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Obesity, Obstructive Sleep Apnea and Metabolic Syndrome

AbstractObstructive sleep apnea (OSA) is increasingly recognized as a major health problem in developed countries. Obesity is the most common risk factor in OSA and hence, the prevalence of OSA is undoubtedly rising given the epidemic of obesity. Recent data also suggest that OSA is highly associated with the metabolic syndrome, and it is postulated that OSA contributes to cardiometabolic dysfunction, and subsequently vasculopathy.Current evidence regarding the magnitude of impact on ultimate cardiovascular morbidity or mortality attributable to OSA‐induced metabolic dysregulation is scarce. Given the known pathophysiological triggers of intermittent hypoxia and sleep fragmentation in OSA, the potential mechanisms of OSA‐obesity‐metabolic syndrome interaction involve sympathetic acti...

Obesity And Craniofacial Structure As Risk Factors For Obstructive Sleep Apnea – Impact Of Ethnicity

AbstractObstructive sleep apnoea (OSA) is the result of structural and functional abnormalities which promote the repetitive collapse of the upper airway during sleep. This common disorder is estimated to occur in approximately 4% of men and 2% of women with prevalence studies from North America, Australia, Europe and Asia indicating that occurrence is relatively similar across the globe. Anatomic factors, such as obesity and craniofacial morphology, are key determinants of the predisposition to airway collapse; however their relative importance for OSA risk likely varies between ethnicities. Direct inter‐ethnic studies comparing craniofacial phenotypes in OSA are limited. However available data suggest Asian OSA populations primarily display features of craniofacial skeletal restriction...

Outcomes of hospitalized patients with bacteraemic and non-bacteraemic community-acquired pneumonia caused by Streptococcus pneumoniae.

In contrast to bacteraemic pneumococcal community-acquired pneumonia (CAP), there is a paucity of data on the clinical characteristics and outcomes of non-bacteraemic pneumococcal CAP.

This retrospective study compared the outcome of hospitalized patients with bacteraemic and non-bacteraemic pneumococcal CAP treated at a medical centre from 2004 to 2008. Data on clinical outcomes including all-cause mortality, length of hospital stay, need for intensive-care unit admission and extrapulmonary involvement were analysed. In all, 221 patients with pneumococcal pneumonia (87 bacteraemic, 134 non-bacteraemic) were included.

Patients with bacteraemic pneumococcal pneumonia (BPP) were older than those with non-BPP (46·2 ± 30·7 years vs. 21·7 ± 30·8 years, P<0·001) and were more likely to have underlying medical diseases (66·7% vs. 33·6%, P<0·001). The overall mortality rates at 7, 14, and 30 days were significantly higher in BPP than non-BPP patients (12·6% vs. 2·2%, 14·9% vs. 3·7%, 19·5% vs. 5·1%, all P<0·01). Multivariate logistic regression analysis showed that pneumococcal bacteraemia was correlated with extrapulmonary involvement (odds ratio 5·46, 95% confidence interval 1·97-15·16, P=0·001).

In conclusion, S. pneumoniae bacteraemia increased the risk of mortality and extrapulmonary involvement in patients with pneumococcal CAP.

Classification algorithms to improve the accuracy of identifying patients hospitalized with community-acquired pneumonia using administrative data.

In epidemiological studies of community-acquired pneumonia (CAP) that utilize administrative data, cases are typically defined by the presence of a pneumonia hospital discharge diagnosis code. However, not all such hospitalizations represent true CAP cases.

We identified 3991 hospitalizations during 1997-2005 in a managed care organization, and validated them as CAP or not by reviewing medical records. To improve the accuracy of CAP identification, classification algorithms that incorporated additional administrative information associated with the hospitalization were developed using the classification and regression tree analysis. We found that a pneumonia code designated as the primary discharge diagnosis and duration of hospital stay improved the classification of CAP hospitalizations.

Compared to the commonly used method that is based on the presence of a primary discharge diagnosis code of pneumonia alone, these algorithms had higher sensitivity (81-98%) and positive predictive values (82-84%) with only modest decreases in specificity (48-82%) and negative predictive values (75-90%).

Pathogenesis of airway inflammation in bronchial asthma.

Bronchial asthma is a chronic disorder characterized by airway inflammation, reversible airway obstruction, and airway hyperresponsiveness. Eosinophils are believed to play important roles in the pathogenesis of asthma through the release of inflammatory mediators.

In refractory eosinophilic asthma, anti-IL-5 mAb reduces exacerbations and steroid dose, indicating roles of eosinophils and IL-5 in the development of severe eosinophilic asthma. Even in the absence of IL-5, it is likely that the "Th2 network", including a cascade of vascular cell adhesion molecule-1/CC chemokines/GM-CSF, can sufficiently maintain eosinophilic infiltration and degranulation. Cysteinyl leukotrienes can also directly provoke eosinophilic infiltration and activation in the airways of asthma. Therefore, various mechanisms would be involved in the eosinophilic airway inflammation of asthma. In the pathogenesis of severe asthma, not only eosinophils but also mast cells or neutrophils play important roles. Mast cells are much infiltrated to smooth muscle in severe asthma and induce airway remodeling by release of inflammatory mediators such as amphiregulin. Treatment with anti-IgE Ab, which neutralizes circulating IgE and suppresses mast cell functions, reduces asthma exacerbations in severe asthmatic patients. Furthermore, infiltration of neutrophils in the airway is also increased in severe asthma. IL-8 plays an important role in the accumulation of neutrophils and is indeed upregulated in severe asthma. In the absence of chemoattractant for eosinophils, neutrophils stimulated by IL-8 augment the trans-basement membrane migration of eosinophils, suggesting that IL-8-stimulated neutrophils could lead eosinophils to accumulate in the airways of asthma.

In view of these mechanisms, an effective strategy for controlling asthma, especially severe asthma, should be considered.

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