Drug-induced lupus erythematosus causes
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Cafer Zorkun, M.D., Ph.D. [2]
Overview
Drug-induced lupus (DIL) is known to be caused by hundreds of different drugs.[1] They are classified as high, moderate, low, or very low risk. While some drugs have good evidence of association with DIL, there are case reports implicating several other drugs as a possible cause of DIL. In addition, Several herbal medications have also been reported to cause a lupus-like syndrome. Procainamide and hydralazine have the highest incidence of causing DIL, with risks reported as high as 30% with procainamide and 5% to 10% with hydralazine. All anti-TNF agents have been associated with DIL, with the risk being higher with etanercept and infliximab. https://www.medsafe.govt.nz/profs/PUArticles/March2017/DrugInducedLupus.htm https://www.ncbi.nlm.nih.gov/books/NBK441889/
Causes
The processes that lead to drug-induced lupus erythematosus are not entirely understood. The exact processes that occur are not known even after 50 years since its discovery, but many studies present theories on the mechanisms of DIL.
A predisposing factor to developing DIL is N-acetylation speed, or the rate at which the body can metabolize the drug. Acetylation speed is generally a genetic factor. A study showed that 29 of 30 patients with DIL were slow acetylators. In addition, these patients had more hydralazine metabolites in their urine than fast acetylators.[2] These metabolites (byproducts of the interactions between the drug and constituents in the body) of hydralazine are said to have been created when leukocytes (white blood cells) have been activated, meaning they are stimulated to produce a respiratory burst.[3] Respiratory burst in white blood cells induces an increased production of free radicals and oxidants such as hydrogen peroxide.[4] These oxidants have been found to react with hydralazine to produce a reactive species that is able to bond to protein.[5] Monocytes, one type of leukocyte, detect the antigen and relay the recognition to T helper cells, creating antinuclear antibodies leading to an immune response.[6] Further studies on the interactions between oxidants and hydralazine are necessary to understand the processes involved in DIL.
Of the drugs that cause DIL, hydralazine has been found to cause a higher incidence. Hydralazine is a medication used to treat high blood pressure. Approximately 12% of the patients who have taken hydralazine over long periods of time and in high doses have shown DIL-like symptoms.[7] Many of the other drugs have a low to very low risk to develop DIL. The following table shows the risk of development of DIL of some of these drugs on a very to high scale.
- High risk:
- Moderate to low risk:
- Herbal medications have also been linked to more lupus flares. These include:
- alfalfa sprouts.
- echinacea.
- melatonin.
https://www.ncbi.nlm.nih.gov/books/NBK441889/
References
- ↑ Bojinca VC, Bojinca M, Gheorghe M, Birceanu A, Iosif CI, Balanescu SM; et al. (2018). "Stevens-Johnsons syndrome or drug-induced lupus - a clinical dilemma: A case report and review of the literature". Biomed Rep. 9 (1): 37–41. doi:10.3892/br.2018.1098. PMC 6007037. PMID 29930803.
- ↑ Lahita, Robert G. (1987). Systemic Lupus Erythematosus. New York: John Wiley & Sons. pp. p. 859. ISBN 0-471-87388-8.
- ↑ Uetrecht J, Zahid N, Rubin R (1988). "Metabolism of procainamide to a hydroxylamine by human neutrophils and mononuclear leukocytes". Chem Res Toxicol. 1 (1): 74–8. PMID 2979715.
- ↑ Stites, Daniel P. (1994). Basic & Clinical Immunology. Norwalk, CT: Appleton & Lange. p. 373. ISBN 0-8385-0561-9. Unknown parameter
|coauthors=ignored (help) - ↑ Hofstra A, Matassa L, Uetrecht J (1991). "Metabolism of hydralazine by activated leukocytes: implications for hydralazine induced lupus". J Rheumatol. 18 (11): 1673–80. PMID 1664857.
- ↑ Hofstra A (1994). "Metabolism of hydralazine: relevance to drug-induced lupus". Drug Metab Rev. 26 (3): 485–505. PMID 7924901.
- ↑ Schur, Peter H. et al. (1983), p. 223.