drug-induced lupus erythematosus
Jump to navigation
Jump to search
Etiology
- general
- low levels of hepatic acetyltransferase may play a role.
- drugs that are metabolized by acetylation are most commonly involved
- antiarrhythmic agents
- procainamide*
- almost all patients develop anti-histone antibodies
- antibodies of IgM class in asymptomatic patients
- IgG antibodies to H2A-H2B dimer in symptomatic patients (also IgM)
- 50% of patients treated with procainamide develop anti-nuclear antibody (ANA) after 1 year
- quinidine
- practolol
- procainamide*
- antihypertensive agents
- hydralazine*
- anti-nuclear Ab (ANA)
- anti-histone Ab
- antibodies to H2A-H2B dimer
- antibodies to H3-H4 complex
- IgM > IgG
- methyldopa (Aldomet)
- beta-blockers
- calcium channel blockers, diltiazem*[3]
- anti-nuclear Ab (ANA), anti-SSA/Ro Ab, anti-histone Ab (rare)
- thiazide diuretics
- anti-nuclear Ab (ANA), anti-SSA/Ro Ab, anti-histone Ab (rare)
- ACE inhibitors[3]
- anti-nuclear Ab (ANA), anti-SSA/Ro Ab, anti-histone Ab (rare)
- hydralazine*
- antibiotics
- anticonvulsive agents
- antituberculous agents
- phenothiazines
- thyroid medications
- biologicals
- interferon-alpha
- anti-nuclear Ab (ANA) in 23-57%
- anti-dsDNA (common)
- anti-histone Ab (rare)
- interleukin-2
- TNF-alpha inhibitors*[3][5][6]
- interferon-alpha
- chemotherapy
- others
- oral contraceptives
* common causes ** minocycline appeared twice in MKSAP questions[3]
Epidemiology
more common in older white patients
Clinical manifestations
- arthralgias & arthritis (90%)
- fever & malaise (40%)
- pleural effusion (50%)
- pulmonary infiltrates (30%)
- serositis
- non-blanching purpuric rash[3]
- renal disease is rare
- low-grade proteinuria[3]
- microscopic hematuria, few WBC in urine; described as active urine sediment[3]
- may be more common with TNF-alpha inhibitor
- neurologic & cutaneous involvement may be more common with TNF-alpha inhibitor[11]
- clinical improvement upon withdrawing the drug
Laboratory
- complete blood count: anemia, leukopenia
- erythrocyte sedimentation rate elevated
- positive antinuclear antibody (ANA) is positive in 100%
- almost all have anti-histone antibodies with older agents
- more variable with newer agents[3]
- anti-histone antibodies less common with TNF-alpha inhibitor[11]
- almost all have anti-histone antibodies with older agents
- lupus erythematous (LE) cell clot (75%)
- low complement levels in 70%; complement levels normal[4]
- antinuclear antibody, anti-histone Ab & anti-ssDNA Ab is typical
- anti-double-stranded DNA (anti-dsDNA) is uncommon, unless caused by TNF-alpha inhibitor
- rheumatoid factor (RF) is positive in 33%
- anti-RNP Ab is uncommon
- anti-Sm Ab is uncommon
- anti-U1 RNP Ab is uncommon
- anti-SSA, anti-SSB uncommon
Management
- identify & stop offending agent
- symptoms resolve 4-6 weeks after stopping offending agent[3]
More general terms
Additional terms
References
- ↑ Clinical Diagnosis & Management by Laboratory Methods, 19th edition, J.B. Henry (ed), W.B. Saunders Co., Philadelphia, PA. 1996, pg 1017-18
- ↑ Mayo Internal Medicine Board Review, 1998-99, Prakash UBS (ed) Lippincott-Raven, Philadelphia, 1998, pg 760-61
- ↑ 3.00 3.01 3.02 3.03 3.04 3.05 3.06 3.07 3.08 3.09 3.10 3.11 3.12 Medical Knowledge Self Assessment Program (MKSAP) 11, 14, 15, 16, 17, 18. American College of Physicians, Philadelphia 1998, 2006, 2009, 2012, 2015, 2018.
Medical Knowledge Self Assessment Program (MKSAP) 19 Board Basics. An Enhancement to MKSAP19. American College of Physicians, Philadelphia 2022 - ↑ 4.0 4.1 Geriatrics Review Syllabus, American Geriatrics Society, 5th edition, 2002-2004
- ↑ 5.0 5.1 Wetter DA and Davis MDP. Lupus-like syndrome attributable to anti-tumor necrosis factor therapy in 14 patients during an 8-year period at Mayo Clinic. Mayo Clin Proc 2009 Nov; 84:979. PMID: https://www.ncbi.nlm.nih.gov/pubmed/19880688
- ↑ 6.0 6.1 Williams EL, Gadola S, Edwards CJ. Anti-TNF-induced lupus. Rheumatology (Oxford). 2009 Jul;48(7):716-20 PMID: https://www.ncbi.nlm.nih.gov/pubmed/19416947
- ↑ Sontheimer RD, Henderson CL, Grau RH. Drug-induced subacute cutaneous lupus erythematosus: a paradigm for bedside-to-bench patient-oriented translational clinical investigation. Arch Dermatol Res. 2009 Jan;301(1):65-70 PMID: https://www.ncbi.nlm.nih.gov/pubmed/18797894
- ↑ Katz U, Zandman-Goddard G. Drug-induced lupus: an update. Autoimmun Rev. 2010 Nov;10(1):46-50. Review. PMID: https://www.ncbi.nlm.nih.gov/pubmed/20656071
- ↑ Chang C, Gershwin ME. Drug-induced lupus erythematosus: incidence, management and prevention. Drug Saf. 2011 May 1;34(5):357-74 PMID: https://www.ncbi.nlm.nih.gov/pubmed/21513360
- ↑ Lowe GC, Henderson CL, Grau RH, Hansen CB, Sontheimer RD. A systematic review of drug-induced subacute cutaneous lupus erythematosus. Br J Dermatol. 2011 Mar;164(3):465-72 PMID: https://www.ncbi.nlm.nih.gov/pubmed/21039412
- ↑ 11.0 11.1 11.2 NEJM Knowledge+ Rheumatology