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Related Experiment Video

Updated: Jul 7, 2026

Optimized LC-MS/MS Method for the High-throughput Analysis of Clinical Samples of Ivacaftor, Its Major Metabolites, and Lumacaftor in Biological Fluids of Cystic Fibrosis Patients

Optimized LC-MS/MS Method for the High-throughput Analysis of Clinical Samples of Ivacaftor, Its Major Metabolites, and Lumacaftor in Biological Fluids of Cystic Fibrosis Patients

Published on: October 15, 2017

Stavudine plasma concentrations and lipoatrophy.

Hadewych J M ter Hofstede¹, Peter P Koopmans, David M Burger

¹Department of Internal Medicine, Radboud University Nijmegen Medical Center, Nijmegen, The Netherlands. h.terhofstede@aig.umcn.nl

The Journal of Antimicrobial Chemotherapy

|February 19, 2008

Summary

This summary is machine-generated.

Higher stavudine concentrations in patients correlate with lipoatrophy (LA). Monitoring drug levels may help prevent this adverse event, improving treatment adherence.

Related Experiment Videos

Last Updated: Jul 7, 2026

Optimized LC-MS/MS Method for the High-throughput Analysis of Clinical Samples of Ivacaftor, Its Major Metabolites, and Lumacaftor in Biological Fluids of Cystic Fibrosis Patients

Optimized LC-MS/MS Method for the High-throughput Analysis of Clinical Samples of Ivacaftor, Its Major Metabolites, and Lumacaftor in Biological Fluids of Cystic Fibrosis Patients

Published on: October 15, 2017

Area of Science:

Pharmacokinetics and Drug Metabolism
HIV/AIDS Therapeutics
Adverse Drug Reactions

Background:

Stavudine is an antiretroviral drug used in HIV treatment.
Lipoatrophy (LA) is a significant side effect of stavudine therapy, leading to treatment discontinuation.
Understanding the relationship between drug concentration and LA is crucial for patient management.

Purpose of the Study:

To investigate the correlation between plasma stavudine concentrations and the incidence of lipoatrophy (LA).
To identify potential predictors for stavudine-induced lipoatrophy.

Main Methods:

Retrospective analysis of plasma stavudine concentrations in patients on stavudine-containing regimens for at least 12 months.
Comparison of drug concentrations between patients with LA and a control group without LA or neuropathy.
Multivariate analysis to identify independent predictors of LA.

Main Results:

Patients with LA exhibited higher plasma stavudine concentrations (geometric CRs 0.978 vs. 0.741, P=0.04).
A higher percentage of LA patients had stavudine concentrations above the normal population curve (46% vs. 23%, P=0.02).
Both longer duration of stavudine therapy and higher drug concentrations were independently associated with LA (P=0.05 and P=0.02, respectively).

Conclusions:

Plasma stavudine concentration monitoring can aid in preventing stavudine-related lipoatrophy.
Identifying patients with elevated drug exposure may allow for early intervention to mitigate LA risk.
This finding supports personalized dosing strategies to minimize stavudine toxicity.