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The aim of this study is to evaluate the presence of neurocognitive dysfunctions, depression and anxiety and the effect of positive airway pressure (PAP) therapy on these alterations in Obesity Hypoventilation Syndrome (OHS) patients. Ten healthy normal and obese controls, 10 OHS and 10 OSAS patients were included in the study. Short form-36, Beck Depression Scale and State-Trade Anxiety Inventory (STAI 1-2) were performed. Wisconsin Card Sorting Test (WCST), Montreal Cognitive Assessment Scale (MOCA), Enhanced Cued Recall (ECR) and Mini Mental Test (MMT) were used for neurocognitive evaluation. All tests were repeated after one night PAP therapy in OHS and OSAS groups. OHS patients had the lowest scores of physical (PF) and social functioning (SF) in SF-36. The total number of persistent errors and incorrect answers were the highest in OHS group in WCST. The scores of MOCA, ECR and MMT were lower; depression and anxiety scores were higher in OHS group than in controls (p= 0,00). There was a significant increase in the completed categories in OHS after PAP therapy (p= 0,03). There were also significant increases in MOCA, ECR and MMT scores and significant decreases in depression and anxiety scores with respect to PAP therapy. Cognitive dysfunction, depression and anxiety are important under-recognized comorbidities in OHS. It is suggested that short term PAP therapy had positive effects on neurocognitive functions, depression and anxiety but further multicentre, prospective studies with large number of cases are needed to evaluate the effect of long term PAP therapy on these parameters.

To evaluate the effects of montelukast in smoke-induced lung injury. 28 Wistar-Albino rats were enrolled into 4 groups with 7 rats per group. The healthy control group was exposed to fresh air while all rats in the 3 experimental groups were exposed to cigarette smoke for 20 weeks for 2 hours per day. After histopathological verification of smoke induced lung injury, montelukast (0.1 mg/kg) dissolved in Na2CO3was given in one group (MON), Na2CO3only was given in another group (MON control) and placebo was injected in the third group (COPD control) intraperitoneally for 21 days. At the end of this period blood samples were obtained for serum TNF-α assessment and light and electron microscopy analyses were performed on the lung tissues of sacrificed rats. Serum TNF-α levels in the MON group were significantly lower than in the MON control and COPD control groups (38.84 ± 4.9 pg/ml, 77.5 ± 5.8 pg/ml and 79.2 ± 6.9 pg/ml respectively, p < 0.05). Furthermore there was no statistically significant difference between the MON group and healthy controls with respect to serum TNF-α levels (38.84 ± 4.9 pg/ml vs. 29.5 ± 3.6 pg/ml, p > 0.05). Light and electron microscopic evaluation of the lungs demonstrated that the total histopathological damage score of the lung samples was significantly lower in the MON group than in MON controls and COPD controls (5.14 ± 0.5, 8.4 ± 0.6 and 8.7 ± 0.4 respectively, p < 0.05), while there was no significant difference between the MON group and healthy controls (5.1 ± 0.6 vs 2.3 ± 0.2, p > 0.05). These findings suggest that montelukast might have a protective effect on smoke-induced lung injury in rats both from a histopathological and inflammatory point of view. Valutare gli effetti del montelukast sui danni polmonari indotti dal fumo. 28 ratti Wistar-Albino sono stati suddivisi in 4 gruppi di 7 ratti per gruppo. Il gruppo di controlli normali è stato esposto ad aria pura, mentre tutti i ratti dei 3 gruppi sperimentali sono stati esposti a fumo di sigaretta per 20 settimane per 2 ore al giorno. Dopo la verifica istopatologica del danno polmonare indotto da fumo ad un gruppo è stato somministrato montelukast (0,1 mg/kg) disciolto in Na2CO3 (MON), ad un altro gruppo è stato somministrato il solo Na2CO3 (controlli MON) e nel terzo gruppo è stato iniettato placebo (controlli COPD) per via intraperitoneale per 21 giorni. Al termine di questo periodo sono stati effettuati prelievi di sangue per il dosaggio del TNF-α serico e sul tessuto polmonare dei ratti sacrificati sono state effettuate analisi al microscopio ottico ed elettronico. I livelli serici di TNF-α nel gruppo MON erano significativamente inferiori ai controlli MON e ai controlli COPD (38,84 ± 4,9 pg/ml, 77,5 ± 5,8 pg/ml e 79,2 ± 6,9 pg/ml rispettivamente; p < 0,05). non vi erano inoltre differenze statisticamente significative tra il gruppo MON ed i controlli sani nei livelli serici di TNF-α (38,84 ± 4,9 pg/ml vs. 29,5 ± 3,6 pg/ml, p > 0,05). La valutazione al microscopio ottico ed elettronico dei tessuti polmonari dimostravano che lo score complessivo di danno istopatologico dei campioni di polmone era significativamente minore nel gruppo MON rispetto ai controlli MON e ai controlli COPD (5,14 ± 0,5, 8,4 ± 0,6 and 8,7 ± 0,4 rispettivamente, p < 0,05), mentre non vi erano differenze significative tra il gruppo MON ed i controlli sani (5,1 ± 0,6 vs 2,3 ± 0,2; p > 0,05). Questi risultati suggeriscono che il montelukast possa avere un effetto protettivo sul danno polmonare indotto da fumo nei ratti sia dal punto di vista istopatologico che da quello infiammatorio.

BACKGROUND: Clarithromycin is an antimicrobial agent that can be used for treatment of chronic obstructive pulmonary disease (COPD) exacerbations with bronchodilator therapy. However, it has also been shown that clarithromycin has antiinflammatory effects by the inhibition of cytokine production.OBJECTIVE: To evaluate the antiinflammatory effect of clarithromycin on serum and sputum interleukin-8 (IL-8), tumor necrosis factor-α (TNF-α), and leukotriene B4levels in patients with COPD.METHODS: Thirty men with mild to moderate COPD were enrolled in this prospective, single-center, double-blind, placebo-controlled study. None of the patients was receiving systemic or inhaled corticosteroids during the study. Subjects received either clarithromycin or placebo for 14 days. Before and after this treatment period, spirometric tests and arterial blood gas analysis were performed, blood was drawn for measurement of serum inflammatory markers, and sputum was induced.RESULTS: There were no statistically significant differences in baseline clinical or laboratory parameters between the groups. After the treatment, the induced sputum total cell counts, and IL-8 and TNF-α levels decreased significantly in the clarithromycin group compared with pretreatment levels (mean ± SD IL-8 1606 ± 367.3 vs 882 ± 143.6 pg/mL, p = 0.001; TNF-α 638.2 ± 287.5 vs 390 ± 235 pg/mL, p = 0.001). Similarly, decreases in serum inflammatory markers were found in the clarithromycin group while there was no significant change in the placebo group.CONCLUSIONS: This study demonstrated that the decrease in IL-8 and TNF-α levels might be related to the antiinflammatory effect of clarithromycin. Thus, we suggest that the use of clarithromycin in COPD exacerbations may either treat the infection or help control the inflammation. Future studies are needed to determine the clinical significance of these findings.