Chemotherapy-induced nausea and vomiting (CINV) is a prevalent and distressing adverse effect of cancer chemotherapy that significantly reduces patients' quality of life and can be treatment-limiting. CINV is classified into acute (within 24 hours of chemotherapy), delayed (after 24 hours), and anticipatory (conditioned response before treatment) forms. The pathophysiology involves serotonin release from enterochromaffin cells activating vagal afferents via 5-HT3 receptors, substance P acting on NK1 receptors in the area postrema (chemoreceptor trigger zone), and central nervous system pathways. Modern antiemetic regimens combining 5-HT3 receptor antagonists, NK1 receptor antagonists, and corticosteroids can prevent vomiting in 70-80% of patients, though control of nausea remains suboptimal.
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name: Chemotherapy-Induced Nausea and Vomiting
creation_date: '2026-04-03T00:00:00Z'
updated_date: '2026-05-08T20:47:43Z'
category: Iatrogenic
description: >-
Chemotherapy-induced nausea and vomiting (CINV) is a prevalent and distressing
adverse effect of cancer chemotherapy that significantly reduces patients' quality
of life and can be treatment-limiting. CINV is classified into acute (within 24
hours
of chemotherapy), delayed (after 24 hours), and anticipatory (conditioned response
before treatment) forms. The pathophysiology involves serotonin release from
enterochromaffin cells activating vagal afferents via 5-HT3 receptors, substance
P
acting on NK1 receptors in the area postrema (chemoreceptor trigger zone), and
central nervous system pathways. Modern antiemetic regimens combining 5-HT3 receptor
antagonists, NK1 receptor antagonists, and corticosteroids can prevent vomiting
in
70-80% of patients, though control of nausea remains suboptimal.
parents:
- Gastrointestinal Disorder
- Drug Adverse Reaction
has_subtypes:
- name: Acute CINV
description: >-
Nausea and vomiting occurring within the first 24 hours after chemotherapy
administration. Primarily mediated by serotonin release from enterochromaffin
cells activating 5-HT3 receptors on vagal afferents.
evidence:
- reference: PMID:17208005
reference_title: "Comparative activity of antiemetic drugs."
supports: SUPPORT
snippet: >-
Chemotherapy-induced nausea and vomiting (CINV) are classified as acute,
occurring within the first 24h, or delayed, occurring after the first 24h.
explanation: >-
Directly defines the classification of acute CINV as occurring within the
first 24 hours after chemotherapy.
- name: Delayed CINV
description: >-
Nausea and vomiting occurring more than 24 hours after chemotherapy, often
lasting several days. Less well controlled by standard antiemetics and involves
substance P/NK1 receptor pathways.
evidence:
- reference: PMID:17208005
reference_title: "Comparative activity of antiemetic drugs."
supports: SUPPORT
snippet: >-
The pathophysiology of delayed emesis is less well understood, and multiple
mechanisms may contribute, including substance P.
explanation: >-
Identifies substance P as a contributor to delayed emesis pathophysiology
and notes that it is less well understood than acute emesis.
- name: Anticipatory CINV
description: >-
A conditioned response occurring before or during chemotherapy administration,
triggered by sensory cues associated with prior emetic episodes. Driven by
central nervous system conditioning rather than direct chemotherapy effects.
evidence:
- reference: PMID:30328690
reference_title: "Overview of the prevention and management of CINV."
supports: SUPPORT
snippet: >-
The different types of CINV (ie, acute, delayed, anticipatory, breakthrough,
and refractory) are controlled through various pathways and neurotransmitters,
so the pharmacologic approach to prevention and treatment varies based on the
type of CINV.
explanation: >-
Identifies anticipatory CINV as a distinct type controlled through different
pathways, supporting the classification.
pathophysiology:
- name: Serotonin Release from Enterochromaffin Cells
description: >-
Chemotherapy induces the release of serotonin (5-HT) from enterochromaffin
cells in the small intestinal mucosa. This serotonin activates 5-HT3 receptors
on vagal afferent neurons innervating the gastrointestinal tract, initiating
the emetic reflex. This is the primary mechanism driving acute CINV.
downstream:
- target: Vagal Afferent 5-HT3 Receptor Activation
description: >-
Released serotonin stimulates vagal afferent nerves via 5-HT3 receptors.
evidence:
- reference: PMID:1387926
reference_title: "Mechanism of the anti-emetic activity of 5-HT3 receptor antagonists."
supports: SUPPORT
snippet: >-
Evidence suggests that chemotherapy induces the release of 5-HT from
enterochromaffin cells in the small intestine. This stimulates vagal afferent
nerves via 5-HT3 receptors. Information is then relayed, via the vagus nerve,
to the central vomiting system.
explanation: >-
Directly describes the mechanistic link between enterochromaffin cell
serotonin release, vagal afferent stimulation, and relay to the central
vomiting system.
biological_processes:
- preferred_term: Serotonin secretion
term:
id: GO:0001820
label: serotonin secretion
modifier: INCREASED
cell_types:
- preferred_term: Enterochromaffin cell
term:
id: CL:0000577
label: type EC enteroendocrine cell
evidence:
- reference: PMID:1387926
reference_title: "Mechanism of the anti-emetic activity of 5-HT3 receptor antagonists."
supports: SUPPORT
snippet: >-
Evidence suggests that chemotherapy induces the release of 5-HT from
enterochromaffin cells in the small intestine.
explanation: >-
Establishes that chemotherapy triggers serotonin release from enterochromaffin
cells as a key initiating event in the emetic reflex.
- reference: PMID:29057666
reference_title: "Granisetron: a review of pharmacokinetics and clinical experience in chemotherapy induced - nausea and vomiting."
supports: SUPPORT
snippet: >-
Serotonin and substance P are the major neurotransmitters involved in the
pathophysiology of CINV
explanation: >-
Confirms serotonin as one of the two major neurotransmitters in CINV
pathophysiology.
- name: Vagal Afferent 5-HT3 Receptor Activation
description: >-
Serotonin released by enterochromaffin cells activates 5-HT3 receptors on vagal
afferent neurons innervating the gastrointestinal tract. Signals are relayed via
the vagus nerve to the central vomiting system, initiating the emetic reflex.
downstream:
- target: Central Emetic Signaling via Area Postrema
description: >-
Vagal afferent signals are relayed to the hindbrain vomiting center, where the
area postrema provides a second site of 5-HT3 receptor-mediated activation.
biological_processes:
- preferred_term: Chemical synaptic transmission
term:
id: GO:0007268
label: chemical synaptic transmission
cell_types:
- preferred_term: Vagal afferent sensory neuron
term:
id: CL:0000101
label: sensory neuron
evidence:
- reference: PMID:1387926
reference_title: "Mechanism of the anti-emetic activity of 5-HT3 receptor antagonists."
supports: SUPPORT
snippet: >-
Ondansetron, a potent and highly selective 5-HT3 receptor antagonist, prevents
emesis following chemotherapy by antagonising the action of 5-hydroxytryptamine
(5-HT) at 5-HT3 receptors on vagal afferent neurons that innervate the
gastrointestinal tract and 5-HT3 receptors in the central vomiting system.
explanation: >-
Describes 5-HT3 receptor activation on vagal afferent neurons as the peripheral
mechanism of emesis following chemotherapy.
- name: Central Emetic Signaling via Area Postrema
description: >-
The area postrema (chemoreceptor trigger zone) in the hindbrain contains 5-HT3
receptors, providing a second central site for emetic activation. This area lies
outside the blood-brain barrier and integrates peripheral and central emetic inputs.
downstream:
- target: Substance P/NK1 Receptor Signaling
description: >-
Prolonged emetic signaling involves substance P acting on NK1 receptors,
contributing especially to delayed CINV.
biological_processes:
- preferred_term: Signal transduction
term:
id: GO:0007165
label: signal transduction
evidence:
- reference: PMID:1387926
reference_title: "Mechanism of the anti-emetic activity of 5-HT3 receptor antagonists."
supports: SUPPORT
snippet: >-
5-HT3 receptors are also found in the hind-brain vomiting system including
the area postrema (the site of the chemoreceptor trigger zone for emesis).
Therefore, following chemotherapy, 5-HT activates 5-HT3 receptors at 2 sites
to induce emesis.
explanation: >-
Identifies the area postrema/chemoreceptor trigger zone as a second site where
5-HT3 receptor activation drives emesis.
- name: Substance P/NK1 Receptor Signaling
description: >-
Substance P acting on neurokinin-1 (NK1) receptors contributes to the emetic
response, particularly in delayed CINV. This pathway is distinct from the
serotonin-mediated acute phase and is targeted by NK1 receptor antagonists
such as aprepitant.
evidence:
- reference: PMID:17208005
reference_title: "Comparative activity of antiemetic drugs."
supports: SUPPORT
snippet: >-
The development of acute emesis is known to depend on serotonin. The
pathophysiology of delayed emesis is less well understood, and multiple
mechanisms may contribute, including substance P.
explanation: >-
Identifies substance P as a key contributor to delayed emesis, distinct from
the serotonin-dependent acute phase.
- reference: PMID:29057666
reference_title: "Granisetron: a review of pharmacokinetics and clinical experience in chemotherapy induced - nausea and vomiting."
supports: SUPPORT
snippet: >-
Serotonin and substance P are the major neurotransmitters involved in the
pathophysiology of CINV
explanation: >-
Confirms substance P as one of the two major neurotransmitters in CINV.
phenotypes:
- category: Gastrointestinal
name: Nausea
frequency: VERY_FREQUENT
description: >-
Persistent sensation of stomach discomfort and urge to vomit, often the most
distressing symptom for patients. Control of nausea remains suboptimal even
with modern antiemetic therapy.
evidence:
- reference: PMID:17208005
reference_title: "Comparative activity of antiemetic drugs."
supports: SUPPORT
snippet: >-
With modern antiemetic therapy, vomiting can be prevented in 70-80% of
patients, whereas the control of nausea remains suboptimal.
explanation: >-
Highlights that nausea is highly prevalent and more difficult to control
than vomiting in CINV.
phenotype_term:
preferred_term: Nausea
term:
id: HP:0002018
label: Nausea
- category: Gastrointestinal
name: Vomiting
frequency: VERY_FREQUENT
description: >-
Forceful expulsion of stomach contents, which can be acute (within 24 hours),
delayed (after 24 hours), or anticipatory (conditioned response). Can lead
to dehydration, electrolyte imbalance, and nutritional compromise.
evidence:
- reference: PMID:17208005
reference_title: "Comparative activity of antiemetic drugs."
supports: SUPPORT
snippet: >-
Nausea and vomiting continues to be an important problem for cancer patients
receiving chemotherapy.
explanation: >-
Confirms vomiting as a major problem for chemotherapy patients.
phenotype_term:
preferred_term: Vomiting
term:
id: HP:0002013
label: Vomiting
- category: Constitutional
name: Poor Appetite
frequency: FREQUENT
description: >-
Decreased appetite and food intake commonly accompany CINV, contributing to
weight loss and nutritional compromise during cancer treatment.
phenotype_term:
preferred_term: Poor appetite
term:
id: HP:0004396
label: Poor appetite
- category: Constitutional
name: Dehydration
frequency: OCCASIONAL
description: >-
Fluid loss from persistent vomiting can lead to dehydration and electrolyte
imbalances, occasionally requiring hospitalization for intravenous fluid
replacement.
phenotype_term:
preferred_term: Dehydration
term:
id: HP:0001944
label: Dehydration
treatments:
- name: 5-HT3 Receptor Antagonists
description: >-
First-line antiemetics (ondansetron, granisetron, palonosetron) that block
serotonin action at 5-HT3 receptors on vagal afferents and in the area postrema.
Highly effective for acute CINV prevention, typically co-administered with
dexamethasone and NK1 antagonists for highly emetogenic chemotherapy.
evidence:
- reference: PMID:1387926
reference_title: "Mechanism of the anti-emetic activity of 5-HT3 receptor antagonists."
supports: SUPPORT
snippet: >-
Ondansetron, a potent and highly selective 5-HT3 receptor antagonist, prevents
emesis following chemotherapy by antagonising the action of 5-hydroxytryptamine
(5-HT) at 5-HT3 receptors on vagal afferent neurons that innervate the
gastrointestinal tract and 5-HT3 receptors in the central vomiting system.
explanation: >-
Describes the mechanism by which 5-HT3 antagonists prevent chemotherapy-induced
emesis by blocking receptors at peripheral and central sites.
- reference: PMID:29057666
reference_title: "Granisetron: a review of pharmacokinetics and clinical experience in chemotherapy induced - nausea and vomiting."
supports: SUPPORT
snippet: >-
According to current literature, granisetron 2 mg orally or 0,01mg/kg (1 mg)
intravenously per day, co-administered with dexamethasone and NK-1 antagonists
is the recommended regime for highly emetogenic chemotherapy.
explanation: >-
Confirms 5-HT3 antagonist granisetron as part of the recommended triple
antiemetic regimen for highly emetogenic chemotherapy.
treatment_term:
preferred_term: 5-HT3 receptor antagonist therapy
term:
id: NCIT:C15986
label: Pharmacotherapy
- name: NK1 Receptor Antagonists
description: >-
Aprepitant, fosaprepitant, and netupitant block substance P binding to
neurokinin-1 receptors, providing benefit particularly for delayed CINV.
Used in combination with 5-HT3 antagonists and corticosteroids.
evidence:
- reference: PMID:28235999
reference_title: "Concise review of the management of iatrogenic emesis using cannabinoids: emphasis on nabilone for chemotherapy-induced nausea and vomiting."
supports: SUPPORT
snippet: >-
Despite seemingly numerous options, such as antimuscarinic anticholinergics,
antihistamines, 5-HT3 receptor antagonists, dopamine receptor antagonists, and
neurokinin-1 receptor antagonists, preventative therapies are often inadequately
effective, particularly for "delayed CINV"-leaving an important unmet clinical
need.
explanation: >-
Lists NK1 receptor antagonists among established antiemetic options while noting
that delayed CINV remains an unmet need.
- reference: PMID:17208005
reference_title: "Comparative activity of antiemetic drugs."
supports: SUPPORT
snippet: >-
A number of antiemetic agents are available for the management of nausea and
vomiting, including 5-HT3-receptor-antagonists, corticosteroids,
NK-1-receptor-antagonists, dopamine-receptor antagonists, benzodiazepines,
neuroleptics and cannabinoids.
explanation: >-
Confirms NK1 receptor antagonists as an established class of antiemetic agents.
treatment_term:
preferred_term: NK1 receptor antagonist therapy
term:
id: NCIT:C15986
label: Pharmacotherapy
- name: Corticosteroids
description: >-
Dexamethasone is a key component of antiemetic regimens, providing synergistic
benefit when combined with 5-HT3 and NK1 antagonists. Effective for both acute
and delayed CINV.
evidence:
- reference: PMID:29057666
reference_title: "Granisetron: a review of pharmacokinetics and clinical experience in chemotherapy induced - nausea and vomiting."
supports: SUPPORT
snippet: >-
granisetron 2 mg orally or 0,01mg/kg (1 mg) intravenously per day,
co-administered with dexamethasone and NK-1 antagonists is the recommended
regime for highly emetogenic chemotherapy.
explanation: >-
Confirms dexamethasone as part of the recommended triple antiemetic regimen.
treatment_term:
preferred_term: corticosteroid therapy
term:
id: NCIT:C122080
label: Systemic Corticosteroid Therapy
- name: Cannabinoid-Based Antiemetics
description: >-
Synthetic cannabinoid receptor agonists (nabilone, dronabinol) are approved
for treatment of CINV. Nabilone is superior to placebo and prochlorperazine
but does not add benefit beyond 5-HT3 receptor antagonists. These agents offer
a useful additional option particularly when standard antiemetics are inadequate,
though side effects including euphoria, drowsiness, and dizziness are more
frequent than with conventional antiemetics.
notes: >-
Cannabis and cannabinoid-based therapies have been used for decades to manage
CINV. While synthetic cannabinoids like nabilone are FDA-approved for this
indication, the role of botanical cannabis remains an area of active debate.
Cannabinoid receptor agonists act through a unique mechanism distinct from
5-HT3 and NK1 antagonists. However, they have been underutilized historically
due to legal restrictions and the notoriety of marijuana. Current evidence
suggests they are most useful as adjunctive or rescue therapy rather than
first-line treatment, as they do not add benefit to 5-HT3 antagonist-based
regimens.
evidence:
- reference: PMID:28235999
reference_title: "Concise review of the management of iatrogenic emesis using cannabinoids: emphasis on nabilone for chemotherapy-induced nausea and vomiting."
supports: SUPPORT
snippet: >-
Cannabinoid receptor agonists, by virtue of their unique mechanism of action
and efficacy and safety data reported in clinical trials, appear to offer a
useful additional option.
explanation: >-
Supports the role of cannabinoid receptor agonists as a useful additional
antiemetic option based on clinical trial data.
- reference: PMID:28235999
reference_title: "Concise review of the management of iatrogenic emesis using cannabinoids: emphasis on nabilone for chemotherapy-induced nausea and vomiting."
supports: SUPPORT
snippet: >-
The mechanistic value of cannabinoids has been well known for many years, but
these agents may have been underutilized in the past because of the notoriety
and legal status of marijuana.
explanation: >-
Notes the historical underutilization of cannabinoids despite established
efficacy, due to legal and social factors.
- reference: PMID:18095921
reference_title: "Oral nabilone capsules in the treatment of chemotherapy-induced nausea and vomiting and pain."
supports: SUPPORT
snippet: >-
Nabilone is superior to placebo, domperidone and prochlorperazine but not
metoclopramide or chlorpromazine. Cannabinoids do not add to benefits of
5-HT(3) receptor antagonists.
explanation: >-
Establishes that nabilone is effective compared to placebo and some conventional
antiemetics, but does not augment 5-HT3 antagonist efficacy.
- reference: PMID:18095921
reference_title: "Oral nabilone capsules in the treatment of chemotherapy-induced nausea and vomiting and pain."
supports: SUPPORT
snippet: >-
Side effects are greater for nabilone than for prochlorperazine, in most
studies patients prefered nabilone over prochlorperazine.
explanation: >-
Notes that while nabilone has more side effects than conventional antiemetics,
patients tend to prefer it, suggesting better subjective antiemetic control.
treatment_term:
preferred_term: cannabinoid antiemetic therapy
term:
id: NCIT:C15986
label: Pharmacotherapy
notes: >-
The prevention of CINV is critically important both for reducing morbidity and
healthcare costs. Multiple CINV types (acute, delayed, anticipatory, breakthrough,
refractory) are controlled through different pathways and neurotransmitters,
requiring tailored pharmacologic approaches. With modern triple antiemetic therapy
(5-HT3 antagonist + NK1 antagonist + dexamethasone), vomiting can be prevented
in 70-80% of patients, but nausea control remains suboptimal. Cannabinoid-based
antiemetics (nabilone, dronabinol) are approved for CINV and offer a unique
mechanism of action, but current evidence does not support their use as first-line
therapy over established 5-HT3/NK1 antagonist regimens.
references:
- reference: DOI:10.1007/s00520-023-08220-5
title: Emetic risk classification and evaluation of the emetogenicity of antineoplastic agents—updated MASCC/ESMO consensus recommendation
found_in:
- Chemotherapy_Induced_Nausea_and_Vomiting-deep-research-falcon.md
findings:
- statement: Our goal was to identify new anticancer agents approved by the US Food and Drug Administration (FDA) and the European Medical Agency (EMA) since the 2016 MASCC/ESMO antiemetic update and classify their emetic potential.
supporting_text: Our goal was to identify new anticancer agents approved by the US Food and Drug Administration (FDA) and the European Medical Agency (EMA) since the 2016 MASCC/ESMO antiemetic update and classify their emetic potential.
evidence:
- reference: DOI:10.1007/s00520-023-08220-5
reference_title: Emetic risk classification and evaluation of the emetogenicity of antineoplastic agents—updated MASCC/ESMO consensus recommendation
supports: SUPPORT
evidence_source: OTHER
snippet: Our goal was to identify new anticancer agents approved by the US Food and Drug Administration (FDA) and the European Medical Agency (EMA) since the 2016 MASCC/ESMO antiemetic update and classify their emetic potential.
explanation: Deep research cited this publication as relevant literature for Chemotherapy Induced Nausea and Vomiting.
- reference: DOI:10.1007/s00520-023-08221-4
title: '2023 updated MASCC/ESMO consensus recommendations: prevention of nausea and vomiting following high-emetic-risk antineoplastic agents'
found_in:
- Chemotherapy_Induced_Nausea_and_Vomiting-deep-research-falcon.md
findings:
- statement: This systematic review updates the MASCC/ESMO recommendations for high-emetic-risk chemotherapy (HEC) published in 2016–2017.
supporting_text: This systematic review updates the MASCC/ESMO recommendations for high-emetic-risk chemotherapy (HEC) published in 2016–2017.
evidence:
- reference: DOI:10.1007/s00520-023-08221-4
reference_title: '2023 updated MASCC/ESMO consensus recommendations: prevention of nausea and vomiting following high-emetic-risk antineoplastic agents'
supports: SUPPORT
evidence_source: OTHER
snippet: This systematic review updates the MASCC/ESMO recommendations for high-emetic-risk chemotherapy (HEC) published in 2016–2017.
explanation: Deep research cited this publication as relevant literature for Chemotherapy Induced Nausea and Vomiting.
- reference: DOI:10.1007/s00520-023-08224-1
title: '2023 updated MASCC/ESMO consensus recommendations: prevention of nausea and vomiting following multiple-day chemotherapy, high-dose chemotherapy, and breakthrough nausea and vomiting'
found_in:
- Chemotherapy_Induced_Nausea_and_Vomiting-deep-research-falcon.md
findings:
- statement: This review is an update of the MASCC/ESMO 2015 recommendations for the prophylaxis of acute and delayed nausea and vomiting induced by multiple-day chemotherapy, high-dose chemotherapy, and breakthrough nausea and vomiting.
supporting_text: This review is an update of the MASCC/ESMO 2015 recommendations for the prophylaxis of acute and delayed nausea and vomiting induced by multiple-day chemotherapy, high-dose chemotherapy, and breakthrough nausea and vomiting.
evidence:
- reference: DOI:10.1007/s00520-023-08224-1
reference_title: '2023 updated MASCC/ESMO consensus recommendations: prevention of nausea and vomiting following multiple-day chemotherapy, high-dose chemotherapy, and breakthrough nausea and vomiting'
supports: SUPPORT
evidence_source: OTHER
snippet: This review is an update of the MASCC/ESMO 2015 recommendations for the prophylaxis of acute and delayed nausea and vomiting induced by multiple-day chemotherapy, high-dose chemotherapy, and breakthrough nausea and vomiting.
explanation: Deep research cited this publication as relevant literature for Chemotherapy Induced Nausea and Vomiting.
- reference: DOI:10.1007/s00520-024-08939-9
title: 'Antiemetic medications for preventing chemotherapy-induced nausea and vomiting in children: a systematic review and Bayesian network meta-analysis'
found_in:
- Chemotherapy_Induced_Nausea_and_Vomiting-deep-research-falcon.md
findings:
- statement: Children continue to experience chemotherapy-induced nausea and vomiting (CINV), despite effective antiemetic medications.
supporting_text: Children continue to experience chemotherapy-induced nausea and vomiting (CINV), despite effective antiemetic medications.
evidence:
- reference: DOI:10.1007/s00520-024-08939-9
reference_title: 'Antiemetic medications for preventing chemotherapy-induced nausea and vomiting in children: a systematic review and Bayesian network meta-analysis'
supports: SUPPORT
evidence_source: HUMAN_CLINICAL
snippet: Children continue to experience chemotherapy-induced nausea and vomiting (CINV), despite effective antiemetic medications.
explanation: Deep research cited this publication as relevant literature for Chemotherapy Induced Nausea and Vomiting.
- reference: DOI:10.1007/s12254-025-01098-5
title: Antiemetic therapy
found_in:
- Chemotherapy_Induced_Nausea_and_Vomiting-deep-research-falcon.md
findings:
- statement: Chemotherapy-induced nausea and vomiting (CINV) remains one of the most distressing adverse effects of antineoplastic therapy despite major advances in antiemetic management.
supporting_text: Chemotherapy-induced nausea and vomiting (CINV) remains one of the most distressing adverse effects of antineoplastic therapy despite major advances in antiemetic management.
evidence:
- reference: DOI:10.1007/s12254-025-01098-5
reference_title: Antiemetic therapy
supports: SUPPORT
evidence_source: OTHER
snippet: Chemotherapy-induced nausea and vomiting (CINV) remains one of the most distressing adverse effects of antineoplastic therapy despite major advances in antiemetic management.
explanation: Deep research cited this publication as relevant literature for Chemotherapy Induced Nausea and Vomiting.
- reference: DOI:10.1186/s40780-023-00293-y
title: 'Olanzapine treatment effectively relieves breakthrough chemotherapy-induced nausea and vomiting: a real-world experience'
found_in:
- Chemotherapy_Induced_Nausea_and_Vomiting-deep-research-falcon.md
findings:
- statement: Olanzapine treatment prevents chemotherapy-induced nausea and vomiting (CINV) in patients receiving highly emetogenic chemotherapy (HEC).
supporting_text: Olanzapine treatment prevents chemotherapy-induced nausea and vomiting (CINV) in patients receiving highly emetogenic chemotherapy (HEC).
evidence:
- reference: DOI:10.1186/s40780-023-00293-y
reference_title: 'Olanzapine treatment effectively relieves breakthrough chemotherapy-induced nausea and vomiting: a real-world experience'
supports: SUPPORT
evidence_source: HUMAN_CLINICAL
snippet: Olanzapine treatment prevents chemotherapy-induced nausea and vomiting (CINV) in patients receiving highly emetogenic chemotherapy (HEC).
explanation: Deep research cited this publication as relevant literature for Chemotherapy Induced Nausea and Vomiting.
- reference: DOI:10.1186/s40780-024-00403-4
title: Pharmacist intervention and identification of adverse events related to treatment efficacy in cancer chemotherapy to improve clinical outcomes
found_in:
- Chemotherapy_Induced_Nausea_and_Vomiting-deep-research-falcon.md
findings:
- statement: Adverse events (AEs) induced by cancer chemotherapy reduce not only patient quality of life (QOL) but also the efficacy of treatment.
supporting_text: Adverse events (AEs) induced by cancer chemotherapy reduce not only patient quality of life (QOL) but also the efficacy of treatment.
evidence:
- reference: DOI:10.1186/s40780-024-00403-4
reference_title: Pharmacist intervention and identification of adverse events related to treatment efficacy in cancer chemotherapy to improve clinical outcomes
supports: SUPPORT
evidence_source: HUMAN_CLINICAL
snippet: Adverse events (AEs) induced by cancer chemotherapy reduce not only patient quality of life (QOL) but also the efficacy of treatment.
explanation: Deep research cited this publication as relevant literature for Chemotherapy Induced Nausea and Vomiting.
- reference: DOI:10.18203/2320-6012.ijrms20251304
title: A retrospective drug utilization study in chemotherapy-induced nausea and vomiting
found_in:
- Chemotherapy_Induced_Nausea_and_Vomiting-deep-research-falcon.md
findings:
- statement: Chemotherapy-induced nausea and vomiting (CINV) significantly impacts patients' quality of life.
supporting_text: Chemotherapy-induced nausea and vomiting (CINV) significantly impacts patients' quality of life.
evidence:
- reference: DOI:10.18203/2320-6012.ijrms20251304
reference_title: A retrospective drug utilization study in chemotherapy-induced nausea and vomiting
supports: SUPPORT
evidence_source: HUMAN_CLINICAL
snippet: Chemotherapy-induced nausea and vomiting (CINV) significantly impacts patients' quality of life.
explanation: Deep research cited this publication as relevant literature for Chemotherapy Induced Nausea and Vomiting.
CINV is a common, distressing adverse effect of antineoplastic therapy characterized by nausea and/or vomiting that occurs temporally in relation to chemotherapy exposure, with clinically relevant subtypes defined by timing and response to prophylaxis. Acute CINV occurs in the first 24 hours, delayed CINV occurs from 24–120 hours, and some sources additionally describe long-delayed/persistent symptoms beyond 120 hours; these later phases remain a major clinical challenge. (jeryczynski2026antiemetictherapy pages 1-2)
Definitions supported by guideline and expert consensus sources include: - Acute CINV: within 0–24 h after chemotherapy. (jeryczynski2026antiemetictherapy pages 1-2, uchiike2023olanzapinetreatmenteffectively pages 1-2) - Delayed CINV: 24–120 h after chemotherapy; one consensus also highlights a common window of 24–72 h. (jeryczynski2026antiemetictherapy pages 1-2, montes2026ttdexpertconsensus pages 3-5) - Long-delayed/persistent CINV: >120 h after chemotherapy. (jeryczynski2026antiemetictherapy pages 1-2) - Anticipatory CINV: conditioned response occurring before treatment (linked to prior negative experiences). (montes2026ttdexpertconsensus pages 3-5, dhabhar2025expertconsensusguidance pages 5-6) - Breakthrough CINV: nausea/vomiting occurring despite guideline-directed prophylaxis; MASCC/ESMO explicitly defines it as occurring “during chemotherapy regardless of prophylaxis with guideline-directed antiemetics.” (rapoport20242023updatedmasccesmo pages 5-6) - Refractory CINV: symptoms recurring in subsequent cycles despite management in prior cycles. (montes2026ttdexpertconsensus pages 3-5)
A structured subtype table with suggested HPO mappings is provided in Artifact 00.
| Phenotype/subtype | Definition/time window | Putative dominant mediator(s) | Suggested HPO term(s) |
|---|---|---|---|
| Acute CINV | Nausea/vomiting occurring within 0–24 h after chemotherapy; may peak at ~5–6 h (jeryczynski2026antiemetictherapy pages 1-2, montes2026ttdexpertconsensus pages 3-5) | Predominantly serotonin signaling via 5-HT3 receptors (montes2026ttdexpertconsensus pages 3-5) | Nausea (HP:0002018); Vomiting (HP:0002013) |
| Delayed CINV | Nausea/vomiting occurring 24–120 h after chemotherapy; Montes notes delayed phase commonly 24–72 h (jeryczynski2026antiemetictherapy pages 1-2, montes2026ttdexpertconsensus pages 3-5) | Predominantly substance P signaling via NK1 receptors (montes2026ttdexpertconsensus pages 3-5) | Nausea (HP:0002018); Vomiting (HP:0002013) |
| Long-delayed / persistent CINV | Symptoms persisting beyond 120 h after chemotherapy (jeryczynski2026antiemetictherapy pages 1-2) | Not specifically assigned in provided snippets; likely mixed/uncertain | Nausea (HP:0002018) candidate; Vomiting (HP:0002013) candidate |
| Anticipatory CINV | Conditioned nausea/vomiting occurring before treatment, typically in anticipation of chemotherapy (montes2026ttdexpertconsensus pages 3-5) | Conditioned/behavioral response; specific neurotransmitter not defined in provided snippets | Nausea (HP:0002018) candidate; Vomiting (HP:0002013) candidate; Anticipatory nausea candidate |
| Breakthrough CINV | Nausea/vomiting occurring despite guideline-directed prophylaxis during/after chemotherapy; one source also describes it as arising beyond the fifth day despite prophylaxis (rapoport20242023updatedmasccesmo pages 5-6, montes2026ttdexpertconsensus pages 3-5) | Not specifically assigned in provided snippets; likely mixed/uncertain | Nausea (HP:0002018) candidate; Vomiting (HP:0002013) candidate; Breakthrough vomiting candidate |
| Refractory CINV | Nausea/vomiting occurring in subsequent chemotherapy cycles despite prior antiemetic management (montes2026ttdexpertconsensus pages 3-5) | Not specifically assigned in provided snippets; likely mixed/uncertain | Nausea (HP:0002018) candidate; Vomiting (HP:0002013) candidate; Refractory nausea/vomiting candidate |
Table: This table summarizes the clinically recognized temporal and response-pattern subtypes of chemotherapy-induced nausea and vomiting, along with the dominant mediators supported by the cited evidence. It also suggests best-effort HPO mappings for structured phenotype annotation.
CINV is caused by chemotherapy-triggered activation of peripheral and central emetic pathways, including gastrointestinal mucosal injury with neurotransmitter release and central chemoreceptor trigger zone/vomiting center activation. (aher2025aretrospectivedrug pages 1-3, montes2026ttdexpertconsensus pages 3-5)
Emetogenicity of the antineoplastic regimen is a key determinant. - High-emetic-risk chemotherapy (HEC) is defined as >90% risk of vomiting in the first 24 h without prophylaxis and includes cisplatin and the anthracycline–cyclophosphamide (AC) combination (in women with breast cancer), among others. (herrstedt20242023updatedmasccesmo pages 1-2) - MASCC/ESMO updated the classification of newer antineoplastic agents (FDA/EMA approvals 2015–2023), revising oral-agent classification to two categories (minimal–low vs moderate–high) to align with ASCO, while retaining the four-category schema for IV agents; the panel emphasized large heterogeneity and imprecision for oral agents. (jordan2024emeticriskclassification pages 1-2)
Expert consensus and meta-analytic evidence highlight: - Female sex and younger age (e.g., <50) as major risk factors. (montes2026ttdexpertconsensus pages 3-5) - Prior CINV predicting subsequent cycles; MASCC/ESMO notes prior history significantly predicts later-cycle CINV. (rapoport20242023updatedmasccesmo pages 5-6) - History of pregnancy emesis and motion sickness as additional risk factors. (montes2026ttdexpertconsensus pages 3-5) - Anxiety and fatigue as risk factors in platinum-based chemotherapy meta-analysis (OR 1.689 and OR 1.413, respectively). (suzukichiba2024comparisonofolanzapine pages 5-7)
A clinically relevant pharmacogenomic point is that CYP2D6 ultra-rapid metabolizers may be undertreated with standard 5-HT3 receptor antagonist dosing, implying reduced antiemetic efficacy for some patients. (montes2026ttdexpertconsensus pages 3-5)
Concomitant exposures and clinical context can modulate risk, including opioids/NSAIDs and radiotherapy site/dose. (montes2026ttdexpertconsensus pages 3-5)
Protective “factors” are largely iatrogenic/behavioral (preventive pharmacotherapy and implementation): - Guideline-concordant primary prophylaxis (prophylaxis before chemotherapy rather than rescue) is emphasized as key for preventing CINV and reducing later problems such as anticipatory CINV. (jeryczynski2026antiemetictherapy pages 1-2, dhabhar2025expertconsensusguidance pages 5-6)
A structured risk/protective/implementation table is provided in Artifact 02.
| Category | Factor or metric | Effect/notes | Population/setting | Source context IDs |
|---|---|---|---|---|
| Risk | High emetogenic chemotherapy (HEC) | Defined as >90% risk of vomiting within 24 h without prophylaxis; includes cisplatin, carmustine, dacarbazine, mechlorethamine, streptozocin, high-dose cyclophosphamide, and anthracycline-cyclophosphamide in women with breast cancer | Guideline classification for IV antineoplastic agents | (herrstedt20242023updatedmasccesmo pages 1-2) |
| Risk | Moderate/low/minimal emetogenicity classification | IV agents remain classified in 4 categories; oral agents revised to 2 categories (minimal-low, moderate-high); emetogenicity for oral agents is less precise and heterogeneous across studies | MASCC/ESMO emetogenicity classification update | (jordan2024emeticriskclassification pages 1-2, jordan2024emeticriskclassification pages 4-5) |
| Risk | Female sex | Repeatedly identified as a major patient-related risk factor for CINV; meta-analysis in platinum-treated patients found OR 2.363 (95% CI 1.363-4.096) | General CINV risk; platinum-based chemotherapy | (montes2026ttdexpertconsensus pages 3-5, suzukichiba2024comparisonofolanzapine pages 5-7) |
| Risk | Younger age / age <50 | Reported as a risk factor in expert guidance and risk models; younger age is repeatedly incorporated into prediction tools | General adult oncology populations | (montes2026ttdexpertconsensus pages 3-5, suzukichiba2024comparisonofolanzapine pages 5-7) |
| Risk | Prior CINV / prior vomiting during chemotherapy | Strong predictor of subsequent-cycle CINV; prior history significantly predicts later-cycle events; history of vomiting during chemotherapy OR 2.728 in platinum meta-analysis | Subsequent chemotherapy cycles; platinum-based chemotherapy | (rapoport20242023updatedmasccesmo pages 5-6, suzukichiba2024comparisonofolanzapine pages 5-7) |
| Risk | History of pregnancy-related emesis | Listed as a patient-related risk factor | General CINV risk assessment | (montes2026ttdexpertconsensus pages 3-5) |
| Risk | Motion sickness history | Listed as a patient-related risk factor; platinum meta-analysis OR 1.816 (95% CI 1.266-2.605) | General and platinum-based chemotherapy | (montes2026ttdexpertconsensus pages 3-5, suzukichiba2024comparisonofolanzapine pages 5-7) |
| Risk | Anxiety | Included in risk models and meta-analysis; platinum meta-analysis OR 1.689 (95% CI 1.057-2.700) | General and platinum-based chemotherapy | (suzukichiba2024comparisonofolanzapine pages 5-7) |
| Risk | Fatigue | Associated with increased platinum-related CINV risk; meta-analysis OR 1.413 (95% CI 1.145-1.744) | Platinum-based chemotherapy | (suzukichiba2024comparisonofolanzapine pages 5-7) |
| Risk | Concomitant opioids, NSAIDs, radiotherapy site/dose | Co-medications and concomitant radiotherapy may increase emesis burden and modify risk | Clinical practice risk stratification | (montes2026ttdexpertconsensus pages 3-5) |
| Risk | Gastric mucosa retained / no gastrectomy | Review notes gastric mucosa as a primary site of toxicity and that patients without gastrectomy may have higher symptom burden | Gastric cancer/supportive care context | (jeryczynski2026antiemetictherapy pages 1-2) |
| Risk | CYP2D6 ultrarapid metabolizer status | Pharmacogenomic risk factor: may be undertreated with standard 5-HT3 receptor antagonist dosing, implying reduced efficacy in some patients | Precision antiemetic selection / dosing consideration | (montes2026ttdexpertconsensus pages 3-5) |
| Protective | Lower-risk chemotherapy regimens | Receiving lower or minimal emetogenic regimens confers lower baseline CINV risk compared with HEC/MEC | Regimen-level protection by exposure class | (jeryczynski2026antiemetictherapy pages 1-2, jordan2024emeticriskclassification pages 1-2) |
| Protective | Guideline-concordant primary prophylaxis | Prevention before chemotherapy is emphasized as superior to rescue; using recommended 5-HT3 RA/NK1 RA/dexamethasone/olanzapine combinations reduces CINV burden | Across emetogenic risk groups, especially HEC and multiple-day cisplatin | (jeryczynski2026antiemetictherapy pages 1-2, herrstedt20242023updatedmasccesmo pages 1-2, rapoport20242023updatedmasccesmo pages 5-6, herrstedt20242023updatedmasccesmo media aa8b3b03) |
| Protective | Optimal control in cycle 1 | Good control of acute/delayed CINV in the first cycle may help prevent anticipatory CINV in later cycles | Longitudinal supportive care strategy | (dhabhar2025expertconsensusguidance pages 5-6) |
| Implementation | Guideline-consistent prophylaxis use | Review reports only ~50% guideline-consistent use in more recent real-world data; older studies showed only 11-29% appropriate prophylaxis | Real-world oncology practice | (jeryczynski2026antiemetictherapy pages 1-2) |
| Implementation | Physician risk-factor assessment gaps | 11% of surveyed oncologists did not discuss additional personal CINV risk factors with patients | Multinational THRIVE survey, 446 patients | (jeryczynski2026antiemetictherapy pages 1-2) |
| Implementation | MEC prophylaxis underuse of NK1 RA | In patients with additional risk factors on MEC, 39% of surveyed physicians did not include an NK1 RA | Multinational THRIVE survey | (jeryczynski2026antiemetictherapy pages 1-2) |
| Implementation | Delayed CINV assessment gap | 35% of physicians relied only on spontaneous patient reports for delayed CINV assessment | Multinational THRIVE survey | (jeryczynski2026antiemetictherapy pages 1-2) |
| Implementation | Pharmacist intervention | Improved adherence to prophylaxis pharmacotherapy and significantly decreased CINV incidence after pharmacist intervention | Practice-improvement / supportive oncology programs | (suzukichiba2024comparisonofolanzapine pages 1-2) |
| Effectiveness | Breakthrough CINV prevalence despite prophylaxis | Guideline review cites a prospective Japanese multicenter study in which almost half of 1,910 patients experienced breakthrough nausea/vomiting despite prophylactic antiemetics | Patients receiving MEC or HEC | (rapoport20242023updatedmasccesmo pages 5-6) |
| Effectiveness | Olanzapine for breakthrough CINV: overall response | In 127 real-world patients, olanzapine 2.5/5/10 mg/day improved symptoms in 83% and achieved complete response in 33% | Retrospective real-world breakthrough CINV cohort | (uchiike2023olanzapinetreatmenteffectively pages 1-2) |
| Effectiveness | Olanzapine for breakthrough CINV: adverse effects | 27% had olanzapine-related adverse events, mainly somnolence; no grade >=3 adverse events observed | Same breakthrough cohort | (uchiike2023olanzapinetreatmenteffectively pages 1-2) |
| Effectiveness | Olanzapine dose comparison in prophylaxis | Nationwide Japanese database study found 2.5 mg associated with more additional antiemetic use than 5 mg (36% vs 31%, p<0.001) | Patients with lung cancer receiving HEC | (suzukichiba2024comparisonofolanzapine pages 2-4) |
| Effectiveness | Dexamethasone-sparing in AC chemotherapy | Network meta-analysis found essentially no difference in delayed-phase complete response between multiple vs single dexamethasone doses when combined with palonosetron and NK1 RA (difference 0.1%, 95% CI -12.4 to 12.5) | Anthracycline-cyclophosphamide breast cancer regimens | (suzukichiba2024comparisonofolanzapine pages 8-9, herrstedt20242023updatedmasccesmo pages 1-2) |
| Effectiveness | Pediatric antiemetic optimization | In children, NK1 antagonists with ondansetron plus dexamethasone ranked highest for complete/partial response; post hoc analysis suggested added benefit from olanzapine | Pediatric MEC/HEC, 16 RCTs and 3,115 patients | (suzukichiba2024comparisonofolanzapine pages 7-8) |
| Burden | Persistent real-world burden despite advances | Review states that despite advances, over 40% of patients in clinical practice still experience CINV | Clinical practice, especially cisplatin-based settings | (walker2024antiemeticmedicationsfor pages 1-2) |
Table: This table summarizes evidence-backed CINV risk factors, limited protective factors, and real-world implementation/effectiveness findings, including pharmacogenomic risk, adherence gaps, and olanzapine outcomes. It is useful for knowledge-base curation and risk-stratified supportive care planning.
CINV is described as one of the most distressing adverse effects of chemotherapy and a contributor to interruptions/discontinuation in cancer therapy; persistent nausea is emphasized as a key residual problem. (jeryczynski2026antiemetictherapy pages 1-2, herrstedt20242023updatedmasccesmo pages 7-8)
CINV is not a monogenic disorder and does not have “causal genes” in the Mendelian sense. Evidence in the provided corpus supports a pharmacogenomic modifier concept (e.g., CYP2D6 affecting 5-HT3 receptor antagonist exposure/effect), but does not provide specific variants/allele frequencies suitable for ClinVar-style annotation. (montes2026ttdexpertconsensus pages 3-5)
For CINV, “environmental” contributors are best conceptualized as clinical context exposures: - Concomitant medications (opioids, NSAIDs) and radiation parameters can influence emesis risk. (montes2026ttdexpertconsensus pages 3-5)
Specific mediator timing: - Acute CINV: linked to serotonin → 5-HT3 receptor signaling (GI tract and CNS), with vagal and splanchnic afferent involvement. (montes2026ttdexpertconsensus pages 3-5, aher2025aretrospectivedrug pages 1-3) - Delayed CINV: linked to substance P → NK1 receptor signaling. (montes2026ttdexpertconsensus pages 3-5, aher2025aretrospectivedrug pages 1-3) - Inflammation/cytokines: IL-1β, TNF-α, IL-6 can sensitize vagal afferents; IL-33 may stimulate serotonin release, connecting inflammation to emesis. (montes2026ttdexpertconsensus pages 3-5, montes2026ttdexpertconsensus pages 2-3)
Ontology suggestions (candidates; not exhaustively validated in this corpus): - UBERON: stomach, gastrointestinal tract, medulla oblongata, area postrema; vagus nerve. - CL: enterochromaffin cell. - GO biological process: emesis; regulation of neurotransmitter secretion; inflammatory response; vagus nerve signaling.
Primary “affected” systems are functional emesis circuits spanning: - Digestive system (gastric mucosa, GI tract). (aher2025aretrospectivedrug pages 1-3, jeryczynski2026antiemetictherapy pages 1-2) - Nervous system (vagus nerve, brainstem/medullary emetic circuitry). (aher2025aretrospectivedrug pages 1-3, montes2026ttdexpertconsensus pages 3-5)
CINV is not inherited in a Mendelian pattern. Population differences may arise from treatment distributions and pharmacogenomics (e.g., CYP2D6 metabolizer phenotypes), but detailed population genetics are not present in the provided corpus. (montes2026ttdexpertconsensus pages 3-5)
CINV is clinically diagnosed and monitored using symptom grading and patient-reported measures.
MASCC/ESMO emphasizes considering non-chemotherapy causes of persistent nausea/vomiting, including: - Gastrointestinal: constipation, mucositis, hepatic metastases. - Neurological: CNS metastases. - Metabolic: electrolyte abnormalities. - Drug-related: narcotics, antibiotics. - Psychophysiological causes. (rapoport20242023updatedmasccesmo pages 5-6)
CINV rarely affects long-term survival directly but substantially impacts tolerability and supportive-care burden.
In clinical practice, “over 40%” of patients still experience CINV despite major antiemetic advances. (sun2024theevolvinglandscape pages 1-2)
A 2024 analysis of 156 cisplatin-based RCTs reported stepwise improvements in vomiting control aligned with major antiemetic eras: - No-vomiting improved from 40.30% → 54.18% after 5-HT3RA-based doublets and then to 66.01% after NK1RA-based triplets. (sun2024theevolvinglandscape pages 2-5) - Acute-phase no-vomiting improved from 50.46% → 76.98% with 5-HT3RA+glucocorticoid vs 5-HT3RA alone, and to 91.30% after adding an NK1RA. (sun2024theevolvinglandscape pages 2-5) However, nausea control improvements were modest and nausea outcomes were frequently underreported in antiemetic trials. (sun2024theevolvinglandscape pages 1-2, sun2024theevolvinglandscape pages 2-5)
The MASCC/ESMO 2023 update for high-emetic-risk chemotherapy emphasizes: - Olanzapine as a fixed component of a four-drug prophylactic regimen for both AC and non-AC HEC. (herrstedt20242023updatedmasccesmo pages 1-2) - Steroid-sparing for AC HEC: “no need to prescribe steroids (dexamethasone) beyond day 1 after AC HEC,” while non-AC HEC retains a multi-day dexamethasone regimen. (herrstedt20242023updatedmasccesmo pages 1-2, herrstedt20242023updatedmasccesmo pages 7-8) Visual evidence from the guideline summary table is provided in Table 2 image (MASCC/ESMO high-risk update). (herrstedt20242023updatedmasccesmo media aa8b3b03)
A structured regimen summary is provided in Artifact 01.
| Setting | Recommended prophylaxis/rescue regimen components | Dexamethasone schedule notes | Olanzapine notes | Evidence/remarks |
|---|---|---|---|---|
| High-emetic-risk chemotherapy (HEC), anthracycline-cyclophosphamide (AC) | 4-drug prophylaxis: 5-HT3 receptor antagonist + NK1 receptor antagonist + dexamethasone + olanzapine (herrstedt20242023updatedmasccesmo pages 1-2, herrstedt20242023updatedmasccesmo media aa8b3b03) | No need to prescribe dexamethasone beyond day 1 after AC HEC; day-1-only steroid approach supported in the 2023 update (herrstedt20242023updatedmasccesmo pages 1-2, herrstedt20242023updatedmasccesmo media aa8b3b03) | Olanzapine is now a fixed part of the 4-drug regimen; Table 2 notes dosing before chemotherapy on day 1 then daily on days 2-4, with 5 mg a starting option if sedation is a concern (herrstedt20242023updatedmasccesmo pages 7-8, herrstedt20242023updatedmasccesmo media aa8b3b03) | MASCC/ESMO 2023 high-risk update identified 46 relevant references and concluded olanzapine should be incorporated into both AC and non-AC HEC prophylaxis (herrstedt20242023updatedmasccesmo pages 1-2) |
| High-emetic-risk chemotherapy (HEC), non-AC (e.g., cisplatin-based) | 4-drug prophylaxis: 5-HT3 receptor antagonist + NK1 receptor antagonist + dexamethasone + olanzapine (herrstedt20242023updatedmasccesmo pages 1-2, herrstedt20242023updatedmasccesmo media aa8b3b03) | For non-AC HEC, a 4-day dexamethasone regimen is recommended; evidence for limiting dexamethasone after cisplatin/non-AC HEC was considered inconclusive (herrstedt20242023updatedmasccesmo pages 1-2, herrstedt20242023updatedmasccesmo pages 7-8, herrstedt20242023updatedmasccesmo media aa8b3b03) | Olanzapine is recommended as a fixed part of prophylaxis; Table 2 indicates administration before chemotherapy on day 1 and daily on days 2-4, commonly 10 mg with 5 mg reasonable if sedation risk is important (herrstedt20242023updatedmasccesmo pages 7-8, herrstedt20242023updatedmasccesmo media aa8b3b03) | The guideline found no major differences between 5-HT3 receptor antagonists or between NK1 receptor antagonists for HEC prophylaxis (herrstedt20242023updatedmasccesmo pages 1-2) |
| Multiple-day cisplatin chemotherapy | 5-HT3 receptor antagonist once daily on chemotherapy days + dexamethasone once daily from day 1 until 2 days post-chemotherapy + aprepitant 125 mg day 1 then 80 mg daily from day 2 until 2 days post-chemotherapy + olanzapine 5 mg once daily from day 1 until 2 days post-chemotherapy (rapoport20242023updatedmasccesmo pages 1-2, rapoport20242023updatedmasccesmo pages 5-6) | Continue dexamethasone daily from day 1 through 2 days after chemotherapy; concern about late corticosteroid toxicity is specifically noted in the discussion (rapoport20242023updatedmasccesmo pages 5-6) | Olanzapine 5 mg once daily from day 1 until 2 days post-chemotherapy; note recommends giving olanzapine at bedtime (rapoport20242023updatedmasccesmo pages 5-6) | Recommendation graded I/A overall, but II/B for number of days; palonosetron may be used on days 1, 3, and 5 if chemotherapy lasts 5 days (rapoport20242023updatedmasccesmo pages 5-6) |
| High-dose chemotherapy with stem cell transplant / HSCT | 5-HT3 receptor antagonist + dexamethasone + aprepitant recommended; olanzapine may be considered as part of the regimen (rapoport20242023updatedmasccesmo pages 1-2) | Specific dexamethasone day-by-day schedule not detailed in the extracted evidence; recommendation is to include dexamethasone in combination prophylaxis (rapoport20242023updatedmasccesmo pages 1-2) | Olanzapine is not mandatory in the extracted wording but may be considered; guideline notes it as an important advance for improving prevention in high-dose chemotherapy/autologous transplant settings (rapoport20242023updatedmasccesmo pages 1-2) | The 2023 update reviewed literature from 2015-2023 and updated recommendations for HDC/HSCT patients, emphasizing persistent clinical significance of nausea in this population (rapoport20242023updatedmasccesmo pages 1-2) |
| Breakthrough CINV | Use olanzapine if not used for primary prophylaxis; evidence supports a single daily dose for 3 days (rapoport20242023updatedmasccesmo pages 1-2, rapoport20242023updatedmasccesmo pages 5-6) | No dexamethasone rescue schedule recommendation identified in the extracted guideline evidence (rapoport20242023updatedmasccesmo pages 1-2, rapoport20242023updatedmasccesmo pages 5-6) | Some evidence supports olanzapine 10 mg once daily for 3 days; meta-analytic evidence favored olanzapine in the breakthrough setting, and 5 mg may be considered to reduce side effects although optimal dose remains unsettled (rapoport20242023updatedmasccesmo pages 1-2, rapoport20242023updatedmasccesmo pages 5-6) | Breakthrough CINV is defined as nausea/vomiting during chemotherapy despite guideline-directed prophylaxis; guideline recommendation level reported as II/B (rapoport20242023updatedmasccesmo pages 5-6) |
Table: This table summarizes the key 2023-2024 MASCC/ESMO guideline-update recommendations for major CINV settings supported by the retrieved evidence. It highlights regimen components, dexamethasone duration, and where olanzapine is fixed, optional, or recommended for rescue.
For multiple-day cisplatin, MASCC/ESMO recommends 5-HT3RA + dexamethasone + aprepitant + olanzapine, with explicit dosing schedules and bedtime olanzapine suggested. (rapoport20242023updatedmasccesmo pages 5-6)
For high-dose chemotherapy with stem cell transplantation, MASCC/ESMO recommends 5-HT3RA + dexamethasone + aprepitant, with olanzapine as a consideration. (rapoport20242023updatedmasccesmo pages 1-2)
MASCC/ESMO recommends olanzapine for breakthrough CINV if it was not used in prophylaxis, with evidence supporting daily dosing for 3 days. (rapoport20242023updatedmasccesmo pages 1-2, rapoport20242023updatedmasccesmo pages 5-6)
A 2024 pediatric NMA (16 RCTs; 3115 patients) found that, when given with dexamethasone, NK1 antagonists with ondansetron ranked highest for several complete/partial response outcomes; palonosetron performed better than ondansetron for delayed/overall CR and nausea prevention; and post hoc analysis suggested benefit from adding olanzapine to aprepitant+ondansetron regimens. (walker2024antiemeticmedicationsfor pages 1-2)
Primary prevention is largely pharmacologic prophylaxis matched to emetogenic risk, emphasizing correct upfront regimens over rescue therapy. (jeryczynski2026antiemetictherapy pages 1-2, rapoport20242023updatedmasccesmo pages 5-6)
A key prevention concept is that optimal control in cycle 1 helps prevent anticipatory CINV in later cycles. (dhabhar2025expertconsensusguidance pages 5-6)
Not applicable as a naturally occurring disease entity; this is iatrogenic and treatment-triggered.
Not represented in the retrieved corpus; mechanistic understanding in these sources is primarily human clinical/pharmacologic.
References
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(suzukichiba2024comparisonofolanzapine pages 1-2): Hiroe Suzuki-Chiba, Takaaki Konishi, Shotaro Aso, Kanako Makito, Hiroki Matsui, Taisuke Jo, Kiyohide Fushimi, and Hideo Yasunaga. Comparison of olanzapine 2.5 mg and 5 mg in the prevention of chemotherapy-induced nausea and vomiting: a japanese nationwide database study. International Journal of Clinical Oncology, 29:1762-1773, Aug 2024. URL: https://doi.org/10.1007/s10147-024-02603-2, doi:10.1007/s10147-024-02603-2. This article has 2 citations and is from a peer-reviewed journal.
(suzukichiba2024comparisonofolanzapine pages 2-4): Hiroe Suzuki-Chiba, Takaaki Konishi, Shotaro Aso, Kanako Makito, Hiroki Matsui, Taisuke Jo, Kiyohide Fushimi, and Hideo Yasunaga. Comparison of olanzapine 2.5 mg and 5 mg in the prevention of chemotherapy-induced nausea and vomiting: a japanese nationwide database study. International Journal of Clinical Oncology, 29:1762-1773, Aug 2024. URL: https://doi.org/10.1007/s10147-024-02603-2, doi:10.1007/s10147-024-02603-2. This article has 2 citations and is from a peer-reviewed journal.
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(suzukichiba2024comparisonofolanzapine pages 7-8): Hiroe Suzuki-Chiba, Takaaki Konishi, Shotaro Aso, Kanako Makito, Hiroki Matsui, Taisuke Jo, Kiyohide Fushimi, and Hideo Yasunaga. Comparison of olanzapine 2.5 mg and 5 mg in the prevention of chemotherapy-induced nausea and vomiting: a japanese nationwide database study. International Journal of Clinical Oncology, 29:1762-1773, Aug 2024. URL: https://doi.org/10.1007/s10147-024-02603-2, doi:10.1007/s10147-024-02603-2. This article has 2 citations and is from a peer-reviewed journal.
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(fujii2024pharmacistinterventionand pages 1-2): Hironori Fujii. Pharmacist intervention and identification of adverse events related to treatment efficacy in cancer chemotherapy to improve clinical outcomes. Journal of Pharmaceutical Health Care and Sciences, Dec 2024. URL: https://doi.org/10.1186/s40780-024-00403-4, doi:10.1186/s40780-024-00403-4. This article has 5 citations.