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P.3.012 Olanzapine-induced leucopenia and neutropenia a case report
P3 Psychotic disorders and antipsychotics
$460
and insufficient efficacy (HAL 38%, FLU 48%, ZUC 38%) of previous therapy. The completion rates were 76%, 82% and 71% for the HAL, FLU and ZUC groups, respectively. The most frequent reason for trial discontinuation was due to adverse events or withdrawal of consent (HAL, 11 and 12 patients; FLU, 4 and 7 patients; ZUC, 4 and 14 patients) (Table 1). There were significant reductions from baseline to endpoint (p < 0.001) in the mean total PANSS score in all three groups (HAL 76.2 vs 64.1, FLU 70.7 vs 59.6, ZUC 70.3 vs 63.6). At endpoint, improvement ,,d20% in the PANSS total score was seen in 43%, 41% and 32% of patients in the HAL, FLU and ZUC groups, respectively. A significant decrease (p <0.001) in the PANSS negative subscale score was seen in all groups; 18.6 vs 15.7; 20.9 vs 16.9 and 19.8 vs 17.1 in the HAL, FLU and ZUC groups respectively. Patient satisfaction with treatment also improved significantly in all groups, with marked increases from baseline to endpoint in the proportion of patients rating their satisfaction as "very good" (HAL 0% vs 24%, FLU 0% vs 40%, ZUC 6% vs 27%). There was an improvement in quality of life (SF-36 scores) in all three groups. The severity of movement disorders decreased significantly during the 6-month study. Patients in all three groups had reductions from baseline to endpoint (p <0.05) in mean scores on all ESRS subscales. Treatment emergent AEs were reported in 60, 59 and 70% of the patients in the HAL, FLU and ZUC groups respectively. Conclusion: Patients experienced significant improvements in movement disorders after treatment change to RLAI regardless of the previous conventional drug regimen. Satisfaction with therapy after the change was improved significantly probably as a result of better symptom control and less movement disorders as when treated with RLAI. RLAI is a valuable alternative to depot neuroleptics for patients requiring long-term antipsychotic therapy. Table 1. Most frequent adverse event mentioned as reason for treatment change or trial discontinuation
Extrapyramidal disorders Parkinsonism Akathi sia Rigor Total
Haloperidol
Fluphaneazine
Zuclopenthixol
28 13 10 1 83
14 7 14 5 44
21 4 12 6 71
We report the case of patient who developed leucopenia and neutropenia during treatment with olanzapine. G.B. was a 69 yearold man with a diagnosis of severe major depression with psychotic and catatonic features. His initial laboratory tests showed mild leucopenia and neutropenia [his white blood cells (WBC) count was 3500 cells and his absolute neutrophilic count was 1600 cells], anaemia, which was attributed to low levels of folic acid, as well as mild uraemia due to dehydration. The patient was treated with 10mg/day of olanzapine, 20mg/day of citalopram, and 5mg/day of lorazepam. He showed a gradual decrease in his WBC and his absolute neutrophilic count. His WBC count decreased to 2500 cells and his absolute neutrophilic count to 1400 cells after 17 days of treatment. Olanzapine was stopped as a possible cause of leucopenia and was replaced by 4mg/day risperidone. The patient had an increase of his WBC count and his absolute neutrophilic count 7 days after the discontinuation of treatment with olanzapine; the WBC count went up to 3700 cells with an absolute neutrophilic count of 2.1 cells. One month later the WBC count was 4200 cells and the absolute neutrophilic count 2000 cells. Thirteen cases, including our own, of olanzapine-induced leucopenia and neutropenia have been reported so far. In the majority of these cases haematological toxicity occurred within the first month after the initiation of treatment with olanzapine and recovery of the WBC and neutrophilic count after olanzapine withdrawal was the rule. Clinicians should be aware of the possibility that these drugs might induce leucopenia and consider close WBC monitoring, at least during initiation of treatment with atypical antipsychotics.
References [1] Tolosa-Vilella, C., Ruiz-Ripoll, A., Marl-Alfonso, B., Naval-Sendra, E., 2002. Olanzapine-induced agranulocytosis. A case report and review of the literature. Progress in Neuro-Psychopharmacology and Biological Psychiatry 26, 411417.
•
Depression in schizophrenia: comparison between I and II generation antipsychotic drugs
M.C. Mauri*, A. Colasanti, L.S. Volonteri, A. Fiorentini, V.M.S. Ferrari. Clinical Psychiatty, IRCCS Ospedale Maggiore
Policlinico, Milan, Italy References [1] Cloninger, C.R., 1991. D2 dopamine receptor gene is associated but not linked with alcoholism. JAMA 266, 861 868.
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Olanzapine-induced leucopenia and neutropenia a case report
V. Stergiou, V.R Bozikas*, G. Garyfallos, N. Nikolaidis, G. Lavrentiadis, K. Fokas. Aristotle University of Psychiatry, 2rid
Department of Psychiatry, Giannitsa, Greece Newer atypical antipsychotics, like olanzapine, risperidone, and quetiapine, were expected to be safe alternatives to clozapine regarding leucopenia and neutropenia in treating patients with psychotic disorders. However, there have been several reports in the literature of olanzapine-, risperidone-, and quetiapine-induced leucopenia and neutropenia.
Depressive symptoms are frequent in Schizophrenia but they are often misunderstood and misdiagnosed. Therapeutic interventions directed to treat the depressive symptomatology in Schizophrenic patients may be helpful in improving individual patient's quality of life and compliance to therapeutic projects. The aim of this study is to compare the impact of different antipsychotic drugs on the depressive dimension in Schizophrenic patients. 255 patients (185 males and 70 females) with Schizophrenia were retrospectively examined during a phase of acute reexacerbation of symptoms; 8 antipsychotic drugs, including haloperidol, haloperidol decanoate, fluphenazine decanoate, 1-sulpiride, risperidone, olanzapine, quetiapine, and clozapine were evaluated in the study. Clinical improvement was assessed by BPRS, EPSE, and ACS at baseline and 6 weeks after the beginning of the treatment. The depressive symptomatology was evaluated by BPRS items: depression, guilt, and motor retardation. The results evidenced depressive symptoms in 66.3% of the patients [1]. Clinical improvement in depressive dimension was significantly correlated with the amelioration of negative and
$460
and insufficient efficacy (HAL 38%, FLU 48%, ZUC 38%) of previous therapy. The completion rates were 76%, 82% and 71% for the HAL, FLU and ZUC groups, respectively. The most frequent reason for trial discontinuation was due to adverse events or withdrawal of consent (HAL, 11 and 12 patients; FLU, 4 and 7 patients; ZUC, 4 and 14 patients) (Table 1). There were significant reductions from baseline to endpoint (p < 0.001) in the mean total PANSS score in all three groups (HAL 76.2 vs 64.1, FLU 70.7 vs 59.6, ZUC 70.3 vs 63.6). At endpoint, improvement ,,d20% in the PANSS total score was seen in 43%, 41% and 32% of patients in the HAL, FLU and ZUC groups, respectively. A significant decrease (p <0.001) in the PANSS negative subscale score was seen in all groups; 18.6 vs 15.7; 20.9 vs 16.9 and 19.8 vs 17.1 in the HAL, FLU and ZUC groups respectively. Patient satisfaction with treatment also improved significantly in all groups, with marked increases from baseline to endpoint in the proportion of patients rating their satisfaction as "very good" (HAL 0% vs 24%, FLU 0% vs 40%, ZUC 6% vs 27%). There was an improvement in quality of life (SF-36 scores) in all three groups. The severity of movement disorders decreased significantly during the 6-month study. Patients in all three groups had reductions from baseline to endpoint (p <0.05) in mean scores on all ESRS subscales. Treatment emergent AEs were reported in 60, 59 and 70% of the patients in the HAL, FLU and ZUC groups respectively. Conclusion: Patients experienced significant improvements in movement disorders after treatment change to RLAI regardless of the previous conventional drug regimen. Satisfaction with therapy after the change was improved significantly probably as a result of better symptom control and less movement disorders as when treated with RLAI. RLAI is a valuable alternative to depot neuroleptics for patients requiring long-term antipsychotic therapy. Table 1. Most frequent adverse event mentioned as reason for treatment change or trial discontinuation
Extrapyramidal disorders Parkinsonism Akathi sia Rigor Total
Haloperidol
Fluphaneazine
Zuclopenthixol
28 13 10 1 83
14 7 14 5 44
21 4 12 6 71
We report the case of patient who developed leucopenia and neutropenia during treatment with olanzapine. G.B. was a 69 yearold man with a diagnosis of severe major depression with psychotic and catatonic features. His initial laboratory tests showed mild leucopenia and neutropenia [his white blood cells (WBC) count was 3500 cells and his absolute neutrophilic count was 1600 cells], anaemia, which was attributed to low levels of folic acid, as well as mild uraemia due to dehydration. The patient was treated with 10mg/day of olanzapine, 20mg/day of citalopram, and 5mg/day of lorazepam. He showed a gradual decrease in his WBC and his absolute neutrophilic count. His WBC count decreased to 2500 cells and his absolute neutrophilic count to 1400 cells after 17 days of treatment. Olanzapine was stopped as a possible cause of leucopenia and was replaced by 4mg/day risperidone. The patient had an increase of his WBC count and his absolute neutrophilic count 7 days after the discontinuation of treatment with olanzapine; the WBC count went up to 3700 cells with an absolute neutrophilic count of 2.1 cells. One month later the WBC count was 4200 cells and the absolute neutrophilic count 2000 cells. Thirteen cases, including our own, of olanzapine-induced leucopenia and neutropenia have been reported so far. In the majority of these cases haematological toxicity occurred within the first month after the initiation of treatment with olanzapine and recovery of the WBC and neutrophilic count after olanzapine withdrawal was the rule. Clinicians should be aware of the possibility that these drugs might induce leucopenia and consider close WBC monitoring, at least during initiation of treatment with atypical antipsychotics.
References [1] Tolosa-Vilella, C., Ruiz-Ripoll, A., Marl-Alfonso, B., Naval-Sendra, E., 2002. Olanzapine-induced agranulocytosis. A case report and review of the literature. Progress in Neuro-Psychopharmacology and Biological Psychiatry 26, 411417.
•
Depression in schizophrenia: comparison between I and II generation antipsychotic drugs
M.C. Mauri*, A. Colasanti, L.S. Volonteri, A. Fiorentini, V.M.S. Ferrari. Clinical Psychiatty, IRCCS Ospedale Maggiore
Policlinico, Milan, Italy References [1] Cloninger, C.R., 1991. D2 dopamine receptor gene is associated but not linked with alcoholism. JAMA 266, 861 868.
•
Olanzapine-induced leucopenia and neutropenia a case report
V. Stergiou, V.R Bozikas*, G. Garyfallos, N. Nikolaidis, G. Lavrentiadis, K. Fokas. Aristotle University of Psychiatry, 2rid
Department of Psychiatry, Giannitsa, Greece Newer atypical antipsychotics, like olanzapine, risperidone, and quetiapine, were expected to be safe alternatives to clozapine regarding leucopenia and neutropenia in treating patients with psychotic disorders. However, there have been several reports in the literature of olanzapine-, risperidone-, and quetiapine-induced leucopenia and neutropenia.
Depressive symptoms are frequent in Schizophrenia but they are often misunderstood and misdiagnosed. Therapeutic interventions directed to treat the depressive symptomatology in Schizophrenic patients may be helpful in improving individual patient's quality of life and compliance to therapeutic projects. The aim of this study is to compare the impact of different antipsychotic drugs on the depressive dimension in Schizophrenic patients. 255 patients (185 males and 70 females) with Schizophrenia were retrospectively examined during a phase of acute reexacerbation of symptoms; 8 antipsychotic drugs, including haloperidol, haloperidol decanoate, fluphenazine decanoate, 1-sulpiride, risperidone, olanzapine, quetiapine, and clozapine were evaluated in the study. Clinical improvement was assessed by BPRS, EPSE, and ACS at baseline and 6 weeks after the beginning of the treatment. The depressive symptomatology was evaluated by BPRS items: depression, guilt, and motor retardation. The results evidenced depressive symptoms in 66.3% of the patients [1]. Clinical improvement in depressive dimension was significantly correlated with the amelioration of negative and