Understanding Drug Induced Lupus

We all know that lupus is an autoimmune disorder/disease which can effect the internal organs. We also know that lupus effects each and everyone of us differently, but what exactly is Drug Induced Lupus? Are the affects the same as lupus erythematosus? What drugs causes drug induced lupus? You'll find out what you need to know regarding this, so let's get started.

Drug-induced lupus is a lupus-like disease caused by certain prescription drugs. The drugs most commonly connected with drug-induced lupus are: hydralazine (used to treat high blood pressure or hypertension) procainamide (used to treat irregular heart rhythms) isoniazid (used to treat tuberculosis).

This form also accounts for about 10% of all lupus cases. It is caused by high doses of certain medications. The symptoms of drug-induced lupus are like those of SLE but rarely affect major organs. These symptoms usually disappear within 6 months of stopping the medicine that caused them. Drug-induced lupus erythematosus (DIL) is a subset of lupus defined as a lupus-like syndrome that develops in temporal relation to exposure to a drug and resolves after cessation of the drug exposure.

Anti ds DNA is usually absent cerebral and renal involvement are rare. Antihistone antibodies in 95% complement deficiencies are uncommon. DIL develops after long-term use of certain medications. To meet the criteria for DIL, a patient should have exposure to a suspected drug, no prior history of idiopathic SLE prior to the use of drug, development of ANAs, and at least one clinical feature of SLE and rapid improvement of symptoms with gradual decline in ANAs following drug discontinuation. DIL is most common in men over 50 years old. DIL symptoms are similar to SLE.

Which drugs can cause DIL?


Signs and Symptoms of DIL

Signs and symptoms of drug-induced lupus erythematosus include the following:

  • Joint pain (arthralgia) and muscle pain (myalgia)

  • Fatigue

  • Serositis —inflammation of the tissues lining the heart and lungs.

  • Anti-histone antibodies in 95% of cases among those taking procainamide, hydralazine, chlorpromazine, and quinidine; however, these antibodies have been found in a smaller proportion of patients associated with other medications, including minocycline, propylthiouracil, and statins.

These signs and symptoms are not side effects of the drugs taken which occur during short term use. DIL occurs over long-term and chronic use of the medications listed below. While these symptoms are similar to those of systemic lupus erythematosus, they are generally not as severe unless they are ignored which leads to more harsh symptoms, and in some reported cases, death.




References


  1. ^ Jump up to:a b Rubin, Robert L. (2005-02-04). "Drug-Induced Lupus Erythematosus". Lupus Foundation of America. Archived from the original on 2006-10-13. Retrieved 2006-11-03.

  2. ^ Schur, Peter H., ed. (July 1983). The Clinical Management of Systemic Lupus Erythematosus. New York: Grune & Stratton. p. 221. ISBN 978-0-8089-1543-0.

  3. ^ Lahita, Robert G. (1987). Systemic Lupus Erythematosus. New York: John Wiley & Sons. p. 859. ISBN 978-0-471-87388-4.

  4. ^ 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. doi:10.1021/tx00001a013. PMID 2979715.

  5. ^ Stites, Daniel P (1994). Terr, Abba I.; Parslow, Tristram G. (eds.). Basic & Clinical Immunology. Norwalk, CT: Appleton & Lange. p. 373. ISBN 978-0-8385-0561-8.

  6. ^ 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.

  7. ^ Hofstra A (1994). "Metabolism of hydralazine: relevance to drug-induced lupus". Drug Metab Rev. 26 (3): 485–505. doi:10.3109/03602539408998315. PMID 7924901.

  8. ^ Schur, Peter H. et al. (1983), p. 223.

  9. ^ Chang, Christopher; Gershwin, M. Eric (2010). "Drugs and autoimmunity – A contemporary review and mechanistic approach". Journal of Autoimmunity. 34 (3): J266–J275. doi:10.1016/j.jaut.2009.11.012. PMID 20015613.


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