Related Experiment Video
Updated: Apr 15, 2026
04:48
Chemotherapy-induced Vascular Toxicity - Real-time In vivo Imaging of Vessel Impairment
Published on: January 7, 2015
7.9K
Nail toxicities induced by systemic anticancer treatments.
Caroline Robert1, Vincent Sibaud2, Christina Mateus3
1Gustave Roussy, Département de Médicine Oncologique, Service de Dermatologie, Villejuif, France; Université Paris-Sud, Faculté de Médecine, Le Kremlin Bicetre, France.
The Lancet. Oncology
|April 8, 2015
Summary
Cancer drug nail side effects, including pain and functional issues, are common with taxanes and EGFR inhibitors. This review covers nail changes from chemotherapy and targeted drugs, discussing prevention and treatment.
Area of Science:
- Oncology
- Dermatology
- Pharmacology
Background:
- Systemic anticancer drugs can cause nail changes, impacting patient quality of life.
- Nail toxicities are particularly noted with taxanes and epidermal growth factor receptor (EGFR) inhibitors.
- These changes affect the nail plate, nail bed, and surrounding skin (perionychium).
Purpose of the Study:
- To review nail changes induced by conventional chemotherapies.
- To discuss nail toxicities associated with targeted anticancer drugs.
- To explore preventive and curative strategies for drug-induced nail toxicities.
Main Methods:
- Literature review of nail changes from conventional chemotherapy.
- Analysis of nail toxicities linked to targeted anticancer agents (e.g., EGFR and MEK inhibitors).
- Synthesis of reported preventive and curative options for nail side effects.
Main Results:
- Common nail changes include melanonychia, leukonychia, onycholysis, onychomadesis, Beau's lines, and onychorrhexis with conventional chemotherapy.
- Paronychia and pyogenic granuloma are frequent in the periungual area with targeted therapies like EGFR and MEK inhibitors.
- Nail toxicities can lead to pain and functional impairment, significantly affecting quality of life.
Conclusions:
- Nail changes are a significant, though often overlooked, toxicity of systemic anticancer treatments.
- Understanding the specific nail toxicities associated with different drug classes is crucial for patient management.
- Further research into effective preventive and curative interventions is warranted to improve patient outcomes and quality of life.
Related Concept Videos
01:24Drug Toxicity: Dose-Dependent Reactions
211
Drug toxicities can be stratified into pharmacological, pathological, or genotoxic based on their mechanisms. The incidence and severity of these toxicities generally increase with the drug's concentration in the body and exposure time.Pharmacological toxicity is evident when the therapeutic effects of drugs overshoot into adverse reactions in a predictable, dose-dependent manner. Central nervous system (CNS) depression from barbiturates is a classic example, with effects escalating from...
211
01:28Chemotherapy-Induced Nausea and Vomiting: Neurokinin-1 Receptor Antagonists
785
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...
785
01:26Toxic Reactions: Overview
4.0K
When toxic substances penetrate the human body, they disseminate to various tissues, undergoing metabolic changes. This process yields reactive metabolites that may covalently bind with specific target molecules, resulting in toxicity.
Toxicity falls into two primary categories: local and systemic.
Local toxicity appears at the exposure site, such as protein denaturation caused by caustic substances.
In contrast, systemic toxicity requires the toxic agent's absorption and distribution,...
Toxicity falls into two primary categories: local and systemic.
Local toxicity appears at the exposure site, such as protein denaturation caused by caustic substances.
In contrast, systemic toxicity requires the toxic agent's absorption and distribution,...
4.0K
01:00Drug Toxicity: Overview
256
Drug toxicity quantifies the harm a compound causes to an organism, varying by dose and potentially impacting whole systems or specific organs like the liver. Toxic reactions may arise from venomous insect or spider bites, with effects ranging from mild symptoms to severe outcomes such as brain damage or death. Common forms of acute poisoning include ethanol intoxication and overdose of pain or fever medications, with substances like GHB and heroin being particularly lethal at doses close to...
256
01:30Drug toxicity: Drug–Drug Interaction
376
Drug–drug interactions can precipitate toxicity through multiple mechanisms. Absorption interactions alter how drugs enter the body, exemplified when ranitidine increases the absorption of basic drugs, while cholestyramine decreases the levels of propranolol. Protein binding interactions occur when drugs share the same binding sites on plasma proteins. Drugs like aspirin and warfarin, when bound in excess, can lead to increased free drug concentrations, enhancing the potential for...
376
01:16Drug toxicity: Idiosyncratic Reactions
197
Idiosyncratic drug reactions represent abnormal chemical responses that vary significantly among individuals, ranging from extreme sensitivity to low doses to insensitivity to high doses. These reactions often occur due to the drug's covalent binding with serum proteins, forming a foreign hapten that triggers an immunotoxicological response. The variability in drug reactions has a strong pharmacogenetic foundation, with genetic differences crucial in how individuals metabolize drugs. For...
197