Written by: Jessie Signorelli PharmD, BCOP, Massachusetts General Hospital

DOWNLAD HERE

Description: This PQI will aim to review ponatinib efficacy and safety data as well as clinical pearls regarding supportive care and adverse event management.1

Background: Ponatinib (Iclusig®) is a third-generation tyrosine kinase inhibitor (TKI) with activity directed at BCR-ABL mutant kinase in patients with chronic phase (CP) chronic myeloid leukemia (CML) with intolerance to at least two prior TKIs or with a T315I mutation. Ponatinib is also approved for accelerated phase (AP) or blast phase (BP) CML or Philadelphia chromosome positive acute lymphoblastic leukemia (Ph+ ALL) for whom no other TKIs are indicated or who have a T315I mutation.

Safety and efficacy data of ponatinib in patients with CML or Ph+ ALL was first demonstrated in a single-arm, open-label, international, and multicenter trial, the PACE trial, which included patients with unacceptable side effects from dasatinib or nilotinib or a T315I mutation. A major molecular response (MMR) was achieved in 40% of patients with CP-CML (35% relapsed/intolerant to previous TKI, 58% in patients with T315I mutation). A major hematologic response (MaHR) was demonstrated in 61%, 31%, and 41% in the AP-CML, BP-CML, and Ph+ ALL, respectively. Median time to MaHR was 0.8 months (range 0.4-6.3), 1 month (range 0.4-4 months), and 0.7 months (range 0.4-6 months) in the AP-CML, BP-CML, and Ph+ ALL groups, respectively.2

The OPTIC trial was a dose optimization trial to explore the relationship between ponatinib dose and both adverse events and response. This trial demonstrated ponatinib can be safely decreased to 15 mg in CP-CML once BCR-ABL1 < 1%.3

Ponatinib carries black box warnings for arterial occlusive events (AOEs), venous thromboembolic events (VTEs), heart failure (HF), and hepatoxicity. Other warnings associated with ponatinib include hypertension, pancreatitis, ocular toxicity, myelosuppression, and impaired wound healing.1 Grade 3 or 4 adverse events (AEs) were seen in 89% and 67% of patients in the PACE and OPTIC populations, respectively.2,3 Because there is a lag time between dose change and event risk, patients with CP-CML should be decreased to 15 mg once BCR-ABL1 is <1%.4  Due to the number of AEs with ponatinib, monitoring and patient education are vital to decrease risk of serious AEs.

PQI Process: Upon receipt of new prescription for ponatinib:

  • Verify patient has BCR-ABL1 mutation and one of the following indications:
    • CP-CML with resistance or intolerance to at least two prior TKIs
    • AP/BP-CML or Ph+ ALL whom no other TKIs are indicated (ex: developed AP/BP while on alternate TKI)
    • CML or Ph+ ALL with T315I mutation
    • TKI resistance in CP-CML per NCCN: Patients with >10% BCR-ABL1 IS at 6 and 12 months
  • Verify dosing:
    • CP-CML: 45mg once daily with a decrease to 15 mg once daily once BCR-ABL1 <1%
    • AP-CML, BP-CML, and Ph+ ALL: 45 mg once daily
    • Hepatic impairment (Child-Pugh A, B, or C): decrease starting dose from 45 mg to 30 mg
    • Consider decreased starting dose of 30 mg in patients who may not tolerate a starting dose of 45 mg (ex: severe coronary artery disease, history of severe pancreatitis, or advanced HF)
  • Dispensing information:
    • Ponatinib is a limited distribution medication; will first go to AcariaHealth pharmacy
    • If ponatinib is needed urgently, prescription should read “blast crisis” or “emergency”
    • For more information on dispensing, visit: Iclusigdirect.com or call 1-833-291-2773. Hours of operation are 8:30am to 8:00pm EST
    • Ponatinib is available as 10 mg, 15 mg, 30 mg, and 45 mg tablets
  • Screen for drug interactions:
    • Advise patients to avoid grapefruit products as it may increase the amount of ponatinib in their blood and therefore increase their risk of adverse reactions
    • Avoid coadministration with CYP3A4 strong inducers
    • Increase QTc monitoring with concomitant QTc prolonging medications
    • If coadministration with CYP3A4 inhibitors cannot be avoided, decrease dose as follows:
Recommended ponatinib dose for coadministration with strong CYP3A4 inhibitors
Current ponatinib doseRecommended ponatinib dose with strong CYP3A4 inhibition
45 mg once daily30 mg once daily
30 mg once daily15 mg once daily
15 mg once daily10 mg once daily
10 mg once dailyAvoid coadministration

 

  • Laboratory monitoring:
    • Baseline: CBC, CMP, ECG, Mg, fasting glucose, lipid panel, blood pressure, comprehensive eye exam, TLS labs, consider baseline ECHO/MUGA, clinical cardiovascular assessment
    • Every 2 weeks for the first 3 months, then monthly or as clinically indicated: CBC
    • Every 2 weeks for the first 2 months then monthly or as clinically indicated: lipase
    • Monthly or as clinically indicated: LFTs, ECG
    • If concern for pancreatitis: amylase, lipase, triglycerides
  • Dosage modification for adverse reactions: See supplemental
Dose reductionDosage for Patients with CP-CMLDosage for patients with AP-CML, BP-CML, and Ph+ ALL
First30 mg once daily30 mg once daily
Second15 mg once daily15 mg once daily
Third10 mg once dailyPermanently discontinue in patients unable to tolerate 15mg once daily
Subsequent reductionPermanently discontinue in patients unable to tolerate 10mg once daily

 

  • Supportive care:
    • Patients with cardiovascular risk factors should be referred to a cardiologist5
    • Blood pressure should be well controlled prior to starting ponatinib if possible
    • Consider optimizing cardiovascular disease (CAD) risk factors including diabetes, hypertension, hyperlipidemia, history of CAD including myocardial infarction
    • Consider statin therapy if indicated: to decrease risk of drug interactions, consider a statin that is not a substrate of CYP3A4 including rosuvastatin or pravastatin, especially if for the treatment of Ph+ ALL where patients will be on multiple chemotherapy and supportive care medications
    • Consider aspirin 81 mg PO daily for CAD event prophylaxis, however, there has not yet been data demonstrating the benefit of this intervention6

 

Patient Centered Activities:

  • Provide Oral Chemotherapy Education (OCE) sheet
  • Administer with or without food
  • If a dose is missed, skip the dose and take the next dose at the regularly scheduled time
  • Educate patients how to monitor their blood pressure, log recordings and bring to appointments
  • Monitor patients for signs or symptoms of bleeding and advise patient to contact provider with any of the following: vomiting blood or vomit that looks like coffee grounds, pink/brown urine or red/black/tary stools, coughing up blood/clots, unusual bleeding/bruising of skin, menstrual bleeding that is heavier than normal, unusual vaginal bleeding, nose bleeds that happen often, drowsiness/difficulty being awakened, confusion, headache, or change in speech 2
  • Educate patients to contact provider if surgery is planned, as ponatinib can impair wound healing
    • Withhold ponatinib treatment for ≥ 1 week prior to elective surgery and do not administer for ≥ 2 weeks following major surgery and until adequate wound healing 1
  • Patient Assistance: NCODA Financial Assistance Tool

 

References:

  1. ICLUSIG (ponatinib) [prescribing information]. Lexington, MA: Takeda Pharmaceuticals America, Inc.
  2. Cortes JE, Kim DW, Pinilla-Ibarz J, et al. Ponatinib efficacy and safety in Philadelphia chromosome-positive leukemia: final 5-year results of the phase 2 PACE trial. Blood. 2018 Jul 26;132(4):393-404.
  3. Cortes JE, Apperley J, Lomaia E, et al. OPTIC primary analysis: a dose-optimization study of 3 starting doses of ponatinib. J Clin Oncol. 2021;39(15).
  4. Dorer DJ, Knickerbocker RK, Baccarani M, et al. Impact of dose intensity of ponatinib on selected adverse events: Multivariate analyses from a pooled population of clinical trial patients. Leuk Res. 2016 Sep;48:84-91. doi: 10.1016/j.leukres.2016.07.007. Epub 2016 Jul 22. PMID: 27505637.
  5. NCCN Clinical Practice Guidelines in Oncology. Chronic myeloid leukemia. Version 1.2022. Available at: https://www.nccn.org/professionals/physician_gls/pdf/cml.pdf.
  6. Steegmann JL, Baccarani M, Breccia M, et al. European LeukemiaNet recommendations for the management and avoidance of adverse events of treatment in chronic myeloid leukaemia. Leukemia. 2016 Aug;30(8):1648-71. doi: 10.1038/leu.2016.104. Epub 2016 Apr 28. PMID: 27121688; PMCID: PMC4991363.

 

 

 

Recommended dose modifications for ponatinib for adverse reactions
Adverse reactionSeverity Ponatinib dose modifications
Arterial occlusive event (AOE)

Cardiovascular or cerebrovascular

Grade 1Interrupt ponatinib until resolved, then resume at same dose
Grade 2Interrupt ponatinib until Grade 0 or 1, then resume at next lower dose

Discontinue ponatinib if recurrence

Grade 3 or 4Discontinue ponatinib
AOE: peripheral or vascular and other OR venous thromboembolismGrade 1Interrupt ponatinib until resolved, then resume at same dose
Grade 2Interrupt ponatinib until Grade 0 or 1, then resume at same dose

If recurrence interrupt until resolution, then resume at next lower dose

Grade 3Interrupt ponatinib until Grade 0 or 1, then resume at next lower dose

Discontinue ponatinib if recurrence

Grade 4Discontinue ponatinib
Heart FailureGrade 2 or 3Interrupt ponatinib until Grade 0 or 1, then resume at next lower dose

Discontinue ponatinib if recurrence

Grade 4Discontinue ponatinib
HepatotoxicityAST or ALT > 3x ULNInterrupt ponatinib until Grade 0 or 1, then resume at next lower dose
AST/ALT > 3x ULN, bilirubin > 2x ULN, ALP < 2x ULNDiscontinue ponatinib
Pancreatitis and elevated lipaseSerum lipase > 1-1.5 x ULNConsider interrupting until resolution, then resume at same dose
Serum lipase > 1.5-2 x ULN, 2-5 x ULN and asymptomatic, or radiologic pancreatitisInterrupt until Grade 0 or 1 (< 1.5 x ULN) then resume at next lower dose
Serum lipase > 2-5 x ULN and symptomatic, symptomatic Grade 3 pancreatitis, or serum lipase > 5 x ULN and asymptomaticInterrupt ponatinib until complete resolution of symptoms and after recovery of lipase elevation Grade 0 or 1, then resume at next lower dose
Symptomatic pancreatitis and serum lipase > 5x ULNDiscontinue ponatinib
MyelosuppressionANC < 1 x 109/L

OR

Platelets < 50 x 109/L

Interrupt ponatinib until ANC > 1.5 x 109/L and platelets at least 75 x 109/L, then resume at the same dose

If recurrence interrupt until resolution, then resume at next lower dose

Other non-hematologic adverse reactionsGrade 1Interrupt ponatinib until resolved, then resume at same dose
Grade 2Interrupt ponatinib until Grade 0 or 1, then resume at same dose

If recurrence, interrupt until Grade 0 or 1, and resume at next lower dose

Grade 3 or 4Interrupt until Grade 0 or 1, then resume at next lower dose

Discontinue ponatinib if recurrence

ANC: absolute neutrophil count; ALT: alanine aminotransferase; ALP: alkaline phosphatase; AST: aspartate aminotransferase; ULN: upper limit of normal

Important notice: NCODA has developed this Positive Quality Intervention platform. This platform represents a brief summary of medication uses and therapy options derived from information provided by the drug manufacturer and other resources. This platform is intended as an educational aid and does not provide individual medical advice and does not substitute for the advice of a qualified healthcare professional.  This platform does not cover all existing information related to the possible uses, directions, doses, precautions, warning, interactions, adverse effects, or risks associated with the medication discussed in the platform and is not intended as a substitute for the advice of a qualified healthcare professional. The materials contained in this platform are for informational purposes only and do not constitute or imply endorsement, recommendation, or favoring of this medication by NCODA, which assumes no liability for and does not ensure the accuracy of the information presented.  NCODA does not make any representations with respect to the medications whatsoever, and any and all decisions, with respect to such medications, are at the sole risk of the individual consuming the medication. All decisions related to taking this medication should be made with the guidance and under the direction of a qualified healthcare professional.
Read More

Written by: Sara Moran Smith, PharmD, BCOP | M Health Fairview

DOWNLOAD HERE

Purpose: Rash occurs in approximately 90% of patients treated with epidermal growth factor receptor (EGFR)  inhibitors1 with 10-20% developing severe eruption.1 Studies have shown that the presence of this rash is indicative of response to treatment.1 Therefore, it is important to prevent and manage this side effect appropriately  in an effort to avoid holding or decreasing the dose of EGFR inhibitors.

Background: EGFR inhibitors are in integral part of treatment for advanced lung, pancreatic, colorectal, and head and neck cancers. These include monoclonal antibodies (amivantamab, cetuximab, panitumumab) and small-molecule tyrosine kinase inhibitors (afatinib, dacomitinib, erlotinib, gefitinib, osimertinib). A common side effect of these agents is a papulopustular or “acneiform” rash. EGFR inhibitor induced rash can decrease the quality of life for patients and result in dose interruptions or discontinuation by patients. The rash affects areas rich in sebaceous glands, such as the scalp, face, nose, cheeks, nasolabial folds, and perioral region. In addition, the rash can extend to the upper trunk and the “V” region of the neck and chest. Patients commonly report itching, pain, irritation, and stinging. Symptoms can begin as early as the first week of therapy, commonly with an abnormal sensation with redness and edema. As therapy progresses through the first 3 weeks, papules and pustules begin to develop. By the end of the first month of therapy, crusting from the purulent material forms and there is persistent redness and dryness. These initial pustules are sterile; however, a secondary infection can occur with bacteria, fungus, or viruses. These symptoms wax and wane despite continued EGFR inhibitor therapy.1 There are a few risk factors for developing severe form of the rash. Patients with pale skin that do not tan can increase their risk of a grade 3 to 4 rash.1 Incidence of grade 3 rash was higher in patients treated with combination therapy that included an EGFR inhibitor versus single agent.1 Patients with non-small cell lung cancer on erlotinib who also smoked had a lower incidence of skin eruption, possibly due to enhanced clearance of the drug.1 

PQI Process:

  • Identify patients starting EGFR inhibitor therapy
  • After patients start therapy, monitor symptoms of rash on a biweekly basis
  • Grade rash as symptoms develop according to NCCN CTCAE Criteria as well as impact on quality of life
CTCAE(v4) Grade 1           Continue EGFRi at current dose 
<10% body surface area (BSA) papules and/or pustules;

With or without symptoms  of pruritus or tenderness

Topical steroid moderate strength*

Topical antibiotic* bid

 

CTCAE(v4) Grade 2           Continue EGFRi at current dose 
10 – 30% BSA papules and/or pustules;

With or without symptoms of pruritus or tenderness;

Psychosocial impact;

Limiting instrumental activities of daily living (ADL)

Oral antibiotic for 6 weeks (doxycycline 100 mg bid; minocycline 100 mg bid)

Stop topical antibiotic if being used

Topical steroid moderate strength*

CTCAE(v4) Grade ≥3         Interrupt EGFRi and monitor
>30% BSA papules and/or pustules;

With or without symptoms of pruritus or tenderness;

Limiting self-care ADL;

Associated with local superinfection with oral antibiotics indicated

 

Oral antibiotic for 6 weeks (doxycycline 100 mg bid; minocycline 100 mg bid)

If infection suspected (yellow crusts, purulent discharge, painful skin/nares):

o  Switch oral antibiotic to broad spectrum/gram negative coverage

o  Consider skin swab for bacterial culture

Topical steroid moderate strength*

* Example topical steroids and antibiotics 
Topical steroids moderate strengthTriamcinolone acetonide 0.025%; Desonide 0.05%; Fluticasone proprionate 0.05%; Aclometasone 0.05% 
Topical antibioticsClindamycin 1 – 2%; Erythromycin 1% -2% ; Metronidazole 1% 

Patient Centered Activities:

  • Monitor skin and call provider if rash worsens
  • Counsel on the importance of preventative measures to decrease severity of rash
    • Patients should limit sun exposure and use sunscreen (SPF 30 or higher)
    • Mild cleansers and shampoos and avoid fragrant soaps and detergents
    • Use lukewarm water for bathing
    • Use thick, alcohol-free emollients twice daily
    • When starting therapy, an oral antibiotic for a minimum of 6 weeks of therapy is indicated
    • Patients should be counseled on not treating acneiform rash with any products for acne, such as benzoyl peroxide, salicylic acid, and other exfoliating scrubs (may worsen rash)
    • Apply topical steroid cream on commonly affected areas once a day (avoid eyes)
      • Prolonged use may cause steroid-induced rash (especially on face and scalp)
      • Referral to dermatology warranted if a steroid-induced rash suspected

References:

  1. Lacouture, M. E., Anadkat, M. J., Bensadoun, R. J., Bryce, J., Chan, A., Epstein, J. B., Eaby-Sandy, B., Murphy, B. A., & MASCC Skin Toxicity Study Group (2011). Clinical practice guidelines for the prevention and treatment of EGFR inhibitor-associated dermatologic toxicities. Supportive care in cancer : official journal of the Multinational Association of Supportive Care in Cancer19(8), 1079–1095. https://doi.org/10.1007/s00520-011-1197-6.
Important notice: NCODA has developed this Positive Quality Intervention platform. This platform represents a brief summary of medication uses and therapy options derived from information provided by the drug manufacturer and other resources. This platform is intended as an educational aid and does not provide individual medical advice and does not substitute for the advice of a qualified healthcare professional.  This platform does not cover all existing information related to the possible uses, directions, doses, precautions, warning, interactions, adverse effects, or risks associated with the medication discussed in the platform and is not intended as a substitute for the advice of a qualified healthcare professional. The materials contained in this platform are for informational purposes only and do not constitute or imply endorsement, recommendation, or favoring of this medication by NCODA, which assumes no liability for and does not ensure the accuracy of the information presented.  NCODA does not make any representations with respect to the medications whatsoever, and any and all decisions, with respect to such medications, are at the sole risk of the individual consuming the medication. All decisions related to taking this medication should be made with the guidance and under the direction of a qualified healthcare professional.
Read More

Written by: Dan Hertz, PharmD, PhD – University of Michigan College of Pharmacy

DOWNLOAD HERE

Description: The purpose of this PQI is to review recommendations for DPYD testing prior to initiation of treatment with fluoropyrimidine based chemotherapy and increase awareness of the clinical benefit of pre-treatment DPYD testing. 

Background: Fluoropyrimidine (5-fluorouracil or capecitabine) chemotherapy is highly effective for several solid tumor types, including colorectal and breast cancer. FP treatment is associated with substantial risk of severe toxicities including neutropenia, diarrhea, mucositis, and hand-foot syndrome that can cause hospitalization and death. Approximately 7% of patients carry pathogenic germline variants in DPYD, the gene encoding the DPD enzyme. These pathogenic variants reduce DPD activity and substantially increase risk of severe (>50%)1, 2 and sometimes fatal (2%-4%)3 toxicity. This increased toxicity risk is acknowledged in the FDA-approved drug labeling as well as in clinical practice guidelines published by the National Comprehensive Cancer Network (NCCN).4

The Clinical Pharmacogenetics Implementation Consortium (CPIC) assigned DPYD/fluoropyrimidines as Level A, indicating that “[DPYD] information should be used to change prescribing of [fluoropyrimidines],” and published consensus dosing recommendations based on DPYD genotype.5 Briefly, patients are assigned a DPD activity score (AS) based on their DPYD genotype, and the AS is used to determine whether the patient should receive standard or reduced dosing or should avoid FP treatment, if possible. Two prospective single-arm clinical trials have demonstrated that pre-treatment testing and DPYD-guided FP dose-reduction significantly reduces severe toxicity and overall healthcare costs.6, 7 The NCCN Guidelines for Colon Cancer acknowledge that pre-treatment DPYD testing has been demonstrated to reduce toxicity and be cost effective.4

Pre-treatment DPYD/DPD testing is recommended by the European Society of Medical Oncology (ESMO)8 and is standard of care throughout Europe. However, in the United States, pre-treatment testing has not been recommended by the FDA or by the NCCN4, and pre-treatment testing is not the prevailing standard of care. Nevertheless, based on the demonstrated clinical benefit, NCODA supports pre-treatment DPYD testing.

PQI Process:

Patient Centered Activities: The patient should be informed that:

  • Testing may take 5-10 days and may not be appropriate when there is an urgent need to start treatment as soon as possible
  • A positive DPYD test does not guarantee they will experience toxicity from standard FP dosing (risk of toxicity 50%-90%) and a negative test does not guarantee they will not experience toxicity (risk of toxicity ~30%)
  • The best available studies suggest that reduced dose chemotherapy in DPYD carriers should achieve treatment effectiveness similar to standard dosing in DPYD non-carriers; however, definitive studies have not been conducted
  • The dose may need to be re-adjusted after the first or second treatment based on whether they are tolerating treatment
  • Insurance coverage of pre-treatment DPYD testing varies by insurance provider and geographic region, and testing may have out of pocket costs of up to $300

Supplemental Section:

Recommended dosing of fluoropyrimidines (5-fluorouracil or capecitabine) by DPD phenotype

PhenotypeImplications for Phenotypic measuresDosing recommendationsClassification of recommendation
DPYD normal metabolizerNormal DPD activity and “normal” risk for fluoropyrimidine toxicity.

 

Based on genotype, there is no indication to change dose or therapy. Use label-recommended dosage and administration.

 

Strong
DPYD intermediate metabolizer

 

Decreased DPD activity (leukocyte DPD activity at 30% to 70% that of the normal population) and increased risk for severe or even fatal drug toxicity when treated with fluoropyrimidine drugs.

 

Reduce starting dose based on activity score followed by titration of dose based on toxicity or therapeutic drug monitoring (if available).

 

Activity score 1 or 1.5: Reduce dose by 50%

 

 

Activity score 1: Strong

 

Activity score 1.5: Moderate

 

DPYD poor metabolizer

 

Complete DPD deficiency and increased risk for severe or even fatal drug toxicity when treated with fluoropyrimidine drugs.

 

Activity score 0.5: Avoid use of 5-fluorouracil or 5-fluorouracil prodrug-based regimens. In the event, based on clinical advice, where alternative agents are not considered a suitable therapeutic option, 5-fluorouracil should be administered at a strongly reduced dose with early therapeutic drug monitoring.

 

Activity score 0: Avoid use of 5-fluorouracil or 5-fluorouracil prodrug-based regimens.

Strong

References:

  1. Lee AM, Shi Q, Pavey E, et al. DPYD variants as predictors of 5-fluorouracil toxicity in adjuvant colon cancer treatment (NCCTG N0147). J Natl Cancer Inst. 2014;106.
  2. Meulendijks D, Henricks LM, Sonke GS, et al. Clinical relevance of DPYD variants c.1679T>G, c.1236G>A/HapB3, and c.1601G>A as predictors of severe fluoropyrimidine-associated toxicity: a systematic review and meta-analysis of individual patient data. Lancet Oncol. 2015;16:1639-1650.
  3. Sharma BB, Rai K, Blunt H, Zhao W, Tosteson TD, Brooks GA. Pathogenic DPYD variants and treatment-related mortality in patients receiving fluoropyrimidine chemotherapy: A systematic review and meta-analysis. Oncologist. 2021;10:13967.
  4. Referenced from the NCCN Clinical Practice Guidelines in Oncology (NCCN Guidelines®) for Colon Cancer V.1.2015. © National Comprehensive Cancer Network, Inc 2014.  All rights reserved.  Accessed [August 22, 2014].  To view the most recent and complete version of the guideline, go online to www.nccn.org.  NATIONAL COMPREHENSIVE CANCER NETWORK®, NCCN®, NCCN GUIDELINES®, and all other NCCN Content are trademarks owned by the National Comprehensive Cancer Network, Inc.
  5. Amstutz U, Henricks LM, Offer SM, et al. Clinical Pharmacogenetics Implementation Consortium (CPIC) Guideline for Dihydropyrimidine Dehydrogenase Genotype and Fluoropyrimidine Dosing: 2017 Update. Clin Pharmacol Ther. 2018;103:210-216.
  6. Deenen MJ, Meulendijks D, Cats A, et al. Upfront Genotyping of DPYD*2A to Individualize Fluoropyrimidine Therapy: A Safety and Cost Analysis. J Clin Oncol. 2016;34:227-234.
  7. Henricks LM, Lunenburg C, de Man FM, et al. DPYD genotype-guided dose individualisation of fluoropyrimidine therapy in patients with cancer: a prospective safety analysis. Lancet Oncol. 2018;19:1459-1467.
  8. Argilés G, Tabernero J, Labianca R, et al. Localised colon cancer: ESMO Clinical Practice Guidelines for diagnosis, treatment and follow-up. Ann Oncol. 2020;31:1291-1305. doi: 1210.1016/j.annonc.2020.1206.1022. Epub 2020 Jul 1220.
Important notice: NCODA has developed this Positive Quality Intervention platform. This platform represents a brief summary of medication uses and therapy options derived from information provided by the drug manufacturer and other resources. This platform is intended as an educational aid and does not provide individual medical advice and does not substitute for the advice of a qualified healthcare professional.  This platform does not cover all existing information related to the possible uses, directions, doses, precautions, warning, interactions, adverse effects, or risks associated with the medication discussed in the platform and is not intended as a substitute for the advice of a qualified healthcare professional. The materials contained in this platform are for informational purposes only and do not constitute or imply endorsement, recommendation, or favoring of this medication by NCODA, which assumes no liability for and does not ensure the accuracy of the information presented.  NCODA does not make any representations with respect to the medications whatsoever, and any and all decisions, with respect to such medications, are at the sole risk of the individual consuming the medication. All decisions related to taking this medication should be made with the guidance and under the direction of a qualified healthcare professional.
Read More