Psychosomatics 44:175-176, April 2003
© 2003 The Academy of Psychosomatic Medicine
Olanzapine and Quick-Response Hyperglycemia
Nasreen Abdullah, M.D.,
Liouda Voronovitch, M.D.,
Stephen Taylor, B.M., and
Steven Lippmann, M.D., Louisville, Ky.
TO THE EDITOR: Olanzapine is a commonly prescribed atypical antipsychotic drug that is usually well tolerated and has a low incidence of side effects.1 Some of the concerns with olanzapine, however, include metabolic changes such as weight gain, glucose dysregulation, and hyperlipidemia. Glucose intolerance with new-onset diabetes mellitus, exacerbation of type 2 diabetes, and severe instances of ketoacidosis have been reported in people taking olanzapine.2 We describe a case of transient, immediate hyperglycemia observed in a patient who started olanzapine and who experienced rapid resolution upon discontinuation of this pharmacotherapy.
Case Report
Ms. A, a 29-year-old African American woman, was hospitalized after a suicide attempt by drug overdose. On arrival, she expressed hopelessness and exhibited paranoia. She was moderately overweight. The results of a blood chemistry profile, including a fasting blood sugar level of 84 mg/dl, were within normal limits, except for modest hypokalemia—3.4 meq/liter. Ms. A was psychotic, so risperidone, 2 mg/day, orally with potassium supplement was prescribed. The next day, her risperidone dose was increased to 4 mg/day. Her serum chemistries were closely monitored to assess electrolyte concentrations; her potassium level returned to normal, and her fasting blood sugar level was 89 mg/dl.
Olanzapine was added to her drug regimen adjunctively on day 3 because of escalating agitation with significant psychosis and insomnia; Ms. A's blood glucose level was 102 mg/dl. On day 4, her fasting blood sugar level became abnormal—167 mg/dl—and was unexpected after the finding of normal potassium levels. Because Ms. A's hyperglycemia was presumably related to olanzapine therapy, this medicine was stopped. After olanzapine discontinuation, the next day's serum glucose concentration was normal—90 mg/dl. No other pharmaceuticals were used during the hospital course. Ms. A's hypokalemia remained corrected.
Discussion
Glucose intolerance is documented secondary to the administration of olanzapine, as illustrated by this vignette. Although the exact mechanism of this metabolic alteration is unclear, it is hypothesized that serotonin antagonism may decrease the responsiveness of pancreatic beta cells.3 Such hyperglycemia may also be associated with, or precipitated by, other risk factors for diabetes. Our patient did not have a family history of diabetes, but she was slightly obese, which is well established as associated with glucose intolerance.4
Reports of olanzapine-induced glycemic dyscontrol vary by time of onset and the length of time required for serum glucose levels to return to normal after discontinuation of olanzapine;5 however, in this patient, the changes from a normal blood sugar concentration to an elevation and back to the normal range were almost immediate. This pattern appeared to correlate with the patient's olanzapine exposure.
Although olanzapine-induced hyperglycemia does not always occur, the possibility does exist.1–3 Physicians should remain vigilant about this potential adverse metabolic effect. Olanzapine has a known diabetogenic property. Consequently, it is important to identify all other potential risk factors, including lipid disorders, family predisposition, and/or obesity. In addition, clinicians should conduct appropriate laboratory monitoring of blood sugar and lipid profiles, as indicated, when prescribing olanzapine.
REFERENCES
- Bettinger TL, Mendelson SC, Dosson PG, Crismon ML: Olanzapine-induced glucose dysregulation. Ann Pharmacother 2000; 34:865-867[Abstract]
- Newcomer JW: Metabolic disturbances associated with antipsychotic use. J Clin Psychiatry 2001; 62(suppl 27):3-4; discussion, 62(suppl 27):40-41
- Wirshing DA, Spellberg BJ, Erhart SM, Marder SR, Wirshing WC: Novel antipsychotics and new-onset diabetes. Biol Psychiatry 1998; 44:778-783[CrossRef][Medline]
- Berstein J: Psychotropic drug induced weight gain: mechanism and management. Clin Neuropharmacol 1988; 11:S194-S206
- Melkersson K, Hulting A, Brismar K: Different influences of classical antipsychotics and clozapine on glucose-insulin homeostasis in patients with schizophrenia or related psychoses. J Clin Psychiatry 1999; 60:783-791[Medline]
Get information about faster international access.
Privacy Policy
Copyright © 2003
Academy of Psychosomatic Medicine.
All rights reserved.
Home
| Search
| Current Issue
| Past Issues
| Subscribe
| All APPI Journals
| Help
| Contact Us
|
