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DNA single strand-breaks in human lymphocytes after therapy with antirheumatic drugs
1Department of Physiological Chemistry, University of Mainz, Fed. Rep. of Germany,
Abstract:
In rheumatic patients the proportion of DNA single strand-breaks in peripheral lymphocytes was investigated after a long-term treatment. The antirheumatic drugs indomethacin, diclofenac, D-penicillamine, auranofin, and chloroquine support the formation of DNA single strand-breaks. The highest rate of DNA single strand-breaks can be seen after treatment with the non-steroidal antirheumatic drugs indomethacin and diclofenac as well as after treatment with the combination of non-steroidal anti-rheumatic drugs with auranofin. In case of treatment with non-steroidal antirheumatic drugs in combination with D-penicillamine the rate of DNA single strand-breaks is lower than by other forms of treatment. The observation support the suspicion of an increased susceptibility to cancer in rheumatic patients after a long-term treatment.
Insights
Long-term antirheumatic drug use, including NSAIDs like indomethacin and diclofenac, increases DNA strand breaks in rheumatic patients. This finding suggests a potential heightened cancer risk with prolonged treatment.
Area of Science:
- Rheumatology
- Genotoxicology
- Pharmacology
Background:
- Rheumatic diseases require long-term management with various medications.
- Concerns exist regarding the potential genotoxicity of antirheumatic drugs.
- Understanding drug-induced DNA damage is crucial for patient safety.
Purpose of the Study:
- To investigate the genotoxic effects of commonly used antirheumatic drugs on peripheral lymphocytes in rheumatic patients.
- To compare the DNA single-strand break induction potential of different drug classes and combinations.
Main Methods:
- Analysis of DNA single-strand breaks in peripheral lymphocytes.
- Long-term treatment assessment of patients with indomethacin, diclofenac, D-penicillamine, auranofin, and chloroquine.
- Comparative analysis of genotoxic effects across different treatment regimens.
Main Results:
- All tested antirheumatic drugs, including indomethacin, diclofenac, D-penicillamine, auranofin, and chloroquine, induced DNA single-strand breaks.
- Non-steroidal anti-rheumatic drugs (NSAIDs) like indomethacin and diclofenac, and NSAIDs combined with auranofin, showed the highest rates of DNA damage.
- Combinations of NSAIDs with D-penicillamine resulted in lower DNA single-strand break rates compared to other treatments.
Conclusions:
- Long-term treatment with antirheumatic drugs can lead to DNA damage in rheumatic patients.
- NSAIDs and certain drug combinations may pose a higher genotoxic risk.
- These findings support concerns about increased cancer susceptibility in rheumatic patients undergoing long-term drug therapy.