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Toxic Reactions: Overview

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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,...

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Updated: Mar 1, 2026

Author Spotlight: Integrating Mechanical and Biological Analysis in Tendinopathy Research

Author Spotlight: Integrating Mechanical and Biological Analysis in Tendinopathy Research

Published on: March 1, 2024

Mini-Review: Toxic Tendinopathy.

¹1 GEMpath, Inc., Longmont, Colorado, USA.

Toxicologic Pathology

|May 30, 2017

Summary

This summary is machine-generated.

Certain medications, including aromatase inhibitors, fluoroquinolones, glucocorticoids, and statins, can cause toxic tendinopathy, a progressive tendon degeneration. This condition, particularly affecting the Achilles tendon, can lead to rupture and requires careful monitoring during drug safety assessments.

Keywords:

review tendinopathy tendinosis tendon toxic tendinopathy toxicity

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Last Updated: Mar 1, 2026

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Area of Science:

Pharmacology
Orthopedics
Toxicology

Background:

Toxic tendinopathy is a rare but documented adverse effect associated with several drug classes.
Commonly implicated drugs include aromatase inhibitors, fluoroquinolone antibiotics, glucocorticoids, and statins.
Less consistent links exist with anabolic steroids, antiretroviral agents, metalloproteinase inhibitors, and isotretinoin.

Purpose of the Study:

To review the clinical presentation and proposed pathogenesis of drug-induced toxic tendinopathy.
To highlight the specific tendons affected and the risk of rupture.
To recommend incorporating tendon evaluation in nonclinical drug safety assessments.

Main Methods:

Review of existing literature on drug-induced tendinopathy.
Analysis of clinical presentations, including affected tendons and time to onset.
Discussion of proposed pathogenetic mechanisms.

Main Results:

Drug-induced tendinopathies typically manifest as tendinosis, except for aromatase inhibitor-associated tenosynovitis.
Load-bearing tendons, particularly the Achilles tendon, are most frequently affected by fluoroquinolones, glucocorticoids, and statins, with a 30-40% rupture rate.
Symptom onset varies from days to years depending on the causative agent.

Conclusions:

Toxic tendinopathy is a significant complication of certain medications, necessitating awareness among clinicians and researchers.
Understanding the pathogenesis, including cellular and molecular mechanisms, is crucial for risk mitigation.
Routine tendon pathology evaluation in nonclinical safety assessments for relevant drug classes is recommended to prevent adverse events.