Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Drug Toxicity: Allergic Reactions

Drug Toxicity: Allergic Reactions

Drug-related allergies are immune-mediated responses triggered by the administration of pharmacological agents. These hypersensitivity reactions are classified based on the immune mechanisms involved. The four primary types—Type I, II, III, and IV—are mediated by different immunological pathways and exhibit distinct clinical manifestations.Type I Hypersensitivity/ IgE-Mediated Reactions: Immunoglobulin E (IgE) immediately mediates Type I hypersensitivity reactions. Upon initial exposure to a...

Drug toxicity: Idiosyncratic Reactions

Drug toxicity: Idiosyncratic Reactions

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...

Drug Toxicity: Dose-Dependent Reactions

Drug Toxicity: Dose-Dependent Reactions

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...

Drug Toxicity: Risk factors

Drug Toxicity: Risk factors

Adverse Drug Reactions (ADRs) are potential complications that arise during pharmacotherapy, influenced by multiple risk factors. Age plays a significant role; both neonates and the elderly are at heightened risk due to their respective immature and diminished metabolic and elimination processes. Gender also impacts ADRs, with females experiencing a 1.5 to 1.7-fold greater risk than males, which may be linked to pharmacokinetic, pharmacodynamic, and hormonal differences. Notably, neonates, the...

Drug Toxicity: Overview

Drug Toxicity: Overview

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...

Toxic Reactions: Overview

Toxic Reactions: Overview

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,...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by

Same author

Outcomes of patients with Richter transformation who received no prior chemoimmunotherapy for their CLL.

Blood cancer journal·2025

Same author

Inhaled colistimethate sodium in patients with bronchiectasis and Pseudomonas aeruginosa infection: results of PROMIS-I and PROMIS-II, two randomised, double-blind, placebo-controlled phase 3 trials assessing safety and efficacy over 12 months.

The Lancet. Respiratory medicine·2024

Same author

Real-world treatment patterns, health care resource utilization, and costs in a US Medicare population with bronchiectasis.

Journal of managed care & specialty pharmacy·2024

Same author

Nebulized hypertonic saline and positive expiratory pressure device use in patients with bronchiectasis: Analysis from the United States Bronchiectasis and NTM research registry.

Respiratory medicine and research·2024

Same author

Five-Year Outcomes among U.S. Bronchiectasis and NTM Research Registry Patients.

American journal of respiratory and critical care medicine·2024

Same author

Hypertension treatment for patients receiving ibrutinib: a multicenter retrospective study.

Blood advances·2024

Search research articles

Related Experiment Video

Updated: May 31, 2026

Chemical Inactivation of the E3 Ubiquitin Ligase Cereblon by Pomalidomide-based Homo-PROTACs

Chemical Inactivation of the E3 Ubiquitin Ligase Cereblon by Pomalidomide-based Homo-PROTACs

Published on: May 15, 2019

Reversible pulmonary toxicity due to lenalidomide.

Stephanie Coates¹, Alan Barker, Stephen Spurgeon

¹Division of Pulmonary and Critical Care Medicine, Oregon Health and Science University, Portland, OR 97239, USA. coates@ohsu.edu

Journal of Oncology Pharmacy Practice : Official Publication of the International Society of Oncology Pharmacy Practitioners

|July 12, 2011

Summary

Lenalidomide can cause serious lung toxicity, presenting as shortness of breath and interstitial pneumonia. This pulmonary toxicity appears reversible upon medication discontinuation, offering hope for affected patients.

Related Experiment Videos

Last Updated: May 31, 2026

Chemical Inactivation of the E3 Ubiquitin Ligase Cereblon by Pomalidomide-based Homo-PROTACs

Chemical Inactivation of the E3 Ubiquitin Ligase Cereblon by Pomalidomide-based Homo-PROTACs

Published on: May 15, 2019

Area of Science:

Pulmonology
Oncology
Pharmacology

Background:

Lenalidomide, a thalidomide derivative, is approved for myelodysplastic syndrome and multiple myeloma.
Pulmonary toxicity is a known risk with thalidomide, but less documented with lenalidomide.

Observation:

A patient presented with severe dyspnea and decreased exercise tolerance.
Imaging revealed new ground-glass opacities and reticulation, indicative of nonspecific interstitial pneumonia.

Findings:

High clinical suspicion for lenalidomide-induced pulmonary toxicity led to drug discontinuation.
The patient experienced rapid symptom improvement within two weeks and complete resolution in eight weeks.
Computed tomography scans showed resolving interstitial changes, confirming reversibility.

Implications:

Lenalidomide-induced pulmonary toxicity, though debilitating, appears to be reversible.
This case highlights the importance of monitoring for pulmonary complications in patients treated with lenalidomide.
Early recognition and discontinuation of lenalidomide can lead to favorable patient outcomes.