[show abstract][hide abstract] ABSTRACT: The vascular endothelial growth factor (VEGF) signaling, which modulates angiogenesis and neurogenesis within the neurovascular unit, might play an important role in the neuro-endocrine-immune (NEI) stress-adaptation system. Recent evidence suggests that VEGF is involved in the pathophysiology of a number of diseases including major depressive disorder (MDD) and is affected by some treatments, including antidepressants. The objective of the study was to investigate the VEGF level variations in MDD patients during antidepressant treatment with duloxetine, a relatively new SNRI.
A total of 30 MDD patients and 32 healthy controls were assessed using the Hamilton Depression Scale (HAM-D) and monitored for VEGF plasma levels at baseline, week 6 and week 12 of duloxetine treatment (60mg/day) and at baseline, respectively.
According to early clinical response to duloxetine (defined at week 6 by reduction>50% of baseline HAM-D score), the MDD patients were divided into early responders (ER) and early non-responders (ENR). During duloxetine treatment, we found an opposite trend in the VEGF levels between ER and ENR: in ER the VEGF levels significantly increased in association with clinical response at W6, while in ENR the VEGF levels significantly decreased in association with an overall clinical response at W12.
Small sample size.
The opposite trends in VEGF levels, increasing in ER and decreasing in ENR, might reflect differential Norepinephrine/Serotonin effects of duloxetine on differential neurobiological backgrounds of depressive syndromes. Overall, the modulation of VEGF signaling within the neurovascular unit during antidepressant treatment could hypothetically favor the remodeling of neural circuitry, contributing to adaptive adjustment of the NEI stress-adaptation system.
Journal of affective disorders 07/2013; · 3.76 Impact Factor
[show abstract][hide abstract] ABSTRACT: BACKGROUNDS: Nerve growth factor (NGF) is involved in the modulation of the neuro-endocrine-immune (NEI) system, whereas alterations in neuroplasticity and NEI homeostasis seem to play a role in the pathophysiology of major depressive disorder (MDD). Objective of the study was to investigate NGF levels variations in MDD patients during antidepressant treatment with duloxetine, a relatively newer SNRI. METHODS: 30 MDD patients and 32 healthy controls were assessed using Hamilton depression scale (HAM-D) and monitored for NGF serum levels at baseline, week 6 and week 12 of duloxetine treatment (60mg/day) and at baseline, respectively. RESULTS: According to early clinical response to duloxetine (defined at week 6 by reduction >50% of baseline HAM-D score), MDD patients were distinguished in early responders (ER) and early non-responders (ENR), who overall reached clinical response at week 12. Laboratory analysis showed overall significant lower baseline NGF levels among depressed patients compared to healthy controls, not significantly in ER and significantly in ENR. During duloxetine treatment NGF levels further decreased in association with clinical response, reaching significantly lower values in ER at W6 compared to controls, and in ENR at W12 compared to baseline. CONCLUSIONS: A decrease in NGF levels during duloxetine treatment in association to clinical response could be indicative of a relative restoring of NEI stress-adaptation system, since stressors, inducing neuronal instability due to neurotrophins activity changes, permits circuitry remodeling as background in the selection of alternative adaptive behaviors. However, the lower baseline NGF levels found in MDD patients that further decrease during the treatment could represent a lower neurotrophin set point, possibly reflecting a functional impairment in stress-adaptive neuroplasticity in depressive disorders.
[show abstract][hide abstract] ABSTRACT: The circadian rhythm hypothesis of bipolar disorder (BD) suggests a role for melatonin in regulating mood, thus extending the interest toward the melatonergic antidepressant agomelatine as well as type I (acute) or II cases of bipolar depression.
Twenty-eight depressed BD-II patients received open label agomelatine (25 mg/bedtime) for 6 consecutive weeks as an adjunct to treatment with lithium or valproate, followed by an optional treatment extension of 30 weeks. Measures included the Hamilton depression scale, Pittsburgh Sleep Quality Index, the Clinical Global Impression Scale-Bipolar Version, Young Mania Rating Scale, and body mass index.
Intent to treat analysis results demonstrated that 18 of the 28 subjects (64%) showed medication response after 6 weeks (primary study endpoint), while 24 of the 28 subjects (86%) responded by 36 weeks. When examining primary mood stabilizer treatment, 12 of the 17 (70.6%) valproate and six of the 11 (54.5%) lithium patients responded by the first endpoint. At 36 weeks, 14 valproate treated (82.4%) and 10 lithium treated (90.9%) subjects responded. At 36 weeks, there was a slight yet statistically significant (P = 0.001) reduction in body mass index and Pittsburgh Sleep Quality Index scores compared to respective baseline values, regardless of mood stabilizer/outcome. Treatment related drop-out cases included four patients (14.28%) at week 6 two valproate-treated subjects with pseudo-vertigo and drug-induced hypomania, respectively, and two lithium-treated subjects with insomnia and mania, respectively. Week 36 drop outs were two hypomanic cases, one per group.
Agomelatine 25 mg/day was an effective and well-tolerated adjunct to valproate/lithium for acute depression in BD-II, suggesting the need for confirmation by future double blind, controlled clinical trials.
Neuropsychiatric Disease and Treatment 01/2013; 9:243-51. · 2.00 Impact Factor
[show abstract][hide abstract] ABSTRACT: To evaluate the impact of Eating Disorders (EDs) lifetime co-morbidity among female with Bipolar Disorders (BDs) and to compare clinical and cognitive features among EDs subgroups.
A hundred and forty eight women with a lifetime history of Diagnostic and Statistical Manual, Fourth Edition (DSM-IV)-defined Bipolar-I, Bipolar-II and/or Cyclothymia, were consecutively enrolled to determinate the prevalence of co-morbid DSM-IV-defined Anorexia Nervosa [AN], Bulimia Nervosa [BN] or Binge Eating Disorder [BED]. Measures included the Structured Clinical Interview for the DSM-IV Axis I Disorders (SCID-I), the Clinical Global Impression (CGI) rating scale, the Eating Disorder Examination Questionnaire (EDE-Q) and BMI record.
Forty six patients (31%) reported lifetime history of at least one ED: AN was the most common ED (n=23, 15.5%), followed by BED (n=21, 14.2%), and BN (n=8, 5.4%); 6 patients (4.1%) reported multiple lifetime EDs. As expected, BMI was highest in BED patients and lowest in those with AN. Clinical characteristics were similar in the 3 groups, while rapid cycling and co-morbid drug abuse were more common in BED compared to AN or No-ED group. As expected cognitive eating symptoms assessed by the EDE-Q were all more represented in AN than in No-ED patients. AN and BED only differed in restricting behavior and weight concerns.
Our results prompt for the recognition of co-morbid EDs among bipolar patients, indicating that BED, along with other EDs, may influence in different ways both clinical characteristics and course of the illness. Further perspective studies are necessary to better define the relationships between different EDs and Bipolar Spectrum disorders.
Journal of affective disorders 07/2009; 121(1-2):147-51. · 3.76 Impact Factor
[show abstract][hide abstract] ABSTRACT: Our aim was to present a comprehensive, updated survey on obsessive-compulsive disorder (OCD) and obsessive-compulsive related disorders (OCRDs) and their clinical management via literature review, critical analysis and synthesis. Information on OCD and OCRD current nosography, clinical phenomenology and etiology, may lead to a better comprehension of their management. Clinicians should become familiar with the broad spectrum of OCD disorders, since it is a pivotal issue in current clinical psychiatry.
Annals of General Psychiatry 06/2009; 8:13. · 1.57 Impact Factor
[show abstract][hide abstract] ABSTRACT: While many ancient cultures contributed to our current knowledge about medicine and psychiatry origins, Ancient Greeks were among the best observers of feelings and moods patients could express toward medicine and toward what today referred as "psychopathology". Myths and religious references were used to explain what elsewhere impossible to understand or easily communicated. Most of ancient myths focus on ambiguous feelings patients could have towards drugs, especially psychotropic ones. Interestingly, such prejudices are common yet today. Recalling ancient findings and descriptions made using myths, should represent a valuable knowledge for modern physicians, especially for psychiatrists, and their patients, with the aim of better understanding each other and therefore achieving a better clinical outcome. The paper explores many human aspects and feelings toward doctors and their cures, referring to ancient myths, focusing on the perception of mental illness.
[show abstract][hide abstract] ABSTRACT: Obsessive-compulsive disorder is associated with a relevant impairment in social and interpersonal functioning and severe disability. This seems to be particularly true for the poor insight subtype, characterised by a lack of consciousness of illness and, consequently, compliance with treatment. Poor responsiveness to serotonergic drugs in poor insight obsessive-compulsive patients may also require an augmentation therapy with atypical antipsychotics.
We reviewed a case in which a patient with a long history of poor insight obsessive-compulsive disorder was treated with a high dosage of serotonin reuptake inhibitors.
The treatment resulted in a poor outcome. This patient was therefore augmentated with aripiprazole.
Doctors should consider aripiprazole as a possible augmentation strategy for serotonergic poor responder obsessive-compulsive patients, but further research on these subjects is needed.
Annals of General Psychiatry 01/2009; 7:26. · 1.57 Impact Factor
[show abstract][hide abstract] ABSTRACT: The density of the serotonin transporter in the plasma membranes of blood platelets was evaluated by labelled paroxetine binding in three different groups. These groups were: normal controls, epileptic patients having undergone a recent seizure (less than 4 days before) and patients who equally recently presented psychogenic non-epileptic seizures (pseudoseizures). Real seizures resulted in a significant decrease of membrane serotonin transporter density. In the instances of pseudoseizures, its membrane density was undistinguishable from that of normal controls. These data lend further support to the idea that down regulation of serotonin transporter may play a homeostatic role in the cessation of epileptic seizures.
Neurochemical Research 05/2008; 33(11):2263-8. · 2.13 Impact Factor