Article
Pityriasis rosea-like drug eruption due to bupropion: A case report
Human and Experimental Toxicology 1–3 ª The Author(s) 2014 Reprints and permission: sagepub.co.uk/journalsPermissions.nav DOI: 10.1177/0960327113478444 het.sagepub.com
¨ . Uzun2, I. ¨ rs1 and C _ O M. Polat1, O ¸ . Boran3
Abstract Pityriasis rosea (PR) is a common, acute, and self-limited inflammatory skin disease. The typical clinical presentation includes the appearance of a primary ‘‘herald’’ patch followed within days to weeks by the onset of secondary scaly skin eruptions distributed along the skin tension line in most cases. Although PR is a well-known and relatively common disease, its cause is still not completely understood. However, viral agents, autoimmunity, psychogenic status, and numerous drugs have been proposed as possible factors to PR. Bupropion is known to cause hypersensitivity reactions. We present a clinical case of PR eruption caused by the use of bupropion. To the best of our knowledge, this is the first published case of PR associated with bupropion use. Keywords Pityriasis rosea; bupropion; drug eruption
Introduction Pityriasis rosea (PR) is an acute, self-limited, and papulosquamous skin eruption that occurs most commonly among teenagers and young adults.1 Although PR is a well-known and relatively common disease, and its cause is still not completely understood. Although no aetiology has been proven, viral agents (especially human herpes virus 6 and 7), autoimmunity psychogenic status, and drugs have been proposed as possible risk factors for PR.1,2 Bupropion (Zyban1) is a non-tricyclic antidepressant that is currently used in the treatment of smoking addiction. The main mechanism of action of bupropion seems to be the inhibition of noradrenaline and dopamine reuptake. The literature describes cutaneous manifestations of bupropion hypersensitivity including anaphylactic reactions,3 atopic dermatitis,4 erythema multiforme,5 angiooedema,6 Stevens–Johnson syndrome with acute psoriatic exacerbation,7 and generalised pustular and erythrodermic psoriasis.8 Here, we describe the first clinical case of PR eruption caused by the use of bupropion.
taking bupropion (150 mg/day) for smoking addiction. She was not taking any other medication concurrently and had not suffered any intercurrent infections before. She had neither a history of previous rashes nor a family history of psoriasis. An examination revealed a widespread mildly pruritic rash mainly involving the trunk and proximal upper limbs (Figure 1). The eruption was characterised by numerous erythematous plaques measuring 1–3 cm in diameter, many of which had peripheral scales (Figure 2). The patient did not report the appearance of a ‘‘herald’’ patch prior to the generalised eruption on either occasion. A number of lesions on her back were oval shaped with their long axes parallel to the line of the ribs, whereas some of the lesions on her chest and upper abdomen were circular with central clearing. The results of routine laboratory analyses were within
1
Department of Dermatology, Medical Faculty, Abant Izzet Baysal University, Bolu, Turkey 2 Department of Pharmacology, Medical Faculty, Abant Izzet Baysal University, Bolu, Turkey 3 Department of Pathology, Medical Faculty, Abant Izzet Baysal University, Bolu, Turkey
Case report A 46-year-old woman was admitted to our clinic with a skin rash on her trunk and proximal limbs that had developed approximately 10 days after she started
Corresponding author: Mualla Polat, Department of Dermatology, Izzet Baysal Medical Faculty, 14280 Golkoy, Bolu, Turkey. Email: [email protected]
2
Figure 1. Erythematous, papulosquamous plaques on the trunk and proximal upper limbs.
Human and Experimental Toxicology
Figure 3. Superficial perivascular infiltration of lymphocytes/histiocytes, with occasional eosinophils and scattered extravasated erythrocytes (hematoxylin and eosin, 100).
Discussion
Figure 2. Close-up of the papulosquamous lesions on the breast showing fine collarettes of scales.
normal limits. Venereal Disease Research Laboratory, human immunodeficiency virus antibody, and antinuclear antibody tests were negative. A potassium hydroxide preparation for fungal infection was negative. There were no stigmata of either psoriasis or tinea. The clinical appearance was suggestive of PR. The biopsy of a representative plaque on the trunk showed slight papillary oedema in the superficial dermis, and perivascular and superficial dermal interstitial infiltrate by lymphocytes, plasma cells, and small numbers of eosinophils and extravasated erythrocytes (Figure 3). A diagnosis of PR was made because of the typical clinicopathologic features. The patient stopped taking bupropion and was treated with oral antihistamine and a mid-potency topical steroid cream. At the scheduled 2-week follow-up visit, the skin lesions had improved.
PR was probably first described by the Edinburgh dermatologist Robert Willan under another name in 1798. The macular variety of PR was first named as such by the French dermatologist Camille Melchoir Gibert in 1860.1 Aetiology of PR has long been suspected to have an infectious, mainly viral, aetiology because of a distinct clinical course akin to that of a viral exanthems. That most sufferers will not have a relapse in their lifetime is suggestive of immunity against the virus upon the first attack.1 Although drug-induced PR has been reported for a variety of agents including barbiturates, bismuth, clonidine, captopril, and gold, no reported cases were induced by bupropion.9,10 The mechanism by which bupropion causes PR, which is a papulosquamous disease, is unknown. It has been reported that bupropion also causes another papulosquamous disease: the exacerbation of psoriasis.8 The bupropion-induced exacerbation of psoriasis is more likely to occur due to an idiosyncratic reaction rather than a pharmacological action on receptors whose role in psoriasis is uncertain.8 Our diagnosis of bupropion-induced PR is based on the following criteria: the strong relationship between the onset of the reaction and the initiation of bupropion treatment and improvement in the patient’s symptoms with treatment withdrawal; the patient was taking no other medication when the symptoms of PR developed, and the results of a histopathological examination of the lesion were examined. A histopathological examination revealed signs of a drug hypersensitivity
Polat M. et al.
reaction, including increased numbers of dermal eosinophils. Even if the diagnosis is based on seeing an increase in drug-induced eruption following resumption of the drug, we avoided giving bupropion to our patient again for fear that the current eruption would spread. Therefore, we confirmed the diagnosis based on the clinical and histopathological data. A limitation of this case report is that we did not perform a patch test or oral provocation test. Factors in the differential diagnosis include diffuse nummular eczema, tinea corporis, tinea versicolor pityriasis lichenoides, guttate psoriasis, viral exanthem, lichen planus, and secondary syphilis.11 Although PR does not cause a worse clinical outcome except for erythroderma, the lesions worry patients. Smoking is very common in Turkey; however, thanks to the smoking cessation campaigns launched in recent years; we assume that the use of bupropion will increase. For this reason, individuals should be alerted to bupropion-induced drug eruptions. Funding This research received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors.
References 1. Chuh A, Lee A, Zawar V, et al. Pityriasis rosea—an update. Indian J Dermatol Venereol Leprol 2005; 71: 311–315.
3 2. Chuh A, Chan H, and Zawar V. Pityriasis rosea—evidence for and against an infectious aetiology. Epidemiol Infect 2004; 132: 381–390. 3. West R. Bupropion SR for smoking cessation. Expert Opin Pharmacother 2003; 4: 533–540. 4. Gonza´lez E, Sanguino RM, and Franco MA. Bupropion in atopic dermatitis.Pharmacopsychiatry 2006; 39: 229. 5. Lineberry TW, Peters GE, Jr, and Bostwick JM. Bupropion-induced erythema multiforme. Mayo Clin Proc 2001; 76: 664–666. 6. Tackett AE and Smith KM. Bupropion-induced angioedema. Am J Health Syst Pharm 2008; 65: 1627–1630. 7. Surovik J, Riddel C, and Chon SY. A case of bupropion-induced Stevens–Johnson syndrome with acute psoriatic exacerbation. J Drugs Dermatol 2010; 9:1010–1012. 8. Cox NH, Gordon PM, and Dodd H. Generalized pustular and erythrodermic psoriasis associated with bupropion treatment. Br J Dermatol 2002; 146: 1061–1063. 9. Stulberg DL and Wolfrey J. Pityriasis Rosea. Am Fam Physician 2004; 69: 87–91. 10. Buckley C. Pityriasis rosea-like eruption in a patient receiving omeprazole. Br J Dermatol 1996; 135: 660–661. 11. Stulberg DL and Wolfrey J. Pityriasis rosea. Am Fam Physician 2004; 69(1): 87–91.
Pityriasis rosea-like drug eruption due to bupropion: A case report
Human and Experimental Toxicology 1–3 ª The Author(s) 2014 Reprints and permission: sagepub.co.uk/journalsPermissions.nav DOI: 10.1177/0960327113478444 het.sagepub.com
¨ . Uzun2, I. ¨ rs1 and C _ O M. Polat1, O ¸ . Boran3
Abstract Pityriasis rosea (PR) is a common, acute, and self-limited inflammatory skin disease. The typical clinical presentation includes the appearance of a primary ‘‘herald’’ patch followed within days to weeks by the onset of secondary scaly skin eruptions distributed along the skin tension line in most cases. Although PR is a well-known and relatively common disease, its cause is still not completely understood. However, viral agents, autoimmunity, psychogenic status, and numerous drugs have been proposed as possible factors to PR. Bupropion is known to cause hypersensitivity reactions. We present a clinical case of PR eruption caused by the use of bupropion. To the best of our knowledge, this is the first published case of PR associated with bupropion use. Keywords Pityriasis rosea; bupropion; drug eruption
Introduction Pityriasis rosea (PR) is an acute, self-limited, and papulosquamous skin eruption that occurs most commonly among teenagers and young adults.1 Although PR is a well-known and relatively common disease, and its cause is still not completely understood. Although no aetiology has been proven, viral agents (especially human herpes virus 6 and 7), autoimmunity psychogenic status, and drugs have been proposed as possible risk factors for PR.1,2 Bupropion (Zyban1) is a non-tricyclic antidepressant that is currently used in the treatment of smoking addiction. The main mechanism of action of bupropion seems to be the inhibition of noradrenaline and dopamine reuptake. The literature describes cutaneous manifestations of bupropion hypersensitivity including anaphylactic reactions,3 atopic dermatitis,4 erythema multiforme,5 angiooedema,6 Stevens–Johnson syndrome with acute psoriatic exacerbation,7 and generalised pustular and erythrodermic psoriasis.8 Here, we describe the first clinical case of PR eruption caused by the use of bupropion.
taking bupropion (150 mg/day) for smoking addiction. She was not taking any other medication concurrently and had not suffered any intercurrent infections before. She had neither a history of previous rashes nor a family history of psoriasis. An examination revealed a widespread mildly pruritic rash mainly involving the trunk and proximal upper limbs (Figure 1). The eruption was characterised by numerous erythematous plaques measuring 1–3 cm in diameter, many of which had peripheral scales (Figure 2). The patient did not report the appearance of a ‘‘herald’’ patch prior to the generalised eruption on either occasion. A number of lesions on her back were oval shaped with their long axes parallel to the line of the ribs, whereas some of the lesions on her chest and upper abdomen were circular with central clearing. The results of routine laboratory analyses were within
1
Department of Dermatology, Medical Faculty, Abant Izzet Baysal University, Bolu, Turkey 2 Department of Pharmacology, Medical Faculty, Abant Izzet Baysal University, Bolu, Turkey 3 Department of Pathology, Medical Faculty, Abant Izzet Baysal University, Bolu, Turkey
Case report A 46-year-old woman was admitted to our clinic with a skin rash on her trunk and proximal limbs that had developed approximately 10 days after she started
Corresponding author: Mualla Polat, Department of Dermatology, Izzet Baysal Medical Faculty, 14280 Golkoy, Bolu, Turkey. Email: [email protected]
2
Figure 1. Erythematous, papulosquamous plaques on the trunk and proximal upper limbs.
Human and Experimental Toxicology
Figure 3. Superficial perivascular infiltration of lymphocytes/histiocytes, with occasional eosinophils and scattered extravasated erythrocytes (hematoxylin and eosin, 100).
Discussion
Figure 2. Close-up of the papulosquamous lesions on the breast showing fine collarettes of scales.
normal limits. Venereal Disease Research Laboratory, human immunodeficiency virus antibody, and antinuclear antibody tests were negative. A potassium hydroxide preparation for fungal infection was negative. There were no stigmata of either psoriasis or tinea. The clinical appearance was suggestive of PR. The biopsy of a representative plaque on the trunk showed slight papillary oedema in the superficial dermis, and perivascular and superficial dermal interstitial infiltrate by lymphocytes, plasma cells, and small numbers of eosinophils and extravasated erythrocytes (Figure 3). A diagnosis of PR was made because of the typical clinicopathologic features. The patient stopped taking bupropion and was treated with oral antihistamine and a mid-potency topical steroid cream. At the scheduled 2-week follow-up visit, the skin lesions had improved.
PR was probably first described by the Edinburgh dermatologist Robert Willan under another name in 1798. The macular variety of PR was first named as such by the French dermatologist Camille Melchoir Gibert in 1860.1 Aetiology of PR has long been suspected to have an infectious, mainly viral, aetiology because of a distinct clinical course akin to that of a viral exanthems. That most sufferers will not have a relapse in their lifetime is suggestive of immunity against the virus upon the first attack.1 Although drug-induced PR has been reported for a variety of agents including barbiturates, bismuth, clonidine, captopril, and gold, no reported cases were induced by bupropion.9,10 The mechanism by which bupropion causes PR, which is a papulosquamous disease, is unknown. It has been reported that bupropion also causes another papulosquamous disease: the exacerbation of psoriasis.8 The bupropion-induced exacerbation of psoriasis is more likely to occur due to an idiosyncratic reaction rather than a pharmacological action on receptors whose role in psoriasis is uncertain.8 Our diagnosis of bupropion-induced PR is based on the following criteria: the strong relationship between the onset of the reaction and the initiation of bupropion treatment and improvement in the patient’s symptoms with treatment withdrawal; the patient was taking no other medication when the symptoms of PR developed, and the results of a histopathological examination of the lesion were examined. A histopathological examination revealed signs of a drug hypersensitivity
Polat M. et al.
reaction, including increased numbers of dermal eosinophils. Even if the diagnosis is based on seeing an increase in drug-induced eruption following resumption of the drug, we avoided giving bupropion to our patient again for fear that the current eruption would spread. Therefore, we confirmed the diagnosis based on the clinical and histopathological data. A limitation of this case report is that we did not perform a patch test or oral provocation test. Factors in the differential diagnosis include diffuse nummular eczema, tinea corporis, tinea versicolor pityriasis lichenoides, guttate psoriasis, viral exanthem, lichen planus, and secondary syphilis.11 Although PR does not cause a worse clinical outcome except for erythroderma, the lesions worry patients. Smoking is very common in Turkey; however, thanks to the smoking cessation campaigns launched in recent years; we assume that the use of bupropion will increase. For this reason, individuals should be alerted to bupropion-induced drug eruptions. Funding This research received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors.
References 1. Chuh A, Lee A, Zawar V, et al. Pityriasis rosea—an update. Indian J Dermatol Venereol Leprol 2005; 71: 311–315.
3 2. Chuh A, Chan H, and Zawar V. Pityriasis rosea—evidence for and against an infectious aetiology. Epidemiol Infect 2004; 132: 381–390. 3. West R. Bupropion SR for smoking cessation. Expert Opin Pharmacother 2003; 4: 533–540. 4. Gonza´lez E, Sanguino RM, and Franco MA. Bupropion in atopic dermatitis.Pharmacopsychiatry 2006; 39: 229. 5. Lineberry TW, Peters GE, Jr, and Bostwick JM. Bupropion-induced erythema multiforme. Mayo Clin Proc 2001; 76: 664–666. 6. Tackett AE and Smith KM. Bupropion-induced angioedema. Am J Health Syst Pharm 2008; 65: 1627–1630. 7. Surovik J, Riddel C, and Chon SY. A case of bupropion-induced Stevens–Johnson syndrome with acute psoriatic exacerbation. J Drugs Dermatol 2010; 9:1010–1012. 8. Cox NH, Gordon PM, and Dodd H. Generalized pustular and erythrodermic psoriasis associated with bupropion treatment. Br J Dermatol 2002; 146: 1061–1063. 9. Stulberg DL and Wolfrey J. Pityriasis Rosea. Am Fam Physician 2004; 69: 87–91. 10. Buckley C. Pityriasis rosea-like eruption in a patient receiving omeprazole. Br J Dermatol 1996; 135: 660–661. 11. Stulberg DL and Wolfrey J. Pityriasis rosea. Am Fam Physician 2004; 69(1): 87–91.
