Delirium After Pregabalin Withdrawal.

Pregabalin is a γ-amino butyric acid analogue drug that is used in fibromyalgia, neuropathic pain associated with diabetic peripheral neuropathy, spinal cord injury, and postherpetic neuralgia. Symptoms reported in association with pregabalin withdrawal include insomnia, gastrointestinal distress, tachycardia, and headache. This case report describes a 68-year-old patient who developed delirium after experiencing pregabalin withdrawal. Clinicians should be aware of the possibility of pregabalin withdrawal delirium.

The effects of adding long-acting injectable antipsychotic drugs to clozapine on relapse and hospitalization in patients with treatment-resistant schizophrenia: a mirror-image retrospective study.

The literature assessing the addition of long-acting injectable antipsychotics (LAIs) to clozapine is limited. The aim of this retrospective study was to determine the safety and effectiveness of adding LAIs to clozapine in patients with treatment-resistant schizophrenia (TRS). Patients aged 18-65 years with TRS, who were treated with first-generation (FGA-LAIs) and second-generation (SGA-LAIs) for at least 1 year after clozapine use, were included retrospectively by registration system scanning. Effectiveness measures included relapses and hospitalizations and days of hospitalization. Safety outcomes included levels of neutrophils, fasting blood sugar, total cholesterol, triglycerides, high-density lipoprotein (HDL), low-density lipoprotein (LDL), and prolactin. The data of 29 patients who met the study criteria were evaluated. The numbers and days of hospitalizations and the numbers of relapses significantly decreased after LAI addition. Comparisons of the neutrophil counts and the total cholesterol, triglyceride, HDL, LDL, prolactin, and fasting blood glucose levels as safety indicators of the clozapine and LAI combination revealed no statistically significant change in these values before and after LAI addition. Adding LAIs to clozapine is apparently well tolerated in patients with TRS and may have a positive effect on the course of the disease.

Impact of initiating long-acting injectable paliperidone palmitate on relapse and hospitalization in patients with bipolar I disorder: A mirror image retrospective study.

Literature assessing the use of long-acting injectable paliperidone palmitate in patients with bipolar I disorder is limited. The aim of this retrospective study was to determine the effectiveness of long-acting injectable paliperidone palmitate treatment on relapse and hospitalization in a real-world setting. Patients with bipolar I disorder aged 18-65 years, who were treated with paliperidone palmitate once-monthly (PP1M) for at least one year, were included. The rate of relapse, hospitalization, and length of hospital stay were collected. Safety outcomes included levels of prolactin, fasting blood sugar, total cholesterol, triglyceride, high density lipoprotein, and low density lipoprotein. The data of 36 patients who met the study criteria were evaluated. Number and length of hospitalizations, number of manic and mixed episodes significantly decreased after PP1M addition. When we compared the prolactin, fasting blood sugar, total cholesterol, triglyceride, high density lipoprotein, and low density lipoprotein levels as an indicator of the safety of treatment, there was no statistically significant change in these values before and after PP1M addition. Our findings suggested PP1M may be effective in reducing manic and mixed episodes. Limitations include a mirror image retrospective design and small sample size.

Acamprosate modulates alcohol-induced hippocampal NMDA receptors and brain microsomal Ca2+-ATPase but induces oxidative stress in rat.

We investigated the effects of acamprosate on alcohol-induced oxidative toxicity, microsomal membrane Ca(2+)-ATPase (MMCA) activity and N-methyl-D: -aspartate receptor (NMDAR) subunits in rat brain. Forty male rats were equally divided into four groups. The first group was used as control, and the second group received ethanol. Acamprosate and acamprosate plus ethanol each day were administered to rats constituting the third and fourth groups for 21 days, respectively. Brain cortical and hippocampal samples were taken from the four groups after 21 days. Brain cortical lipid peroxidation (LP) levels and MMCA activity were higher in the alcohol group than in control, although glutathione peroxidase (GSH-Px), vitamin C, vitamin E and ß-carotene values were lower in the alcohol group than in control. LP levels were further increased in the acamprosate and alcohol + acamprosate groups compared with the alcohol group. GSH-Px, vitamin A, vitamin C, vitamin E and ß-carotene in the acamprosate and alcohol + acamprosate groups were further decreased compared with the alcohol group. Hippocampal NMDAR 2A and 2B subunit concentrations were lower in the alcohol group than in control, although they were increased by acamprosate and alcohol + acamprosate. Brain cortical MMCA activity was higher in the acamprosate group than in the alcohol-treated rats, although its activity was lower in the alcohol + acamprosate group than in the acamprosate group. Brain cortical reduced glutathione levels were not found to be statistically different in any of the groups. Oxidative stress has been proposed to explain the biological side effects of experimental alcohol intake. Acamprosate and alcohol-induced oxidative stress decreased brain antioxidant vitamins in the alcoholic rats.