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Neurology India, Vol. 59, No. 1, January-February, 2011, pp. 72-73 Topic of the Issue: Letter to Editor Fever, mild elevation in liver function tests, leucopenia of carbamazepine-induced anticonvulsant hypersensitivity syndrome Hua-Jun Chang, Nian Wang, Ya-Ping Quan, Xue-Mei Xing Department of Neurology, Taizhou Affiliated Hospital of Nanjing University of Chinese Medicine, Taizhou, Jiangsu, China Date of Submission: 18-Oct-2010 Code Number: ni11018 PMID: 21339666 Sir, Anticonvulsant hypersensitivity syndrome (AHS), a rare adverse drug event, is most commonly seen with carbamazepine, phenytoin, and phenobarbital therapy. It typically presents with fever, cutaneous eruption, and internal organ involvement. All the features described may not be present in all the patients; only fever was the clinical feature in a report of three AHS patients with carbamazepine therapy [1],[2] and fever, hepatitis, and agranulocytosis without cutaneous eruption were the clinical features in a report of two other patients. [3] Here we report a rare case of AHS, which developed fever, mild elevation in liver function tests, and leucopenia. A 43-year-old Chinese man was admitted for recurrent left focal motor seizures. He developed left hemiplegia and focal motor seizures after an operation (25 years ago) for brain abscess. On examination, he was febrile and neurologic examination revealed grade 3/5 motor power on the left side. Computed tomography scan revealed right frontal and temporal skull defect and gliotic scar in the same regions. Hematological and biochemical investigations were normal. He was started on carbamazepine 600 mg/d after which his seizures were controlled. His fever subsided on the second day of admission. On day 13, he was discharged. But he developed a moderate fever the next day, and was readmitted on day 20. On examination, he was febrile, and his body temperature was 38.3ºC. Investigations revealed the following results: white blood cell count (WBC) 3.5 Χ 10 9 /L, neutrophils 0.577, hemoglobin (Hb) 136.4 g/L, platelets 152 Χ 10 9 /L, alanine aminotransferase (ALT) 63 IU/L, aspartate aminotransferase (AST) 55 IU/L, and γ-glutamyl transpeptidase (GGT) 135IU/L. His body temperature varied between 37.9ºC and 39.9ºC. He was prescribed sodium valproate 200 mg thrice a day and carbamazepine was tapered, and his fever subsided within a week. On day 24, repeat blood tests showed: WBC 2.5 Χ 10 9 /L, neutrophils 0.472, Hb 136.3 g/L, and platelets 91 Χ 10 9 /L. He received recombinant human granulocyte colony stimulating factor, 75 μg, once. On day 25, cabamazepine was stopped completely. The liver function tests were abnormal; ALT, AST, and GGT levels 421, 227, and 218 IU/L respectively. Then sodium valproate was also discontinued and topiramate was started at a dose of 25 mg twice a day. On day 36, repeat blood tests showed: WBC 5.6 Χ 10 9 /L, neutrophils 0.594, Hb 152.0g/L, platelets 136 Χ 10 9 /L, ALT 64 IU/L, AST 40 IU/L, and GGT 123 IU/L. Subsequent in the course he was free of seizures. Anticonvulsant hypersensitivity syndrome was first described by Chaiken et al. [4] In addition to carbamazepine, phenytoin, and phenobarbital, AHS has been described in association with oxcarbazepine, lamotrigine, and gabapentin therapy. Skin rash (87%), fever (94%), hepatitis (51%), and hematologic abnormalities (51%) are the common clinical features. [3] Fever usually precedes the onset of the cutaneous eruptions by several days, but both the features can occur concurrently. [5],[6] Cutaneous eruptions may not be seen in all the patients with AHS. [3] Our patient did not have skin rash; because carbamazepine was tapered as soon as he was readmitted. Our patient fulfils the criteria for the diagnosis of AHS. [3],[7] In our patient fever subsided over one week after carbamazepine was tapered. AHS is classified as mild, moderate, and severe, [8] and our patient had a milder form. We suggest patient with AHS and without skin rash should be considered as a mild case. The good recovery observed in our patient could be attributed to the early discontinuation of carbamazepine. However, the liver function tests deteriorated, which was probably related to the use of sodium valproate. In patients who develop AHS, it may be appropriate to use non-enzyme inducing and non-hepatotoxic antiepileptic drugs. Acknowledgment We are grateful to Dr. Shugang Zhang, Department of Neurology, Nanjing Medical University Affiliated Brain Hospital for revising the manuscript. References
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