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Lichen planus induced by carbamazepine: A case report
Epilepsy & Behavior 24 (2012) 269–271
Contents lists available at SciVerse ScienceDirect
Epilepsy & Behavior journal homepage: www.elsevier.com/locate/yebeh
Case Report
Lichen planus induced by carbamazepine: A case report S. Hajnsek a, b, c,⁎, V. Milavec-Puretic a, b, d, S. Nankovic a, b, c, Z. Petelin Gadze a, b, c, I. Filipcic a, b, e, A. Bujan Kovac a, b, c, D. Stulhofer Buzina a, b, d a
University Hospital Center Zagreb, Zagreb, Croatia School of Medicine, Zagreb, Croatia Department of Neurology, Referral Center for Epilepsy of the Ministry of Health of the Republic of Croatia, Kišpatićeva 12, 10000 Zagreb, Croatia d Department of Dermatology and Venereology, Referral Center for Contact Allergy of the Ministry of Health of the Republic of Croatia, Salata 2, 10000 Zagreb, Croatia e Department of Psychiatry, Kišpatićeva 12, 10000 Zagreb, Croatia b c
a r t i c l e
i n f o
Article history: Received 20 March 2012 Accepted 27 March 2012 Available online 6 May 2012 Keywords: Epilepsy Long-term carbamazepine therapy Lichen planus
a b s t r a c t We report a case of Lichen planus in a female patient who has been treated for epilepsy in the Referral Center for Epilepsy of the Ministry of Health of the Republic of Croatia. She was diagnosed with mesio-temporal lobe epilepsy with secondary generalization and had been treated for years with carbamazepine. In Novemeber 2009, erythematous papulosquamous papules were noticed on her trunk and under her breasts which spread to her legs. Dermatohistological testing confirmed the diagnosis of Lichen planus. Replacement of carbamazepine with oxcarbazepine and application of steroid therapy resulted in regression of skin changes. © 2012 Elsevier Inc. All rights reserved.
1. Introduction Lichen planus is a chronic papulosquamous dermatosis of unclear etiology, usually thought to be caused by viruses and/or autotoxic reactions. It was first described by Kaposi in 1982, as Lichen ruber pemphigoides. Clinically, it presents as a typical eruption of lichen red and blue papules on the skin surface of a waxy shine. After a while, papules change color and become brown [1]. Diagnosis is made on the basis of clinical presentation and histological and immunological findings. Some medications have been implicated with the development of Lichen planus, usually beta blockers, methyldopa, penicillamine, quinidine, quinine and rarely angiotensin converting enzyme inhibitors, sulfonylurea agents, carbamazepine, gold, lithium, and nonsteroidal antiinflammatory agents [2]. We report a case of a patient with a history of complex partial seizures with secondary generalization, who developed Lichen planus as a side effect of long-term carbamazepine therapy. 2. Case report We report a case of a 71-year-old female patient, with no family history for epilepsy, as well as with normal premorbid medical history until 1952, when she suffered head trauma and concussion.
⁎ Corresponding author at: Department of Neurology, Referral Center for Epilepsy of the Ministry of Health of the Republic of Croatia, Kišpatićeva 12, 10000 Zagreb, Croatia. Fax: + 385 1 2376021. E-mail address: [email protected] (S. Hajnsek). 1525-5050/$ – see front matter © 2012 Elsevier Inc. All rights reserved. doi:10.1016/j.yebeh.2012.03.037
In 1958, at the age of 19 and during her first pregnancy, she started having seizures. According to the clinical semiology, they were complex partial seizures of mesial temporal lobe origin. Seizures were preceded by elementary auditory hallucinations (“ringing in the ears”) and followed by temporal pseudoabsence with oroalimentary automatisms. In the postictal phase, she was confused for a short period of time, with headaches and non-fluent motor dysphasia. The seizures lasted for several minutes. At first, seizures were very rare, but since 1966, they began to emerge once a month, mostly in the morning and showed a catamenial character. On three occasions, seizures with secondary generalization were observed. She was referred to the Referral Center for Epilepsy of the Ministry of Health of the Republic of Croatia in September 1966. Electroencephalogram (EEG) at that time pointed to a left temporal focus. She was treated with several antiepileptic drugs (AEDs) — phenytoin, methylphenobarbitone, sulthiame, and primidone, but only when carbamazepine was introduced as monotherapy in 1984 did her seizures go into remission. Considering the fact that she was in remission for a long period of time, in the last 5 years, carbamazepine was reduced to a maintenance dose of 400 mg BID (b.i.d). During the course of her treatment at the Center for Epilepsy, brain CT and brain MRI were normal. In Novemeber 2009, non-itching erythematous papulosquamous papules were first noticed on her trunk and under her breasts which spread to her legs. Thus, carbamazepine was discontinued, and the patient was hospitalized in the Department of Dermatology and Venereology, University Hospital Center Zagreb. The prominent symptom at admission was itching of the feet. Erythematosquamous papules were noted, 5 mm in diameter on the lower part of the abdomen and in the scapular region, confluating and forming larger plaques
270
S. Hajnsek et al. / Epilepsy & Behavior 24 (2012) 269–271 Table 1 Skin side effects caused by carbamazepine therapy. Modified according to Litt J [6]. Skin side effects
Fig. 1. Typical changes of the skin — erythematosquamous papules, 5 mm in diameter on the back, confluating and forming larger plaques.
(Fig. 1). On the wrist and on both ankles, they had waxy shine, while the palmar and plantar skin was yellowish-erythematous with desquamation and with a clearly marked edge (Fig. 2). During the hospitalization, complete immunological testing was done; results of which were normal. A skin biopsy showed that it was Lichen planus in exanthematous form. In vitro lymphocyte transformation test (TTL) was performed, which turned out positive for carbamazepine. We conducted a combined therapy with corticosteroids and neutral preparations under occlusion on the affected areas of the skin, which resulted in regression of skin changes and which made the skin typically brown pigmented. After discharge, she continued topical betamethasone treatment in a neutral base. Upon the occurrence of exanthema, carbamazepine was excluded from the therapy, and oxcarbazepine was introduced at a dose of 600 mg BID, on which the patient remains seizure free. 3. Discussion We present a single case report of carbamazepine-associated Lichen planus in a woman with temporal lobe epilepsy. Lichen planus is a chronic papulosquamous dermatosis of unclear etiology, which affects 1–2% of the population [3,4]. Clinically, it is manifested by the typical eruption of lichen red and blue papules on the skin surface of a waxy shine. In the regression phase, papule color changes and becomes brown [1]. Administration of carbamazepine may lead to an eruption of various skin lesions (Table 1), but lichenoid eruptions are rare after prolonged use of the drug [5–7]. Atkin et al. reported a case of lichenoid skin eruption following a 3-month administration of carbamazepine in a dose of 100 mg TID [8], and Yasuda et al. reported a case of photosensitive lichenoid reaction after receiving 200 mg of carbamazepine daily for 1 year [9]. Skin side effects following carbamazepine therapy should always be taken seriously, and carbamazepine treatment must immediately be stopped in nearly all instances. In our patient, long-term carbamazepine treatment resulted in skin changes in the form of erythematosquamous papules on the trunk,
Hypersensitivity Toxic epidermal necrolysis (TEN) Stevens–Johnson syndrome (SJS) Lupus erythematosus Exfoliative dermatitis or erythroderma Exanthems DRESS syndrome Erythema multiforme Rash Diaphoresis Anticonvulsant hypersensitivity syndrome Urticaria Fixed eruptions Photosensitivity Purpura Dermatitis Acute generalized exanthematous pustulosis (AGEP) Lichenoid eruption Pruritus Pseudolymphoma Angioedema Lymphoproliferative disease Pustules Vasculitis Bullous dermatitis Mycosis fungoides Toxic pustuloderma Eczema Lymphoma Erythema nodosum (EN)
Incidence
(1–10%) (1–10%)
(> 5)
(> 10%) (1–10%)
(b1%)
(b1%) (b1%)
(b1%)
Number of cases in the literature 53 46 45 34 34 27 17 17 17 16 12 10 9 8 7 6 6 6 6 5 5 5 5 4 3 3 2 2
(b1%)
Rare side effects (one case described in the literature): acne keloid, collagen disease, edema, eosinophilic pustular folliculitis (Ofuji), bullous epidermolysis, erythema (sheet-like), facial edema, linear IgA bullous dermatosis, pemphigus, peripheral edema, petechiae, pigmentation, psoriasis, Schamberger's disease, toxic-allergic shock, and toxicoderma.
on both wrists and ankles, with a waxy shine and with yellowisherythematous desquamation of the palms and soles. Testing done excluded immunological etiology of the condition [10,11], in vitro lymphocyte transformation test (TTL) was performed and turned out positive for carbamazepine [12,13], while dermatohistological testing confirmed the diagnosis of Lichen planus [1]. Combined topical therapy with corticosteroids was applied that led to the regression of skin changes, and consistent with the literature, the skin pigmentation became brown [1]. Contributors' statement All authors have equally contributed to this article including literature search, data collection, interpretation and writing. Role of the funding source We confirm that no funding source had any involvement in creating this article. Patients' consent and permission to publish We confirm that we have obtained patient's consent and permission to publish. References
Fig. 2. Skin changes of the palms — yellowish-erythematous skin with desquamation.
[1] Lipozenčić J. Lichen planus. In: Lipozenčić J, et al, editor. Dermatovenerologija, Zagreb: Medicinska naklada; 2008. p. 234–7. [2] Thompson DF, Skaehill PA. Drug induced lichen planus. Pharmacotherapy 1994;14:561–71.
S. Hajnsek et al. / Epilepsy & Behavior 24 (2012) 269–271 [3] DeRossi SS, Ciarrocca KN. Lichen planus, lichenoid drug reactions, and lichenoid mucositis. Dent Clin N Am 2005;49:77–89. [4] Scully C, Eisen D, Carrozzo M. Management of oral lichen planus. Am J Clin Dermatol 2000;1:287–306. [5] Litt J. Drug eruption reference manual. 2000 Millennium Edition. New York: The Parthenon, Publishing Group; 2000. pp. 635–636. [6] Litt J. Litt's drug eruptions and reactions manual. Seventeenth Edition. London: Informa; 2011. pp. 102–104. [7] Roberts DL, Marks R. Skin reactions to carbamazepine. Arch Dermatol 1981;117:273–5. [8] Atkin SL, McKenzie TMM, Stevenson CJ. Carmabazepine-induced lichenoid eruption. Clin Exp Dermatol 1990;15:382–3.
271
[9] Yasuda S, Mizuno N, Kawabe Y, Sakakibara S. Photosensitive lichenoid reaction accompanied by nonphotosensitive subacute prurigo caused by carbamazepine. Photodermatol 1988;5:206–10. [10] Roujeau JC. Immune mechanisms in drug allergy. Allergol Int 2006;55:27–33. [11] Livni E, Halevy S, Stahl B, Joshua H. The appearance of macrophage migration–inhibition factor in drug reactions. J Allergy Clin Immunol 1987;80(6): 843–9. [12] Warrington RJ, Tse KS. The lymphocyte transformation studies in drug hypersensitivity. Can Med Assoc J 1979;120:1089–94. [13] Nyfeler B, Pichler WJ. The lymphocyte transformation test for diagnosis of drug allergy: sensitivity and specificity. Clin Exp Allergy 1997;27:175–81.
Contents lists available at SciVerse ScienceDirect
Epilepsy & Behavior journal homepage: www.elsevier.com/locate/yebeh
Case Report
Lichen planus induced by carbamazepine: A case report S. Hajnsek a, b, c,⁎, V. Milavec-Puretic a, b, d, S. Nankovic a, b, c, Z. Petelin Gadze a, b, c, I. Filipcic a, b, e, A. Bujan Kovac a, b, c, D. Stulhofer Buzina a, b, d a
University Hospital Center Zagreb, Zagreb, Croatia School of Medicine, Zagreb, Croatia Department of Neurology, Referral Center for Epilepsy of the Ministry of Health of the Republic of Croatia, Kišpatićeva 12, 10000 Zagreb, Croatia d Department of Dermatology and Venereology, Referral Center for Contact Allergy of the Ministry of Health of the Republic of Croatia, Salata 2, 10000 Zagreb, Croatia e Department of Psychiatry, Kišpatićeva 12, 10000 Zagreb, Croatia b c
a r t i c l e
i n f o
Article history: Received 20 March 2012 Accepted 27 March 2012 Available online 6 May 2012 Keywords: Epilepsy Long-term carbamazepine therapy Lichen planus
a b s t r a c t We report a case of Lichen planus in a female patient who has been treated for epilepsy in the Referral Center for Epilepsy of the Ministry of Health of the Republic of Croatia. She was diagnosed with mesio-temporal lobe epilepsy with secondary generalization and had been treated for years with carbamazepine. In Novemeber 2009, erythematous papulosquamous papules were noticed on her trunk and under her breasts which spread to her legs. Dermatohistological testing confirmed the diagnosis of Lichen planus. Replacement of carbamazepine with oxcarbazepine and application of steroid therapy resulted in regression of skin changes. © 2012 Elsevier Inc. All rights reserved.
1. Introduction Lichen planus is a chronic papulosquamous dermatosis of unclear etiology, usually thought to be caused by viruses and/or autotoxic reactions. It was first described by Kaposi in 1982, as Lichen ruber pemphigoides. Clinically, it presents as a typical eruption of lichen red and blue papules on the skin surface of a waxy shine. After a while, papules change color and become brown [1]. Diagnosis is made on the basis of clinical presentation and histological and immunological findings. Some medications have been implicated with the development of Lichen planus, usually beta blockers, methyldopa, penicillamine, quinidine, quinine and rarely angiotensin converting enzyme inhibitors, sulfonylurea agents, carbamazepine, gold, lithium, and nonsteroidal antiinflammatory agents [2]. We report a case of a patient with a history of complex partial seizures with secondary generalization, who developed Lichen planus as a side effect of long-term carbamazepine therapy. 2. Case report We report a case of a 71-year-old female patient, with no family history for epilepsy, as well as with normal premorbid medical history until 1952, when she suffered head trauma and concussion.
⁎ Corresponding author at: Department of Neurology, Referral Center for Epilepsy of the Ministry of Health of the Republic of Croatia, Kišpatićeva 12, 10000 Zagreb, Croatia. Fax: + 385 1 2376021. E-mail address: [email protected] (S. Hajnsek). 1525-5050/$ – see front matter © 2012 Elsevier Inc. All rights reserved. doi:10.1016/j.yebeh.2012.03.037
In 1958, at the age of 19 and during her first pregnancy, she started having seizures. According to the clinical semiology, they were complex partial seizures of mesial temporal lobe origin. Seizures were preceded by elementary auditory hallucinations (“ringing in the ears”) and followed by temporal pseudoabsence with oroalimentary automatisms. In the postictal phase, she was confused for a short period of time, with headaches and non-fluent motor dysphasia. The seizures lasted for several minutes. At first, seizures were very rare, but since 1966, they began to emerge once a month, mostly in the morning and showed a catamenial character. On three occasions, seizures with secondary generalization were observed. She was referred to the Referral Center for Epilepsy of the Ministry of Health of the Republic of Croatia in September 1966. Electroencephalogram (EEG) at that time pointed to a left temporal focus. She was treated with several antiepileptic drugs (AEDs) — phenytoin, methylphenobarbitone, sulthiame, and primidone, but only when carbamazepine was introduced as monotherapy in 1984 did her seizures go into remission. Considering the fact that she was in remission for a long period of time, in the last 5 years, carbamazepine was reduced to a maintenance dose of 400 mg BID (b.i.d). During the course of her treatment at the Center for Epilepsy, brain CT and brain MRI were normal. In Novemeber 2009, non-itching erythematous papulosquamous papules were first noticed on her trunk and under her breasts which spread to her legs. Thus, carbamazepine was discontinued, and the patient was hospitalized in the Department of Dermatology and Venereology, University Hospital Center Zagreb. The prominent symptom at admission was itching of the feet. Erythematosquamous papules were noted, 5 mm in diameter on the lower part of the abdomen and in the scapular region, confluating and forming larger plaques
270
S. Hajnsek et al. / Epilepsy & Behavior 24 (2012) 269–271 Table 1 Skin side effects caused by carbamazepine therapy. Modified according to Litt J [6]. Skin side effects
Fig. 1. Typical changes of the skin — erythematosquamous papules, 5 mm in diameter on the back, confluating and forming larger plaques.
(Fig. 1). On the wrist and on both ankles, they had waxy shine, while the palmar and plantar skin was yellowish-erythematous with desquamation and with a clearly marked edge (Fig. 2). During the hospitalization, complete immunological testing was done; results of which were normal. A skin biopsy showed that it was Lichen planus in exanthematous form. In vitro lymphocyte transformation test (TTL) was performed, which turned out positive for carbamazepine. We conducted a combined therapy with corticosteroids and neutral preparations under occlusion on the affected areas of the skin, which resulted in regression of skin changes and which made the skin typically brown pigmented. After discharge, she continued topical betamethasone treatment in a neutral base. Upon the occurrence of exanthema, carbamazepine was excluded from the therapy, and oxcarbazepine was introduced at a dose of 600 mg BID, on which the patient remains seizure free. 3. Discussion We present a single case report of carbamazepine-associated Lichen planus in a woman with temporal lobe epilepsy. Lichen planus is a chronic papulosquamous dermatosis of unclear etiology, which affects 1–2% of the population [3,4]. Clinically, it is manifested by the typical eruption of lichen red and blue papules on the skin surface of a waxy shine. In the regression phase, papule color changes and becomes brown [1]. Administration of carbamazepine may lead to an eruption of various skin lesions (Table 1), but lichenoid eruptions are rare after prolonged use of the drug [5–7]. Atkin et al. reported a case of lichenoid skin eruption following a 3-month administration of carbamazepine in a dose of 100 mg TID [8], and Yasuda et al. reported a case of photosensitive lichenoid reaction after receiving 200 mg of carbamazepine daily for 1 year [9]. Skin side effects following carbamazepine therapy should always be taken seriously, and carbamazepine treatment must immediately be stopped in nearly all instances. In our patient, long-term carbamazepine treatment resulted in skin changes in the form of erythematosquamous papules on the trunk,
Hypersensitivity Toxic epidermal necrolysis (TEN) Stevens–Johnson syndrome (SJS) Lupus erythematosus Exfoliative dermatitis or erythroderma Exanthems DRESS syndrome Erythema multiforme Rash Diaphoresis Anticonvulsant hypersensitivity syndrome Urticaria Fixed eruptions Photosensitivity Purpura Dermatitis Acute generalized exanthematous pustulosis (AGEP) Lichenoid eruption Pruritus Pseudolymphoma Angioedema Lymphoproliferative disease Pustules Vasculitis Bullous dermatitis Mycosis fungoides Toxic pustuloderma Eczema Lymphoma Erythema nodosum (EN)
Incidence
(1–10%) (1–10%)
(> 5)
(> 10%) (1–10%)
(b1%)
(b1%) (b1%)
(b1%)
Number of cases in the literature 53 46 45 34 34 27 17 17 17 16 12 10 9 8 7 6 6 6 6 5 5 5 5 4 3 3 2 2
(b1%)
Rare side effects (one case described in the literature): acne keloid, collagen disease, edema, eosinophilic pustular folliculitis (Ofuji), bullous epidermolysis, erythema (sheet-like), facial edema, linear IgA bullous dermatosis, pemphigus, peripheral edema, petechiae, pigmentation, psoriasis, Schamberger's disease, toxic-allergic shock, and toxicoderma.
on both wrists and ankles, with a waxy shine and with yellowisherythematous desquamation of the palms and soles. Testing done excluded immunological etiology of the condition [10,11], in vitro lymphocyte transformation test (TTL) was performed and turned out positive for carbamazepine [12,13], while dermatohistological testing confirmed the diagnosis of Lichen planus [1]. Combined topical therapy with corticosteroids was applied that led to the regression of skin changes, and consistent with the literature, the skin pigmentation became brown [1]. Contributors' statement All authors have equally contributed to this article including literature search, data collection, interpretation and writing. Role of the funding source We confirm that no funding source had any involvement in creating this article. Patients' consent and permission to publish We confirm that we have obtained patient's consent and permission to publish. References
Fig. 2. Skin changes of the palms — yellowish-erythematous skin with desquamation.
[1] Lipozenčić J. Lichen planus. In: Lipozenčić J, et al, editor. Dermatovenerologija, Zagreb: Medicinska naklada; 2008. p. 234–7. [2] Thompson DF, Skaehill PA. Drug induced lichen planus. Pharmacotherapy 1994;14:561–71.
S. Hajnsek et al. / Epilepsy & Behavior 24 (2012) 269–271 [3] DeRossi SS, Ciarrocca KN. Lichen planus, lichenoid drug reactions, and lichenoid mucositis. Dent Clin N Am 2005;49:77–89. [4] Scully C, Eisen D, Carrozzo M. Management of oral lichen planus. Am J Clin Dermatol 2000;1:287–306. [5] Litt J. Drug eruption reference manual. 2000 Millennium Edition. New York: The Parthenon, Publishing Group; 2000. pp. 635–636. [6] Litt J. Litt's drug eruptions and reactions manual. Seventeenth Edition. London: Informa; 2011. pp. 102–104. [7] Roberts DL, Marks R. Skin reactions to carbamazepine. Arch Dermatol 1981;117:273–5. [8] Atkin SL, McKenzie TMM, Stevenson CJ. Carmabazepine-induced lichenoid eruption. Clin Exp Dermatol 1990;15:382–3.
271
[9] Yasuda S, Mizuno N, Kawabe Y, Sakakibara S. Photosensitive lichenoid reaction accompanied by nonphotosensitive subacute prurigo caused by carbamazepine. Photodermatol 1988;5:206–10. [10] Roujeau JC. Immune mechanisms in drug allergy. Allergol Int 2006;55:27–33. [11] Livni E, Halevy S, Stahl B, Joshua H. The appearance of macrophage migration–inhibition factor in drug reactions. J Allergy Clin Immunol 1987;80(6): 843–9. [12] Warrington RJ, Tse KS. The lymphocyte transformation studies in drug hypersensitivity. Can Med Assoc J 1979;120:1089–94. [13] Nyfeler B, Pichler WJ. The lymphocyte transformation test for diagnosis of drug allergy: sensitivity and specificity. Clin Exp Allergy 1997;27:175–81.