased bone marrow function leading to a low number of white blood cells).
This effect can lower your body's ability to fight an infection. Your doctor will monitor you closely and check your blood often during treatment. If your white blood cell count is too low, you should not receive this medication. Tell your doctor right away if you develop any signs of infection (such as sore throat that doesn't go away, fever, chills, painful/difficult urination).
The following icd codes are available for PACLITAXEL (paclitaxel)'s list of indications:
| Epithelial ovarian cancer | |
| C48.1 | Malignant neoplasm of specified parts of peritoneum |
| C48.2 | Malignant neoplasm of peritoneum, unspecified |
| C48.8 | Malignant neoplasm of overlapping sites of retroperitoneum and peritoneum |
| C56 | Malignant neoplasm of ovary |
| C56.1 | Malignant neoplasm of right ovary |
| C56.2 | Malignant neoplasm of left ovary |
| C56.3 | Malignant neoplasm of bilateral ovaries |
| C56.9 | Malignant neoplasm of unspecified ovary |
| C57.01 | Malignant neoplasm of right fallopian tube |
| C57.02 | Malignant neoplasm of left fallopian tube |
| Kaposi's sarcoma | |
| C46 | Kaposi's sarcoma |
| C46.0 | Kaposi's sarcoma of skin |
| C46.1 | Kaposi's sarcoma of soft tissue |
| C46.2 | Kaposi's sarcoma of palate |
| C46.3 | Kaposi's sarcoma of lymph nodes |
| C46.4 | Kaposi's sarcoma of gastrointestinal sites |
| C46.5 | Kaposi's sarcoma of lung |
| C46.50 | Kaposi's sarcoma of unspecified lung |
| C46.51 | Kaposi's sarcoma of right lung |
| C46.52 | Kaposi's sarcoma of left lung |
| C46.7 | Kaposi's sarcoma of other sites |
| C46.9 | Kaposi's sarcoma, unspecified |
| Locally advanced breast carcinoma | |
| C50 | Malignant neoplasm of breast |
| C50.1 | Malignant neoplasm of central portion of breast |
| C50.11 | Malignant neoplasm of central portion of breast, female |
| C50.111 | Malignant neoplasm of central portion of right female breast |
| C50.112 | Malignant neoplasm of central portion of left female breast |
| C50.119 | Malignant neoplasm of central portion of unspecified female breast |
| C50.12 | Malignant neoplasm of central portion of breast, male |
| C50.121 | Malignant neoplasm of central portion of right male breast |
| C50.122 | Malignant neoplasm of central portion of left male breast |
| C50.129 | Malignant neoplasm of central portion of unspecified male breast |
| C50.2 | Malignant neoplasm of upper-inner quadrant of breast |
| C50.21 | Malignant neoplasm of upper-inner quadrant of breast, female |
| C50.211 | Malignant neoplasm of upper-inner quadrant of right female breast |
| C50.212 | Malignant neoplasm of upper-inner quadrant of left female breast |
| C50.219 | Malignant neoplasm of upper-inner quadrant of unspecified female breast |
| C50.22 | Malignant neoplasm of upper-inner quadrant of breast, male |
| C50.221 | Malignant neoplasm of upper-inner quadrant of right male breast |
| C50.222 | Malignant neoplasm of upper-inner quadrant of left male breast |
| C50.229 | Malignant neoplasm of upper-inner quadrant of unspecified male breast |
| C50.3 | Malignant neoplasm of lower-inner quadrant of breast |
| C50.31 | Malignant neoplasm of lower-inner quadrant of breast, female |
| C50.311 | Malignant neoplasm of lower-inner quadrant of right female breast |
| C50.312 | Malignant neoplasm of lower-inner quadrant of left female breast |
| C50.319 | Malignant neoplasm of lower-inner quadrant of unspecified female breast |
| C50.32 | Malignant neoplasm of lower-inner quadrant of breast, male |
| C50.321 | Malignant neoplasm of lower-inner quadrant of right male breast |
| C50.322 | Malignant neoplasm of lower-inner quadrant of left male breast |
| C50.329 | Malignant neoplasm of lower-inner quadrant of unspecified male breast |
| C50.4 | Malignant neoplasm of upper-outer quadrant of breast |
| C50.41 | Malignant neoplasm of upper-outer quadrant of breast, female |
| C50.411 | Malignant neoplasm of upper-outer quadrant of right female breast |
| C50.412 | Malignant neoplasm of upper-outer quadrant of left female breast |
| C50.419 | Malignant neoplasm of upper-outer quadrant of unspecified female breast |
| C50.42 | Malignant neoplasm of upper-outer quadrant of breast, male |
| C50.421 | Malignant neoplasm of upper-outer quadrant of right male breast |
| C50.422 | Malignant neoplasm of upper-outer quadrant of left male breast |
| C50.429 | Malignant neoplasm of upper-outer quadrant of unspecified male breast |
| C50.5 | Malignant neoplasm of lower-outer quadrant of breast |
| C50.51 | Malignant neoplasm of lower-outer quadrant of breast, female |
| C50.511 | Malignant neoplasm of lower-outer quadrant of right female breast |
| C50.512 | Malignant neoplasm of lower-outer quadrant of left female breast |
| C50.519 | Malignant neoplasm of lower-outer quadrant of unspecified female breast |
| C50.52 | Malignant neoplasm of lower-outer quadrant of breast, male |
| C50.521 | Malignant neoplasm of lower-outer quadrant of right male breast |
| C50.522 | Malignant neoplasm of lower-outer quadrant of left male breast |
| C50.529 | Malignant neoplasm of lower-outer quadrant of unspecified male breast |
| C50.6 | Malignant neoplasm of axillary tail of breast |
| C50.61 | Malignant neoplasm of axillary tail of breast, female |
| C50.611 | Malignant neoplasm of axillary tail of right female breast |
| C50.612 | Malignant neoplasm of axillary tail of left female breast |
| C50.619 | Malignant neoplasm of axillary tail of unspecified female breast |
| C50.62 | Malignant neoplasm of axillary tail of breast, male |
| C50.621 | Malignant neoplasm of axillary tail of right male breast |
| C50.622 | Malignant neoplasm of axillary tail of left male breast |
| C50.629 | Malignant neoplasm of axillary tail of unspecified male breast |
| C50.8 | Malignant neoplasm of overlapping sites of breast |
| C50.81 | Malignant neoplasm of overlapping sites of breast, female |
| C50.811 | Malignant neoplasm of overlapping sites of right female breast |
| C50.812 | Malignant neoplasm of overlapping sites of left female breast |
| C50.819 | Malignant neoplasm of overlapping sites of unspecified female breast |
| C50.82 | Malignant neoplasm of overlapping sites of breast, male |
| C50.821 | Malignant neoplasm of overlapping sites of right male breast |
| C50.822 | Malignant neoplasm of overlapping sites of left male breast |
| C50.829 | Malignant neoplasm of overlapping sites of unspecified male breast |
| C50.9 | Malignant neoplasm of breast of unspecified site |
| C50.91 | Malignant neoplasm of breast of unspecified site, female |
| C50.911 | Malignant neoplasm of unspecified site of right female breast |
| C50.912 | Malignant neoplasm of unspecified site of left female breast |
| C50.919 | Malignant neoplasm of unspecified site of unspecified female breast |
| C50.92 | Malignant neoplasm of breast of unspecified site, male |
| C50.921 | Malignant neoplasm of unspecified site of right male breast |
| C50.922 | Malignant neoplasm of unspecified site of left male breast |
| C50.929 | Malignant neoplasm of unspecified site of unspecified male breast |
| Malignant neoplasm of the ovary | |
| C56 | Malignant neoplasm of ovary |
| C56.1 | Malignant neoplasm of right ovary |
| C56.2 | Malignant neoplasm of left ovary |
| C56.3 | Malignant neoplasm of bilateral ovaries |
| C56.9 | Malignant neoplasm of unspecified ovary |
| Metastatic breast carcinoma | |
| C50 | Malignant neoplasm of breast |
| C50.1 | Malignant neoplasm of central portion of breast |
| C50.11 | Malignant neoplasm of central portion of breast, female |
| C50.111 | Malignant neoplasm of central portion of right female breast |
| C50.112 | Malignant neoplasm of central portion of left female breast |
| C50.119 | Malignant neoplasm of central portion of unspecified female breast |
| C50.12 | Malignant neoplasm of central portion of breast, male |
| C50.121 | Malignant neoplasm of central portion of right male breast |
| C50.122 | Malignant neoplasm of central portion of left male breast |
| C50.129 | Malignant neoplasm of central portion of unspecified male breast |
| C50.2 | Malignant neoplasm of upper-inner quadrant of breast |
| C50.21 | Malignant neoplasm of upper-inner quadrant of breast, female |
| C50.211 | Malignant neoplasm of upper-inner quadrant of right female breast |
| C50.212 | Malignant neoplasm of upper-inner quadrant of left female breast |
| C50.219 | Malignant neoplasm of upper-inner quadrant of unspecified female breast |
| C50.22 | Malignant neoplasm of upper-inner quadrant of breast, male |
| C50.221 | Malignant neoplasm of upper-inner quadrant of right male breast |
| C50.222 | Malignant neoplasm of upper-inner quadrant of left male breast |
| C50.229 | Malignant neoplasm of upper-inner quadrant of unspecified male breast |
| C50.3 | Malignant neoplasm of lower-inner quadrant of breast |
| C50.31 | Malignant neoplasm of lower-inner quadrant of breast, female |
| C50.311 | Malignant neoplasm of lower-inner quadrant of right female breast |
| C50.312 | Malignant neoplasm of lower-inner quadrant of left female breast |
| C50.319 | Malignant neoplasm of lower-inner quadrant of unspecified female breast |
| C50.32 | Malignant neoplasm of lower-inner quadrant of breast, male |
| C50.321 | Malignant neoplasm of lower-inner quadrant of right male breast |
| C50.322 | Malignant neoplasm of lower-inner quadrant of left male breast |
| C50.329 | Malignant neoplasm of lower-inner quadrant of unspecified male breast |
| C50.4 | Malignant neoplasm of upper-outer quadrant of breast |
| C50.41 | Malignant neoplasm of upper-outer quadrant of breast, female |
| C50.411 | Malignant neoplasm of upper-outer quadrant of right female breast |
| C50.412 | Malignant neoplasm of upper-outer quadrant of left female breast |
| C50.419 | Malignant neoplasm of upper-outer quadrant of unspecified female breast |
| C50.42 | Malignant neoplasm of upper-outer quadrant of breast, male |
| C50.421 | Malignant neoplasm of upper-outer quadrant of right male breast |
| C50.422 | Malignant neoplasm of upper-outer quadrant of left male breast |
| C50.429 | Malignant neoplasm of upper-outer quadrant of unspecified male breast |
| C50.5 | Malignant neoplasm of lower-outer quadrant of breast |
| C50.51 | Malignant neoplasm of lower-outer quadrant of breast, female |
| C50.511 | Malignant neoplasm of lower-outer quadrant of right female breast |
| C50.512 | Malignant neoplasm of lower-outer quadrant of left female breast |
| C50.519 | Malignant neoplasm of lower-outer quadrant of unspecified female breast |
| C50.52 | Malignant neoplasm of lower-outer quadrant of breast, male |
| C50.521 | Malignant neoplasm of lower-outer quadrant of right male breast |
| C50.522 | Malignant neoplasm of lower-outer quadrant of left male breast |
| C50.529 | Malignant neoplasm of lower-outer quadrant of unspecified male breast |
| C50.6 | Malignant neoplasm of axillary tail of breast |
| C50.61 | Malignant neoplasm of axillary tail of breast, female |
| C50.611 | Malignant neoplasm of axillary tail of right female breast |
| C50.612 | Malignant neoplasm of axillary tail of left female breast |
| C50.619 | Malignant neoplasm of axillary tail of unspecified female breast |
| C50.62 | Malignant neoplasm of axillary tail of breast, male |
| C50.621 | Malignant neoplasm of axillary tail of right male breast |
| C50.622 | Malignant neoplasm of axillary tail of left male breast |
| C50.629 | Malignant neoplasm of axillary tail of unspecified male breast |
| C50.8 | Malignant neoplasm of overlapping sites of breast |
| C50.81 | Malignant neoplasm of overlapping sites of breast, female |
| C50.811 | Malignant neoplasm of overlapping sites of right female breast |
| C50.812 | Malignant neoplasm of overlapping sites of left female breast |
| C50.819 | Malignant neoplasm of overlapping sites of unspecified female breast |
| C50.82 | Malignant neoplasm of overlapping sites of breast, male |
| C50.821 | Malignant neoplasm of overlapping sites of right male breast |
| C50.822 | Malignant neoplasm of overlapping sites of left male breast |
| C50.829 | Malignant neoplasm of overlapping sites of unspecified male breast |
| C50.9 | Malignant neoplasm of breast of unspecified site |
| C50.91 | Malignant neoplasm of breast of unspecified site, female |
| C50.911 | Malignant neoplasm of unspecified site of right female breast |
| C50.912 | Malignant neoplasm of unspecified site of left female breast |
| C50.919 | Malignant neoplasm of unspecified site of unspecified female breast |
| C50.92 | Malignant neoplasm of breast of unspecified site, male |
| C50.921 | Malignant neoplasm of unspecified site of right male breast |
| C50.922 | Malignant neoplasm of unspecified site of left male breast |
| C50.929 | Malignant neoplasm of unspecified site of unspecified male breast |
| Non-small cell lung cancer | |
| C34 | Malignant neoplasm of bronchus and lung |
| C34.0 | Malignant neoplasm of main bronchus |
| C34.00 | Malignant neoplasm of unspecified main bronchus |
| C34.01 | Malignant neoplasm of right main bronchus |
| C34.02 | Malignant neoplasm of left main bronchus |
| C34.1 | Malignant neoplasm of upper lobe, bronchus or lung |
| C34.10 | Malignant neoplasm of upper lobe, unspecified bronchus or lung |
| C34.11 | Malignant neoplasm of upper lobe, right bronchus or lung |
| C34.12 | Malignant neoplasm of upper lobe, left bronchus or lung |
| C34.2 | Malignant neoplasm of middle lobe, bronchus or lung |
| C34.3 | Malignant neoplasm of lower lobe, bronchus or lung |
| C34.30 | Malignant neoplasm of lower lobe, unspecified bronchus or lung |
| C34.31 | Malignant neoplasm of lower lobe, right bronchus or lung |
| C34.32 | Malignant neoplasm of lower lobe, left bronchus or lung |
| C34.8 | Malignant neoplasm of overlapping sites of bronchus and lung |
| C34.80 | Malignant neoplasm of overlapping sites of unspecified bronchus and lung |
| C34.81 | Malignant neoplasm of overlapping sites of right bronchus and lung |
| C34.82 | Malignant neoplasm of overlapping sites of left bronchus and lung |
| C34.9 | Malignant neoplasm of unspecified part of bronchus or lung |
| C34.90 | Malignant neoplasm of unspecified part of unspecified bronchus or lung |
| C34.91 | Malignant neoplasm of unspecified part of right bronchus or lung |
| C34.92 | Malignant neoplasm of unspecified part of left bronchus or lung |
| C39.9 | Malignant neoplasm of lower respiratory tract, part unspecified |
Formulary Reference Tool