ChloroquineV1, Istex, Corpus, bibRecord, 000097

Antimalarial lichenoid tissue reactions in patients with pre-existing lupus erythematosus

Identifieur interne : 000097 ( Istex/Corpus ); précédent : 000096; suivant : 000098

Antimalarial lichenoid tissue reactions in patients with pre-existing lupus erythematosus

Auteurs : P. Geraminejad ; M S Stone ; R D Sontheimer

Source :

Lupus [ 0961-2033 ] ; 2004-06.

RBID : ISTEX:EF10B91F688CCB789B5182F71C853BE4BA244474

English descriptors

Teeft :
- Acad dermatol, Aminoquinolone antimalarials, Antimalarial, Antimalarial lichenoid tissue reactions, Apoptosis, Arch dermatol, Basal, Basal vacuolopathy, Cutaneous, Cutaneous lupus erythematosus, Dermatitis, Dermatol, Eruption, Erythematosus, Hydroxychloroquine, Idiopathic, Idiopathic cutaneous, Keratinocyte, Keratinocytes, Lesion, Lichenoid, Lichenoid drug eruptions, Lichenoid drug reactions, Lichenoid tissue reaction, Lupus, Medication, Other medications, Paucicellular interface dermatitis, Quinacrine, Skin disease, Skin lesions, Subacute, Subacute cutaneous lupus erythematosus, Systemic lupus erythematosus.

Abstract

Recently a number of cases of drug induction or exacerbation of lupus erythematosus (LE) specific skin disease have been described in the literature. Many of the responsible medications are also known for their ability to induce a lichenoid tissue reaction. Aminoquinoline antimalarials are currently the first line of therapy in cutaneous LE specific skin disease. Lichenoid tissue reactions are among the most common cutaneous side effects of aminoquinolone antimalarials. We report three cases of aminoquinolone antimalarial induced or exacerbated LE specific skin disease. We also review the pathophysiology of LE specific skin disease and propose a mechanism by which induction of the lichenoid tissue reaction may result in Koebnerization of LE specific skin lesions.

Url:

https://api.istex.fr/ark:/67375/M70-2Z4K7L39-F/fulltext.pdf

DOI: 10.1191/0961203304lu1056cr

Links to Exploration step

ISTEX:EF10B91F688CCB789B5182F71C853BE4BA244474

Le document en format XML

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<abstract xml:lang="en"><p>Recently a number of cases of drug induction or exacerbation of lupus erythematosus (LE) specific skin disease have been described in the literature. Many of the responsible medications are also known for their ability to induce a lichenoid tissue reaction. Aminoquinoline antimalarials are currently the first line of therapy in cutaneous LE specific skin disease. Lichenoid tissue reactions are among the most common cutaneous side effects of aminoquinolone antimalarials. We report three cases of aminoquinolone antimalarial induced or exacerbated LE specific skin disease. We also review the pathophysiology of LE specific skin disease and propose a mechanism by which induction of the lichenoid tissue reaction may result in Koebnerization of LE specific skin lesions.</p>
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         <contrib-group><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>Geraminejad</surname>
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            <p>Recently a number of cases of drug induction or exacerbation of lupus erythematosus                 (LE) specific skin disease have been described in the literature. Many of the                 responsible medications are also known for their ability to induce a lichenoid                 tissue reaction. Aminoquinoline antimalarials are currently the first line of                 therapy in cutaneous LE specific skin disease. Lichenoid tissue reactions are among                 the most common cutaneous side effects of aminoquinolone antimalarials. We report                 three cases of aminoquinolone antimalarial induced or exacerbated LE specific skin                 disease. We also review the pathophysiology of LE specific skin disease and propose                 a mechanism by which induction of the lichenoid tissue reaction may result in                 Koebnerization of LE specific skin lesions.</p>         
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<meta-value> CASE REPORT Antimalarial lichenoid tissue reactions in patients with             pre-existing lupus erythematosus P Geraminejad, MS Stone and RD Sontheimer\Delta             Department of Dermatology, University of Iowa, Iowa city, IA, USA Recently a number of             cases of drug induction or exacerbation of lupus erythematosus (LE) specific skin             disease have been described in the literature. Many of the responsible medications are             also known for their ability to induce a lichenoid tissue reaction. Aminoquinoline             antimalarials are currently the first line of therapy in cutaneous LE specific skin             disease. Lichenoid tissue reactions are among the most common cutaneous side effects of             aminoquinolone antimalarials. We report three cases of aminoquinolone antimalarial             induced or exacerbated LE specific skin disease. We also review the pathophysiology of             LE specific skin disease and propose a mechanism by which induction of the lichenoid             tissue reaction may result in Koebnerization of LE specific skin lesions. Lupus (2004)             13, 473-477. Key words: antimalarials; cutaneous lupus; lichenoid drug eruptions; lupus             erythematosus Introduction Basal epidermal keratinocyte apoptosis is a key feature of             several inflammatory skin diseases. Lichen planus (LP) and cutaneous lupus erythematosus             (LE) fall into this category. Drug eruptions which resemble these conditions are also             characterized by basal keratinocyte apoptosis.1 A lichenoid tissue reaction is also a             significant feature of idiopathic and drug induced LP as well as LE specific skin             lesions.2 Although there are definite histologic differences, the pathomechanisms are             thought to be similar. Aminoquinolone antimalarials are currently the first line of             systemic therapy in cutaneous LE. The ability of antimalarials to induce lichenoid             reactions has been well documented.3,4 However, the induction of cutaneous LE or the             exacerbation of pre-existing cutaneous LE by antimalarials has been less well described             and can result in a particularly confusing scenario for the clinician. The histology of             drug induced cutaneous LE is commonly indistinguishable from idiopathic cutaneous LE.             However, clinicopathologic correlation can help establish the diagnosis. We present a             series of three cases of patients who developed drug induced cutaneous LE secondary to             antimalarial therapy. We also discuss a possible mechanism for these reactions and             provide some clinical guidelines for the diagnosis. Case 1 A 46-year old woman with a             four-year history of systemic lupus erythematosus (SLE) was referred to our department             by her rheumatologist for an extremely pruritic, persistent, erythematous, scaly,             annular eruption with central clearing involving the face, extensor arms and trunk             extending from her shoulders to her upper thighs (Figure 1). Lesions covered both             sunexposed and sun-protected areas. There was no sign of pterygium, pitting or other             nail changes. There was no follicular keratosis of the scalp. Her initial presentation             to rheumatology consisted of inflammatory pulmonary and joint disease. Prednisone and             hydroxychloroquine were initiated by her rheumatologist. She was on no other active             medications at that time. Over the ensuing one to two month period she developed the             above described eruption. As her lungs and joints continued to be symptomatic,             azathioprine was added which allowed good control of disease activity. However, her rash             persisted for several years unimproved. Eventually quinacrine (mepacrine) was added and             the rash flared several weeks later with increased redness and inflammation as well as             further extension along the arms and thighs including a significant proportion of non             sun-exposed skin. \Delta Correspondence: Richard D Sontheimer, Department of             Dermatology, University of Iowa, BT2045-1, 200 Hawkins Drive, Iowa City, IA 52242, USA.             E-mail: richard-sontheimer@uiowa.edu Received 17 November 2003; accepted 10 February             2004 Lupus (2004) 13, 473-477 www.lupus-journal.com # Arnold 2004             10.1191/0961203304lu1056cr Other medications initiated between the initial flare and the             initiation of quinacrine include buspirone, lansoprazole, atenolol, amitryptiline and             coumadin, all of which had been used for at least one year prior to the initiation of             the quinacrine. Clinically her rash was consistent with annular subacute cutaneous LE             (SCLE), however it was slightly more extensive than typical involving not only the upper             trunk but the lower trunk and parts of the upper thighs. A biopsy from the right upper             back showed interface dermatitis with basal vacuolopathy, perivascular lymphocytic             infiltrate and mucin deposition of the dermis consistent with cutaneous LE. There were             no neutrophils or eosinophils (Figure 2). Hydroxychloroquine and quinacrine were             simultaneously discontinued. All other medications remained unchanged. Over the next             three months with no other therapy, the patient experienced marked clearing of lesions.             The patient has now been followed for an eight-month period extending from November when             the hydroxychloroquine was discontinued until July and continues to be clear of skin             changes, which had persisted for four years while on hydroxychloroquine. Case 2 A             51-year old female with a six-year history of SLE on hydroxychloroquine was seen in             referral for persistent erythema and superficial erosion of the lower lip consistent             with lupus cheilitis. Quinacrine was initiated in addition to the hydroxychloroquine.             The patient's only other medications were prempro, lanoxin and arthrotek, all of which             she had been using for several years. Over the next four weeks the patient developed             pruritic thick scaly erythematous papules and plaques on the arms, hands, abdomen and             lower legs (Figure 3a and b). The plaques contained follicular keratotic papules and             upon pealing the plaque a positive carpet tack sign could be elicited. The lesions were             clinically consistent with discoid lupus erythematosus (DLE). The lesions were not             restricted to sun-exposed areas. The patient's only cutaneous involvement previous to             this was her lip. A biopsy from the right dorsal hand showed alternating areas of             lichenoid infiltrate and paucicellular interface dermatitis with basal vacuolopathy and             prominent keratinocyte necrosis. Areas of alternating epidermal hyperplasia and             epidermal attenuation were also present. Numerous plasma cells as well as rare             eosinophils were present in the lichenoid infiltrate (Figure 4). GMS, gram stain, AFB             and Steiner stain were negative for organisms. There was mildly increased mucin. The             pathologic findings were consistent with cutaneous LE. Hydroxychloroquine and quinacrine             were discontinued. The trunkal and extremity skin lesions resolved over the next three             months, however many healed with atrophic scarring. The lesion on the lip persisted. At             four-year follow up the patient remains without trunkal or extremity skin lesions. Case             3 A 47-year old female with history of SCLE was seen for evaluation of a one-year             history of persistent but stable erythematous papulosquamous plaques on the face, upper             trunk, upper back and bilateral upper extensor arms. The lesions were predominantly in a             sun-exposed distribution. There were no nail changes and there was no obvious follicular             keratosis of the scalp. Biopsy from the right upper back revealed hyperkeratosis and             parakeratosis with follicular plugging with irregular acanthosis of the epidermis. There             were discontiguous islands of atypical keratinocytes in the upper dermis. There was             prominent interface dermatitis with Figure 1 Annular plaques with central clearing and             yellowish collarette scale in patient 1. Figure 2 Interface dermatitis with apoptotic             keratinocytes and abundant dermal mucin in patient 1. Hematoxylin and eosin stained at             100\Theta original magnification. Antimalarial lichenoid tissue reactions in cutaneous             LE P Geraminejad et al. 474 Lupus dyskeratotic keratinocytes and increased dermal mucin             consistent with LE (Figure 5). Her only treatment was topical steroids. The patient's             only other medication was a daily multivitamin. Over the previous year the patient             failed multiple trials of topical steroids. The patient was started on             hydroxychloroquine and over the next four weeks developed progression of lesions to the             lower arms, hands and upper legs as well as worsening pruritus of lesions. Both             sun-exposed and non sun-exposed areas were involved. The lesions were clinically             indistinguishable from those on the upper torso present prior to initiation of the             medication. Therefore it was felt that no further histologic examination was necessary.             Hydroxychloroquine was discontinued and her disease returned to its previous state over             the next several months, involving only the upper arms, upper back and chest. At             two-year follow up her lesions remain stable with no subsequent progression. Discussion             Many of the drugs reported as capable of inducing cutaneous LE (predominantly SCLE) are             also well known for their ability to cause lichenoid drug eruptions. These include             thiazide diuretics, diltiazem, terbinafine, phenytoin, TNF (tumor necrosis factor)             inhibitors, antihistamines, cilazapril, griseofulvin, piroxicam, penicillamine,             procainamide, oxyprenolol, ACE inhibitors and PUVA.5 - 14 Antimalarials such as             hydroxychloroquine, chloroquine and quinacrine are also capable of inducing lichenoid             tissue reactions.4 Experience with quinacrine used for malaria prophylaxis in the second             world war shows that lichenoid skin eruptions were the most common adverse effect of             this drug.3 However, it should be remembered that higher daily doses of quinacrine (300-             400 mg/day) were Figure 3 (a, b) Thick scaly erythematous papules and plaques on the             arms and hands of patient 2. Figure 4 Alternating lichenoid and paucicellular interface             dermatitis with basal vacuolopathy and prominent keratinocytes apoptosis/necrosis.             Hematoloxylin and eosin stained at 100\Theta original magnification. Figure 5 Prominent             interface dermatitis with dyskeratotoic keratinocytes and increased dermal mucin             consistent with LE. Hematoxylin and eosin stained at 100\Theta original magnification.             Antimalarial lichenoid tissue reactions in cutaneous LE P Geraminejad et al. 475 Lupus             commonly used than compared to today (100 mg/day).15 Induction or exacerbation of             cutaneous LE by antimalarials has been reported informally but not well documented.16,17             The development of lichenoid drug eruptions and cutaneous LE as a result of many of the             same medications may be explained by a review of the pathophysiology of these respective             conditions. Keratinocyte apoptosis is the most prominent mechanism of cell death in             lichenoid drug reactions. Lichenoid drug reactions refer to those drug reactions showing             a bandlike infiltrate of lymphocytes at the dermoepidermal junction associated with             vacuolopathic degeneration of basal keratinocytes and colloid body formation.             Ultrastructural detail reveals intracellular vacuoles and separation of basal cells from             each other as well as the lamina lucida, consistent with apoptotic cell death.18             Although a precise pathomechanism with ordered events is not known for cutaneous LE, a             number of likely key events have been described. Apoptosis or necrosis of basal layer             keratinocytes, induced by UV light or other causes, is likely among the initiating             events.18 Other factors include increased expression of dermal and epidermal             inflammatory mediators such as TNF, IL-1a (interleukin-1 alpha), LFA-1 (leukocyte             function associated antigen-1) and ICAM-1(intercellular adhesion molecule-1),             respectively.19 It is also thought that immunization to neoantigens exposed either by             necrosis or apoptosis by inflammatory cells recruited by chemokine and adhesion molecule             expression including LFA-1 and ICAM-1 occurs. In the case of SCLE, Ro may be one of             these significant antigens.20 Recent evidence has shown that many of the antigens             involved in autoantibody formation in LE, are more susceptible to cleavage by enzymes of             the apoptotic cascade.21-24 This may enhance the immunogenicity of these auto-antigens.             Finally, defects or deficiency of complement components is thought to play a role.25 One             possible explanation for this is the recent observation that keratinocyte apoptotic             blebs are removed by direct binding to the C1q complement component.26 Considering these             observations, it is not inconceivable that drugs capable of causing lichenoid drug             eruptions and basal keratinocyte apoptosis may also result in cutaneous LE reactions in             patients with certain predisposing immunologic phenotypes. The induction of basal             keratinocyte apoptosis in these individuals may be best conceptualized as a             Koebnerizining phenomenon which initiates the subsequent cascade of events described             earlier which leads to LE specific lesions. (Koebnerization in dermatologic conditions             refers to the appearance of the dermatologic condition in traumatized skin.) These             patients commonly form anti-Ro antibodies supporting the concept that these are true LE             specific skin lesions. In the majority of patients without LE predisposing factors, a             routine lichenoid drug eruption may develop. Overlap between cutaneous LE and LP is well             recognized. Drug induced cutaneous LE and lichenoid drug reactions can also show some             overlap. However, there are some distinguishing features. Drug induced LE typically has             both areas of paucicellular interface dermatitis and lichenoid dermatitis in the same             histologic section. Drug induced LE also typically has mucin in the dermis. The             epidermis in drug induced LE lacks the typical epidermal features of lichen planus such             as wedge shaped hypergranulosis and saw toothing. Lastly, drug induced LE often shows an             atrophic epidermis or atrophy alternating with areas of hyperplasia. All patients in our             series had histologic characteristics suggestive of idiopathic or drug induced cutaneous             LE by all these criteria. Our patient's clinical characteristics were also consistent             with classic descriptions of cutaneous LE. The histopathology of drug induced LE             specific lesions typically cannot be distinguished from idiopathic cutaneous LE. Tissue             or blood eosinophilia may support a drug induced etiology. Additionally preferential             migration of lymphocytes into acrosyrngium and small foci of palisading interstitial             granulomatous inflammation can suggest a drug reaction.27 However, the absence of any of             these features does not preclude the possibility of drug induced LE specific lesions.             Patient 1 had a biopsy consistent with typical LE and distinction from idiopathic LE             could not be made on histologic findings alone. Patient 2 had a denser lichenoid             infiltrate as well as areas of more paucicellular interface dermatitis with rare             eosinophils. Prominent involvement of the acrosyrngium was also seen. These are features             consistent with drug induced LE. As is typically the case, clinicopathologic correlation             was necessary to determine the drug induced nature of the LE specific lesions. Direct             immunofluorescence was not obtained in any of our patients. The test is positive in 60%             of SCLE patients in lesional skin and can also be positive in drug induced cases of             SCLE28 It is also commonly positive in nonlesional skin of SLE patients as well as             actinically damaged skin. Patients 1 and 2 from our series had SLE. Thus if a lupus band             was present in a skin lesion of one of our patients it would not have necessarily             distinguished between drug induced and idiopathic cutaneous LE. It is also of interest             that the skin lesions in each of our three cases that were thought to have resulted from             drug exposure were pruritic. Idiopathic LE-specific skin lesions are characteristically             non-pruritic. It is the authors' impressions that a considerable majority of patients             with lichenoid drug reactions experience pruritus, often being quite severe.             Antimalarial lichenoid tissue reactions in cutaneous LE P Geraminejad et al. 476 Lupus             In a large majority of patients with cutaneous LE a good response would be expected from             a combination of two antimalarials. Therefore the development of a flare four to eight             weeks following the initiation of aminoquinolone antimalarials and progression of skin             lesions to non sun-exposed skin, particularly below the waist, can be a valuable clue to             the diagnosis. However, we have also considered the possibility that these patients             happened to have a natural flare of cutaneous LE after starting antimalarials. It is             also possible that they were particularly resistant to antimalarials and their disease             course remitted at the same time the medications were discontinued. While patient 1 has             been followed for eight months, patients 2 and 3 have been followed for a range of three             to six years and have not flared while off of antimalarials. In light of the severity of             the cutaneous reaction in our patients we did not rechallenge with the suspected             antimalarials. Patients 1 and 2 had most improvement with the removal of both             hydroxychloroquine and quinacrine, suggesting both medications were involved. However,             in the event of an eruption with hydroxychloroquine, rechallenge with chloroquine would             not be an unreasonable option as there is often no crossreactivity noted clinically             (personal unpublished experience, RDS). Although our patients had a strong background             predisposition for LE, reports in the literature include patients with no history of             cutaneous or systemic LE developing drug induced LE specific lesions.7 It has been             reported that the incidence of lichenoid drug eruptions is significantly higher among             dermatomyositis patients relative to LE patients,29 although this has not been the             experience of the senior author (RDS). The reason for this is unclear, one contributing             factor may be the tendency for drug reactions causing basal layer apoptosis to progress             to LE specific lesions rather than typical lichenoid drug reactions, in the LE             predisposed patient. These lesions may be indistinguishable from the rest of the             patient's skin disease resulting in under recognition of this condition. 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<mods version="3.6"><titleInfo lang="en"><title>Antimalarial lichenoid tissue reactions in patients with pre-existing lupus erythematosus</title>
</titleInfo>
<titleInfo type="alternative" lang="en" contentType="CDATA"><title>Antimalarial lichenoid tissue reactions in patients with pre-existing lupus erythematosus</title>
</titleInfo>
<name type="personal"><namePart type="given">P</namePart>
<namePart type="family">Geraminejad</namePart>
<affiliation>Department of Dermatology, University of Iowa, Iowa city, IA, USA</affiliation>
</name>
<name type="personal"><namePart type="given">M S</namePart>
<namePart type="family">Stone</namePart>
<affiliation>Department of Dermatology, University of Iowa, Iowa city, IA, USA</affiliation>
</name>
<name type="personal"><namePart type="given">R D</namePart>
<namePart type="family">Sontheimer</namePart>
<affiliation>Department of Dermatology, University of Iowa, Iowa city, IA, USA,</affiliation>
<affiliation>E-mail: richard-sontheimer@uiowa.edu</affiliation>
</name>
<typeOfResource>text</typeOfResource>
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<originInfo><publisher>Sage Publications</publisher>
<place><placeTerm type="text">Sage CA: Thousand Oaks, CA</placeTerm>
</place>
<dateIssued encoding="w3cdtf">2004-06</dateIssued>
<copyrightDate encoding="w3cdtf">2004</copyrightDate>
</originInfo>
<language><languageTerm type="code" authority="iso639-2b">eng</languageTerm>
<languageTerm type="code" authority="rfc3066">en</languageTerm>
</language>
<abstract lang="en">Recently a number of cases of drug induction or exacerbation of lupus erythematosus (LE) specific skin disease have been described in the literature. Many of the responsible medications are also known for their ability to induce a lichenoid tissue reaction. Aminoquinoline antimalarials are currently the first line of therapy in cutaneous LE specific skin disease. Lichenoid tissue reactions are among the most common cutaneous side effects of aminoquinolone antimalarials. We report three cases of aminoquinolone antimalarial induced or exacerbated LE specific skin disease. We also review the pathophysiology of LE specific skin disease and propose a mechanism by which induction of the lichenoid tissue reaction may result in Koebnerization of LE specific skin lesions.</abstract>
<subject><genre>keywords</genre>
<topic>antimalarials</topic>
<topic>cutaneous lupus</topic>
<topic>lichenoid drug eruptions</topic>
<topic>lupus erythematosus</topic>
</subject>
<relatedItem type="host"><titleInfo><title>Lupus</title>
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<identifier type="ISSN">0961-2033</identifier>
<identifier type="eISSN">1477-0962</identifier>
<identifier type="PublisherID">LUP</identifier>
<identifier type="PublisherID-hwp">splup</identifier>
<part><date>2004</date>
<detail type="volume"><caption>vol.</caption>
<number>13</number>
</detail>
<detail type="issue"><caption>no.</caption>
<number>6</number>
</detail>
<extent unit="pages"><start>473</start>
<end>477</end>
</extent>
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Antimalarial lichenoid tissue reactions in patients with pre-existing lupus erythematosus

Antimalarial lichenoid tissue reactions in patients with pre-existing lupus erythematosus

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