Carbamazepine
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Reactions 1251 - 9 May 2009 S Carbamazepine Kikuchi-Fujimoto’s disease and systemic lupus erythematosus following hypersensitivity syndrome: case report A 36-year-old man, who had previously received carbamazepine for encephalitis and had experienced drug- induced hypersensitivity syndrome (DIHS) leading to reactivation of Epstein-Barr virus (EBV), developed Kikuchi- Fujimoto’s disease and systemic lupus erythematosus (SLE). The man was hospitalised in June 2006 with a high-grade fever, painless cervical lymphadenopathy and an erythematous papular eruption. In January 2002, he had received carbamazepine [dosage not stated] for encephalitis. Twenty days after starting carbamazepine, he had developed a generalised erythematous skin eruption, severe liver dysfunction, high-grade fever and reactivations of EBV and human herpesvirus 6; at that time, he was diagnosed with DIHS. He had completely recovered 3 months later and remained asymptomatic until 2006. A physical examination during his current admission revealed enlarged lymph nodes (3cm in diameter) extending from just below his ears to his supraclavicular area bilaterally, and non-confluent erythematous papules on his face, chest and back. Blood tests revealed the following; WBC count 3.1 × 10 3 /µL, AST 51 IU/L, ALT 63 IU/L, ANA 1:80, CRP 2.7 mg/dL. A cervical lymph node biopsy revealed massive necrosis with abundant nuclear debris and he was diagnosed with Kikuchi-Fujimoto’s disease. His lymphadenopathy persisted for over 2 weeks and his skin eruptions worsened, evolving into dusty red, slightly infiltrated plaques. A skin biopsy from a macule on his cheek revealed perifollicular lymphocytic infiltration and liquefaction degeneration. A subsequent lupus band test was positive. Further tests revealed pancytopenia, marked proteinuria (10g/day) and decreased serum complement levels. He was diagnosed with SLE. In addition, EBV- encoded RNA and EBV-DNA were detected in his lymph nodes. The man was treated with prednisolone and his symptoms immediately resolved. At 4-months’ follow-up, he was taking prednisolone and ciclosporin for his renal symptoms, which were subsequently diagnosed as lupus nephritis. Author comment: "In view of the unique ability of EBV to infect, activate and latently persist in B cells, EBV repeatedly reactivated during the course of DIHS and again at the time of the lymphadenitis might have contributed to the induction of SLE in this patient. Our case suggests the importance of recognising DIHS as a risk factor for eventually developing autoimmune diseases." Aota N, et al. Systemic lupus erythematosus presenting with Kikuchi-Fujimoto’s disease as a long-term sequela of drug-induced hypersensitivity syndrome: a possible role of Epstein-Barr virus reactivation. Dermatology 218: 275-277, No. 3, Feb 2009 - Japan 801139848 1 Reactions 9 May 2009 No. 1251 0114-9954/10/1251-0001/$14.95 © 2010 Adis Data Information BV. All rights reserved
Transcript of Carbamazepine
Reactions 1251 - 9 May 2009
SCarbamazepine
Kikuchi-Fujimoto’s disease and systemic lupuserythematosus following hypersensitivitysyndrome: case report
A 36-year-old man, who had previously receivedcarbamazepine for encephalitis and had experienced drug-induced hypersensitivity syndrome (DIHS) leading toreactivation of Epstein-Barr virus (EBV), developed Kikuchi-Fujimoto’s disease and systemic lupus erythematosus(SLE).
The man was hospitalised in June 2006 with a high-gradefever, painless cervical lymphadenopathy and anerythematous papular eruption. In January 2002, he hadreceived carbamazepine [dosage not stated] forencephalitis. Twenty days after starting carbamazepine, hehad developed a generalised erythematous skin eruption,severe liver dysfunction, high-grade fever and reactivationsof EBV and human herpesvirus 6; at that time, he wasdiagnosed with DIHS. He had completely recovered3 months later and remained asymptomatic until 2006. Aphysical examination during his current admission revealedenlarged lymph nodes (3cm in diameter) extending fromjust below his ears to his supraclavicular area bilaterally,and non-confluent erythematous papules on his face, chestand back. Blood tests revealed the following; WBC count3.1 × 103/µL, AST 51 IU/L, ALT 63 IU/L, ANA 1:80, CRP2.7 mg/dL. A cervical lymph node biopsy revealed massivenecrosis with abundant nuclear debris and he wasdiagnosed with Kikuchi-Fujimoto’s disease. Hislymphadenopathy persisted for over 2 weeks and his skineruptions worsened, evolving into dusty red, slightlyinfiltrated plaques. A skin biopsy from a macule on hischeek revealed perifollicular lymphocytic infiltration andliquefaction degeneration. A subsequent lupus band testwas positive. Further tests revealed pancytopenia, markedproteinuria (10g/day) and decreased serum complementlevels. He was diagnosed with SLE. In addition, EBV-encoded RNA and EBV-DNA were detected in his lymphnodes.
The man was treated with prednisolone and hissymptoms immediately resolved. At 4-months’ follow-up,he was taking prednisolone and ciclosporin for his renalsymptoms, which were subsequently diagnosed as lupusnephritis.
Author comment: "In view of the unique ability of EBV toinfect, activate and latently persist in B cells, EBV repeatedlyreactivated during the course of DIHS and again at the timeof the lymphadenitis might have contributed to the inductionof SLE in this patient. Our case suggests the importance ofrecognising DIHS as a risk factor for eventually developingautoimmune diseases."Aota N, et al. Systemic lupus erythematosus presenting with Kikuchi-Fujimoto’sdisease as a long-term sequela of drug-induced hypersensitivity syndrome: apossible role of Epstein-Barr virus reactivation. Dermatology 218: 275-277, No. 3,Feb 2009 - Japan 801139848
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Reactions 9 May 2009 No. 12510114-9954/10/1251-0001/$14.95 © 2010 Adis Data Information BV. All rights reserved
