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• W3034485957 abstract "Levetiracetam [LEV] was initially approved as adjunctive therapy for partial-onset seizures but later also approved as adjunctive therapy for primary generalized tonic-clonic seizures and myoclonic seizures [[1]Rashid M. Rajan A.K. Chhabra M. Kashyap A. Levetiracetam and cutaneous adverse reactions: a systematic review of descriptive studies.Seizure. 2020; 75: 101-109Abstract Full Text Full Text PDF PubMed Scopus (8) Google Scholar]. Drug eruptions, Stevens-Johnson syndrome and angioedema precipitated by Levetiracetam have previously been described [[1]Rashid M. Rajan A.K. Chhabra M. Kashyap A. Levetiracetam and cutaneous adverse reactions: a systematic review of descriptive studies.Seizure. 2020; 75: 101-109Abstract Full Text Full Text PDF PubMed Scopus (8) Google Scholar]. Stevens-Johnson syndrome [SJS] is a serious mucocutaneous reaction induced by immune complex mediated hypersensitivity reaction. Anti-epileptic drugs are one of the commonest causes of Stevens-Johnson syndrome. Incidence of Carbamazepine [CBZ] induced Stevens-Johnson syndrome is around 14–20 per 100,000 [[2]Patel P.P. Gandhi A.M. Desai C.K. Desai M.K. Dikshit R.K. An analysis of drug induced Stevens-Johnson syndrome.Indian J Med Res. 2012; 136: 1051-1053PubMed Google Scholar,[3]Frey N. Bodmer M. Bircher A. Rüegg S. Jick S.S. Meier C.R. et al.The risk of Stevens-Johnson syndrome and toxic epidermal necrolysis in new users of antiepileptic drugs.Epilepsia. 2017; 58: 2178-2185Crossref PubMed Scopus (39) Google Scholar]. Studies have found an increased risk of CBZ induced SJS in Asians especially those with a positive HLA-B*15:02 profile [[2]Patel P.P. Gandhi A.M. Desai C.K. Desai M.K. Dikshit R.K. An analysis of drug induced Stevens-Johnson syndrome.Indian J Med Res. 2012; 136: 1051-1053PubMed Google Scholar]. LEV and CBZ combination is frequently used in clinical practice for partial onset seizures. We report a case in which addition of Levetiracetam to Carbamazepine precipitated Stevens-Johnson syndrome. A 22-year female presented to Neurology OPD of our institute with history of seizures for the past two and a half years. Seizure were characterized by right sided head version followed by generalized tonic-clonic movements with loss of consciousness. Birth and developmental histories were normal. There was no history of febrile seizures or encephalitis like illness in childhood. There was no family history of seizures. There was history of fall from roof with loss of consciousness for 5−10 min without any external trauma at the age of 5 years. Neuroimaging was not done at the time of head trauma. MRI Brain done at our institute was normal. She was being treated with phenytoin for past two and a half years and the seizures were well controlled. However, she developed phenytoin induced gingival hyperplasia and wanted to switch over to another drug. She was advised CBZ which was gradually built upto 600 mg/day and phenytoin was tapered. At 8 weeks serum level of CBZ was 8.8 mcg/mL. After 14 weeks of CBZ monotherapy, she developed breakthrough seizures on 3 occasions. Levetiracetam was prescribed as add-on therapy at a dose of 250 mg BD which was increased to 500 mg BD after 7 days. However, 2 days after increasing the Levetiracetam dose to 500 mg BD, patient developed generalized erythematous papules and vesicles on her face, limbs, thighs, breasts, ear lobes and hips. Some of the lesions demonstrated hemorrhagic crusting. Around 10 % of body area was involved. Nicolsky’s sign was positive. Ocular congestion and lid edema with mucopurulent discharge was visible. Patient also had oral ulcers with gingivostomatitis and pharyngitis with odynophagia accompanied by fever. There was no history to suggest a viral infection preceding these muco-cutaneous symptoms. The lesions were diagnosed as Stevens-Johnson syndrome and patient was hospitalized. Symptomatic treatment including intra-venous steroids, local steroid creams, cyclosporine, antibiotics and ophthalmic ointments was initiated. Both Carbamazepine and Levetiracetam were stopped immediately and patient was put on Clobazam. Serum CBZ level was 8.6 mcg/mL. Facilities for checking serum Carbamazepine-epoxide levels were not available at our institute and the same could not be measured. Patient improved and the lesions regressed in 3 weeks leaving no significant sequelae. During follow up, HLA-B*15:02 testing was done, and the patient tested positive. Patient remained seizure free on clobazam monotherapy for the next 11 months without any recurrence of the muco-cutaneous lesions. After 11 months of clobazam monotherapy she had a breakthrough seizure. As she was shortly planning a pregnancy our choice of antiepileptic was limited. Levetiracetam was reinitiated and the dose was slowly titrated to 1000 mg/day. Patient did not develop any dermal lesions and her seizures were controlled. Patient has been seizure free for almost 2 years now on Levetiracetam. The above case demonstrates the potential for LEV to have pharmacodynamic interactions with CBZ and cause adverse effects including Stevens-Johnson syndrome. Sisodiya et al. [[4]Sisodiya S.M. Sander J.W. Patsalos P.N. Carbamazepine toxicity during combination therapy with levetiracetam: a pharmacodynamic interaction.Epilepsy Res. 2002; 48: 217-219Crossref PubMed Scopus (56) Google Scholar] reported 4 cases where addition of Levetiracetam to Carbamazepine precipitated Carbamazepine toxicity. However, in all these 4 cases, serum levels of Carbamazepine and Carbamazepine-epoxide were unaltered prompting them to postulate that a pharmacodynamic interaction between LEV and CBZ was responsible for symptoms of CBZ toxicity caused by addition of LEV. Lamotrigine (LAM) also has similar pharmacodynamic interaction with CBZ. CBZ toxicity features have been reported on addition of LAM without any increase in CBZ or CBZ epoxide levels [[5]Besag F.M. Berry D.J. Pool F. Newbery J.E. Subel B. Carbamazepine toxicity with lamotrigine: pharmacokinetic or pharmacodynamic interaction?.Epilepsia. 1998; 39: 183-187Crossref PubMed Scopus (138) Google Scholar]. In an animal study, Luszczki et al. [[6]Luszczki J.J. Andres M.M. Czuczwar P. Cioczek-Czuczwar A. Wojcik-Cwikla J. Ratnaraj N. et al.Levetiracetam selectively potentiates the acute neurotoxic effects of topiramate and carbamazepine in the rotarod test in mice.Eur Neuropsychopharmacol. 2005; 15: 609-616Crossref PubMed Scopus (41) Google Scholar] found that addition of LEV potentiated the neurotoxicity of CBZ without influencing the brain levels of CBZ clearly showing a pharmacodynamic interaction to be at play Temporal analysis of the available data in our case can probably implicate LEV as the immediate culprit since LEV induced SJS is also well described [[1]Rashid M. Rajan A.K. Chhabra M. Kashyap A. Levetiracetam and cutaneous adverse reactions: a systematic review of descriptive studies.Seizure. 2020; 75: 101-109Abstract Full Text Full Text PDF PubMed Scopus (8) Google Scholar]. Moreover, the patient had very well tolerated CBZ for more than 90 days and more than 90 % cases of SJS with antiepileptics occurred in the first 63 days of treatment [[2]Patel P.P. Gandhi A.M. Desai C.K. Desai M.K. Dikshit R.K. An analysis of drug induced Stevens-Johnson syndrome.Indian J Med Res. 2012; 136: 1051-1053PubMed Google Scholar]. Drug causality was assessed using the specific Algorithm of Drug Causality for Epidermal Necrolysis (ALDEN) which yielded possible equal score of +2 for both drugs [[7]Sassolas B. Haddad C. Mockenhaupt M. Dunant A. Liss Y. Bork K. et al.ALDEN, an algorithm for assessment of drug causality in Stevens-Johnson Syndrome and toxic epidermal necrolysis: comparison with case-control analysis.Clin Pharmacol Ther. 2010; 88: 60-68Crossref PubMed Scopus (346) Google Scholar]. (Table 1)Table 1Details of the algorithm of drug causality for epidermal necrolysis (ALDEN).CriterionCarbamazepineLevetiracetamDescriptionScoreDescriptionScoreDelay from initial drug intake to onset of reaction (index day)>56 days−1(Unlikely)5−28 days(Suggestive)+3Drug present in body on index dayDrug continued upto index day0(Definite)Drug continued upto index day0(Definite)Prechallenge/RechallengeNot done0(Unknown)Exposure to this drug without any reaction (before/ after reaction)−2(Negative)DechallengeDrug Stopped0Drug Stopped0Type of Drug/ NotorietyDrug of high-risk list according to previous case-control studies+3(Strongly associated)Several reports, ambiguous epidemiology results+1(Suspected)Intermediate Score+2+2Other CausesNo intermediate score >3, so no -1 for any of the drugFinal score+2+2Causality2−3 (Possible)Possible2−3 (Possible)Possible Open table in a new tab Our patient was HLA-B*15:02 positive and this strongly implicates CBZ as the causative drug. Later addition of LEV was totally uneventful which completely negates the possibility of LEV being the culprit. Thus, SJS in our patient was possibly a manifestation of increased CBZ activity in a genetically susceptible individual owing to LEV induced pharmacodynamic interaction [[4]Sisodiya S.M. Sander J.W. Patsalos P.N. Carbamazepine toxicity during combination therapy with levetiracetam: a pharmacodynamic interaction.Epilepsy Res. 2002; 48: 217-219Crossref PubMed Scopus (56) Google Scholar,[5]Besag F.M. Berry D.J. Pool F. Newbery J.E. Subel B. Carbamazepine toxicity with lamotrigine: pharmacokinetic or pharmacodynamic interaction?.Epilepsia. 1998; 39: 183-187Crossref PubMed Scopus (138) Google Scholar]. LEV seems to share a complex relationship with CBZ. LEV when added to CBZ, increased CBZ activity without altering the serum CBZ or epoxide levels and patient developed features of CBZ toxicity. LEV may precipitate CBZ induced SJS in a genetically susceptible patient. Brivaracetam, a newer analogue of LEV, has been found to increase CBZ epoxide levels without causing any clinical toxicity features or adverse effects [[8]Stockis A. Sargentini-Maier M.L. Brodie M.J. Pharmacokinetic interaction of brivaracetam on carbamazepine in adult patients with epilepsy, with and without valproate co-administration.Epilepsy Res. 2016; 128: 163-168Crossref PubMed Scopus (18) Google Scholar]. It remains to be seen whether addition of Brivaracetam to CBZ will produce similar effect as LEV in our case. In conclusion, our case highlights the need for vigilance be maintained for muco-cutaneous reactions while not only initiating Levetiracetam as monotherapy but also when it is used as add on therapy with CBZ. HLA testing is not a routine in many countries despite US FDA recommendation for the same. There are limitations in the availability of testing in many parts of world. Based on our case, it can be recommended that HLA testing should be performed before adding LEV, even in those patients who have previously tolerated Carbamazepine well. None. We acknowledge support of Dr Pooja Gupta, Associate Professor of Clinical Pharmacology at AIIMS, New Delhi for doing drug causality analysis using ALDEN." @default.
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• W3034485957 title "Stevens-Johnson syndrome triggered by Levetiracetam—Caution for use with Carbamazepine" @default.
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