Zur Vorlage Bei der Versicherungsanstalt







Wien, am 29. 10. 2002





Betrifft:	Antrag auf Kur zur Gewichtsreduktion bei Neuroleptika induzierter

Adipositas des Patienten HANS BERNHARD, Geb. 23.7.1973





Sehr geehrter Frau Kollegin, Sehr geehrter Herr Kollege,







Bei meinem Patienten , Herrn HANS BERNHARD kam es anfang 2002 zu einer 

Erstmanifestation einer Manische Depressiven Erkrankung  (ICD 10 F 31.2). Ihm

Rahmen der akuten und subakuten Behandlung erhielt der Pat. Zyprexa (Olanzapin)

verschrieben auf welches der Pat sehr gut respondierte.



Im Rahmen dieser Behandlung wurde natuerlich jeweils versucht die niedrigst

moegliche Dosis zu finden. Trotz dieses Versuchs sowie Aufklaerungsmažnahmen und

eines baldigen Ausschleichens der Medikation kam es dennoch zu einer massiven

Gewichtszunahme. Diese Gewichtzunahme unter Zyprexa (Olanzapin) ist in der

Literatur gut bekannt (Gupta, Droney et al. 1998; Gupta, Droney et al. 1999;

Osser, Najarian et al. 1999; Karagianis 2000; Sacchetti, Guarneri et al. 2000;

Ball, Coons et al. 2001; Baptista and Beaulieu 2001; Basson, Kinon et al. 2001;

Eder, Mangweth et al. 2001; Floris, Lejeune et al. 2001; Ganguli, Brar et al.

2001; Haapasalo-Pesu and Saarijarvi 2001; Kinon, Basson et al. 2001; Gothelf,

Falk et al. 2002; Malyuk, Gibson et al. 2002; Meyer 2002; Poyurovsky, Pashinian

et al. 2002; Ramankutty 2002; Ratzoni, Gothelf et al. 2002; Riccitelli and Baker

2002; Virkkunen, Wahlbeck et al. 2002).



So wie in der Literatur beschrieben, wurde der Patient ueber die Nebenwirkung

aufgeklaert. In der Akutphase der Behandlung wurde versucht noch waehrend des

stationaeren Aufenthalts eine Reduktionskost zu verordnen. Nach Entlassung aus der

stationaeren Pflege erfolgte eine Besprechung der Moeglichkeiten  mit den durch

Zyprexa verstaerkten Hungergefuehlen umzugehen. Der Pat. erhielt eine Broschuere

(speziell zu diesem Zweck von Lilly herausgegeben) und diese wurde gemeinsam

besprochen. Aužerdem begann der Pat regelmaežig Bewegung sowie Ausdauersport

(Inline Skaten um die Gelenke nicht zu ueberlasten) zu machen. Nachdem es trotz

Information weiterhin zu einer Gewichtszunahme kam, wurde die Dosis so schnell

wie psychiatrisch moeglich weiter reduziert und der Pat. gebeten ein Esstagebuch

zu fuehren. Aufgrund der Daten des Tagebuches erfolgten weitere Schulungen und

Gespraeche. Zu diesem Zeitpunkt kam es zwar zu einer deutlichen Verlangsamung der

Gewichtszunahme die jedoch erst nach voelligem Ausschleichen der Therapie

sistierte.



Insgesamt kam es jedoch zwischen Maerz 2002 Aufnahmegewicht von 90 Kg bei 175 cm

Koerpergroeže (BMI 29.4) zu einer Gewichtszunahme von 25kg mit einem Maximalgewicht

von 115 Kg. (BMI 37.6) und somit zu einer manifesten behandlungsbeduerftigen

Adipositas im Juni 2002. Trotz bereits durchgefuehrter Schulungen, des

Bewegungsprogramms gelang es dem Pat bis jetzt (29.10.2002) nicht das Gewicht

wesentlich zu reduzieren, dieses Pendelt trotz Gegenmažnahmen zwischen 111 und

114 Kg.



Dies bedeutet, dass es im Rahmen der notwendigen psychiatrischen Behandlung,

trotz Aufklaerung, Bewegungsprogrammen und diaetischer Einschraenkungen zu einer

massiven Gewichtzunahme kam.



Nachdem diese Gewichtszunahme als Folge der notwendigen Behandlung der MDK

anzusehen ist, und es dem Pat. bis jetzt nicht gelungen ist sein Gewicht wieder

zu normalisieren, empfehle ich fuer Hrn. HANS BERNHARD einen Kuraufenthalt wo er

die notwenigen Verhaltensaenderungen und weitergehenden Informationen erlernen

kann, um sie in weiterer Folge anzuwenden.



Aufgrund der guten Kognitiven Faehigkeiten des Patienten und seiner bisherigen

guten Erfahrungen bei der Befolgung von konkreten aerztlichen Anweisungen, sehe

ich einen Kuraufenthalt zum Erlernen einer gesunden  fettarmen,

kohlenhydratreichen Ernaehrungsweise und eines gesunden Lebensstils als sinnvoll

und indiziert.





In der Hoffnung Ihnen mit diesen Informationen gedient zu haben, verbleibe ich

mit freundlichen Gruessen. Sollten Sie noch weiter Fragen haben zoegern Sie nicht

mit mir  unter Tel: 77- 7777 7777 Kontakt aufzunehmen.







Hochachtungsvoll







OA.Dr. S. D. Schindler 

Leiter der Ambulanz















Anhang:	Literaturliste teilweise. mit Abstakt zu Gewichtzunahme unter

Olanzapin Literaturliste:





Ball, M. P., V. B. Coons, et al. (2001). "A program for treating

olanzapine-related weight gain." Psychiatr Serv 52(7): 967-9. This study

evaluated the effectiveness of a Weight Watchers program for patients with

schizophrenia who had olanzapine-related weight gain and ascertained whether the

severity of patients' psychiatric symptoms was correlated with the patients'

success in losing weight. Seven men and four women who had been treated with

olanzapine and who had gained at least 7 percent of their pretreatment body

weight attended Weight Watchers meetings and were offered supervised exercise

sessions. The patients' weight, body mass index, and psychiatric symptoms were

assessed and were compared with those of a matched comparison group who did not

attend the Weight Watchers program. Only the men experienced significant weight

loss. No correlation was found between weight loss and exercise or change in

psychiatric symptoms.



Baptista, T. and S. Beaulieu (2001). "Body weight gain, insulin, and leptin in

olanzapine-treated patients." J Clin Psychiatry 62(11): 902-4.



Basson, B. R., B. J. Kinon, et al. (2001). "Factors influencing acute weight

change in patients with schizophrenia treated with olanzapine, haloperidol, or

risperidone." J Clin Psychiatry 62(4): 231-8. OBJECTIVE: Clinical factors

predicting weight change in patients with schizophrenia and related disorders

during acute treatment with the antipsychotic drugs olanzapine, risperidone, and

haloperidol were sought through retrospective analyses. METHOD: Six-week

body-weight data from 2 trials, study 1 comparing olanzapine and haloperidol (N =

1,369) and study 2 olanzapine and risperidone (N = 268), were analyzed. Effects

of 8 clinically relevant covariates--therapy, clinical outcome (Brief Psychiatric

Rating Scale), baseline body mass index (BBMI), increased appetite, age, gender,

race, and dose--on weight were compared. RESULTS: In study 1, olanzapine (vs.

haloperidol) therapy, better clinical outcome, lower BBMI, and nonwhite race

significantly affected weight gain. Effects of increased appetite and male gender

on weight gain were significant for olanzapine but not for haloperidol. In study

2, better clinical outcome, lower BBMI, and younger age significantly affected

weight gain. Increased appetite was more frequent during olanzapine treatment

than during haloperidol, but not significantly different from risperidone.

Significant differences in effect on weight change were found between olanzapine

and haloperidol but not between olanzapine and risperidone. No evidence was found

that lower antipsychotic drug doses were associated with lower weight gain.

CONCLUSION: This report identifies predictive factors of acute weight change in

patients with schizophrenia. Similar factors across antipsychotic drugs in

predicting greater weight gain included better clinical outcome, low BBMI, and

nonwhite race. Factors differing between conventional (haloperidol) and atypical

(olanzapine) agents included increased appetite and gender. Choice of atypical

antipsychotic drug (olanzapine vs. risperidone) was of minor importance with

regard to influence on acute weight gain.



Eder, U., B. Mangweth, et al. (2001). "Association of olanzapine-induced weight

gain with an increase in body fat." Am J Psychiatry 158(10): 1719-22. OBJECTIVE:

The goal of this study was to explore the pathophysiology of weight gain during

treatment with olanzapine for schizophrenia. METHOD: The authors used a

prospective, controlled, open study comparing body weight, body mass index, and

related biological measures in mentally and physically healthy volunteers and

olanzapine-treated patients with schizophrenia. Weight, eating behavior, leptin

serum levels, body mass index, and body composition were assessed over an 8-week

observation period. RESULTS: A significant increase in body weight, leptin serum

levels, and percentage of body fat was seen in patients treated with olanzapine,

but the drug-free comparison group did not show any significant changes. The

weight gain during antipsychotic treatment with olanzapine was mainly

attributable to an increase in body fat; patients' lean body mass did not change.

CONCLUSIONS: In addition to the original finding that an increase in body fat is

mainly responsible for olanzapine-induced weight gain, these findings confirm

results obtained in other studies showing increases in body weight and serum

leptin levels during treatment with second-generation antipsychotics.



Floris, M., J. Lejeune, et al. (2001). "Effect of amantadine on weight gain

during olanzapine treatment." Eur Neuropsychopharmacol 11(2): 181-2. Patients

treated with olanzapine may gain weight, especially in the first months of

therapy. Amantadine (100-300 mg/day) was started in 12 patients having a mean

weight gain of 7.3 kg during olanzapine treatment. The patients' weight

stabilised and over 3-6 months they lost an average of 3.5 kg. No clinical

deterioration occurred and no adverse effects were reported. These observations

merit confirmation in randomised, controlled trials.



Ganguli, R., J. S. Brar, et al. (2001). "Weight gain over 4 months in

schizophrenia patients: a comparison of olanzapine and risperidone." Schizophr

Res 49(3): 261-7. Weight gain frequently accompanies treatment with

antipsychotics. In order to determine whether newer antipsychotic agents differ

from each other with respect to weight gain, we compared two cohorts of patients

with DSM-IV schizophrenia who had newly started treatment with either risperidone

or olanzapine. After obtaining informed consent, data regarding body weight and

height were culled from existing medical records of 100 patients (50 patients in

each treatment group). Baseline body weight, close to the time of starting the

new medication, and body mass index [BMI = weight (kg)/height (m) squared] were

compared to the body weight and BMI following 4 months of treatment. There was no

significant change in mean body weight or BMI in the group treated with

risperidone (baseline weight = 83.1 kg +/- 20.5, follow-up = 82.8 kg +/- 19.9;

matched pair t = 0.66, P = n.s.; baseline BMI = 29.6 +/- 9.4, follow-up = 29.5

+/- 9.1; matched pair t = 0.79, P = n.s.). However, in the group treated with

olanzapine, there was a significant increase in both mean body weight and BMI

(baseline weight = 84.9 kg +/- 25.0, follow-up = 87.1 kg +/- 25.1; matched pair t

= 4.62, P < 0.001; baseline BMI = 29.5 +/- 7.4, follow-up = 30.3 +/- 7.5; matched

pair t = 4.43, P < 0.001). In this naturalistic study, treatment with olanzapine

was associated with a mean weight gain of about 2 kg from baseline, in patients

with schizophrenia, while treatment with risperidone was associated with no mean

weight change.



Gothelf, D., B. Falk, et al. (2002). "Weight gain associated with increased food

intake and low habitual activity levels in male adolescent schizophrenic

inpatients treated with olanzapine." Am J Psychiatry 159(6): 1055-7. OBJECTIVE:

The authors studied weight gain mechanisms and energy balance in patients treated

with olanzapine. METHOD: The body mass index of male schizophrenic adolescent

inpatients treated with olanzapine (N=10) and of 10 matched patients treated with

haloperidol (N=10) were measured at baseline and after 4 weeks of treatment. For

the patients treated with olanzapine, caloric intake, resting energy expenditure,

and physical activity (determined through accelerometry and heart rate

monitoring) were assessed at baseline and after 4 weeks of treatment. RESULTS:

Body mass index significantly increased in those treated with olanzapine but not

in those given haloperidol. The increase in body mass index was due to an

increase in caloric intake without change in diet composition. Olanzapine had no

significant effect on resting energy expenditure. Daily energy expenditure was

very low before and after treatment. CONCLUSIONS: Olanzapine-induced weight gain

is associated with a general increase in caloric intake.



Gupta, S., T. Droney, et al. (1998). "Olanzapine-induced weight gain." Ann Clin

Psychiatry 10(1): 39.



Gupta, S., T. Droney, et al. (1999). "Olanzapine: weight gain and therapeutic

efficacy." J Clin Psychopharmacol 19(3): 273-5.



Haapasalo-Pesu, K. M. and S. Saarijarvi (2001). "Olanzapine induces remarkable

weight gain in adolescent patients." Eur Child Adolesc Psychiatry 10(3): 205-8.

We present here clinical case reports of three adolescents, aged 14-17 years, who

were treated with olanzapine. The daily dose was 10 mg. Prior to olanzapine, the

patients were unsuccessfully treated with other antipsychotic drugs. The response

to olanzapine for psychotic symptoms was clinically significant in all three

patients. The major adverse effect was excessive weight gain. The increases in

body mass index (BMI) were 9, 8 and 5 kg/m2. One of the patients later lost the

additional weight. Especially in adolescents obesity is a serious side effect and

potential consequences include numerous health problems.



Karagianis, J. (2000). "Olanzapine and weight gain." Can J Psychiatry 45(5): 493.



Kinon, B. J., B. R. Basson, et al. (2001). "Long-term olanzapine treatment:

weight change and weight-related health factors in schizophrenia." J Clin

Psychiatry 62(2): 92-100. BACKGROUND: Weight change and the weight-related health

factors of nonfasting serum glucose, serum cholesterol, and diastolic blood

pressure levels were analyzed in patients with DSM-III-R schizophrenia and

related disorders who received treatment with olanzapine for up to 3 years, and

comparisons were made to patients treated with haloperidol. Baseline body mass

index (BBMI; kg/m2) and dose (mg/day) were investigated as predictors of

long-term weight change experienced during olanzapine treatment. METHOD: This

analysis retrospectively examined 573 patients receiving olanzapine and 103

patients receiving haloperidol for 39 weeks or more from a study of 1,996

patients randomly assigned 2:1 to either olanzapine, 5 to 20 mg/day, or

haloperidol, 5 to 20 mg/day. After 6 weeks of acute therapy, patients continued

for 1 year or more with either double-blind or open-label olanzapine therapy or

double-blind haloperidol therapy. RESULTS: Mean weight gain for

olanzapine-treated patients observed for a median of 2.54 years trended toward a

plateau after the first 39 weeks of treatment with a

last-observation-carried-forward mean weight change of 6.26 kg (13.8 lb) and a

median of 5.90 kg (13.0 lb). This was significantly higher than that for

haloperidol-treated patients, whose mean weight gain was 0.69 kg (1.5 lb) after

1.15 years (p < .001). Patients with higher BBMI (> 27.6) gained significantly

less weight during treatment with olanzapine than their lighter counterparts

(BBMI < 27.6) (p < .001). The effect of olanzapine dose on weight was not

significant (p > or = . 183). Median serum glucose at endpoint was not

significantly associated (p = .096) with weight change for olanzapine. Median

serum cholesterol and diastolic blood pressure for olanzapine- treated patients

at endpoint showed a relationship with weight change that was statistically (p <

or = .001) but not clinically significant. The difference in incidence of

elevated serum glucose, cholesterol, or diastolic blood pressure between

olanzapine and haloperidol therapy groups was not different (p > .05).

CONCLUSION: Mean weight gain during olanzapine treatment trended toward a plateau

after the initial 39 weeks of treatment with no further significant gain out to 3

years. Higher BBMI was predictive of a lower long-term weight gain, while dose

was not a significant predictor of greater longer term weight change. The

relationship between weight change and glucose was not statistically significant.

The association between weight change and changes in cholesterol as well as

changes in diastolic blood pressure was statistically significant but not

considered clinically relevant based on the ranges observed.



Malyuk, R., B. Gibson, et al. (2002). "Olanzapine associated weight gain,

hyperglycemia and neuroleptic malignant syndrome: case report." Int J Geriatr

Psychiatry 17(4): 326-8. We describe here a case of olanzapine associated weight

gain, hyperglycemia and neuroleptic malignant syndrome in a 64 year-old woman

with a significant medical history. Eighteen weeks after initiating olanzapine,

Mrs X lost glycemic control, exhibited signs and symptoms consistent with

neuroleptic malignant syndrome and gained 8.9 kg. We suggest that utilization of

olanzapine in the less medically stable geriatric patient be implemented with

vigilant monitoring for such complications mentioned above.



Meyer, J. M. (2002). "A retrospective comparison of weight, lipid, and glucose

changes between risperidone- and olanzapine-treated inpatients: metabolic

outcomes after 1 year." J Clin Psychiatry 63(5): 425-33. BACKGROUND: Metabolic

side effects have been increasingly noted during therapy with novel

antipsychotics, but there is a dearth of comprehensive comparative data in this

area. The goal of this retrospective study was to examine the changes in weight

parameters, fasting glucose, and fasting lipids in long-term inpatients treated

with either risperidone or olanzapine. METHOD: A retrospective study was

performed by reviewing charts of patients at Oregon State Hospital, Salem, who

were treated during July and August 1999, comparing metabolic outcomes during the

first year of therapy with either risperidone or olanzapine. Data were analyzed

also by age, sex, and concurrent use of lithium or valproate. Included for

analysis were patients at least 18 years old with baseline weights obtained

within 3 weeks of drug initiation, and baseline fasting triglycerides,

cholesterol, and glucose obtained within 3 months prior to drug initiation and at

1 year of treatment (+/- 4 weeks). The patients meeting these criteria in each

drug cohort (risperidone, N = 47; olanzapine, N = 47) included 1 patient with

diagnosed diabetes mellitus prior to onset of treatment. RESULTS: Among those

patients under 60 years old, olanzapine patients (N = 37) experienced

significantly greater increases at 1 year in all metabolic parameters than the

risperidone group (N = 39), except for weight variables: triglycerides +104.8

mg/dL (olanzapine) versus +31.7 mg/dL (risperidone) (p = .037); cholesterol +30.7

mg/dL (olanzapine) versus +7.2 mg/dL (risperidone) (p = .004); glucose +10.8

mg/dL (olanzapine) versus +0.74 mg/dL (risperidone) (p = .030). Patients under 60

years of age with concurrent use of lithium or valproate were associated with

greater weight gain in both drug groups, but this difference was statistically

significant only for the olanzapine cohort. Neither weight change nor use of

lithium or valproate was associated with increases in glucose or lipids among

those under 60 years old for either drug. CONCLUSION: Olanzapine therapy is

associated with significantly greater increases in fasting glucose and lipid

levels for nongeriatric adult patients than risperidone, and the increases are

not correlated with changes in weight parameters. Appropriate monitoring of

fasting glucose and serum lipid levels should be considered during extended

treatment with atypical antipsychotics.



Osser, D. N., D. M. Najarian, et al. (1999). "Olanzapine increases weight and

serum triglyceride levels." J Clin Psychiatry 60(11): 767-70. BACKGROUND:

Previous studies have suggested that clozapine is associated with increases in

both weight and serum triglyceride (but not cholesterol) levels. Because of the

pharmacologic similarities between clozapine and olanzapine, we decided to

evaluate if olanzapine use was associated with an increase in triglycerides.

METHOD: Twenty- five inpatients (21 men, 4 women) were treated with olanzapine,

and their outcomes were tracked prospectively in a medication utilization

evaluation study. RESULTS: After 12 weeks on a mean +/- SD dose of 13.8+/-4.4

mg/day, weight increased a mean of 12 lb (5.4 kg; from 190+/- 37 lb [85.5+/-16.7

kg] to 202+/-30 lb [90.9+/-13.5 kg]), while fasting triglycerides increased a

mean of 60 mg/dL (from 162+/-121 mg/dL to 222+/-135 mg/dL). Both increases were

significant at p < .05. Fasting total cholesterol did not increase. The

triglyceride increase was even larger when we excluded 8 patients who received

various interventions to lower lipid levels (e.g., pravastatin, low-fat diet)

during the olanzapine trial. There was a strong association between weight change

and triglyceride change (p < .02); after controlling for weight, analysis of

covariance showed no independent increase in triglycerides. CONCLUSION: These

results suggest olanzapine has significant effects on weight and serum

triglyceride levels. Clinical implications are discussed.



Poyurovsky, M., A. Pashinian, et al. (2002). "Olanzapine-induced weight gain in

patients with first-episode schizophrenia: a double-blind, placebo-controlled

study of fluoxetine addition." Am J Psychiatry 159(6): 1058-60. OBJECTIVE: Since

olanzapine-induced weight gain may be attributable to the antagonistic activity

of olanzapine at the serotonin-2C receptor, the authors hypothesized that it

might be attenuated by addition of the selective serotonin reuptake inhibitor

fluoxetine. METHOD: First- episode hospitalized schizophrenia patients (N=30)

were randomly assigned in an 8-week double-blind study of olanzapine, 10 mg/day,

coadministered with either fluoxetine, 20 mg/day (N=15), or placebo (N=15).

RESULTS: The group receiving olanzapine plus fluoxetine showed significantly less

improvement in positive and disorganized symptom dimensions than the group

receiving olanzapine plus placebo. The two groups demonstrated similar and

substantial gradual weight gains. CONCLUSIONS: These results suggest that

fluoxetine coadministration is clinically ineffective and cannot attenuate

olanzapine-induced weight gain.



Ramankutty, G. (2002). "Olanzapine-induced destabilization of diabetes in the

absence of weight gain." Acta Psychiatr Scand 105(3): 235-6; discussion 236-7.

OBJECTIVE: To provide evidence that olanzapine can cause glucose dysregulation by

a mechanism other than weight gain. METHOD: I report a case of a diabetic patient

who developed glucose dysregulation soon after initiation of olanzapine

treatment, occurring in the absence of weight gain. I compare this case to

previous case reports. RESULTS: Our patient developed persistent hyperglycaemia

within 3 weeks of initiating treatment with olanzapine. Weight recorded just

prior to commencement and soon after discontinuation of olanzapine were not

significantly different. CONCLUSION: Controlled studies are necessary to

elucidate the mechanism by which olanzapine can cause dysregulation of glucose

homeostasis, and to develop guidelines for the use of olanzapine in patients with

known diabetes as well as in patients with risk factors for diabetes.



Ratzoni, G., D. Gothelf, et al. (2002). "Weight gain associated with olanzapine

and risperidone in adolescent patients: a comparative prospective study." J Am

Acad Child Adolesc Psychiatry 41(3): 337-43. OBJECTIVE: To evaluate weight gain

associated with olanzapine, risperidone, and haloperidol treatment and its

clinical risk factors in adolescent patients. METHOD: The study was conducted at

three adolescent psychiatric departments in two mental health centers in the Tel

Aviv area. All patients were Jewish Israelis. Weight and body mass index (BMI) of

hospitalized adolescents treated with olanzapine (n = 21), risperidone (n = 21),

or haloperidol (n = 8) were prospectively monitored on a weekly basis for the

first 12 weeks of treatment. Various clinical risk factors were tested for

association with weight gain. RESULTS: The olanzapine and risperidone groups

experienced significant weight gain between baseline and endpoint (p < .01),

whereas the average weight of the haloperidol group did not change. Average

weight gain was significantly higher for the olanzapine group (7.2 +/- 6.3 kg,

11.1% +/- 7.8%) than for the risperidone (3.9 +/- 4.8 kg, 6.6% +/- 8.6%) and

haloperidol (1.1 +/- 3.3 kg, 1.5% +/- 6.0%) groups. Extreme weight gain (>7%) was

recorded in 19 patients (90.5%), 9 patients (42.9%), and 1 (12.5%) patient,

respectively Gender (males), low concern about gaining weight (females), low

baseline BMI, and paternal BMI were positively correlated with weight gain,

whereas previous neuroleptic history, neuroleptic dosage, response to treatment,

and illness duration were not. CONCLUSIONS: Olanzapine and risperidone are

associated with extreme weight gain in adolescents, much higher than that

reported in adults. This side effect should be taken into consideration before

prescribing these medications, especially in patients at high risk.



Riccitelli, G. and N. Baker (2002). "Weight gain and hyperglycaemia associated

with olanzapine." Aust N Z J Psychiatry 36(2): 270-1.



Sacchetti, E., L. Guarneri, et al. (2000). "H(2) antagonist nizatidine may

control olanzapine-associated weight gain in schizophrenic patients." Biol

Psychiatry 48(2): 167-8. BACKGROUND: Olanzapine is temporally associated, in a

number of patients with schizophrenia, with weight gain. H(2) antagonists, like

nizatidine, have been shown to control appetite in overweight patients. METHODS:

A patient with olanzapine temporally associated weight gain was treated with

nizatidine as "add-on" therapy. RESULTS: Nizatidine treatment was associated with

good control and subsequent reduction of weight after 4 to 5 weeks of therapy in

a patient with repetitive episodes of weight gain during olanzapine treatment.

Olanzapine was otherwise well tolerated and effective in controlling

psychopathology. CONCLUSIONS: H(2) antagonist treatment with olanzapine may be a

valid medical strategy in preventing and/or reducing weight gain in patients with

schizophrenia. Controlled studies are recommended to confirm this observation.



Virkkunen, M., K. Wahlbeck, et al. (2002). "Decrease of energy expenditure causes

weight increase in olanzapine treatment - a case study." Pharmacopsychiatry

35(3): 124-6. The aim of this study was to evaluate the mechanisms underlying

weight gain induced by the atypical antipsychotic, olanzapine. We performed

euglycemic, hyperinsulinemic clamp combined with indirect calorimetry on a

48-year-old male with antisocial personality disorder, alcohol dependence and

paranoid ideation before and after one month of olanzapine (10 - 15 mg/day)

therapy. The patient gave his informed, written consent for this study. The

results were a weight gain of 6 kg and a decrease in both basal (from 1673 to

1613 kcal/24 h) and 3-hour (from 22.8 to 20.2 cal/kg fat free mass/min) energy

expenditure. Serum thyroid hormone and high-density lipoprotein cholesterol

levels decreased, and the triglyceride and low-density lipoprotein cholesterol

levels increased. Insulin sensitivity did not change. We conclude that decreased

basal energy expenditure may contribute to weight gain in olanzapine treatment.













copyright 2002 HANS BERNHARD