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Related Concept Videos

Treatment for Pulmonary Arterial Hypertension: Endothelin Receptor Antagonists01:18

Treatment for Pulmonary Arterial Hypertension: Endothelin Receptor Antagonists

Endothelins (ETs) are potent vasoactive peptides critical in the human body's various physiological and pathological processes. One of the most promising therapeutic strategies for treating pulmonary arterial hypertension (PAH) involves counteracting the effects of these endothelins using a class of drugs known as endothelin receptor antagonists.
ETs are synthesized through a complex sequence of enzymatic steps, primarily involving an enzyme referred to as endothelin-converting enzyme (ECE). Of...
Treatment for Pulmonary Arterial Hypertension: Receptor Tyrosine Kinase Inhibitors and Calcium Channel Blockers01:26

Treatment for Pulmonary Arterial Hypertension: Receptor Tyrosine Kinase Inhibitors and Calcium Channel Blockers

Receptor tyrosine kinase inhibitors (TKIs) and calcium channel blockers (CCBs) are two critical categories of drugs employed in the treatment of pulmonary artery hypertension (PAH). PAH is a disease that causes high blood pressure in the pulmonary arteries, resulting in chest pain, fatigue, and shortness of breath.
TKIs, such as imatinib (Gleevec), are particularly effective in tackling the growth and mitogenic factors that become upregulated in PAH patients. These factors contribute to the...
Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase01:11

Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase

Genetic polymorphisms in drug targets have emerged as critical determinants of interindividual variability in drug response and toxicity. Pharmacogenomic investigations increasingly focus on identifying these variations to personalize and optimize therapeutic interventions. A drug target may be a receptor, enzyme, or signaling protein involved in pharmacologic responses or disease-related pathways. While early pharmacogenetic studies focused primarily on drug metabolism, current research...

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Pulmonary toxicity associated with erlotinib.

Vincent Liu1, Dorothy A White, Maureen F Zakowski

  • 1Thoracic Oncology Service, Memorial Sloan-Kettering Cancer Center, New York, NY, USA. vinliu@stanford.edu

Chest
|September 18, 2007
PubMed
Summary

Erlotinib may cause fatal interstitial lung disease (ILD), especially in patients with usual interstitial pneumonia (UIP). Physicians should be aware of this risk when prescribing erlotinib for lung cancer.

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Area of Science:

  • Pulmonology
  • Oncology
  • Pharmacology

Background:

  • Interstitial lung disease (ILD) is a known adverse effect of gefitinib therapy.
  • The pulmonary toxicity of erlotinib, another EGFR inhibitor, is less understood.
  • Non-small cell lung cancer (NSCLC) patients are often treated with tyrosine kinase inhibitors like erlotinib.

Observation:

  • A patient with advanced NSCLC developed fatal pulmonary toxicity after receiving erlotinib.
  • This patient had pre-existing usual interstitial pneumonia (UIP) findings on a resected lung specimen before erlotinib treatment.

Findings:

  • This case highlights the potential for erlotinib to cause severe, fatal ILD.
  • Patients with pathological UIP findings or pre-existing pulmonary fibrosis may be at increased risk.
  • Erlotinib-induced ILD can mimic other pulmonary conditions, complicating diagnosis.

Implications:

  • Clinicians should consider erlotinib-induced ILD in patients presenting with new or worsening respiratory symptoms.
  • Pre-treatment screening for pulmonary fibrosis or UIP may be warranted in at-risk patients.
  • Further research is needed to elucidate the mechanisms and incidence of erlotinib-induced pulmonary toxicity.