Psychosomatics 40:438-443, October 1999
© 1999 The Academy of Psychosomatic Medine
New-Onset Diabetes Mellitus and Diabetic Ketoacidosis Associated With Olanzapine Treatment
Lee E. Goldstein, M.D., Ph.D.,
Jonathan Sporn, M.D.,
Susan Brown, M.D.,
Helen Kim, M.D.,
Joan Finkelstein, M.D.,
Gail K. Gaffey, R.N.,
Gary Sachs, M.D., and
Theodore A. Stern, M.D.
Received December 14, 1998; accepted February 10, 1999. From the Department of Psychiatry, Massachusetts General Hospital, Boston, MA; the Department of Psychiatry, University of Massachusetts Medical Center, Worcester, MA; and the Department of Psychiatry, Boston Veterans Affairs Outpatient Clinic, Boston, MA. Address correspondence and reprint requests to Dr. Goldstein, Dept. of Psychiatry, Wang Ambulatory Care Center, Room 812, Massachusetts General Hospital, Boston, MA 02114; email: goldstle{at}helix.mgh.harvard.edu
Key Words: Olanzapine • Diabetes Mellitus • Diabetic Ketoacidosis
Olanzapine, a new, commonly prescribed atypical antipsychotic medication, is highly effective for the treatment of schizophrenia, schizoaffective disorder, and other psychotic disorders. Structurally related to the prototype atypical antipsychotic clozapine, olanzapine exhibits a similar profile for receptor affinity and shares many of its behavioral, neuroendocrine, and electrophysiological properties.1
Here, we describe seven cases of new-onset diabetes mellitus (DM) that developed soon after initiation of olanzapine treatment. Two of these cases presented with diabetic ketoacidosis (DKA). Although recent case reports have documented an association between chronic treatment with clozapine and hyperglycemia,2–7 this report is the first to describe the development of new-onset DM with DKA during treatment with olanzapine. It expands upon a recent report8 of two cases of olanzapine-associated, new-onset DM. Possible mechanisms for the development of DM and DKA are discussed. The present case series includes five cases previously presented in abstract form.9
Case 1.
Ms. A., a 42-year-old white woman with a 20-year history of schizoaffective disorder, did not have a history of DM. Laboratory studies before olanzapine treatment revealed normal random serum glucose levels. Ms. A.'s mother and maternal grandmother had a history of type II diabetes.
Ms. A.'s psychiatric symptoms were controlled with valproic acid and risperidone, each of which she had been taking for approximately 1½ years. Paranoid delusions about her risperidone led to a trial of olanzapine (10 mg qhs). Before starting olanzapine, Ms. A. weighed 138 pounds (height: 5'3''; body mass index [BMI]: 24.5 kg/m2; normal range: 20–25 kg/m2).
After 6 months of olanzapine treatment, Ms. A. had gained 71 pounds (to a weight of 209 pounds; BMI: 36). She complained to her internist of 3 weeks of polydipsia, polyuria, "feeling dazed," decreased appetite, diffuse abdominal pain, and malaise. Routine outpatient blood chemistries revealed a serum glucose of 1,274 mg/dl and a bicarbonate of 19.8 mmol/L. She was contacted and instructed to return to her local community hospital, where she was found to have a glucose level of 882 mg/dl, a bicarbonate of 15 mmol/L, and an anion gap of 30. She was admitted for management of DKA and treated with hydration and insulin. Subsequently, Ms. A. was transferred to a tertiary-care hospital for further care, where she was found to have a positive serum acetone screen without dilution, an elevated white blood cell (WBC) count of 12.1/mm3 without eosinophilia, and 4+ glucose, with 3+ ketones and 4+ protein on urinalysis. An HbA1c measurement was 11.60% (normal range: 3.8%–6.4%). Physical examination revealed evidence of oral thrush and vaginal candidiasis. Ms. A. was hydrated, started on an intravenous (IV) insulin drip, and treated for a fungal infection.
Ms. A. was discharged on Hospital Day 7 on a subcutaneous (sc) insulin regimen of NPH (150 U q A.M. and 70 U q P.M.), and regular insulin (70 U q A.M. and 35 U q P.M.). Over the next 2 months, Ms. A. was tapered off olanzapine and started on quetiapine. Her insulin regimen was decreased (to NPH insulin 30 U q A.M. and 10 U q P.M., and regular insulin 10 U q A.M.) with normalization of her fasting serum glucose measurements.
Case 2.
Ms. B., a 40-year-old, mildly obese (130 pounds; height: 4'10''; BMI: 27.2 kg/m2) white woman with an 18-year history of schizophrenia, was not known to have a personal or family history of DM. Laboratory studies before olanzapine treatment revealed normal random serum glucose levels. Unable to tolerate treatment with clozapine, Ms. B. was switched to olanzapine (10 mg qd), which controlled her psychotic symptoms, but led to a 10- to 15-pound weight gain over 18 months.
Seventeen months after starting olanzapine, Ms. B. developed a sore throat, a minimally productive cough, malaise, anorexia, nausea, and abdominal discomfort. During her week of symptoms, her medication use was limited to olanzapine and an over-the-counter cold elixir, which was taken as directed. Ms. B.'s physical condition worsened, and she became increasingly somnolent.
Ms. B. was taken by ambulance to a local hospital and then transferred to a tertiary-care center for intensive-care treatment. On admission, she was poorly arousable. She had a serum glucose of 1,160 mg/dl, an arterial blood gas pH of 6.82, an anion gap of 21, and a positive serum acetone screen. Several laboratory values were abnormal: amylase, 144 IU/L; lipase, 64.3 IU/dl; alkaline phosphatase, 174 IU/L; SGOT, 49 IU/L; SGPT, 68 IU/L; and LDH, 304 IU/L. Direct and total bilirubin levels were normal. The WBC count was elevated (31.1/mm3) but was without eosinophilia. A urinalysis showed 2+ ketones, 5–10 red blood cells (RBCs), and 10–20 WBCs. A chest X-ray showed a right lower lobe infiltrate. Physical examination revealed a slightly distended, diffusely tender abdomen with decreased bowel sounds. An abdominal CT scan was suggestive of pancreatitis. An ultrasound study revealed a fatty liver without dilation of the common bile duct or other evidence indicative of obstructive pancreatitis. Olanzapine was discontinued. Ms. B. was aggressively hydrated and treated with IV insulin and antibiotics for a presumptive drug-related chemical pancreatitis in the setting of DKA. Her abdominal exam, liver function tests, lipase, and amylase all improved markedly during her hospital stay.
She was discharged on Hospital Day 8, on NPH (15 U sc bid), cefotetan (500 mg bid), omeprazole (20 mg qd), and risperidone (1 mg bid). After discontinuation of olanzapine, her serum glucose levels normalized, and she no longer required either insulin or an oral hypoglycemic agent.
Case 3.
Mrs. C., a 41-year-old white woman with bipolar disorder, obesity, hyperprolactinemia, and amenorrhea, had neither a personal nor a family history of DM. Laboratory studies conducted before treatment with olanzapine revealed normal random serum glucose levels.
At the age 20 years, Mrs. C. had her first episode of psychosis, which required hospitalization and treatment with thiothixene (15 mg tid) and lithium carbonate (1,250 mg qd). When symptoms of depression developed approximately 15 years later, paroxetine was added to her regimen and increased to 60 mg qd. While on this regimen she did well. When her blood urea nitrogen and creatinine levels became elevated, lithium was replaced with valproic acid (1,000 mg q A.M., 1,000 mg q noon, 1,500 mg qhs). Mrs. C. was also treated with medroxyprogesterone 10 mg qd for 10 days each month. Olanzapine (10 mg qhs) was added to her regimen.
Within 1 week of adding olanzapine (10 mg qhs) to her regimen, Mrs. C. complained of increased somnolence and developed 2+ pitting edema in her lower extremities. Olanzapine was stopped and sedation and edema resolved. Olanzapine was reinstituted (5 mg qhs) and was well tolerated. Over the next month, the dose of olanzapine was again increased to 10 mg qhs; Mrs. C. did well on this regimen for approximately 6 months. Thiothixene (15 mg qd) was tapered over several weeks. However, she complained of increasing fatigue and sedation. Olanzapine was again discontinued, but her complaints of fatigue and sedation persisted.
Two weeks after discontinuing olanzapine, Mrs. C. was seen by her gynecologist, who noted that she had a urinary tract infection and a high urine glucose by dipstick. Nitrofurantoin was prescribed, and she was referred to her primary-care provider for next-day follow-up. At this time, Mrs. C. reported several weeks of polydipsia, polyuria with dysuria, and increasing fatigue with weight loss. On physical examination, Mrs. C. had normal vital signs, but was dehydrated. Serum laboratory studies revealed a glucose level of 766 mg/dl, a bicarbonate of 27 mmol/L, a sodium of 120 mEq/L, and a potassium 4.2 mEq/L. She was referred to her local hospital for admission. Laboratory studies upon admission showed a positive serum acetone to dilution of 1:2. Mrs. C. was hydrated and treated with regular and NPH insulin. Treatment with glipizide was also instituted. Her fasting serum glucose levels fell into the 200–300 mg/dl range.
She was discharged to home on Hospital Day 4 on a regimen of Humulin 70/30 40 U q A.M. and 20 U q P.M., troglitazone 400 mg q P.M., as well as her preadmission medications. After 3 weeks of normalized fasting serum glucose levels, Mrs. C.'s insulin was discontinued, but she continued the hypoglycemic agent. Her fasting serum glucose remained normal, and the oral hypoglycemic agent was discontinued without alteration in her serum glucose status.
Case 4.
Mr. D., a 47-year-old white man with a 15-year history of schizoaffective disorder requiring numerous hospitalizations, had no history of DM. A random serum glucose level during a recent psychiatric admission before treatment with olanzapine was normal. His father, as well as a maternal aunt and uncle, had type II diabetes. His medical history was notable for obesity and hypothyroidism, although his recent thyroid indices were normal. Mr. D.'s prior psychopharmacological treatment included trials of neuroleptics (perphenazine, trifluoperazine, haloperidol, risperidone), anticonvulsants (valproic acid), antidepressants (fluoxetine), and anxiolytics (clonazepam, lorazepam, and buspirone).
After several months of noncompliance with his psychotropic regimen, Mr. D. decompensated psychiatrically, which resulted in hospitalization. On admission, olanzapine (10 mg qhs) and clonazepam (2 mg tid) were initiated. After discharge, carbamazepine (400 mg qd) was added to his regimen.
Five weeks after starting olanzapine, Mr. D. developed progressive somnolence, polyuria, and polydipsia. Serum chemistries revealed a serum glucose of 878 mg/dl, normal thyroid indices, and no anion gap. A complete blood cell count showed a WBC count of 8,200/mm3. He weighed 293 pounds (BMI: 40 kg/m2), having gained about 30 pounds since olanzapine was begun. Mr. D. was admitted to an intensive-care unit and treated with hydration and IV insulin. Olanzapine was continued.
Mr. D. was discharged on daily doses of olanzapine (10 mg), clonazepam (6 mg), carbamazepine (800 mg), and Humulin (70/30 insulin twice daily) with poor glucose control. Five months later, he was readmitted for psychiatric symptoms. At that time, he reported having stopped all of his medications for the month prior to the admission. Despite a further weight gain, to 314 pounds, Mr. D. did not require medication for glucose control. In fact, both his fasting serum glucose and hemoglobin A1c levels were normal. He was restarted on olanzapine (10 mg qd) and carbamazepine (800 mg qd). His psychiatric symptoms resolved, and he was discharged from the hospital.
After this discharge, Mr. D. became psychotic again, and olanzapine was increased (to 20 mg qd). His fasting serum glucose levels again rose despite a modest decrease in weight. Several weeks after reinstitution of olanzapine, his fasting serum glucose had risen to 242 mg/dl, and his glycosylated hemoglobin was 10% (normal range: 3.1%–5.5%). An insulin (sc) regimen was begun. Olanzapine was decreased (to 10 mg qd), and gabapentin (1,500 mg qd) was added.
Mr. D. was lost to follow-up for 2 months, during which time he discontinued his use of psychotropics. However, he continued to take Humulin (70/30) and metformin (1 g bid). His daily morning fasting serum glucose levels during this time period averaged 125 mg/dl. Six months later, he was started on quetiapine (300 mg qd) and restarted on clonazepam (6 mg qd). Despite having discontinued olanzapine, Mr. D. still requires insulin.
Case 5.
Mr. E., a 43-year-old, obese, white man with a long history of bipolar disorder requiring multiple psychiatric hospitalizations had neither a personal nor family history of DM. Laboratory studies conducted before treatment with olanzapine revealed normal random serum glucose levels.
Mr. E.'s psychiatric symptoms were treated with lamotrigine (400 mg qd) and lithium (1,200 mg qd). At the time of Mr. E.'s most recent psychiatric hospitalization, he was severely depressed, with suicidal ideation, irritability, affective lability, and paranoia. Paroxetine (20 mg qd) and olanzapine (10 mg qd) were added to his regimen. Mr. E.'s psychiatric symptoms markedly improved. While on olanzapine, his weight increased from 185 to 210 pounds (BMI: 32 kg/m2).
After 5 months on this regimen, Mr. E. complained of restless sleep, morning fatigue, hypersomnia (sleeping 12–15 hours per day), and inattentiveness. He denied feeling depressed or losing interest in his normal activities. Laboratory studies revealed a normal TSH and a lithium level of 0.7 mEq/L. His wife noted that he snored so loudly she would often have to leave the bedroom. Evaluation in a sleep laboratory revealed significant apneas and hypopneas, with an apnea index of 40/hour. Oxygen desaturations to 86% were noted; continuous positive airway pressure was administered, which abolished apneic episodes and desaturations.
One month later, he complained of polyuria and polydipsia. When a serum glucose level of 567 mg/dl was detected, he was admitted to the hospital. On admission, Mr. E. was afebrile and had a normal WBC count. His hemoglobin A1C was markedly elevated (10.4%; normal range: 3.1%–5.5%). He was briefly treated with IV insulin and switched to glyburide, which normalized his fasting serum glucose levels. Six months later, quetiapine was substituted for olanzapine; however, he still required treatment with glyburide.
Case 6.
Mr. F., a 39-year-old white man with a long history of schizoaffective disorder, obesity (272 pounds; height: 5'10'', BMI: 39.1 kg/m2), elevated triglycerides, hypertension, and hypothyroidism secondary to lithium treatment, did not have a history of DM. However, despite recent normal random serum glucose values (95 mg/dl) before treatment with olanzapine, Mr. F. had two documented random serum glucose levels above the normal range (217 mg/dl and 120 mg/dl). Several of his second-degree relatives have type II diabetes.
Mr. F.'s psychiatric symptoms were controlled with haloperidol (2–20 mg qd), lithium (1,800 mg qd), and valproic acid (1,750 mg qd). His medical regimen included hydrochlorothiazide/triamterene (75/30 mg qd), lisinopril (20 mg bid), levothyroxine (0.25 mg qd), atorvastatin (10 mg qd), and lorazepam (0.5–1.0 mg prn). He was started on olanzapine (5 mg qhs) as an adjunct to haloperidol (10 mg qhs). The dose of olanzapine was slowly increased (to 10 mg qhs) over 1½ months, while his haloperidol was tapered and discontinued over a 4-month period.
Three and one-half months after starting olanzapine, Mr. F. presented to his primary-care physician (an endocrinologist) with a complaint of 3–4 weeks of polydipsia, polyuria, and blurry vision. He had lost 6 pounds since starting olanzapine. A random serum glucose measurement was 686 mg/dl. A repeated level was 571 mg/dl. Mr. F. was treated as an outpatient with hydration, a diabetic diet, and glyburide (500 mg po bid). Fasting serum glucose measurements continued in the 120–220 mg/dl range. Mr. F. was then switched to metformin (500 mg bid), which achieved better glucose control.
Over the next several months, Mr. F.'s olanzapine was tapered, and he was started on risperidone (4 mg qd). Symptoms of polydipsia, polyuria, and blurry vision resolved with the diabetic treatment program. Mr. F.'s psychiatric symptoms remained stable after the switch to risperidone.
Case 7.
Mr. G., a 38-year-old white man with a 20-year history of schizophrenia and obsessive-compulsive disorder (OCD), had no history of DM and only a remote family history (great-grandmother) of type II diabetes. His medical history was notable for hypercholesterolemia and obesity. Mr. G. had numerous psychotropic trials for debilitating OCD symptoms and delusions.
Before beginning olanzapine, he took sertraline (50 mg qd) and clozapine (50 mg qd) for approximately 3½ years. Symptom control was fair, and he persistently refused to increase medication dosage. During this period, his weight increased by 21 pounds (to 230 pounds; BMI: 31.3). Random serum glucose measurements were within normal limits.
When the frequency of blood draws and clinic visits associated with clozapine administration began to interfere with his work schedule, he requested that a switch be made to olanzapine. Olanzapine (5 mg qd) was started, and he continued on sertraline (50 mg qd). Mr. G.'s weight remained stable on this regimen.
After 8 months, Mr. G. discontinued olanzapine against medical advice, citing concerns over sexual dysfunction. Two and one-half months later, Mr. G. was admitted to a psychiatric unit with worsening psychotic symptoms—his first psychiatric hospitalization in 5 years. Mr. G. was restarted on olanzapine (5 mg qd) just prior to admission, and his dose was increased (to 10 mg qd) during the hospitalization. A random serum glucose level 1 week after admission was normal.
He was discharged with outpatient follow-up. Three months later, Mr. G. complained of polyuria with urgency, polydipsia, and blurred vision of about 2 weeks' duration. A fasting serum glucose was 372 mg/dl. Olanzapine was discontinued, and dietary changes were initiated. Within 10 days, Mr. G. reported an improvement in symptoms, but continued to have elevated fasting serum glucose levels (316 mg/dl; 323 mg/dl). Referral was made to his primary care physician for continued glucose monitoring and treatment.
Discussion
To our knowledge, this is the first report of an association between treatment with olanzapine and the development of potentially life-threatening DKA in the setting of new-onset DM. The present case series corroborates and extends a recent report of two cases of new-onset DM associated with olanzapine treatment.8 Details of our cases are summarized in Table 1. Three of our patients were diagnosed with schizoaffective disorder, two had schizophrenia, and two had bipolar disorder. Our patients developed new-onset DM between 5 weeks and 17 months (mean 26 weeks; median 20 weeks) after initiation of treatment with olanzapine. Five of these patients required hospitalization to manage hyperglycemia. Roughly half of our patients had known family histories of type II DM, and four patients experienced weight gain while taking olanzapine. Two patients presented with DKA (initial serum glucose values of 1,274 mg/dl, 1,160 mg/dl), a presentation unusual for adults with new-onset DM. One of these patients had symptoms consistent with chemical pancreatitis in a fashion similar to two other case reports of clozapine-associated pancreatitis.10,11 Two patients had an apparent remission of DM after discontinuation of olanzapine treatment; one exhibited a return of hyperglycemia after rechallenge with olanzapine. Of our seven cases, four continue to require medical treatment for DM.
A literature review revealed 13 cases of hyperglycemia or DKA associated with the use of a structurally similar atypical antipsychotic, clozapine, a piperazinyl dibenzodiazepine.2–8 Clozapine-treated patients with hyperglycemia or DKA were predominantly male (12 cases) and black (10 cases). Nine cases had no history of glucose abnormalities, and two cases had preexisting stable type II DM. Four clozapine-treated cases had a family history of DM. Glucose abnormalities typically developed within the first 2 months of treatment with clozapine and ranged from mild hyperglycemia to fulminant ketoacidotic coma. Of these 13 cases, 11 did not require insulin treatment after the resolution of the acute hyperglycemic event. One patient, previously stabilized on an oral hypoglycemic agent for preexisting type II DM, continued on clozapine and required insulin maintenance.
Mechanisms postulated to account for clozapine-induced hyperglycemia include primary damage to the pancreatic islet cells and/or sympathetic nervous system dysregulation, and a secondary phenomenon related to weight gain and insulin resistance. These same putative mechanisms may also apply to hyperglycemia and DKA secondary to olanzapine. Both clozapine and olanzapine may exacerbate subclinical diabetes or promote glucose metabolic abnormalities (e.g., insulin resistance in a patient with a diabetic diathesis). Because weight gain is a common side effect of many antipsychotics,12–16 including olanzapine,17–21 some of our findings may be explained by this factor alone. Since all of our patients were treated with multiple medications, hyperglycemia could be secondary to combinations of medications (e.g., olanzapine coadministered with either lithium or valproic acid). Indeed, valproic acid alone has caused dramatic increases in weight and levels of androgens, as well as insulin resistance, in women.22
Postmarketing surveillance has documented 139 cases of diabetes associated with olanzapine treatment; roughly 10% (14 cases) had no clear diabetic risk factors (Eli Lilly, Indianapolis, IN; data on file). The present case series must be interpreted with caution. Given that olanzapine has been administered to more than 1.2 million patients, chance associations between new-onset DM and initiation of treatment with olanzapine will likely occur. What is unclear is whether the number of cases of olanzapine-related diabetes exceeds the expected incidence for development of diabetes in this patient population. Nevertheless, we were struck by the number of olanzapine-treated patients who developed diabetic complications. It may be prudent to consider periodic serum glucose monitoring in olanzapine-treated patients who have risk factors for diabetes.
Appropriately controlled epidemiological and physiological studies are needed to determine whether a causal relationship exists between treatment with atypical antipsychotics and the development of disordered glucose metabolism.
REFERENCES
-
Janicak P, Davis J, Preskorn S, et al: Principles and Practice of Psychopharmacology, 2nd Edition. Baltimore, MD, Williams & Wilkins, 1997
-
Kamran A, Doraiswamy PM, Jane JL, et al: Severe hyperglycemia associated with high doses of clozapine (letter). Am J Psychiatry 1994; 151:1395
-
Koval MS, Rames LJ, Christie S: Diabetic ketoacidosis associated with clozapine treatment. Am J Psychiatry 1994; 151:1520–1521
-
Kostakoglu AE, Yazici KM, Erbas T, et al: Ketoacidosis as a side-effect of clozapine: a case report. Acta Psychiatr Scand 1996; 93:217–218[Medline]
-
Peterson GA, Byrd SL: Diabetic ketoacidosis from clozapine and lithium cotreatment. Am J Psychiatry 1996; 153:737–738
-
Koren W, Kreis Y, Duchowiczny K, et al: Lactic acidosis and fatal myocardial failure due to clozapine. Ann Pharmacother 1997; 41:168–170
-
Popli AP, Konicki PE, Jurjus GJ, et al: Clozapine and associated diabetes mellitus. J Clin Psychiatry 1997; 58:108–111[Medline]
-
Wirthing DA, Spellberg BJ, Erhart SM, et al: Novel antipsychotics and new-onset diabetes. Biol Psychiatry 1998; 44:778–783[Medline]
-
Sporn J, Goldstein L, Brown S, et al: Hyperglycemia associated with olanzapine (abstract). Annual Meeting of the American Psychiatric Association, May 30–June 4, 1998; Toronto, Canada, p. 250
-
Martin A: Acute pancreatitis associated with clozapine use (letter). Am J Psychiatry 1992; 149:714
-
Jubert P: Clozapine-related pancreatitis: Ann Intern Med 1994; 121:722–723 (published erratum appears in Ann Intern Med 1995; 122:397)
-
Allison DB, Mentore JL, Heo M, et al: Weight gain associated with conventional and newer antipsychotics: a meta-analysis (abstract). Annual Meeting of the New Clinical Drug Evaluation Unit Program, June 10–13, 1998; Boca Raton, FL, p. 113
-
Stanton JM: Weight gain associated with neuroleptic medication: a review. Schizophr Bull 1995; 21:463–472
-
Masand PS: Weight gain associated with atypical antipsychotics. Journal of Psychotic Disorders 1998; 2:4–6
-
Leadbetter R, Shutty M, Pavalonis D, et al: Clozapine-induced weight gain: prevalence and clinical relevance. Am J Psychiatry 1992; 149:68–72[Abstract/Free Full Text]
-
Frankenburg FM, Zanarini MC, Kando J, et al: Clozapine and body mass change. Biol Psychiatry 1998; 43:520–524[Medline]
-
Kraus T, Haack M, Schuld A, et al: Body weight and leptin plasma levels during treatment with antipsychotic drugs. Am J Psychiatry 1999; 156:312–314[Abstract/Free Full Text]
-
Gupta S, Droney T, Al-Samarrai S, et al: Olanzapine-induced weight gain. Ann Clin Psychiatry 1998; 10:39[Medline]
-
Beasley CM, Hamilton SH, Crawford AM, et al: Olanzapine vs. haloperidol: acute phase results of the international double-blind olanzapine trial. Eur Neuropsychopharmacol 1997; 7:125–137[Medline]
-
Osser DN, Najarian D, Berman I, et al: Olanzapine increases weight gain and triglyceride levels (abstract). Annual Meeting of the American Psychiatric Association, 1998, NR688, p. 254
-
Casey DE: Side effect profiles of new antipsychotic agents. J Clin Psychiatry 1996; 11:40–45
-
Isojarvi JIT, Laatikainen TJ, Knip M, et al: Obesity and endocrine disorders in women taking valproate for epilepsy. Ann Neurol 1996; 39:579–584[Medline]
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D. W. Haupt and J. W. Newcomer
Risperidone-Associated Diabetic Ketoacidosis
Psychosomatics,
June 1, 2001;
42(3):
279 - 280.
[Full Text]
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R. R. Conley and R. Mahmoud
A Randomized Double-Blind Study of Risperidone and Olanzapine in the Treatment of Schizophrenia or Schizoaffective Disorder
Am J Psychiatry,
May 1, 2001;
158(5):
765 - 774.
[Abstract]
[Full Text]
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