Evidence of dysregulated affect indicated by high alexithymia in obstructive sleep apnea.

Alexithymia refers to dysregulation of affect characterized by difficulty in identifying and expressing emotions. Obstructive sleep apnea (OSA) is characterized by increased medical/psychiatric comorbidity and possibly by affect dysregulation. In the present case-control study, we examined alexithymia levels with the Toronto Alexithymia Scale (TAS-20) in 23 psychiatrically uncomplicated OSA outpatients and 23 same gender controls one-to-one matched for age, education and subjective depressive symptomatology. General health/quality of life was assessed with the Short-Form 36 Health Survey (SF-36) in the patient group. Hierarchical multivariate regression models were used to evaluate the association of alexithymia with the presence of OSA, and clinical and polysomnographic parameters of this condition. TAS-20 total and subscale scores were associated positively with Beck Depression Inventory (BDI)-21 and negatively with SF-36 scores. After adjusting for all confounders, OSA was positively associated with total TAS-20 score, 'expressing feelings' and 'externally oriented thinking' subscales. The latter was associated with increased sleepiness and reduced blood oxygenation in the OSA group. Finally, 'difficulty describing feelings' and 'externally oriented thinking' significantly predicted risk for OSA. Alexithymia is higher in non-psychiatrically ill patients with OSA compared with carefully matched controls even after adjustment for subjective depressive symptoms and demographic confounders. Total alexithymia is associated with greater subjective depression and poor general health/quality of life, while 'externally oriented thinking' is associated with disease severity and together with 'difficulty describing feelings' may be vulnerability factors for OSA, although reverse causality cannot be excluded.

Angiogenic molecule Tie-2 and VEGF in the pathogenesis of pleural effusions.

BACKGROUND: The role of angiogenesis in the pathogenesis of pleural effusion (PE) has not been determined. The expression of angiogenic factors may represent useful markers for the diagnosis and prediction of disease outcome. To measure the pleural fluid (PF) and serum levels of vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF) and Tie receptor tyrosine kinase (Tie-2) in order to investigate their role in the pathogenesis of PEs. METHODS: Sixty-seven, 17 with transudative PEs due to heart failure and 50 with exudative PEs (malignant, 22; inflammatory, 15; undiagnosed, 13) were included in the study. PF and serum levels of the growth factors (VEGF, bFGF and Tie-2) were measured using enzyme-linked immunosorbent assays. RESULTS: PF and serum VEGF levels but not bFGF and Tie-2 levels were higher (p<0.005) in exudates than in transudates. PF VEGF levels were significantly higher in malignant than inflammatory and undiagnosed PEs (p=0.03). In addition, PF Tie-2 levels were not found different in malignant or in parapneumonic PEs. CONCLUSION: Our results showed that VEGF is one of the main mediators in exudative PEs, but this effect is not mediated through the angiogenetic pathway Ang-1/Tie-2. However, the role of angiogenesis and its pathways in the pathogenesis of exudative PEs needs further exploration.