persistent candidal infections while taking olanzapine. Within 1 week of discontinuing
olanzapine, his {*filter*} glucose levels returned to baseline, and insulin was discontinued.

A patient was treated with olanzapine for 8 months.[9] For 6 weeks before the patient was
hospitalized for ketoacidosis, his olanzapine dosage reached a maximum of 30 mg/day.
Olanzapine was discontinued, and his plasma glucose levels subsequently returned to
normal.

Diabetic ketoacidosis developed in a patient after 1 month of treatment with
olanzapine.[10] The patient was not obese, and had no personal or family history of
diabetes. Olanzapine was discontinued, and the patient's condition was stabilized with
70/30 human insulin.

Olanzapine-associated hyperglycemia in one patient resolved approximately 2 weeks after
olanzapine was stopped.[11] Eight months after discontinuation, the patient was
rechallenged with olanzapine 5 mg at bedtime. Again, the addition of olanzapine resulted
in hyperglycemia, which resolved after discontinuing the drug.

Two patients with olanzapine-associated diabetes were obese with no personal history of
diabetes.[12] Both continued taking olanzapine, so it is uncertain whether their diabetes
would have resolved had the drug been stopped. Their plasma glucose levels were controlled
with glyburide.

Diabetes mellitus developed in seven patients after they started olanzapine.[13]
Ketoacidosis developed in two of these patients. Five required hospitalization for
management of hyperglycemia, which resolved in only two of the patients after olanzapine
was withdrawn.

One patient experienced hyperosmolar, hyperglycemic, nonketonic coma induced by
olanzapine.[14] He did not gain weight after the start of olanzapine. He received acute
treatment with insulin, and his hyperglycemia resolved after olanzapine was discontinued.

One patient died from diabetic ketoacidosis when diabetes developed several weeks after
olanzapine was begun.[16]

Discussion
Although no conclusive evidence exists as to exactly how olanzapine induces glucose
dysregulation, several hypotheses have been put forth. Olanzapine may increase insulin
resistance by altering receptor-binding characteristics.[16] Theoretically, it could cause
primary damage to the pancreatic islet cells, thereby altering insulin production.
However, little or no data support this mechanism other than the observation that in some
patients glucose dysregulation occurred soon after therapy began. Further, no obvious