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Year : 2022  |  Volume : 8  |  Issue : 2  |  Page : 101-104

Discoid lupus erythematosus like lesions after imatinib therapy: A rare case report

1 Department of Dermatology, Military Hospital, Jabalpur, Madhya Pradesh, India
2 Department of Dermatology, Base Hospital, Lucknow, Uttar Pradesh, India
3 Department of Pathology, Command Hospital, Lucknow, Uttar Pradesh, India
4 Department of Medicine, Command Hospital, Lucknow, Uttar Pradesh, India

Date of Submission12-Jul-2021
Date of Decision27-Mar-2022
Date of Acceptance21-Jun-2022
Date of Web Publication5-Jan-2023

Correspondence Address:
Veena Kharayat
Dept of Dermatology, Military Hospital, Jabalpur
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/ijdd.ijdd_31_21

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How to cite this article:
Kharayat V, Sinha P, Madakshira MG, Prashar M. Discoid lupus erythematosus like lesions after imatinib therapy: A rare case report. Indian J Drugs Dermatol 2022;8:101-4

How to cite this URL:
Kharayat V, Sinha P, Madakshira MG, Prashar M. Discoid lupus erythematosus like lesions after imatinib therapy: A rare case report. Indian J Drugs Dermatol [serial online] 2022 [cited 2023 Dec 7];8:101-4. Available from: https://www.ijdd.in/text.asp?2022/8/2/101/367124


Imatinib mesylate is a small molecule tyrosine kinase inhibitor (TYK), an anticancer drug primarily used for chronic myeloid leukemia (CML) and gastrointestinal stromal tumor (GIST). Like other anticancer drugs, imatinib also has various side effects, cutaneous being the commonest. We herein report a case of likely imatinib induced discoid lupus erythematosus (DLE) in a patient of GIST, a side effect which has not been reported till date in the literature.

A 74-year-old male, a known case of GIST on chemotherapy for past one anda half years, presented with asymptomatic multiple dark colored raised and depigmented depressed lesions on the scalp and face of four months duration. The lesions were insidious in onset, initially dark to violaceous in color, gradually progressed in size and number, started flattening and becoming white in the center over the next three months. He had been on imatinib 400 mg daily for the past fifteen months. Apart from imatinib he was receiving only calcium supplements and vitamins.

General and systemic examination was essentially normal. Dermatological examination revealed multiple, well defined,discrete to coalescing, polysized hyperpigmented atrophic plaques distributed over the face predominantly cheeks, eyelids, forehead, nose and the scalp. Few of the plaques were depigmented and few slightly erythematous in the center with a peripheral rim of violaceous hyperpigmentation [Figure 1] and [Figure 2]. Few plaques were covered with white scales. Carpet tack sign was positive.
Figure 1: Multiple, well defined, polysized, hyperpigmented to violaceous atrophic plaques distributed over the face

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Figure 2: Multiple, well defined, polysized, atrophic palques with depigmented to slightly pinkish centre and peripheral rim of hyperpigmentation on the scalp

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Dermoscopy (Illuco IDS 1100, 10x) of the lesions of the scalp revealed follicular plugging, keratin plugs, diminished follicular ostia, white structureless areas, blue grey dots and globules, variable scales and peripheral brown pigmentation.[Figure 3]
Figure 3: Dermoscopy (Illuco IDS 1100,10x) of the lesions of the scalp revealed follicular plugging (blue arrow), keratin plugs (red arrow),diminished follicular ostia, white structureless areas (yellow stars), blue grey dots and globules (green squares),variable scales (yellow arrow) and peripheral brown pigmentation

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Hematological and biochemical investigations revealed no abnormality. Antinuclear antibodies (ANA), antihistone antibodies, anti- extractable nuclear antigens (ENA) and complement 3 and 4 levels were evaluated, however no abnormality was detected.

Histopathology was consistent with features of DLE. Epidermis showed basket weave keratin with follicular plugging, extensive basal cell layer vacuolar degeneration with formation of civatte bodies [Figure 4]. The adjoining dermis showed a band like lymphomononuclear cell infiltrate associated with melanophages. The deeper dermis showed prominent elastotic degeneration.
Figure 4: HandE A(40x), B(400x) and C (400x) Histopathology showed follicular plugging and basal cell vacuolar degeneration with colloid bodies

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On the basis of the clinical, pathological,dermoscopic correlation and in addition with temporal relationship with imatinib treatment, a diagnosis of DLE was made with possible association with imatinib therapy. Patient continues to be on imatinib and is being managed with tab hydroxychloroquine 200 mg twice a day and topically with midpotent steroid cream and sunscreens.

Imatinib, selectively targets TYK, inhibiting the BCR-ABL protein, c-kit, platelet derived growth factor receptors and serine threonine kinase.[1] It was primarily used for chronic myeloid leukemia and GIST initially. However now, it is also used for various other hematological malignancies like relapsed or refractory ALL, myelodysplastic and myeloproliferative disorders and various dermatological conditions like refractory dermatofibrosarcoma protuberance, aggressive systemic mastocytosis, HIV related Kaposi sarcoma and hypereosinophilic syndrome, sclerodermatous graft versus host disease, systemic sclerosis and melanoma with c- kit mutation.[1],[2],[3]

Imatinib has various adverse effects, the most common being fluid retention causing edema, gastrointestinal like nausea, vomiting, dyspepsia, indigestion, abdominal pain and diarrhea, musculoskeletal like muscle cramps, myalgia, fatigue and joint pain. The less frequent side effects anemia, neutropenia and thrombocytopenia, arrhythmias, severe congestive heart failure and left ventricular dysfunction, hemorrhage at any site and hepatic and renal toxicity.[1]

Cutaneous adverse effect of imatinib have been reported in 9.5% to 69% of the patients.[2] Maculopapular rash, periorbital edema, pruritus, angularchelitisandxerosis are the most common and nonspecific side effect. The clinical distinct ones include Stevens Johnsons syndrome, toxic epidermal necrolysis, acute generalized exanthematouspustulosis, lichenoid reaction, psoriasis and psoriasiform rash, pigmentary disorders like generalized hypo and hyperpigmention, vitiligo and melasma like pigmentation, melanonychia and photosensitivityand pityriasis rosea like rash.[3]

The relatively rare adverse effect include neutrophlic dermatoses, porphyria cutaneous tarda, pseuodoporphyria, leucocytoclastic vasculitis, erythema multiforme, palmoplantar erythrodysesthesia syndrome, mycosis fungoides like reaction and pseudolymphoma type drug reaction.[2]

It is postulated that the cutaneous adverse effects are dose dependent as these are usually observed at doses of 400- 800 mg daily and rarely at sub therapeutic doses (25–140 mg) and are a result of toxic pharmacological effect rather than the immunological effect as imatinib has low molecular weight and the effects are dose dependent[1]

However, to the best of our knowledge imatinib induced discoid lupus erythematosus (DLE) or any other type of lupus erythematosus has not been reported in literature until now. Most common drugs causing lupus are procainamide, hydralazine, quinidine, isoniazid, methyldopa, minocycline, biologicals like secukinumab and TNF-αblockers, fluorouracil derivatives, non-steroidal anti-inflammatory drugs and voriconazole.[4],[5]

Drug induced lupus is classified into systemic and cutaneous LE. Drug induced chronic LE is the rarest cutaneous LE and the lesions most commonly resemble DLE. The lesions appear on an average after 8 months of starting the triggering drug. As there are no standard diagnostic criteria for drug induced lupus erythematosus, temporal relation with the drug, at least one symptom of LE, positive ANA and other lupus serology and absence of autoimmune disorders are proposed to be pivotal for the diagnosis. However, ANA is positive in only about 60–75% of cases of drug induced DLE, anti-histone antibody is rarely detected, ENA is negative, anti-dsDNA is absent and blood counts are generally normal.[4],[5]

In our case lesions of DLE appearing denovo in a patient of GIST on Imatinib, temporal relation with drug (lesions of DLE appeared after more than a year after starting imatinib), and absence of any autoimmune disorder favored the diagnosis of imatinib induced DLE.

The pathogenesis underlying the association between the tyrosine kinase inhibitor and DLE in this case cannot be commented upon precisely,however genetic predisposition for drug induced LE may be considered. Further research/ studies are required for better understanding of the pathomechanism of imatinib induced discoid lupus erythematosus.

We report this new rare association to increase awareness of possible occurrence of this side effect with a commonly administered chemotherapy drug.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

  References Top

Guilhot F Indications for imatinib mesylate therapy and clinical management. Oncologist 2004;9:271-81.  Back to cited text no. 1
Scheinfeld N, Schienfeld N A comprehensive review of imatinib mesylate (gleevec) for dermatological diseases. J Drugs Dermatol 2006;5:117-22.  Back to cited text no. 2
PretelIrazabal M, Tuneu- Valls A, Ormaechea- Perez N Efectosadverosos cutaneous del imatinib (inhibidor de la tirosincinasa). ActasDermosifiliogr 2014;105:655-62.  Back to cited text no. 3
Marzano AV, Vezzoli P, Crosti C Drug-induced lupus: An update on its dermatologic aspects. Lupus 2009;18:935-40.  Back to cited text no. 4
Vedove CD, Del Giglio M, Schena D, Girolomoni G Drug-induced lupus erythematosus. Arch Dermatol Res 2009;301:99-105.  Back to cited text no. 5


  [Figure 1], [Figure 2], [Figure 3], [Figure 4]


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