Medication errors in hematology-oncology ward by consultation: The role of the clinical pharmacologist.

BACKGROUND: The aim was to describe, evaluate and document the prevention of medication errors by clinical pharmacologist consultations in patients with cancer. METHODS: We assessed the effect of clinical pharmacologist consultation by the acceptance of interventions recommended due to dosage, frequency, duration of therapy errors and drug-drug interactions (DDIs). All medication errors detected by clinical pharmacologist were reported in the format of medical consultation. A documentation template was designed to collect the patient's data (sex, age, and diagnosis), prescriptions written, and drug-specific recommendations. For the descriptive analysis of medication errors, the unit of analysis was the number and percentage of errors. RESULTS: A total of 296 patients included in this study with a median age of 48.67±19.76 years of which 47.30% were females. 936 prescribing errors were detected and recommended for their correction. The specialist physicians accepted 897 of prescribed errors. DDIs that were detected in 66.22% of patients, were the most errors in this group of errors (47%). Improper dose (17.41%) wrong frequency (16.67%) and drug-food interaction (10.26%) were after that. CONCLUSION: Pharmacological consultation in the hematology-oncology ward revealed many medication errors. The trust of physicians in the views of the clinical pharmacologist led to a large part of these errors being accepted and resolved.

Short-Term Treatment with Silymarin Improved 6-OHDA-Induced Catalepsy and Motor Imbalance in Hemi-Parkisonian Rats.

PURPOSE: Parkinson's disease (PD) is a common neurodegenerative disorder characterized by disabling motor abnormalities, which include tremor, muscle stiffness, paucity of voluntary movements, and postural instability. Silymarin (SM) or milk thistle extract, is known to own antioxidative, anti-apoptotic, anti-inflammatory and neuroprotective effects. In the present study, we investigated the effect of intraperitoneal (i.p) administration of SM, on 6-OHDA-induced motor-impairments (catalepsy and imbalance) in the rats. METHODS: Experimental model of PD was induced by unilateral infusion of 6-hydroxydopamine (6-OHDA; 8 µg/2 µl/rat) into the central region of the substantia nigra pars compacta (SNc). Catalepsy and motor coordination were assessed by using of bar test and rotarod respectively. RESULTS: The results showed a significant (p<0.001) increase in catalepsy of 6-OHDA-lesioned rats whereas; in SM (100, 200 and 300 mg/kg, i.p for 5 days) treated hemi-parkinsonian rats catalepsy was decreased markedly (p<0.001). Furthermore, there was a significant (p<0.001) increase in motor-imbalance of 6-OHDA-lesioned rats. SM improved motor coordination significantly (p<0.001) in a dose dependent manner and increased motor balance. CONCLUSION: In conclusion, we found that short-term treatment with SM could improve 6-OHDA-induced catalepsy and motor imbalance in rats. We suggest that SM can be used as adjunctive therapy along with commonly used anti-parkinsonian drugs. However, further clinical trial studies should be carried out to prove this hypothesis.

Silymarin improved 6-OHDA-induced motor impairment in hemi-parkisonian rats: behavioral and molecular study.

BACKGROUND: Neuroinflammation and oxidative stress has been shown to be associated with the development of Parkinson disease (PD). In the present study, we investigated the effect of intraperitoneal (i.p.) administration of silymarin, on 6-OHDA-induced motor-impairment, brain lipid per-oxidation and cerebrospinal fluid (CSF) levels of inflammatory cytokine in the rats. RESULTS: The results showed that silymarin is able to improve motor coordination significantly (p < 0.001) in a dose dependent manner. There was a significant (p < 0.001) increase in MDA levels of 6-OHDA-lesioned rats whereas; in silymarin (100, 200 and 300 mg/kg, i.p. for 5 days) pre-treated hemi-parkinsonian rats MDA levels was decreased markedly (p < 0.001). Furthermore the CSF levels of IL-1ß was decreased (p < 0.001) in silymarin (100, 200 and 300 mg/kg) pre-treated rats up to the range of normal non-parkinsonian animals. CONCLUSION: We found that pre-treatment with silymarin could improve 6-OHDA-induced motor imbalance by attenuating brain lipid per-oxidation as well as CSF level of IL-1ß as a pro-inflammatory cytokine. We suggest a potential prophylactic effect for silymarin in PD. However, further clinical trial studies should be carried out to prove this hypothesis.

Dose-Dependent Effect of Flouxetine on 6-OHDA-Induced Catalepsy in Male Rats: A Possible Involvement of 5-HT1A Receptors.

PURPOSE: Progressive loss of dopaminergic neurons of the substantia nigra pars compacta (SNc) in Parkinson's disease (PD) leads to impairment of motor skills. Several evidences show that the role of serotonergic system in regulation of normal movement is pivotal and mediates via 5-HT1A receptors. Our previous study has shown that fluoxetine in acute injections able to attenuate catalepsy in 6-hydroxydopamine (6-OHDA)-lesioned rats. Since drugs are used chronically in clinic, in this study we attempted to evaluate effect of chronic administration of fluoxetine on 6-OHDA-induced catalepsy. METHODS: Catalepsy was induced by unilateral infusion of 6-OHDA (8 µg/2 µl/rat) into the central region of SNc and assayed by using bar-test. Fluoxetine (1, 2.5, 5 and 10 mg/kg) was injected intraperitonealy (ip) for 10 days and its anti-cataleptic effect was assessed at the 10th day. RESULTS: Fluoxetine in high doses (5 and 10 mg/kg) worsened 6-OHDA-induced catalepsy while it had anti-cataleptic effect at the dose of 1mg/kg. The anti-cataleptic effect of fluoxetine (1mg/kg) was reversed by co-administration with NAN-190 (0.5 mg/kg, ip), as a5-HT1Areceptor antagonist. CONCLUSION: According to the results it can be concluded that fluoxetine has anti-cataleptic effect in parkinsonian rats only at low doses, whereas at higher doses it worsens catalepsy. It's anti-cataleptic effect is exerted through affecting on 5-HT1Areceptors. However, at high doses other mechanisms may be involved. Further clinical studies are needed to prove it's possible clinical application as an adjuvant therapy in reducing catalepsy of PD.

8-OH-DPAT (5-HT1A agonist) Attenuates 6-Hydroxy- dopamine-induced catalepsy and Modulates Inflammatory Cytokines in Rats.

OBJECTIVE(S): Neuroinflammation in Parkinson disease (PD) is associated with glial cells activation and production of different inflammatory cytokines. In this study, we investigated the effect of chronic administration of 8-OH-DPAT on 6-OHDA-induced catalepsy and levels of inflammatory cytokines in cerebrospinal fluid (CSF). MATERIALS AND METHODS: Catalepsy was induced by unilateral infusion of 6-OHDA (8 µg/2 µl/rat) into the central region of the sabstantia nigra pars compacta (SNc) being assessed by the bar-test, 5, 60, 120 and 180 min after intraperitoneal (IP) administration of 8-OH-DPAT (5-HT1A receptor agonist; 0.25, 0.5 and 1mg/kg, IP for 10 days). CSF samples were collected on the tenth day of 8-OH-DPAT administration and analyzed by ELISA method to measure levels of TNF-α, IL-1ß and IL-6. RESULTS: Chronic injection of 8-OH-DPAT decreased catalepsy in a dose dependent manner when compared with the control group. The most anti-cataleptic effect was observed at the dose of 1 mg/kg of 8-OH-DPAT. Levels of TNF-α in CSF increased three weeks after 6-OHDA injection while there was a significant decrease in TNF-α level of parkinsonian animals treated with 8-OH-DPAT (1 mg/kg, IP for 10 days). IL-1ß and IL-6 decreased and increased in parkinsonian rats and in 8-OH-DPAT-treated parkinsonian rats, respectively. CONCLUSION: Our study indicated that chronic administration of 8-OH-DPAT improves catalepsy in 6-OHDA-induced animal model of PD and restores central concentration of inflammatory cytokines to the basal levels. 5-HT1A receptor agonists can be suggested as potential adjuvant therapy in PD by modulation of cerebral inflammatory cytokines.

The effect of chronic administration of buspirone on 6-hydroxydopamine-induced catalepsy in rats.

PURPOSE: Several evidences show that serotonergic neurons play a role in the regulation of movements executed by the basal ganglia. Recently we have reported that single dose of buspirone improved 6-hydroxydopamine (6-OHDA) and haloperidol-induced catalepsy. This study is aimed to investigate effect of chronic intraperitoneal (i.p.) administration of buspirone on 6-OHDA-induced catalepsy in male Wistar rats. METHOD: Catalepsy was induced by unilateral infusion of 6-OHDA (8 µg/2 µl/rat) into the central region of the SNc and was assayed by the bar-test method 5, 60, 120 and 180 min after drugs administration in 10th day. The effect of buspirone (0.5, 1 and 2 mg/kg, i.p. for 10 days) was assessed in 6-OHDA-lesioned rats. RESULT: The results showed that chronic injection of buspirone (0.5, 1 and 2 mg/kg, i.p. for 10 days) decreased catalepsy when compared with the control group. The best anticataleptic effect was observed at the dose of 1 mg/kg. The catalepsy-improving effect of buspirone was reversed by 1-(2-methoxyphenyl)- 4-[4-(2-phthalimido) butyl]piperazine hydrobromide (NAN-190), 0.5 mg/kg, i.p.,as a 5-HT1A receptor antagonist. CONCLUSION: Our study indicates that chronic administration of buspirone improves catalepsy in a 6-OHDA-induced animal model of parkinson's disease (PD). We also suggest that buspirone may be used as an adjuvant therapy to increase effectiveness of antiparkinsonian drugs. In order to prove this hypothesis, further clinical studies should be done.