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Drug-Induced Lupus Erythematosus

  • Author: Ivan D Camacho, MD; Chief Editor: Dirk M Elston, MD  more...
 
Updated: Jun 14, 2016
 

Background

Drug-induced lupus erythematosus (DILE) is a variant of lupus erythematosus that resolves within days to months after withdrawal of the culprit drug in a patient with no underlying immune system dysfunction. DILE can arise months to years after exposure to drugs prescribed to treat various medical conditions (eg, antihypertensives, antibiotics, anticonvulsants). The most common drugs that cause DILE are hydralazine, procainamide, quinidine, isoniazid, diltiazem, and minocycline (see Etiology).[1]

Drug-induced subacute cutaneous lupus erythematosus (DISCLE) is a DILE variant with predominant skin involvement, temporally related to drug exposure, and resolving after drug discontinuation.[2]

Care must be taken to correctly diagnose the symptoms of DILE and differentiate it from systemic lupus erythematosus (SLE), and DILE should be recognized clinically and serologically for prompt intervention.

Although both SLE and DILE are autoimmune disorders and can have similar clinical and laboratory features (see the Table below), research suggests different mechanistic pathways (see Pathophysiology). Guidelines for diagnosis and management of SLE have been established.[3] Although the pathogenesis of DILE is not completely understood, a genetic predisposition may play a role, as has been shown with certain drugs metabolized by acetylation, such as procainamide or hydralazine.[4]

Table. Comparison of Findings Between Drug-Induced Lupus Erythematosus and Systemic Lupus Erythematosus (Open Table in a new window)

Findings SLE DILE
Clinical Average age of onset of 20-30 y



Affects blacks more than whites



Female-to-male ratio of 9:1



Average age of onset of 50-70 y



Affects whites more than blacks



Female-to-male ratio of 1:1



Laboratory Antihistone antibodies in 50%



Anti-dsDNA present in 80%



C3/C4 levels decrease



Cutaneous findings in >75%



Raynaud phenomenon in 50%



Antinuclear antibodies in >95%



Antihistone antibodies in >95%



Anti-ssDNA present



Anti-dsDNA rare C3/C4 levels normal



Cutaneous findings in ~25%



Raynaud phenomenon in 25%



Antinuclear antibodies in >95%



Immunofluorescence Histopathology Direct immunofluorescence reveals granular deposition of IgG at dermoepidermal junction



Lymphohistiocytic interface dermatitis



Apoptosis basal vacuolization



Same as SLE



Same as SLE



DILE = drug-induced lupus erythematosus, IgG = immunoglobulin G; SLE = systemic lupus erythematosus.

A large systematic review of 117 DISCLE cases demonstrated that white women made up the large majority of cases, and the mean age was 58 years. Antihypertensives and antifungals were most frequently the culprits. Time intervals between drug exposure and appearance of DISCLE varied and were drug-class dependent. Most cases resolved within weeks of drug withdrawal. No significant differences in the clinical, histopathological, or immunopathological features between DISCLE and idiopathic SCLE were detected.[5]

Varying mechanisms leading to the formation of self-recognizing antibodies may explain the differential characteristics of drug effects in persons with DILE and those with SLE. For example, whereas some drugs can cause DILE, others may cause a flare of preexisting SLE.

Drugs such as procainamide, chlorpromazine, and quinidine cause the production of antinuclear antibodies against the histone dimer H2A-H2B. Hydralazine forms antinuclear antibodies to H1 and the H3-H4 complex.[6] Drugs that cause DILE usually take months to years before the associated symptoms occur, whereas flares of SLE due to drugs may occur within hours to days.

Most patients with DILE have 1 or more clinical symptoms of SLE, such as arthralgias, lymphadenopathy, rash, and fever, and have had no prior history of autoimmune disease. However, certain manifestations typical in persons with SLE are not usually observed in persons with DILE (see Clinical).

No specific criteria establish the diagnosis of DILE, and excluding underlying autoimmune disease is not a simple process. DILE is typically diagnosed by a process of elimination to rule out SLE (see Differentials).

Symptoms of DILE usually clear within weeks of stopping the culprit drug. Generally, no other specific treatments are known. Low doses of systemic corticosteroids may be prescribed for short periods if the symptoms are severe (see Treatment).

For patient education resources, see the Blood and Lymphatic System Center and the Arthritis Center, as well as Lupus (Systemic Lupus Erythematosus) and Drug Allergy.

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Pathophysiology

SLE and DILE are both autoimmune diseases that cause the immune system to manufacture autoantibodies against the patient’s own tissues. Molecular mimicry between antibodies directed against infectious agents (eg, bacteria, Epstein-Barr virus [EBV]) and self-antigens has been implicated in SLE. These theories hold that in SLE, the immune system generates autoantibodies to foreign antigens, and these autoantibodies, in turn, attack the patient’s own tissues.

In DILE, autoantibodies are thought to be generated by a mechanism other than molecular mimicry. The medications and other exposures implicated in DILE and flares of SLE produce autoantibodies more often than systemic autoimmune symptoms. Despite these commonalities, research suggests that DILE and SLE have separate and distinct mechanistic pathways. Which drug characteristics cause the autoantibody formation is unclear, but several theories have been proposed.

One is that the metabolites of the drug are subjected to oxidative metabolism and serve as a substrate for myeloperoxidase, which is activated in polymorphonuclear neutrophils. This interaction causes the formation of reactive metabolites that directly affect lymphocyte function in the thymus, disrupting central T-cell tolerance to the patient’s own tissues and producing autoimmune T cells against them. Both mouse models and human studies implicate thymic activity, possibly indicating the persistence of thymic activity into advanced adult life.

Virtually all lupus-inducing drugs undergo oxidative metabolism, whereas analogous non–lupus-inducing drugs do not. In a mouse model, reactive metabolites of procainamide injected into the thymus have been shown to result in lupuslike autoantibodies. Unlike drug hypersensitivity reactions, this process takes months to years of drug exposure for symptoms to develop.

A second theory is that with decreased T-cell methylation, an overexpression of lymphocyte function–associated antigen (LFA-1) occurs. T cells with hypomethylated DNA become autoreactive and cause antibody formation. This is the mechanism by which ultraviolet (UV) light causes flares of lupus.

A third theory is that the genetic differences in an individual’s P450 system causes drugs to be metabolized differently, which results in the generation of toxic metabolites that may facilitate autoimmunity.

Predisposing factors to the development of DILE include a slow drug-acetylator phenotype and advancing patient age. Slower acetylation may play a role in the greater predisposition for elderly persons to develop DILE.[4] However, the higher rates of DILE in elderly persons are also likely to be due to decreased drug clearance and increased medication usage in these individuals.

Biologics such as interleukins (eg, interleukin-2 [IL-2]), interferons (eg, alfa, gamma, beta), and tumor necrosis factor alpha (TNF-α) inhibitors are associated with musculoskeletal symptoms and antibody production suggestive of a lupuslike autoimmune disorder. In 1 study, approximately 14% of rheumatoid arthritis patients treated with anti–TNF-α developed anti-DNA antibodies, whereas fewer than 1% developed lupuslike symptoms.

Recognition of DILE in patients receiving anti–TNF-α agents can be difficult.[7] Making the diagnosis of DILE is even more challenging because cutaneous reactions with and without evidence of autoimmunity are very common in patients treated with anti–TNF-α drugs. It is particularly important to understand the temporal relationship between the onset of symptoms and the initiation of the medication, which can range from weeks to months.

A review by Ramos-Casals et al described 105 patients who developed DILE after starting anti–TNF-α therapy; in this group, lupuslike symptoms appeared at a mean time of 41 weeks after the initiation of anti–TNF-α therapy.[8]

As TNF-α–targeted therapies are being used for an expanding number of autoimmune diseases, the number of reports of their induction of lupuslike syndromes has been growing. When one considers the large number of patients now treated with these biologic agents, the incidence of anti–TNF-α–induced DILE is relatively low.[9] Most case reports have involved the use of etanercept or infliximab. Adalimumab is less often the inciting agent; this may simply be the result of fewer cumulative patient years of exposure to adalimumab.

In a report of 33 cases of anti–TNF-α agents causing DILE, Costa et al found that 21 were due to infliximab, 10 to etanercept, and only 2 to adalimumab.[10] Of the 33 patients, 19 had only cutaneous manifestations. Anti–TNF-α agents induce a higher prevalence of antibodies to double-stranded DNA, hypocomplementemia, a higher incidence of both cutaneous and systemic disease, particularly renal involvement, than classic DILE caused by other drugs. Serositis may be clinically significant.[11]

Cutaneous findings in TNF-α–associated DILE commonly include photosensitivity and the classic cutaneous findings associated with discoid lupus erythematosus and subacute cutaneous lupus erythematosus. Cutaneous manifestations are more frequently observed in patients receiving etanercept, whereas infliximab causes a higher incidence of serositis.

Fever is found in similar incidence in both TNF-α inhibitor–induced DILE and DILE caused by other categories of medications. More than 50% of laboratory results in anti–TNF-α–induced DILE patients show low serum complement levels and anti-dsDNA antibodies, which are usually absent or rare findings in classic DILE.

The use of anti–TNF-α agents is also associated with the emergence of other autoantibodies, such as anticardiolipin antibodies. Classic DILE is more often associated with antihistone antibodies. DeBandt looked at the only case of thrombosis in a patient with anticardiolipin antibodies and anti–TNF-α–induced DILE, although half of the anti–TNF-α–related DILE patients studied (12) had anticardiolipin antibodies.[12]

The mechanism by which anti–TNF-α therapy induces DILE is not understood. One hypothesis is that the binding of the anti–TNF-α drug to the cell surface TNF-α induces cell apoptosis, which causes the release of antinucleosomal autoantigens and the induction of anti-dsDNA antibodies.[10]

A second hypothesis is that the suppression of T-helper type 1 response from the anti–TNF-α therapy would generate an exuberant T-helper 2 response, leading to an overproduction of autoantibodies.[13]

A third suggestion regarding the pathogenesis of DILE from these immunosuppressive agents is that patients on these medications may experience more bacterial infections, which are powerful stimulants that boost polyclonal B-lymphocyte activation and autoantibody production.[14]

A baseline evaluation, including serology to rule out lupus erythematosus, should be considered in patients before the initiation of TNF-α therapy.[10] A study demonstrated that the development of DILE after one TNF-alpha antagonist does not preclude continued treatment with an alternative TNF-alpha antagonist.[15]

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Etiology

DILE may be induced by medications or caused by other compounds in the environment. The most common drugs that cause drug-induced SLE are hydralazine (rate roughly 20%), procainamide (rate roughly 20%, 5-8% if taken for 1 y), quinidine, isoniazid, and minocycline.

Drugs most commonly associated with drug-induced SCLE include calcium-channel blockers, angiotensin-converting enzyme inhibitors, thiazide diuretics, terbinafine, TNF-alpha antagonists.[16]

Several broad drug categories have been linked to DILE, including the following:

  • Antiarrhythmics - Procainamide and quinidine
  • Antibiotics – Minocycline [17] , isoniazid, rifabutin [18]
  • Antifungals - Griseofulvin and voriconazole
  • Anticonvulsants - Valproate, ethosuximide, carbamazepine, [19] and hydantoins
  • Hormonal therapy - Leuprolide acetate
  • Antihypertensives - Hydralazine, methyldopa, and captopril
  • Anti-inflammatories - Penicillamine and sulfasalazine [20]
  • Antipsychotics - Chlorpromazine
  • Cholesterol-lowering agents - Lovastatin, simvastatin (DISCLE), atorvastatin, and gemfibrozil
  • Biologics - Interleukins (eg, IL-2), interferons (eg, alfa, beta, gamma), [21] TNF-α (etanercept, infliximab, adalimumab), [8] and rituximab [22]
  • Inhalers - Tiotropium bromide inhaler [23]
  • Chemotherapy agents -Docetaxel, paclitaxel, cabazitaxel (DISCLE), gemcitabine (DISCLE) [24, 25, 26]
  • Other drug categories - Ophthalmic timolol

Additional drugs that may cause DILE include the following:

  • Acebutolol
  • Amiodarone (SLE and SCLE) [27]
  • Atenolol [28]
  • Bupropion
  • Cefepime
  • Diltiazem [29]
  • Doxorubicin (DISCLE) [30]
  • Doxycycline (DISCLE) [31]
  • Esomeprazole (DISCLE) [32]
  • Fluorouracil [33]
  • Glyburide
  • Gold salt
  • Hydroxychloroquine
  • Imiquimod (DISCLE)
  • Lamotrigine [34, 35]
  • Lansoprazole (DISCLE)
  • Lithium
  • Mephenytoin
  • Methimazole (bullous SLE) [36]
  • Nitrofurantoin
  • Olanzapine
  • Omeprazole (DISCLE)
  • Oral contraceptives
  • Phenytoin
  • Practolol
  • Propylthiouracil
  • Reserpine
  • Rifampin
  • Rifamycin [37]
  • Sertraline [38]
  • Tetracycline
  • Ticlopidine
  • Trimethadione

A genetic predisposition may play a role. Hydralazine-induced DILE has been observed with increased frequency in association with human leukocyte antigen (HLA)-DR4.

Intrinsic genetic susceptibility may help explain why some patients experience DILE as a reaction to drug therapies, whereas others do not. For example, the rate of acetylation is genetically predetermined. In the United States, the population is almost evenly divided between those who are fast acetylators and those who are slow acetylators. Those with slow acetylation rates have a higher prevalence of DILE than those with faster acetylation rates. In contrast, SLE affects individuals with slow and fast acetylation rates approximately equally.

Other causes may induce DILE in certain individuals for no apparent reason, such as sensitivity to the following:

  • Insecticide compounds
  • Certain metallic compounds
  • Eosin (a fluorescent acid dye found in some lipsticks)

Drugs that cause flares of SLE are as follows:

  • Cimetidine
  • Hydralazine
  • Hydrochlorothiazide
  • Golimumab (SCLE) [39]
  • Mesantoin
  • Omeprazole (SCLE) [40]
  • Para-aminobenzoic acid (PABA)
  • Penicillin
  • Phenylbutazone
  • Sulfonamides
  • Terbinafine [41]
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Epidemiology

As many as 10% of the approximately 500,000 cases of lupus erythematosus in the United States may be DILE. Patients with DILE tend to be older (50-70 y) than those with SLE (average age 29 y at diagnosis). Elderly persons generally are more susceptible to DILE.

In DILE, no significant statistical difference is apparent in the prevalence for males versus females. In contrast, SLE affects women with considerably higher frequency than men (female-to-male ratio of 9:1). More whites than blacks develop DILE; more blacks than whites present with SLE.

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Prognosis

Prognosis is excellent once the causative medication is discontinued. Recovery generally occurs within days or weeks.

Death from DILE is extremely rare and may result from renal involvement (see Complications). In diagnosing this condition, it is extremely crucial to first exclude the possibility that the patient has renal idiopathic lupus rather than DILE with renal involvement.

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Contributor Information and Disclosures
Author

Ivan D Camacho, MD Dermatologist, Private Practice; Voluntary Assistant Professor of Dermatology, Department of Dermatology and Cutaneous Surgery, University of Miami, Leonard M Miller School of Medicine

Ivan D Camacho, MD is a member of the following medical societies: American Academy of Dermatology, American Medical Association, American Society for Dermatologic Surgery, American Society for MOHS Surgery, Florida Medical Association, International Society of Dermatology, Women's Dermatologic Society

Disclosure: Nothing to disclose.

Coauthor(s)

Catharine Lisa Kauffman, MD, FACP Georgetown Dermatology and Georgetown Dermpath

Catharine Lisa Kauffman, MD, FACP is a member of the following medical societies: American Academy of Dermatology, Royal Society of Medicine, Women's Dermatologic Society, American Medical Association, Society for Investigative Dermatology

Disclosure: Nothing to disclose.

Arden E Fredeking Georgetown University School of Medicine

Arden E Fredeking is a member of the following medical societies: American Medical Student Association/Foundation

Disclosure: Nothing to disclose.

Chief Editor

Dirk M Elston, MD Professor and Chairman, Department of Dermatology and Dermatologic Surgery, Medical University of South Carolina College of Medicine

Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

Acknowledgements

Jeffrey P Callen, MD Professor of Medicine (Dermatology), Chief, Division of Dermatology, University of Louisville School of Medicine

Jeffrey P Callen, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American College of Physicians, and American College of Rheumatology

Disclosure: Amgen Honoraria Consulting; Abbott Honoraria Consulting; Electrical Optical Sciences Consulting fee Consulting; Celgene Honoraria Safety Monitoring Committee; GSK - Glaxo Smith Kline Consulting fee Consulting; TenXBioPharma Consulting fee Safety Monitoring Committee

Craig A Elmets, MD Professor and Chair, Department of Dermatology, Director, UAB Skin Diseases Research Center, University of Alabama at Birmingham School of Medicine

Craig A Elmets, MD is a member of the following medical societies: American Academy of Dermatology, American Association of Immunologists, American College of Physicians, American Federation for Medical Research, and Society for Investigative Dermatology

Disclosure: Palomar Medical Technologies Stock None; Astellas Consulting fee Review panel membership; Massachusetts Medical Society Salary Employment; Abbott Laboratories Grant/research funds Independent contractor; UpToDate Salary Employment; Biogen Grant/research funds Independent contractor; Clinuvel Independent contractor; Covan Basilea Pharmaceutical Grant/research funds Independent contractor; ISDIN None Consulting; TenX BIopharma Grant/research funds Independent contractor

Michael J Wells, MD Associate Professor, Department of Dermatology, Texas Tech University Health Sciences Center, Paul L Foster School of Medicine

Michael J Wells, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, and Texas Medical Association

Disclosure: Nothing to disclose.

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Erythematous macules and papules are seen on face, upper chest, and arms in photodistribution.
Dermis contains interface and superficial and deep perivascular lymphohistiocytic infiltrate (×100, hematoxylin-eosin).
Parakeratosis, apoptosis, and basal vacuolization (×200, hematoxylin-eosin).
Table. Comparison of Findings Between Drug-Induced Lupus Erythematosus and Systemic Lupus Erythematosus
Findings SLE DILE
Clinical Average age of onset of 20-30 y



Affects blacks more than whites



Female-to-male ratio of 9:1



Average age of onset of 50-70 y



Affects whites more than blacks



Female-to-male ratio of 1:1



Laboratory Antihistone antibodies in 50%



Anti-dsDNA present in 80%



C3/C4 levels decrease



Cutaneous findings in >75%



Raynaud phenomenon in 50%



Antinuclear antibodies in >95%



Antihistone antibodies in >95%



Anti-ssDNA present



Anti-dsDNA rare C3/C4 levels normal



Cutaneous findings in ~25%



Raynaud phenomenon in 25%



Antinuclear antibodies in >95%



Immunofluorescence Histopathology Direct immunofluorescence reveals granular deposition of IgG at dermoepidermal junction



Lymphohistiocytic interface dermatitis



Apoptosis basal vacuolization



Same as SLE



Same as SLE



DILE = drug-induced lupus erythematosus, IgG = immunoglobulin G; SLE = systemic lupus erythematosus.
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