To assess whether therapy with two widely used antidepressants influences platelet counts.

In 90 patients hospitalized for treatment of a major depressive episode according to DSM-IV, platelet counts were performed after a 6 d antidepressant-free run-in period and again after 35 d of active standardized treatment with amitriptyline (n = 40) or paroxetine (n = 50).

There was a trend for platelet counts to increase during treatment with amitriptyline (from 245.5 ± 68.6 to 256.8 ± 69 cells × 109 L-1, P < 0.06); no change was observed during treatment with paroxetine (from 232.6 ± 58.3 to 234.6 ± 68.9 cells × 109 L-1, n.s).

Treatment with amitriptyline tends to be associated with elevated platelet counts. The cause for this increase is not known, but may be relevant in terms of patients’ long-term thromboembolic risk.

Preclinical and first clinical studies suggested that the selective γ-aminobutyric acid (GABA)-B receptor agonist baclofen might be effective in the treatment of alcohol dependence. However, previous randomized controlled trials have reported inconsistent results, possibly related to the low to medium dosages of baclofen used in these studies.

To assess the efficacy and safety of individually titrated high-dose baclofen (30-270 mg/d) for the treatment of alcohol dependence.

Fifty-six alcohol-dependent patients were randomized to a double-blind treatment with individually titrated baclofen or placebo. Multiple primary outcome measures were total abstinence and cumulative abstinence duration during a 12-week high-dose phase.

Preliminary results of this clinical trial will be presented.

Brain-derived neurotrophic factor (BDNF) plays important roles in neurotransmitter release and synaptic plasticity and has been hypothesized to be involved in the development and maintenance of addictive disorders. Also, alterations in secretion of stress hormones within the <a name="_Hlk388856744">hypothalamic–pituitary–adrenal </a>(HPA) axis have repeatedly been found in substance-related addictive disorders. It has been suggested that glucocorticoids might modulate behavioural responses to substances of abuse. Therefore, we investigated alterations of BDNF expression and HPA axis activity in non-substance-related addictive disorders, i.e. pathological gambling (PG) and Internet use disorder (IUD).

We measured serum BDNF levels, plasma levels of copeptin, a vasopressin (AVP) surrogate marker, adrenocorticotropic hormone (ACTH) and cortisol in male patients with PG (n=14), IUD (n=11) and carefully matched healthy controls for PG (n=13) and IUD (n=10).

BDNF serum levels were significantly increased in patients with PG in comparison to healthy control subjects (p = 0.016). Furthermore, cortisol plasma levels correlated negatively with the PG-YBOCS total severity score (r² = -.626, p = .039) in patients with PG. There was no significant difference in BDNF serum levels of patients with IUD in comparison to control subjects. Plasma levels of copeptin, ACTH and cortisol in patients with PG and IUD did not differ among groups.

These preliminary results might suggest that the pathophysiology of PG shares some characteristics with substance-related addictive disorders on a neuroendocrinological level, whereas those similarities could not be observed in IUD.