Topiramate is an effective antiepileptic medication. It holds promise in the care of diabetic patients by virtue of its effect on weight loss (1). It is also reported efficacious as an adjunct in the treatment of alcohol dependence (2) and in the management of binge-eating disorder (3). We report a case illustrating the potential anticraving effects of topiramate against chocolate, leading to significantly improved glycemic control in an epileptic patient with concurrent diabetes.
A 67-year-old woman presented to the epilepsy clinic in September 2003 for evaluation of “possible seizures” and was subsequently treated with topiramate. She also had an 11-year history of poorly controlled diabetes and was a recovered alcoholic for 30 years. Medications included levothyroxine, repaglinide, acetylsalicylic acid, and atorvastatin. General examination was remarkable for an obese woman with clinical features of hypothyroidism. She weighed 194 pounds, and neurological examination was significant for symmetrical peripheral neuropathy. Subsequent follow-ups were remarkable for a moderate improvement in seizure control, a total of 34 pounds weight loss, and significant amelioration of her diabetes. She ascribed the improved glycemic control to her recent aversion to chocolates and sweets, which she claimed had occurred since starting the topiramate.
Initial blood work was remarkable for a fasting blood glucose of 14.3 mmol/l (normal 3.3–6.0 mmol/l) and HbA1c (A1C) of 8.9% (normal 4.3–6.1%). Eight months after starting the topiramate, her fasting blood glucose was 6.1 mmol/l, and A1C dropped from 8.9 to 6.1%. We checked fasting blood glucose and A1C every 3–4 months after initiating the topiramate. Average fasting blood glucose and A1C before introduction of topiramate were 10.2 mmol/l and 8.4%, and 8 months later were 8.7 mmol/l and 6.7%, respectively. The dosage of repaglinide was unchanged over the last 2 years. The patient reported a significant aversion to chocolate after starting the topiramate.
Topiramate is one of the preferred agents in obese epileptic patients, and this was one of the reasons for prescribing this agent to our patient. The 34-pound weight loss was most likely related to the use of topiramate. Our patient reported a very strong craving for chocolate in previous years, which together with her obesity was apparently responsible for her poor glycemic control. Topiramate is known to cause weight loss in 15−20% of patients, but the precise mechanism is unknown. There is a possibility that the anticraving effect may in part be responsible for the weight loss.
Topiramate is known to be efficacious as an adjunct treatment for alcohol dependence and in the treatment of binge-eating disorder. The proposed mechanism is facilitation of γ-amino-butyric acid activity and inhibition of glutamate function in the mesocorticolimbic dopamine pathways (2). Similar mechanisms may be responsible for the anticraving effects noted in our patient. Dietary noncompliance can adversely affect glycemic control. Although some patients are aware of this fact, they are unable to avert this craving without pharmacological support, thus leading to failure of oral hypoglycemic agents. By virtue of its potential to cause weight loss, topiramate deserves consideration when treating diabetic patients with epilepsy. Our case illustrates the possibility of another potential mechanism, its anticraving effect, which would support topiramate as a useful adjuvant in the treatment of diabetes.
