Carbamazepine
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Reactions 843 - 17 Mar 2001 S Carbamazepine Hypersensitivity leading to haemolytic anaemia and fulminant type 1 diabetes mellitus in an elderly patient: case report A 77-year-old woman developed carbamazepine-induced cold agglutinin disease leading to haemolytic anaemia and type 1 diabetes mellitus with diabetic ketoacidosis; she had received carbamazepine for postherpetic neuralgia. The woman developed a generalised skin eruption 1 month after starting treatment with carbamazepine 200 mg/day. Treatment with carbamazepine was stopped and she received inpatient treatment with prednisone. Two weeks later, she began to feel thirsty and she developed epigastric discomfort. The next morning she was found to be comatose. She had marked dehydration, a BP of 80/60mm Hg and a body temperature of 33.4°C. Laboratory tests revealed severe hyperglycaemic ketoacidosis. She received standard treatment for diabetic ketoacidosis and, following recovery from her coma, she required multiple injections of insulin for blood glucose control. She then developed thrombocytopenia and anaemia; both of these disorders subsequently spontaneously improved. She had an undetectable haptoglobin level, autoagglutination of her blood film and an increased cold agglutinin titre. Lymphocyte stimulation and patch tests to carbamazepine were positive. Based on these findings, a diagnosis was made of haemolytic anaemia due to carbamazepine-induced cold agglutinin disease. An analysis of a retained sample of the woman’s sera from when she was first hospitalised showed a rapid loss of C- peptide that led to diabetic ketoacidosis within 2 days. Also, there was a transient increase in her pancreatic enzyme levels, followed by a loss of insulin secretion. Human herpesvirus-6 antibodies were detected 1 week before the onset of diabetic ketoacidosis and the virus’s DNA were detected in her serum, but only the antibodies were detected l month later. At 6 months’ follow-up, the woman’s serum C-peptide level remained undetectable, and she exhibited no response to an IV glucagon load. It was found that she had a type 1 diabetes mellitus-resistant human leucocyte antigen haplotype. Author comment: ‘It is possible that an interaction between reactivation of HHV-6 [human herpesvirus-6] and carbamazepine exposure caused a drug hypersensitivity reaction, somehow resulting in both the fulminant-onset DM [diabetes mellitus] and hemolytic anaemia’. Sekine N, et al. Rapid loss of insulin secretion in a patient with fulminant type 1 diabetes mellitus and carbamazepine hypersensitivity syndrome. JAMA: the Journal of the American Medical Association 285: 1153-1154, 7 Mar 2001 - Japan 800852797 1 Reactions 17 Mar 2001 No. 843 0114-9954/10/0843-0001/$14.95 Adis © 2010 Springer International Publishing AG. All rights reserved
Transcript of Carbamazepine
Reactions 843 - 17 Mar 2001
SCarbamazepine
Hypersensitivity leading to haemolytic anaemia andfulminant type 1 diabetes mellitus in an elderlypatient: case report
A 77-year-old woman developed carbamazepine-inducedcold agglutinin disease leading to haemolytic anaemia and type1 diabetes mellitus with diabetic ketoacidosis; she hadreceived carbamazepine for postherpetic neuralgia.
The woman developed a generalised skin eruption 1 monthafter starting treatment with carbamazepine 200 mg/day.Treatment with carbamazepine was stopped and she receivedinpatient treatment with prednisone. Two weeks later, shebegan to feel thirsty and she developed epigastric discomfort.The next morning she was found to be comatose. She hadmarked dehydration, a BP of 80/60mm Hg and a bodytemperature of 33.4°C. Laboratory tests revealed severehyperglycaemic ketoacidosis. She received standard treatmentfor diabetic ketoacidosis and, following recovery from hercoma, she required multiple injections of insulin for bloodglucose control. She then developed thrombocytopenia andanaemia; both of these disorders subsequently spontaneouslyimproved. She had an undetectable haptoglobin level,autoagglutination of her blood film and an increased coldagglutinin titre. Lymphocyte stimulation and patch tests tocarbamazepine were positive. Based on these findings, adiagnosis was made of haemolytic anaemia due tocarbamazepine-induced cold agglutinin disease.
An analysis of a retained sample of the woman’s sera fromwhen she was first hospitalised showed a rapid loss of C-peptide that led to diabetic ketoacidosis within 2 days. Also,there was a transient increase in her pancreatic enzyme levels,followed by a loss of insulin secretion. Human herpesvirus-6antibodies were detected 1 week before the onset of diabeticketoacidosis and the virus’s DNA were detected in her serum,but only the antibodies were detected l month later.
At 6 months’ follow-up, the woman’s serum C-peptide levelremained undetectable, and she exhibited no response to an IVglucagon load. It was found that she had a type 1 diabetesmellitus-resistant human leucocyte antigen haplotype.
Author comment: ‘It is possible that an interaction betweenreactivation of HHV-6 [human herpesvirus-6] andcarbamazepine exposure caused a drug hypersensitivityreaction, somehow resulting in both the fulminant-onset DM[diabetes mellitus] and hemolytic anaemia’.Sekine N, et al. Rapid loss of insulin secretion in a patient with fulminant type 1diabetes mellitus and carbamazepine hypersensitivity syndrome. JAMA: theJournal of the American Medical Association 285: 1153-1154, 7 Mar 2001 -Japan 800852797
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Reactions 17 Mar 2001 No. 8430114-9954/10/0843-0001/$14.95 Adis © 2010 Springer International Publishing AG. All rights reserved
