Drug-induced autoimmune hemolytic anemia in a 78-year-old African-American man with chronic lymphocytic leukemia.
We reviewed the English language literature for drug trials evaluating treatment of ECP in PubMed, Cochrane, and MEDLINE databases from 1968-2012. Standard forms were used to abstract data regarding study design, duration, outcome measures and adverse events, and study quality.
Treatment of negative symptoms in chronic schizophrenia continues to be a major clinical issue.
Familial hypercholesterolemia (FH) is a common cause of a variety of cardiovascular diseases. The aim of this study was to uncover the underlying mechanism of FH and provide a possible treatment project for FH. We tried to identify the differently expressed genes (DEGs) involved in FH by comparing the gene expression profiles between FH and normal cells. We performed GO and biological pathway analysis of differently expressed genes with DAVID. We searched for candidates for FH treatment by analyzing DEGs between normal cells and FH cells and compared the differences with the DEGs caused by the small interfering molecules in The Connectivity Map (CMap). Using a bioinformatics method, we identified the abnormal metabolic processes in the cells of FH patients, including cell adhesion, material transport, signal transduction and gene expression, and found that the small molecule trazodone could be a potential drug in restoring the dysregulated metabolic pathway. In conclusion, candidates for further evaluation as possible therapeutic agents for FH have been identified using bioinformatics analysis of differentially expressed genes. Phenotype targeting using genomic profiling is a rational approach to drug discovery, which provides a new guideline in treatment of FH and a potential new clinical drug for FH patients.
Hypomania or mania has been reported to be induced by multiple classes of antidepressant agents. Agomelatine is a newly approved drug for treating major depression, and its antidepressant effect works through distinct pharmacodynamic mechanisms from most other commonly used antidepressants. Here, we report a middle-aged female patient who presented hypomanic symptoms shortly after shifting from paroxetine to agomelatine.
Thirty patients (mean age, 50 years) with civilian- or military-related PTSD enrolled in an 8-week evaluation of bupropion SR versus placebo assigned in a 2:1 ratio in addition to their usual pharmacological care. Statistical tests included analyzing both study completers and using an intent-to-treat analysis, as well as post hoc examination of responders versus nonresponders.
The effects of amitriptyline, trazodone and placebo on cognitive skills performance were examined in a group of 15 normal volunteers with a minimum age of 60. Each subject was behaviorally tested after single, acute treatments at weekly sessions using a battery of tasks measuring visual search, division of attention, tracking, critical tracking, rate of information processing, and vigilance. Amitriptyline, 50 mg, produced impairment on the vigilance task, the divided attention task and the critical tracking task. In addition, episodes of extended insensitivity to external stimuli similar to short-term sleep occurred. In contrast, trazodone exhibited impairment only on the critical tracking task. This study indicates that trazodone is less likely than amitriptyline to produce impairment of skills performance aspects of cognition.
Fourteen out-patients with major depressive disorder completed a double-blind, randomized, parallel group study using trazodone (n = 6), amitriptyline (n = 5) and matching placebo (n = 3). The average daily doses used were 223 mg and 95.3 mg for trazodone and amitriptyline, respectively, over the 28-day treatment period. Cardiovascular function was monitored with high speed ECG and by determining systolic time intervals. No significant effects of either drug on supine or standing blood pressure were demonstrated. Trazodone increased QTc on Day 1 only, and reduced heart rate and increased the PR interval on Day 15; these effects had disappeared by Day 29. Amitriptyline markedly increased heart rate, PR interval and QTc, and reduced T wave amplitude on Days 15 and 29. Trazodone had no consistent effect on systolic time intervals except to increase the LVET index, whereas amitriptyline increased both PEP index and PEP/LVET ratio on Days 15 and 29. It is concluded that amitriptyline had a much more marked effect on cardiac function than did trazodone.
ECG effects were evaluated in 60 depressed geriatric patients in a drug-free baseline state and weekly during treatment with trazodone, placebo, or imipramine. Eighteen patients underwent crossover from placebo or imipramine to trazodone. Imipramine increased heart rate and was associated with more isolated ECG complications. Trazodone and placebo did not increase heart rate and had no other significant ECG effects.
The effects of antidepressants [(+)-oxaprotiline, (-)-oxaprotiline, imipramine, maprotiline, and trazodone] and antihistamines (mepyramine, dimethindene, ketotifen, methapyrilene, and antazoline) on muricidal behaviour in olfactory bulbectomized rats were investigated. All drugs except for dimethindene, which only minimally passes across the blood-brain barrier, suppressed muricide. The drugs which have high affinity for histamine H1 receptor showed potent suppressive effect on muricide. It is suggested that the central histaminergic system is involved via H1 receptors in the expression of muricide in olfactory bulbectomized rats.