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Chemotherapy-Induced Nausea and Vomiting: Neurokinin-1 Receptor Antagonists01:28

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Neurokinin 1 (NK1) receptors are distributed across the GI tract, vagal afferents, and key CNS regions including the central vomiting center and chemoreceptor trigger zone (CTZ) Chemotherapy agents stimulate enterochromaffin cells in the gastrointestinal (GI) tract to release large amounts of substance P (SP). SP is a neuropeptide released by specific sensory nerves in response to many different stressors, including those in the GI mucosa affected by chemotherapy.  SP binds and activates...
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Chemotherapy-Induced Nausea and Vomiting: Cannabinoids01:21

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Tetrahydrocannabinol (THC) is a phytocannabinoid that primarily interacts with the CB1 receptor, a type of G protein-coupled receptor (GPCR) predominantly in and around the chemoreceptor trigger zone (CTZ) and emetic center. THC also blocks the serotonin receptor activity in the dorsal vagal complex (DVC) by inhibiting serotonin release. THC exerts its anti-emetic effects through these interactions, which are beneficial for patients undergoing chemotherapy.
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Chemotherapy-Induced Nausea and Vomiting: 5-HT3 Receptor Antagonists01:27

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5-HT3 receptor antagonists, such as dolasetron, granisetron (Kytril), ondansetron (Zofran), and palonosetron (Axoli), are crucial in managing chemotherapy-induced nausea and vomiting (CINV) and postoperative nausea. These drugs selectively block 5-HT3 receptors in the visceral vagal and spinal afferent nerves, chemoreceptor trigger zone, and the vomiting center. They have a rapid onset of action and can be given as a single dose before chemotherapy. Ondansetron and granisetron, in particular,...
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Chemotherapy-Induced Nausea and Vomiting: Dopamine Receptor Antagonists01:29

Chemotherapy-Induced Nausea and Vomiting: Dopamine Receptor Antagonists

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Dopamine receptor antagonists, also known as antipsychotic agents, are critical in managing chemotherapy-induced vomiting. These antiemetic agents block dopamine receptors in the chemoreceptor trigger zone (CTZ), inhibiting signal transmission to the vomiting center. Antipsychotic agents encompass phenothiazines (PTZ), butyrophenones, benzamides, and thienobenzodiazepines (Zyprexa), which are utilized for their antiemetic and sedative properties.
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Prokinetic agents are specialized medications that stimulate gastrointestinal (GI) motility, promoting food movement through the GI tract. Dopamine, an inhibitory neurotransmitter, plays a significant role in this process, reducing GI motility and indirectly controlling the speed of digestion. Dopamine receptor antagonists, such as metoclopramide and domperidone, offer a unique advantage as prokinetic agents. By blocking the dopamine receptors, these drugs increase GI motility, improving food...
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Pathophysiology of Vomiting01:22

Pathophysiology of Vomiting

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Vomiting is a complex physiological response to expel harmful or irritating substances from the body. It's a defensive mechanism triggered by stimuli like poisons, microbial toxins, cytotoxic drugs, and mechanical abdominal distension. The process is centrally coordinated by the vomiting (or emetic) center located in the medulla of the brainstem. This area, rich in muscarinic M1, histamine H1, neurokinin 1 (NK1), and serotonin 5-HT3 receptors, coordinates the act of vomiting through...
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Related Experiment Video

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The Association between Molecular Initiating Events and Drug-Induced Hiccups.

Ryuichiro Hosoya1,2, Reiko Ishii-Nozawa3, Tomoko Terajima2

  • 1Department of Medical Molecular Informatics, Meiji Pharmaceutical University, Tokyo 204-8588, Japan.

Pharmaceuticals (Basel, Switzerland)
|March 28, 2024
PubMed
Summary

This study investigated drug-induced hiccups, identifying molecular initiating events (MIEs) linked to hiccups. Transforming growth factor-beta and antioxidant response elements were key factors in males and females, respectively.

Keywords:
FAERSdrug-induced hiccupsnuclear receptorstress response pathways

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Area of Science:

  • Pharmacology
  • Toxicology
  • Computational Biology

Background:

  • Drug-induced hiccups significantly impact patient quality of life.
  • The underlying mechanisms and sex-specific differences of drug-induced hiccups are poorly understood.
  • Limited evidence exists for effective treatment or prevention strategies.

Purpose of the Study:

  • To investigate the molecular initiating events (MIEs) in the pathogenesis of drug-induced hiccups.
  • To identify potential sex-specific pathways contributing to drug-induced hiccups.
  • To explore the utility of adverse event databases and machine learning in understanding drug-induced adverse effects.

Main Methods:

  • Extracted drugs suspected of causing hiccups from the FDA Adverse Event Reporting System.
  • Analyzed data from the overall population and sex-specific subgroups.
  • Utilized the Toxicity Predictor machine-learning model to calculate predicted activity values for nuclear receptors and stress response pathways.

Main Results:

  • Identified transforming growth factor-beta as an independent factor for hiccups in males.
  • Identified antioxidant response elements as an independent factor for hiccups in females.
  • This study provides novel insights into the mechanisms of drug-induced hiccups.

Conclusions:

  • This research elucidates potential molecular initiating events (MIEs) in drug-induced hiccups.
  • Sex-specific factors, including transforming growth factor-beta and antioxidant response elements, play a role in hiccup development.
  • Adverse event databases combined with machine learning offer a valuable approach for hypothesis generation in drug-induced adverse effects.